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Diseases » Grand mal seizures » Causes

Causes of Grand mal seizures

Contents

Grand mal seizures Causes: Book Excerpts

Grand mal seizures as a symptom:

Conditions listing Grand mal seizures as a symptom may also be potential underlying causes of Grand mal seizures. Our database lists the following as having Grand mal seizures as a symptom of that condition:

Medications or substances causing Grand mal seizures:

The following drugs, medications, substances or toxins are some of the possible causes of Grand mal seizures as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

Drug interactions causing Grand mal seizures:

When combined, certain drugs, medications, substances or toxins may react causing Grand mal seizures as a symptom.

The list below is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

Inderal (Propranolol) and Mellaril (Thioridazine) interaction
Inderal (Propranolol) and Thorazine (Chlorpromazine) interaction
Visken (Pindolol) and Mellaril (Thioridazine) interaction
Visken (Pindolol) and Thorazine (Chlorpromazine) interaction
Imipramine and Tranylcypromine interaction
more interactions...»

See full list of 6 drug interactions causing Grand mal seizures

Related information on causes of Grand mal seizures:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Grand mal seizures may be found in:

Causes of Grand mal seizures: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Grand mal seizures.

Aura: Differential Diagnosis
(In a Page: Signs and Symptoms)

Epilepsy
–Recurrent seizures
–Strong family history
Migraine with aura
–Usually visual aura (e.g., scotoma, flashing lights) lasting less than 60 minutes
–Usually fully reversible with rare migrainous infarction (like CVA)
–Migraine headache follows aura within 60 minutes and lasts 4–72 hours; however, aura may occur without headache
- Partial seizure
  –60% of patients with focal seizures have an accompanying aura
  –Aura symptoms are associated with the brain area where they originate (e.g., occipital lobe seizure results in seeing lights)
  –Simple partial seizures result in focal tonic-clonic motor activity without loss of consciousness
  –Complex partial seizures progress to decreased consciousness and unresponsiveness
- Tonic-clonic (grand mal seizure) seizures result in an abrupt loss of consciousness followed by stiffness (tonic); the patient then starts jerking (clonic) for an additional 2–3 minutes; rare aura
- Pituitary adenoma or other underlying pathology that predisposes to migraines, seizures, or altered sensations (taste, smell)
- Hallucinations (not actually an aura)
- Absence seizures (petit mal seizure) only rarely have an aura

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Chorea: Differential Diagnosis
(In a Page: Signs and Symptoms)

Huntington's disease (chronic progressive hereditary chorea)
–Autosomal dominant transmission
–Associated with psychiatric symptoms and progressive dementia
–Caudate atrophy on neuroimaging studies
–Marker on chromosome 4

Sydenham's chorea
–Symptoms follow febrile illness (20–30%
of cases are associated with group A strep)
–Seen in rheumatic fever
–Peak ages: 5–13 years
–More common in females

Systemic lupus erythematosus

AIDS

Hyperthyroidism

Chorea gravidarum
–Develops in the first 4–5 months of
pregnancy
–Resolves following delivery

Drug-induced (e.g., levodopa, stimulants, anticonvulsants, antidepressants, neuroleptics, oral contraceptives)

Stroke

Neoplasm

Wilson's disease
–Autosomal recessive disorder
–Deficiency in copper metabolism
–Associated with hepatic dysfunction,
dystonia, dysarthria

Benign hereditary chorea
–Autosomal dominant
–Onset before age 5
–Symptoms are nonprogressive

Neuroacanthocytosis
–Etiology unknown
–Characterized by chorea and deformed
erythrocytes

DRPLA
–Most common in Japan
–Characterized by chorea, ataxia, epilepsy, and dementia

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Seizures/Convulsions: Differential Diagnosis
(In a Page: Signs and Symptoms)

Partial seizure (involve only part of the brain)
–Simple (no altered consciousness)
–Complex (with altered consciousness)
Generalized seizure (involve both hemispheres)
–Tonic-clonic
–Atonic
–Tonic
–Myoclonic
–Absence
Epilepsy
–Recurrent unprovoked seizures of any or multiple types, which may be idiopathic or symptomatic
- Secondary seizure
  –Metabolic abnormalities (e.g., electrolyte disturbances, hypoglycemia)
  –Drug effects, intoxication, or withdrawal
  –Head injury/trauma
  –Febrile seizures in children
  –Structural lesions (e.g., tumor, subdural hematoma)
  –Cerebrovascular etiologies (e.g., cerebral infarct, intracerebral hemorrhage, subarachnoid hemorrhage
  –Hypoxic-ischemic encephalopathy
  –Infection (e.g., meningitis, encephalitis)
  –Hypoxia
- Nonepileptic seizure
  –Not associated with abnormal electrical activity in the brain
  –Patients with loss of consciousness secondary to cerebral hypoperfusion (fainting, syncope) may occasionally exhibit brief periods of twitching or convulsive movements resembling seizure activity
  –Psychological disturbances (pseudoseizure)
- Inborn errors of metabolism
  –Disorders of amino acid metabolism
  –Organic acidemias
  –Urea cycle disorders
  –Mitochondrial disorders
  –Peroxisomal disorders
  –Glycogen storage disorders
  –Disorders of sugar metabolism
- Rasmussen's encephalitis
  –Causes seizures and progressive hemispheric dysfunction in infants

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Facial Paralysis & Bell's Palsy: Differential Diagnosis
(In a Page: Signs and Symptoms)

Bell's palsy (idiopathic facial palsy of lower motor neuron type)
–Most common cause of facial nerve paralysis

Lyme disease

Tumors that invade the temporal bone (e.g., cholesteatoma, carotid body tumor)

Ramsay Hunt's syndrome
–Association of facial palsy with herpes zoster eruption in the pharynx and external auditory canal
–Eighth cranial nerve often affected as well

Acoustic neuroma
–May compress the facial nerve
Pontine lesions
–Secondary to infarcts, demyelinating processes, or tumors
–Signs of brainstem involvement may be associated
Facial diplegia or bilateral facial palsy
–Guillain-Barré syndrome (associated with ascending areflexic motor paralysis)
–Heerfordt's syndrome (a form of sarcoidosis; also known as uveoparotid fever)

Diabetic neuropathy

Leprosy

Melkersson-Rosenthal syndrome
–Recurrent facial palsy, labial edema, and tongue plication

Sarcoidosis

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Chorea: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Toxins
–Neuroleptics, phenytoin, antiemetics, oral contraceptives, theophylline, L-dopa, stimulants, lithium, carbon monoxide, manganese

Sydenham chorea (in rheumatic fever)
–Migratory chorea, hypotonia, dysarthria, emotional liability
–Usually 4 months after group A β-hemolytic Streptococcus infection
–Molecular mimicry between streptococcal and CNS antigens results in formation of cross-reactive antibodies that disrupt basal ganglia function
–Carditis is present in 80% of Sydenham chorea patients
- Postinfectious: Mycoplasma, HSV, EBV, echovirus 25, varicella
- Encephalitis: viral, mycoplasma, Lyme
- Post-cardiac surgery
  –“Post-pump chorea”
  –Usually 2 weeks after cardiac surgery
- Syndrome or disease associated
  –Wilson disease
  –Hallervorden-Spatz (disorder of iron metabolism with degeneration of globus pallidus)
  –Fahr disease: Encephalopathy and progressive calcification of basal ganglia
  –Lesch-Nyhan syndrome
  –Ataxia-telangiectasia
- Endocrine: Hyperthyroidism, pregnancy (chorea gravidarum)
- Abetalipoproteinemia
- Glutaric aciduria type I
- Neuroacanthocytosis
- Systemic lupus erythematosus
- Kernicterus
- Antiphospholipid antibody syndrome
- Mitochondrial encephalopathies

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Facial Paralysis: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Acquired

Bell palsy
–A diagnosis of exclusion; 40% of cases
Acute otitis media
–From erosion or dehiscence of facial canal
Chronic otitis media
–Nerve compression from granulation tissue

Herpes zoster oticus
–Often infects eighth nerve as well, with hearing loss and vertigo

Lyme disease
–Usually several weeks after inoculation

Tumors
–Temporal bone leukemia, rhabdomyosarcoma of head and neck

Melkersson-Rosenthal syndrome
–Relapsing alternating facial paralysis
–Recurrent facial edema
–Fissured tongue

Temporal bone fracture
–Although most cases involve longitudinal fractures, transverse may also result in hearing loss and vertigo

Facial wounds
–Early repair if clean wound
–Tag nerve for delayed repair if dirty wound

Iatrogenic
–After otologic or parotid surgery

Congenital

Traumatic (associated with prolonged and difficult labor)
Inherited disorders
–Myotonic dystrophy: Progressive muscle weakness, facial paresis at birth
–Albers-Schönberg disease: Osteopetrosis increases bone density, compresses nerve
- Developmental abnormalities
  –Möbius syndrome: Facial paralysis with 6th cranial nerve palsy
  –Association with coloboma, heart defect, choanal atresia, genital hypoplasia, ear anomalies (CHARGE)
  –Goldenhar syndrome, also known as oculoauriculovertebral (OAV) syndrome: First and second branchial arch abnormalities
  –Asymmetric crying facies: Also called congenital unilateral lower lip palsy (CULLP)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Seizures – Childhood: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Febrile seizure
Cerebral dysgenesis: Disorders of neuronal migration, heterotopias, lissencephaly
Epilepsy syndromes
–Childhood absence
–Juvenile absence
–Juvenile myoclonic epilepsy (JME)
–Benign rolandic epilepsy (BRE)
Meningitis/encephalitis (e.g., HSV)
Cerebral abscess
Postinfectious (e.g., ADEM)
Hyponatremia
Hypernatremia
Hypocalcemia
Hypoglycemia
Toxins: Ingestions or sedative withdrawal
Trauma
Pyridoxine deficiency
Neoplasm
Degenerative
–Alpers disease
–Rett syndrome
–Unterricht-Lundborg disease
–Lafora disease
–Neuronal ceroid lipofuscinosis
Genetic
–Angelman syndrome
–Aicardi syndrome

Metabolic
–Medium chain acyl-CoA dehydrogenase deficiency (MCAD)
–Myoclonus epilepsy and ragged-red fibers syndrome (MERRF)
–Sialidosis
–Glucose transporter deficiency
–Urea cycle defects

Vascular: Stroke, hemorrhage, vasculitis
Hashimoto encephalitis
Seizure mimics
–Breath-holding spells
–Syncope, convulsive syncope
–Gastroesophageal reflux
–Cardiac arrhythmia
–Movement disorder
–Migraine
–Benign paroxysmal vertigo
–Parasomnia
–Pseudo-seizure
–Rage attack

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Seizures – Neonatal: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Hypoxic ishemic encephalopathy
Bacterial meningitis/sepsis
Stroke
Cerebral dysgenesis
Electrolyte disturbances
–Hypoglycemia
–Hyponatremia
–Hypomagnesemia
–Hypocalcemia
Maternal drug use
–Drug withdrawal after delivery
–Direct effect of drugs, such as cocaine
Congenital infections (TORCH)
–Toxoplasmosis
–Syphilis
–Rubella
–CMV
–HSV
HSV encephalitis

Intracranial hemorrhage
–Subdural hemorrhage
–Intraparenchymal hemorrhage
–Intraventricular hemorrhage in the premature infant
–Subarachnoid hemorrhage

Urea cycle disturbances
Smith-Lemli-Opitz syndrome
Nonketotic hyperglycinemia
Pyridoxine deficiency
Fructose dysmetabolism
Amino acidurias
–Maple syrup urine disease
–Proprionic acidemia
Molybdenum cofactor deficiency
Mitochondrial encephalopathy
Glucose transporter deficiency

Benign etiologies
–Benign idiopathic neonatal seizures (fifth day fits)
–Benign familial neonatal seizures

Movements commonly mistaken for seizures
–Benign neonatal sleep myoclonus
–Jitteriness (may be secondary to hypoglycemia, drug withdrawal, or idiopathic)
–Gastroesophageal reflux (arching, writhing)
–Breath-holding spell

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Aura: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

❑ Classic migraine headache. A migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

❑ Seizure, generalized tonic-clonic. A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase), and then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Carpopedal spasm: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Hypocalcemia.

Carpopedal spasm is an early sign of hypocalcemia. It's usually accompanied by paresthesia of the fingers, toes, and perioral area; muscle weakness, twitching, and cramping; hyperreflexia; chorea; fatigue; and palpitations. Positive Chvostek's and Trousseau's signs can be elicited. Laryngospasm, stridor, and seizures may appear in severe hypocalcemia.

Chronic hypocalcemia may be accompanied by mental status changes; cramps; dry, scaly skin; brittle nails; and thin, patchy hair and eyebrows.

Tetanus.

Tetanus develops when Clostridium tetani enters a wound in a nonimmunized individual. The patient develops muscle spasms and painful seizures. Difficulty swallowing and a low-grade fever are also present. If the patient isn't treated or treatment is delayed, the mortality rate is very high.

Other causes

Treatments.

Multiple blood transfusions and parathyroidectomy may cause hypocalcemia, resulting in carpopedal spasm. Surgical procedures that impair calcium absorption, such as ileostomy formation and gastric resection with gastrojejunostomy, may also cause hypocalcemia.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Level of consciousness, decreased: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Adrenal crisis

A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of its onset

Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

A decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site

Early signs and symptoms — a constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

The patient’s LOC decreases slowly, from lethargy to coma

He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal

The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in the patient’s LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria

The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 24 to 48 hours after onset, the patient may develop changes in his LOC ranging from lethargy to coma

Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal)

Postvaccinal encephalomyelitisis a life-threatening disorder that produces rapid deterioration in the patient’s LOC, from drowsiness to coma

He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski’s reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma

Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.

With hypoglycemic encephalopathy,the patient’s LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathyproduces a sudden or gradual decrease in the LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski’s reflex; an absent doll’s eye sign; and fixed pupils.

With uremic encephalopathy,the LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Heatstroke

As body temperature increases, the patient’s LOC gradually decreases from lethargy to coma

Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia

Hypernatremia, life threatening if acute, causes the patient’s LOC to deteriorate from lethargy to coma

He is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma

Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia

LOC gradually decreases to lethargy; coma is rare

Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hyponatremia, life threatening if acute, produces a decreased LOC in late stages

Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia(temperature below 90° F [32.2° C]), the patient’s LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity

Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.

Gender cue

Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis

A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Pontine hemorrhage

A sudden, rapid decrease in the patient’s LOC to the point of coma occurs within minutes and death within hours

The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski’s reflex, an absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech

The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in the patient’s LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, a headache, muscle aching, and weakness and may fall into a deep sleep.

An atonic seizureproduces sudden unconsciousness for a few seconds.

Status epilepticus,rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.

Shock

A decreased LOC — lethargy progressing to stupor and coma — occurs late in shock

Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, a cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by a high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

Changes in the patient’s LOC vary in degree and onset, depending on the lesion’s size and location and the presence of edema

A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with the stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, a headache, vomiting, and seizures may occur.

Subdural hemorrhage (acute)

Acute subdural hemorrhageis a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma

The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski’s reflex.

Thyroid storm

The patient’s LOC decreases suddenly and can progress to coma

Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105 ° F (40.5° C).

TIA

The patient’s LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours

Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

West Nile encephalitis is a brain infection that’s caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States

Mild infection is common. Signs and symptoms include a fever, a headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by a high fever, a headache, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Myoclonus: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Alzheimer’s disease

Generalized myoclonus may occur in advanced stages of Alzheimer’s disease, a slowly progressive dementia. Other late findings include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence, delusions, and hallucinations.

Creutzfeldt-Jakob disease

Diffuse myoclonic jerks appear early in Creutzfeldt-Jakob disease, a rapidly progressive dementia. Initially random, they gradually become more rhythmic and symmetrical, usually occurring in response to sensory stimuli. Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and vision disturbances, or possibly, blindness.

Encephalitis (viral)

With viral encephalitis, myoclonus is usually intermittent and either localized or generalized. Associated findings vary, but may include a rapidly decreasing LOC, a fever, a headache, irritability, nuchal rigidity, vomiting, seizures, aphasia, ataxia, hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.

Encephalopathy

Hepatic encephalopathy occasionally produces myoclonic jerks in association with asterixis and focal or generalized seizures.

Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual intention myoclonus.

Uremic encephalopathy commonly produces myoclonic jerks and seizures. Other signs and symptoms include apathy, fatigue, irritability, a headache, confusion, a gradually decreasing LOC, nausea, vomiting, oliguria, edema, and papilledema. The patient may also exhibit elevated blood pressure, dyspnea, arrhythmias, and abnormal respirations.

Epilepsy

With idiopathic epilepsy, localized myoclonus is usually confined to an arm or leg and occurs singly or in short bursts, usually upon awakening. It’s usually more frequent and severe during the prodromal stage of a major generalized seizure, after which it diminishes in frequency and intensity.

Myoclonic jerks are usually the first signs of myoclonic epilepsy, the most common cause of progressive myoclonus. At first, myoclonus is infrequent and localized, but over a period of months, it becomes more frequent and involves the entire body, disrupting voluntary movement (intention myoclonus). As the disease progresses, myoclonus is accompanied by generalized seizures and dementia.

Other causes

Drug withdrawal

Myoclonus may be seen in patients with alcohol, opioid, or sedative withdrawal or delirium tremens.

Poisoning

Acute intoxication with methyl bromide, bismuth, or strychnine may produce an acute onset of myoclonus and confusion.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Paralysis: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

ALS is an invariably fatal disorder that produces spastic or flaccid paralysis in the body’s major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and possibly respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagial drooling, choking, and difficulty chewing.

Bell’s palsy

Bell’s palsy, a disease of CN VII, causes transient, unilateral facial muscle paralysis. The affected muscles sag, and eyelid closure is impossible. Other signs include increased tearing, drooling, and a diminished or absent corneal reflex.

Botulism

Botulism is a bacterial toxin infection that can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after the ingestion of contaminated food. Respiratory muscle paralysis leads to dyspnea and respiratory arrest. Nausea, vomiting, diarrhea, blurred or double vision, bilateral mydriasis, dysarthria, and dysphagia are some early findings.

Brain abscess

Advanced abscess in the frontal or temporal lobe can cause hemiplegia accompanied by other late findings, such as ocular disturbances, unequal pupils, a decreased LOC, ataxia, tremors, and signs of infection.

Brain tumor

A tumor affecting the motor cortex of the frontal lobe may cause contralateral hemiparesis that progresses to hemiplegia. The onset is gradual, but paralysis is permanent without treatment. In early stages, a frontal headache and behavioral changes may be the only indicators. Eventually, seizures, aphasia, and signs of increased ICP (a decreased LOC and vomiting) develop.

Conversion disorder

Hysterical paralysis, a classic symptom of conversion disorder, is characterized by the loss of voluntary movement with no obvious physical cause. It can affect any muscle group, appears and disappears unpredictably, and may occur with histrionic behavior (manipulative, dramatic, vain, irrational) or a strange indifference.

Encephalitis

Variable paralysis develops in the late stages of encephalitis. Earlier signs and symptoms include a rapidly decreasing LOC (possibly coma), a fever, a headache, photophobia, vomiting, signs of meningeal irritation (nuchal rigidity, positive Kernig’s and Brudzinski’s signs), aphasia, ataxia, nystagmus, ocular palsies, myoclonus, and seizures.

Guillain-Barré syndrome

Guillain-Barré syndrome is characterized by a rapidly developing, but reversible, ascending paralysis. It commonly begins as leg muscle weakness and progresses symmetrically, sometimes affecting even the cranial nerves, producing dysphagia, nasal speech, and dysarthria. Respiratory muscle paralysis may be life-threatening. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.

Head trauma

Cerebral injury can cause paralysis due to cerebral edema and increased ICP. The onset is usually sudden. The location and extent vary, depending on the injury. Associated findings also vary, but include a decreased LOC; sensory disturbances, such as paresthesia and loss of sensation; a headache; blurred or double vision; nausea and vomiting; and focal neurologic disturbances.

Multiple sclerosis (MS)

With MS, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, an intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis

With myasthenia gravis, profound muscle weakness and abnormal fatigability may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages, but becomes more persistent as the disease progresses. Associated findings depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient’s jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress — dyspnea, shallow respirations, and cyanosis.

Parkinson’s disease

Tremors, bradykinesia, and lead-pipe or cogwheel rigidity are the classic signs of Parkinson’s disease. Extreme rigidity can progress to paralysis, particularly in the extremities. In most cases, paralysis resolves with prompt treatment of the disease.

Peripheral neuropathy

Typically, peripheral neuropathy produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, a loss of vibration sensation, hypoactive or absent DTRs, neuralgia, and skin changes such as anhidrosis.

Rabies

Rabies is an acute disorder that produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms — a fever; a headache; hyperesthesia; paresthesia, coldness, and itching at the bite site; photophobia; tachycardia; shallow respirations; and excessive salivation, lacrimation, and perspiration — develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupil changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, a high fever, urine retention, drooling, and hydrophobia.

Seizure Disorders

Seizures, particularly focal seizures, can cause transient local paralysis (Todd’s paralysis). Any part of the body may be affected, although paralysis tends to occur contralateral to the side of the irritable focus.

Spinal cord injury

Complete spinal cord transection results in permanent spastic paralysis below the level of injury. Reflexes may return after spinal shock resolves. Partial transection causes variable paralysis and paresthesia, depending on the location and extent of injury. (See Understanding spinal cord syndromes.)

Spinal cord tumors

Paresis, pain, paresthesia, and variable sensory loss may occur along the nerve distribution pathway served by the affected cord segment. Eventually, these symptoms may progress to spastic paralysis with hyperactive DTRs (unless the tumor is in the cauda equina, which produces hyporeflexia) and, perhaps, bladder and bowel incontinence. Paralysis is permanent without treatment.

Stroke

A stroke involving the motor cortex can produce contralateral paresis or paralysis. The onset may be sudden or gradual, and paralysis may be transient or permanent. Associated signs and symptoms vary widely and may include a headache, vomiting, seizures, a decreased LOC and mental acuity, dysarthria, dysphagia, ataxia, contralateral paresthesia or sensory loss, apraxia, agnosia, aphasia, vision disturbances, emotional lability, and bowel and bladder dysfunction.

Subarachnoid hemorrhage

Subarachnoid hemorrhage is a potentially life-threatening disorder that can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are a severe headache, mydriasis, photophobia, aphasia, a sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

Syringomyelia is a degenerative spinal cord disease that produces segmental paresis, leading to flaccid paralysis of the hands and arms. Reflexes are absent, and loss of pain and temperature sensation is distributed over the neck, shoulders, and arms in a capelike pattern.

Transient ischemic attack (TIA)

Episodic TIAs may cause transient unilateral paresis or paralysis accompanied by paresthesia, blurred or double vision, dizziness, aphasia, dysarthria, a decreased LOC, and other site-dependent effects.

West Nile encephalitis

West Nile encephalitis is a brain infection that’s caused by West Nile virus, a mosquito-borne flavivirus endemic to Africa, the Middle East, western Asia, and the United States. Mild infections are common and include a fever, a headache, and body aches, which are sometimes accompanied by a skin rash and swollen lymph glands. More severe infections are marked by a headache, a high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Drugs

The therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.

Electroconvulsive therapy (ECT)

ECT can produce acute, but transient, paralysis.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Seizures, complex partial: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Brain abscess

If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include a headache, nausea, vomiting, generalized seizures, and a decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.

Head trauma

Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.

Herpes simplex encephalitis

The herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include a fever, a headache, coma, and generalized seizures.

Temporal lobe tumor

Complex partial seizures may be the first sign of a temporal lobe tumor. Other signs and symptoms include a headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Seizures, generalized tonic-clonic: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Brain abscess

Generalized seizures may occur in the acute stage of abscess formation or after the abscess disappears. Depending on the size and location of the abscess, a decreased level of consciousness (LOC) varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure (ICP) and include a constant headache, nausea, vomiting, and focal seizures. Typical later features include ocular disturbances, such as nystagmus, impaired vision, and unequal pupils. Other findings vary with the abscess, site but may include aphasia, hemiparesis, abnormal behavior, and personality changes.

Brain tumor

Generalized seizures may occur, depending on the tumor’s location and type. Other findings include a slowly decreasing LOC, a morning headache, dizziness, confusion, focal seizures, vision loss, motor and sensory disturbances, aphasia, and ataxia. Later findings include papilledema, vomiting, increased systolic blood pressure, widening pulse pressure and, eventually, a decorticate posture.

Chronic renal failure

End-stage renal failure produces the rapid onset of twitching, trembling, myoclonic jerks, and generalized seizures. Related signs and symptoms include anuria or oliguria, fatigue, malaise, irritability, decreased mental acuity, muscle cramps, peripheral neuropathies, anorexia, and constipation or diarrhea. Integumentary effects include skin color changes (yellow, brown, or bronze), pruritus, and uremic frost. Other effects include an ammonia breath odor, nausea and vomiting, ecchymoses, petechiae, GI bleeding, mouth and gum ulcers, hypertension, and Kussmaul’s respirations.

Eclampsia

Generalized seizures are a hallmark of eclampsia. Related findings include a severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, a fever of up to 104° (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and a decreased LOC.

Encephalitis

Seizures are an early sign of encephalitis, indicating a poor prognosis; they may also occur after recovery as a result of residual damage. Other findings include a fever, a headache, photophobia, nuchal rigidity, neck pain, vomiting, aphasia, ataxia, hemiparesis, nystagmus, irritability, cranial nerve palsies (causing facial weakness, ptosis, dysphagia), and myoclonic jerks.

Epilepsy (idiopathic)

In most cases, the cause of recurrent seizures is unknown.

Head trauma

In severe cases, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause a decreased LOC, leading to coma; soft-tissue injury of the face, head, or neck; clear or bloody drainage from the mouth, nose, or ears; facial edema; bony deformity of the face, head, or neck; Battle’s sign; and a lack of response to oculocephalic and oculovestibular stimulation. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as a decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit visual deficits, behavioral changes, and a headache.

Hepatic encephalopathy

Generalized seizures may occur late in hepatic encephalopathy. Associated late-stage findings in the comatose patient include fetor hepaticus, asterixis, hyperactive DTRs, and a positive Babinski’s sign.

Hypoglycemia

Generalized seizures usually occur with severe hypoglycemia, accompanied by blurred or double vision, motor weakness, hemiplegia, trembling, excessive diaphoresis, tachycardia, myoclonic twitching, and a decreased LOC.

Hyponatremia

Seizures develop when serum sodium levels fall below 125 mEq/L, especially if the decrease is rapid. Hyponatremia also causes orthostatic hypotension, a headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.

Hypoparathyroidism

Worsening tetany causes generalized seizures. Chronic hypoparathyroidism produces neuromuscular irritability and hyperactive DTRs.

Hypoxic encephalopathy

Besides generalized seizures, hypoxic encephalopathy may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.

Neurofibromatosis

Multiple brain lesions from neurofibromatosis cause focal and generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, monocular blindness, and nystagmus.

Stroke

Seizures (focal more commonly than generalized) may occur within 6 months of an ischemic stroke. Associated signs and symptoms vary with the location and extent of brain damage. They include a decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. The patient may also develop visual deficits, memory loss, poor judgment, personality changes, emotional lability, urine retention or urinary incontinence, constipation, a headache, and vomiting.

Other causes

Arsenic poisoning

Besides generalized seizures, arsenic poisoning may cause a garlicky breath odor, increased salivation, and generalized pruritus. GI effects include diarrhea, nausea, vomiting, and severe abdominal pain. Related effects include diffuse hyperpigmentation; sharply defined edema of the eyelids, face, and ankles; paresthesia of the extremities; alopecia; irritated mucous membranes; weakness; muscle aches; and peripheral neuropathy.

Barbiturate withdrawal

In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.

Diagnostic tests

Contrast agents used in radiologic tests may cause generalized seizures.

Drugs

Toxic blood levels of some drugs, such as theophylline, lidocaine, meperidine, penicillins, and cimetidine, may cause generalized seizures. Phenothiazines, tricyclic antidepressants, amphetamines, isoniazid, and vincristine may cause seizures in patients with preexisting epilepsy.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Seizures, simple partial: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Brain abscess

Seizures can occur in the acute stage of abscess formation or after resolution of the abscess. A decreased LOC varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure and include a constant, intractable headache; nausea; and vomiting. Later signs and symptoms include ocular disturbances, such as nystagmus, decreased visual acuity, and unequal pupils. Other findings vary according to the abscess site and may include aphasia, hemiparesis, and personality changes.

Brain tumor

Focal seizures are commonly the earliest indicators of a brain tumor. The patient may report a morning headache, dizziness, confusion, vision loss, and motor and sensory disturbances. He may also develop aphasia, generalized seizures, ataxia, a decreased LOC, papilledema, vomiting, increased systolic blood pressure, and widening pulse pressure. Eventually, he may assume a decorticate posture.

Head trauma

Any head injury can cause seizures, but penetrating wounds are characteristically associated with focal seizures. The seizures usually begin 3 to 15 months after injury, decrease in frequency after several years, and eventually stop. The patient may develop generalized seizures and a decreased LOC that may progress to coma.

Stroke

A major cause of seizures in patients older than age 50, a stroke may induce focal seizures up to 6 months after its onset. Related effects depend on the type and extent of the stroke, but may include a decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. A stroke may also cause visual deficits, memory loss, poor judgment, personality changes, emotional lability, a headache, urinary incontinence or retention, and vomiting. It may result in generalized seizures.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Seizures, absence: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Idiopathic epilepsy

Some forms of absence seizure are accompanied by learning disabilities.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Vocal cord paralysis: Causes
(Professional Guide to Diseases (Eighth Edition))

Vocal cord paralysis commonly results from the accidental severing of the recurrent laryngeal nerve, or of one of its extralaryngeal branches, during thyroidectomy. Other causes include pressure from a thoracic aortic aneurysm or from an enlarged atrium (in patients with mitral stenosis), bronchial or esophageal carcinoma, hypertrophy of the thyroid gland, trauma (such as neck injuries) and intubation, and neuritis due to infections or metallic poisoning. Vocal cord paralysis can also result from hysteria and, rarely, lesions of the central nervous system.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Aura: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Migraine headache, classic

A classic migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. The headache slowly intensifies; when it peaks, the patient may experience photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic

A generalized tonic-clonic seizure may begin with an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase); then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Carpopedal spasm: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Hypocalcemia

Carpopedal spasm is an early sign of hypocalcemia. It’s usually accompanied by paresthesia of the fingers, toes, and perioral area; muscle weakness, twitching, and cramping; hyperreflexia; chorea; fatigue; and palpitations. Positive Chvostek’s and Trousseau’s signs can be elicited. Laryngospasm, stridor, and seizures may appear in severe hypocalcemia.

Chronic hypocalcemia may be accompanied by mental status changes; cramps; dry, scaly skin; brittle nails; and thin, patchy hair and eyebrows.

Tetanus

Tetanus is an infectious disease that develops when Clostridium tetani enters a wound in a nonimmunized individual. The patient develops muscle spasms, painful seizures, difficulty swallowing, and a low-grade fever. Without prompt treatment, mortality is very high.

Other causes

Treatments

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Level of consciousness, decreased: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Adrenal crisis

Decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms—constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Cerebral contusion

Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.

Diabetic ketoacidosis

This disorder produces a rapid decrease in LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 24 to 48 hours after onset, the patient may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal)

This life-threatening disorder produces rapid LOC deterioration from drowsiness to coma. The patient also experiences rapid onset of fever, headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babinski’s reflex; absent doll’s eye sign; and fixed pupils.

With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Epidural hemorrhage (acute)

This life-threatening posttraumatic disorder produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypercapnia with pulmonary syndrome

LOC decreases gradually from lethargy to coma (usually not prolonged). The patient becomes confused or drowsy and develops asterixis and muscle twitching. He may complain of headache and exhibit mental dullness, papilledema, and small, reactive pupils.

Hypernatremia

This disorder, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hyperventilation syndrome

Brief episodes of unconsciousness follow stress-induced deep, rapid breathing associated with anxiety and agitation. Associated findings include dizziness, circumoral and peripheral paresthesia, twitching, carpopedal spasm, and arrhythmias.

Hypokalemia

LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

This disorder, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

This life-threatening disorder produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

If this serious infection spreads to the nervous system and causes meningitis, signs and symptoms include decreased LOC, fever, headache, and nuchal rigidity. Early signs and symptoms of listeriosis include fever, myalgias, abdominal pain, nausea, vomiting, and diarrhea.

Gender cue Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Myxedema crisis

The patient may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.

Pontine hemorrhage

A sudden, rapid decrease in LOC to the point of coma occurs within minutes and death within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.

Shock

Decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.

Subdural hematoma (chronic)

LOC deteriorates slowly. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.

Subdural hemorrhage (acute)

With this potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.5°C).

TIA

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, staggering or incoordinated gait, aphasia, or dysphagia.

West Nile encephalitis

This brain infection is caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States. Mild infection is common. Signs and symptoms include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Myoclonus: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Alzheimer’s disease

Generalized myoclonus may occur in advanced stages of this slowly progressive dementia. Other late findings include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence, delusions, and hallucinations.

Creutzfeldt-Jakob disease

Diffuse myoclonic jerks appear early in this rapidly progressive dementia. Initially random, they gradually become more rhythmic and symmetrical, often occurring in response to sensory stimuli. Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and visual disturbance, or possibly, blindness.

Encephalitis (viral)

With this disease, myoclonus is usually intermittent and either localized or generalized. Associated findings vary but may include rapidly decreasing level of consciousness, fever, headache, irritability, nuchal rigidity, vomiting, seizures, aphasia, ataxia, hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.

Encephalopathy

Hepatic encephalopathy occasionally produces myoclonic jerks in association with asterixis and focal or generalized seizures.

Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual intention myoclonus.

Uremic encephalopathy commonly produces myoclonic jerks and seizures. Other signs and symptoms include apathy, fatigue, irritability, headache, confusion, gradually decreasing level of consciousness, nausea, vomiting, oliguria, edema, and papilledema. The patient may also exhibit elevated blood pressure, dyspnea, arrhythmias, and abnormal respirations.

Epilepsy

Other causes

Drug withdrawal

Myoclonus may be seen in patients with alcohol, opioid, or sedative withdrawal, or delirium tremens.

Poisoning

Acute intoxication with methyl bromide, bismuth, or strychnine may produce an acute onset of myoclonus and confusion.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Paralysis: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Amyotrophic lateral sclerosis

This invariably fatal disorder produces spastic or flaccid paralysis in the body’s major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and possibly respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagia, drooling, choking, and difficulty chewing.

Bell’s palsy

Bell’s palsy, a disease of cranial nerve VII, causes transient, unilateral facial muscle paralysis. The affected muscles sag and eyelid closure is impossible. Other signs include increased tearing, drooling, and a diminished or absent corneal reflex.

Botulism

This bacterial toxin infection can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after the ingestion of contaminated food. Respiratory muscle paralysis leads to dyspnea and respiratory arrest. Nausea, vomiting, diarrhea, blurred or double vision, bilateral mydriasis, dysarthria, and dysphagia are some early findings.

Brain abscess

Advanced abscessin the frontal or temporal lobe can cause hemiplegia accompanied by other late findings, such as ocular disturbances, unequal pupils, decreased LOC, ataxia, tremors, and signs of infection.

Brain tumor

A tumor affecting the motor cortex of the frontal lobe may cause contralateral hemiparesis that progresses to hemiplegia. Onset is gradual, but paralysis is permanent without treatment. In early stages, frontal headache and behavioral changes may be the only indicators. Eventually, seizures, aphasia, and signs of increased ICP (decreased LOC and vomiting) develop.

Conversion disorder

Encephalitis

Variable paralysis develops in the late stages of this disorder. Earlier signs and symptoms include rapidly decreasing LOC (possibly coma), fever, headache, photophobia, vomiting, signs of meningeal irritation (nuchal rigidity, positive Kernig’s and Brudzinski’s signs), aphasia, ataxia, nystagmus, ocular palsies, myoclonus, and seizures.

Guillain-Barré syndrome

This syndrome is characterized by a rapidly developing, but reversible, ascending paralysis. It commonly begins as leg muscle weakness and progresses symmetrically, sometimes affecting even the cranial nerves, producing dysphagia, nasal speech, and dysarthria. Respiratory muscle paralysis may be life-threatening. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.

Head trauma

Cerebral injury can cause paralysis due to cerebral edema and increased intracranial pressure. Onset is usually sudden. Location and extent vary, depending on the injury. Associated findings also vary but include decreased LOC; sensory disturbances, such as paresthesia and loss of sensation; headache; blurred or double vision; nausea and vomiting; and focal neurologic disturbances.

Migraine headache

Hemiparesis, scotomas, paresthesia, confusion, dizziness, photophobia, or other transient symptoms may precede the onset of a throbbing unilateral headache and may persist after it subsides.

Multiple sclerosis

With this disorder, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis

With this neuromuscular disease, profound muscle weakness and abnormal fatigability may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages but becomes more persistent as the disease progresses. Associated findings depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient’s jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress—dyspnea, shallow respirations, and cyanosis.

Neurosyphilis

Irreversible hemiplegia may occur in the late stages of neurosyphilis. Dementia, cranial nerve palsies, tremors, and abnormal reflexes are other late findings.

Parkinson’s disease

Peripheral nerve trauma

Severe injury to a peripheral nerve or group of nerves results in the loss of motor and sensory function in the innervated area. Muscles become flaccid and atrophied, and reflexes are lost. If transection isn’t complete, paralysis may be temporary.

Peripheral neuropathy

Typically, this syndrome produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, loss of vibration sensation, hypoactive or absent deep tendon reflexes, neuralgia, and skin changes such as anhidrosis.

Poliomyelitis

This disorder can produce insidious, permanent flaccid paralysis and hyporeflexia. Sensory function remains intact, but the patient loses voluntary muscle control.

Rabies

This acute disorder produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms—fever; headache; hyperesthesia; paresthesia, coldness, and itching at the bite site; photophobia; tachycardia; shallow respirations; and excessive salivation, lacrimation, and perspiration—develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupil changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, high fever, urine retention, drooling, and hydrophobia.

Seizure disorders

Spinal cord injury

Spinal cord tumors

Paresis, pain, paresthesia, and variable sensory loss may occur along the nerve distribution pathway served by the affected cord segment. Eventually, these symptoms may progress to spastic paralysis with hyperactive deep tendon reflexes (unless the tumor is in the cauda equina, which produces hyporeflexia) and, perhaps, bladder and bowel incontinence. Paralysis is permanent without treatment.

Stroke

A stroke involving the motor cortex can produce contralateral paresis or paralysis. Onset may be sudden or gradual, and paralysis may be transient or permanent. Associated signs and symptoms vary widely and may include headache, vomiting, seizures, decreased LOC and mental acuity, dysarthria, dysphagia, ataxia, contralateral paresthesia or sensory loss, apraxia, agnosia, aphasia, vision disturbances, emotional lability, and bowel and bladder dysfunction.

Subarachnoid hemorrhage

This potentially life-threatening disorder can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are severe headache, mydriasis, photophobia, aphasia, sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

This degenerative spinal cord disease produces segmental paresis, leading to flaccid paralysis of the hands and arms. Reflexes are absent, and loss of pain and temperature sensation is distributed over the neck, shoulders, and arms in a capelike pattern.

Thoracic aortic aneurysm

Occlusion of spinal arteries by a ruptured thoracic aortic aneurysm may cause sudden onset of transient bilateral paralysis. Severe chest pain radiating to the neck, shoulders, back, and abdomen and a sensation of tearing in the thorax are prominent symptoms. Related findings include syncope, pallor, diaphoresis, dyspnea, tachycardia, cyanosis, diastolic heart murmur, and abrupt loss of radial and femoral pulses or wide variations in pulses and blood pressure between arms and legs. Ironically, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.

Transient ischemic attack (TIA)

Episodic TIAs may cause transient unilateral paresis or paralysis accompanied by paresthesia, blurred or double vision, dizziness, aphasia, dysarthria, decreased LOC, and other site-dependent effects.

West Nile encephalitis

This brain infection is caused by West Nile virus, a mosquito-borne flavivirus endemic to Africa, the Middle East, western Asia, and the United States. Mild infections are common and include fever, headache, and body aches, which are sometimes accompanied by skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Drugs

Therapeutic use of neuromuscular blockers, such as pancuronium, produces paralysis.

Electroconvulsive therapy

This therapy can produce acute, but transient, paralysis.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Seizures, complex partial: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Brain abscess

If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include headache, nausea, vomiting, generalized seizures, and a decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.

Head trauma

Herpes simplex encephalitis

The herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include fever, headache, coma, and generalized seizures.

Temporal lobe tumor

Complex partial seizures may be the first sign of this disorder. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Seizures, generalized tonic-clonic: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Alcohol withdrawal syndrome

i> Sudden withdrawal from alcohol dependence may cause seizures 7 to 48 hours later as well as status epilepticus. The patient may also be restless and exhibit hallucinations, profuse diaphoresis, and tachycardia.

Brain abscess

Generalized seizures may occur in the acute stage of abscess formation or after the abscess disappears. Depending on the size and location of the abscess, decreased level of consciousness (LOC) varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure (ICP) and include constant headache, nausea, vomiting, and focal seizures. Typical later features include ocular disturbances, such as nystagmus, impaired vision, and unequal pupils. Other findings vary with the abscess site but may include aphasia, hemiparesis, abnormal behavior, and personality changes.

Brain tumor

Generalized seizures may occur, depending on the tumor’s location and type. Other findings include a slowly decreasing LOC, morning headache, dizziness, confusion, focal seizures, vision loss, motor and sensory disturbances, aphasia, and ataxia. Later findings include papilledema, vomiting, increased systolic blood pressure, widening pulse pressure, and (eventually) decorticate posture.

Cerebral aneurysm

Occasionally, generalized seizures may occur with an aneurysmal rupture. Premonitory signs and symptoms may last several days, but onset is typically abrupt with severe headache, nausea, vomiting, and decreased LOC. Depending on the site and amount of bleeding, related signs and symptoms vary but may include nuchal rigidity, irritability, hemiparesis, hemisensory defects, dysphagia, photophobia, diplopia, ptosis, and unilateral pupil dilation.

Chronic renal failure

End-stage renal failure produces rapid onset of twitching, trembling, myoclonic jerks, and generalized seizures. Related signs and symptoms include anuria or oliguria, fatigue, malaise, irritability, decreased mental acuity, muscle cramps, peripheral neuropathies, anorexia, and constipation or diarrhea. Integumentary effects include skin color changes (yellow, brown, or bronze), pruritus, and uremic frost. Other effects include ammonia breath odor, nausea and vomiting, ecchymoses, petechiae, GI bleeding, mouth and gum ulcers, hypertension, and Kussmaul’s respirations.

Eclampsia

Generalized seizures are a hallmark of this disorder. Related findings include severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, fever of up to 104° F (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and decreased LOC.

Encephalitis

Seizures are an early sign of this disorder, indicating a poor prognosis; they may also occur after recovery as a result of residual damage. Other findings include fever, headache, photophobia, nuchal rigidity, neck pain, vomiting, aphasia, ataxia, hemiparesis, nystagmus, irritability, cranial nerve palsies (causing facial weakness, ptosis, dysphagia), and myoclonic jerks.

Epilepsy (idiopathic)

In most cases, the cause of recurrent seizures is unknown.

Head trauma

In severe cases, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause a decreased LOC, leading to coma; soft-tissue injury of the face, head, or neck; clear or bloody drainage from the mouth, nose, or ears; facial edema; bony deformity of the face, head, or neck; Battle’s sign; and lack of response to oculocephalic and oculovestibular stimulation. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit visual deficits, behavioral changes, and headache.

Hepatic encephalopathy

Generalized seizures may occur late in this disorder. Associated late-stage findings in the comatose patient include fetor hepaticus, asterixis, hyperactive DTRs, and a positive Babinski’s sign.

Hypertensive encephalopathy

This life-threatening disorder may cause seizures along with severely increased blood pressure, decreased LOC, intense headache, vomiting, transient blindness, paralysis, and (eventually) Cheyne-Stokes respirations.

Hypoglycemia

Hyponatremia

Seizures develop
when serum sodium levels fall below 125 mEq/L, especially if the decrease is rapid. Hyponatremia also causes orthostatic hypotension, headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.

Hypoparathyroidism

Worsening tetany causes generalized seizures. Chronic hypoparathyroidism produces neuromuscular irritability and hyperactive DTRs.

Hypoxic encephalopathy

Besides generalized seizures, this disorder may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.

Multiple sclerosis

This disorder rarely produces generalized seizures. Characteristic findings include vision deficits, paresthesia, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, ataxic gait, dysphagia, dysarthria, impotence, and emotional lability. Urinary frequency, urgency, and incontinence may also occur.

Neurofibromatosis

Multiple brain lesions from this disorder cause focal and generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, monocular blindness, and nystagmus.

Porphyria (intermittent acute)

Generalized seizures are a late sign of this disorder, indicating severe CNS involvement. Acute porphyria also causes severe abdominal pain, tachycardia, psychotic behavior, muscle weakness, and sensory loss in the trunk.

Sarcoidosis

Lesions may affect the brain, causing generalized and focal seizures. Associated findings include a nonproductive cough with dyspnea, substernal pain, malaise, fatigue, arthralgia, myalgia, weight loss, tachypnea, dysphagia, skin lesions, and impaired vision.

Stroke

Seizures (focal more often than generalized) may occur within 6 months of an ischemic stroke. Associated signs and symptoms vary with the location and extent of brain damage. They include decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. The patient may also develop visual deficits, memory loss, poor judgment, personality changes, emotional lability, urine retention or urinary incontinence, constipation, headache, and vomiting.

Other causes

Arsenic poisoning

Barbiturate withdrawal

In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.

Diagnostic tests

Contrast agents used in radiologic tests may cause generalized seizures.

Drugs

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Seizures, simple partial: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Brain abscess

Seizures can occur in the acute stage of abscess formation or after resolution of the abscess. Decreased LOC varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure and include a constant, intractable headache, nausea, and vomiting. Later signs and symptoms include ocular disturbances, such as nystagmus, decreased visual acuity, and unequal pupils. Other findings vary according to the abscess site and may include aphasia, hemiparesis, and personality changes.

Brain tumor

Focal seizures are commonly the earliest indicators of a brain tumor. The patient may report morning headache, dizziness, confusion, vision loss, and motor and sensory disturbances. He may also develop aphasia, generalized seizures, ataxia, decreased LOC, papilledema, vomiting, increased systolic blood pressure, and widening pulse pressure. Eventually, he may assume a decorticate posture.

Head trauma

Multiple sclerosis

Focal or generalized seizures may occur with this disorder, usually during the late stages. Other findings include visual deficits, paresthesia, constipation, muscle weakness, spasticity, paralysis, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, emotional lability, impotence, and urinary frequency, urgency, and incontinence.

Neurofibromatosis

Multiple brain lesions cause focal seizures and, at times, generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, progressive monocular blindness, nystagmus, and endocrine abnormalities.

Sarcoidosis

Multiple lesions from this disorder affect the brain, producing focal and generalized seizures. Associated findings include a nonproductive cough with dyspnea, substernal pain, malaise, fatigue, arthralgia, myalgia, weight loss, tachypnea, dysphagia, skin lesions, and impaired vision.

Stroke

A major cause of seizures in patients older than age 50, a stroke may induce focal seizures up to 6 months after its onset. Related effects depend on the type and extent of the stroke but may include decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. A stroke may also cause visual deficits, memory loss, poor judgment, personality changes, emotional lability, headache, urinary incontinence or retention, and vomiting. It may result in generalized seizures.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Chorea [Choreiform movements]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Cerebral infarction

An infarction that involves the thalamic area produces unilateral or bilateral chorea. The patient may also experience dysarthria, tremors, rigidity, weakness, and sensory disturbances such as paresthesia.

Encephalitis

Chorea may occur in the recovery phase of encephalitis. Low-grade fever and athetosis may also be present, in addition to such focal neurologic signs as hemiparesis, hemiplegia, and facial droop.

Huntington’s disease

In this inherited disease, chorea may be the first sign or it may accompany the intellectual decline that leads to emotional disturbances and dementia. The patient’s movements tend to be choreoathetotic and may be accompanied by dysarthria, dystonia, prancing gait, dysphagia, and facial grimacing.

Wilson’s disease

Chorea and dystonia affecting the arms and legs are early indicators of Wilson’s disease. The patient typically experiences dysarthria, tremors, hoarseness, dysphagia, and slowed body movements; he may also exhibit emotional and behavioral disturbances, drooling, rigidity, and mental deterioration. The pathognomonic Kayser-Fleischer ring in the cornea appears as the disease progresses.

Other causes

Carbon monoxide poisoning

A patient who survives severe carbon monoxide poisoning may have neurologic signs and symptoms, such as chorea, rigidity, dementia, impaired sensory function, masklike facies, generalized seizures, and myoclonus.

Drugs

Phenothiazines (especially the piperazine derivatives), haloperidol, thiothixene, and loxapine commonly produce chorea. Metoclopramide, metyrosine, hormonal contraceptives, levodopa, and phenytoin may also cause this sign.

Lead poisoning

In the later stages, lead poisoning produces chorea in addition to seizures, headache, memory lapses, and severe mental impairment. The patient may also develop masklike facies, footdrop, wristdrop, dizziness, ataxia, weakness, lethargy, abdominal pain, anorexia, nausea, vomiting, constipation, lead line on the gums, and a metallic taste in his mouth.

Manganese poisoning

In miners who have been exposed to manganese dioxide for prolonged periods, chorea characteristically occurs with a propulsive gait, dystonia, and rigidity. Initially, the patient may have masklike facies, a resting tremor, and personality changes; later, extreme muscle weakness and lethargy occur.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Seizures, absence: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Idiopathic epilepsy

Some forms of absence seizure are accompanied by learning disabilities.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Seizures: Differential Overview

(Field Guide to Bedside Diagnosis)

❑ Generalized (grand mal)

❑ Partial (focal)

❑ Complex partial (temporal lobe)

❑ Absence (petit mal)

❑ Vasovagal syncope

❑ Myoclonic

❑ Akinetic (drop attacks)

❑ Psychomotor

❑ Pseudoseizures

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Source: Field Guide to Bedside Diagnosis, 2007

Vocal cord paralysis: Causes
(Handbook of Diseases)

Vocal cord paralysis commonly results from the accidental severing of the recurrent laryngeal nerve or of one of its extralaryngeal branches during thyroidectomy.

Other causes include pressure from an aortic aneurysm or from an enlarged atrium (in patients with mitral stenosis), bronchial or esophageal carcinoma, hypertrophy of the thyroid gland, trauma (such as neck injuries) and intubation, and neuritis due to infections or metallic poisoning. Vocal cord paralysis can also result from hysteria and, rarely, lesions of the central nervous system.

CLINICAL TIP: In some cases, cause isn’t identified and spontaneous recovery can occur within a year.

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Source: Handbook of Diseases, 2003

Carpopedal spasm: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Hypocalcemia.

Chronic hypocalcemia may be accompanied by mental status changes; cramps; dry, scaly skin; brittle nails; and thin, patchy hair and eyebrows. Tetanus is an infectious disease that develops when Clostridium tetani enters a wound in a nonimmunized individual. The patient develops muscle spasms and painful seizures. Difficulty swallowing and low-grade fever are also present. If the patient isn’t treated or treatment is delayed, the mortality rate is very high.

Other causes

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Level of consciousness, decreased: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Adrenal crisis

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms — constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

Cerebral aneurysm (ruptured)

Cerebral contusion

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension, fruity breath odor, and Kussmaul’s respirations, as well as warm, dry skin and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Encephalomyelitis (postvaccinal)

Encephalomyelitis is a life-threatening disorder that produces rapid LOC deterioration from drowsiness to coma. The patient also experiences rapid onset of fever, headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, vision disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion accompanied by hunger, alternate flushing and cold sweats, and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Epidural hemorrhage (acute)

Epidural hemorrhage is a life-threatening posttraumatic disorder that produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

Hypercapnia with pulmonary syndrome

Hypernatremia

Hypernatremia, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse, possibly accompanied by nausea, malaise, fever, thirst, flushed skin, and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma. Early findings include polyuria, polydipsia, hyperglycemia, hyperkalemia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hyperventilation syndrome

Hypokalemia

LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria. The patient may also exhibit weakness, decreased reflexes, and malaise, along with dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hyponatremia, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

Intracerebral hemorrhage

Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

Meningitis

Myxedema crisis

Pontine hemorrhage

Seizure disorders

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock

Decreased LOC — lethargy progressing to stupor and coma — occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.

Subdural hematoma (chronic)

Subdural hemorrhage (acute)

With subdural hemorrhage — a potentially life-threatening disorder — agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.5°C).

Transient ischemic attack (TIA)

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Myoclonus: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Alzheimer’s disease

Generalized myoclonus may occur in advanced stages of Alzheimer’s disease, which is a slowly progressive dementia. Other late findings include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence, delusions, and hallucinations.

Creutzfeldt-Jakob disease

Diffuse myoclonic jerks appear early in Creutzfeldt-Jakob disease — a rapidly progressive dementia. Initially random, they gradually become more rhythmic and symmetrical, often occurring in response to sensory stimuli. Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and vision disturbance, or possibly, blindness.

Encephalitis (viral)

With encephalitis, myoclonus is usually intermittent and either localized or generalized. Associated findings vary but may include rapidly decreasing level of consciousness, fever, headache, irritability, nuchal rigidity, vomiting, seizures, aphasia, ataxia, hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.

Encephalopathy

Hepatic encephalopathy occasionally produces myoclonic jerks in association with asterixis and focal or generalized seizures.

Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual intention myoclonus.

Epilepsy

Other causes

Drug withdrawal

Myoclonus may be seen in patients with alcohol, opioid, or sedative withdrawal, or delirium tremens.

Poisoning

Acute intoxication with methyl bromide, bismuth, or strychnine may produce an acute onset of myoclonus and confusion.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Paralysis: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Amyotrophic lateral sclerosis (ALS)

ALS, an invariably fatal disorder, produces spastic or flaccid paralysis in the body’s major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagia, drooling, choking, and difficulty chewing.

Bell’s palsy

Transient, unilateral facial muscle paralysis occurs in Bell’s palsy, a disease of cranial nerve VII. (See Recognizing unilateral Bell’s palsy.) The affected muscles sag, and eyelid closure may be impossible. Other signs include increased tearing, drooling, diminished or absent corneal reflex, and possible difficulty with hearing or pain in the ear.

Botulism

Botulism, a bacterial toxin infection, can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after eating contaminated food. Respiratory muscle paralysis leads to dyspnea and respiratory arrest. Nausea, vomiting, diarrhea, blurred or double vision, bilateral mydriasis, dysarthria, and dysphagia are some early findings.

Brain abscess

Advanced abscessin the frontal or temporal lobe can cause hemiplegia accompanied by other late findings, such as ocular disturbances, unequal pupils, a decreased LOC, ataxia, tremors, and signs of infection.

Brain tumor

A tumor affecting the motor cortex of the frontal lobe may cause contralateral hemiparesis that progresses to hemiplegia. The onset is gradual, but paralysis is permanent without treatment. In early stages, frontal headache and behavioral changes may be the only indicators. Eventually, seizures, aphasia, and signs of increased ICP (decreased LOC and vomiting) develop.

Conversion disorder

Encephalitis

Variable paralysis develops in the late stages of encephalitis. Earlier signs and symptoms include rapidly decreasing LOC (possibly coma), fever, headache, photophobia, vomiting, signs of meningeal irritation (nuchal rigidity, positive Kernig’s and Brudzinski’s signs), aphasia, ataxia, nystagmus, ocular palsies, myoclonus, and seizures.

Guillain-Barré syndrome

Guillain-Barré syndrome is characterized by a rapidly developing, but reversible, ascending paralysis. It commonly begins as leg muscle weakness and progresses symmetrically, sometimes affecting even the cranial nerves, producing dysphagia, nasal speech, and dysarthria. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.

ALERT: Respiratory muscle paralysis may be life-threatening.

Head trauma

Cerebral injury can cause paralysis due to cerebral edema and increased ICP. The onset is usually sudden. Location and extent vary, depending on the injury. Associated findings also vary, but include a decreased LOC, headache, blurred or double vision, nausea and vomiting, and focal neurologic disturbances. Sensory disturbances, such as paresthesia and loss of sensation, may also occur.

Migraine headache

Hemiparesis, scotomas, paresthesia, confusion, dizziness, photophobia, nausea and vomiting, or other transient symptoms may precede the onset of a throbbing unilateral headache and may persist after it subsides.

Multiple sclerosis (MS)

With MS, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis

With myasthenia gravis, a neuromuscular disease, profound muscle weakness and abnormal fatigability may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages, but becomes more persistent as the disease progresses. Associated findings depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient’s jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress — dyspnea, shallow respirations, and cyanosis.

Neurosyphilis

Irreversible hemiplegia may occur in the late stages of neurosyphilis. Dementia, cranial nerve palsies, tremors, and abnormal reflexes are other late findings.

Parkinson’s disease

Peripheral nerve trauma

Peripheral neuropathy

Typically, peripheral neuropathy produces muscle weakness and sensory disturbances in the extremities that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, loss of vibration sensation, hypoactive or absent DTRs, neuralgia, and skin changes such as anhidrosis.

Poliomyelitis

Poliomyelitis can produce insidious, permanent flaccid paralysis, muscle wasting, and hyporeflexia. Sensory function remains intact, but the patient loses voluntary muscle control. Signs and symptoms before paralysis also include muscle weakness, headache, fever, nuchal rigidity, and nausea and vomiting.

Rabies

Rabies, an acute disorder, produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms — paresthesia and itching at the bite site accompanied by fever, headache, hyperesthesia, photophobia, tachycardia, malaise, alternating rage and calm, hydrophobia, shallow respirations, and excessive salivation, lacrimation, and perspiration — develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupillary changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, high fever, urine retention, and drooling.

Seizure disorders

Spinal cord injury

Spinal cord tumors

Stroke

A stroke involving the motor cortex can produce contralateral paresis or paralysis. The onset may be sudden or gradual, and paralysis may be transient or permanent. Associated signs and symptoms vary widely and may include headache, vomiting, seizures, decreased LOC and mental acuity, dysarthria, dysphagia, ataxia, contralateral paresthesia or sensory loss, apraxia, agnosia, aphasia, vision disturbances, emotional lability, and bowel and bladder dysfunction.

Subarachnoid hemorrhage

A potentially life-threatening disorder, subarachnoid hemorrhage can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are severe headache, mydriasis, photophobia, aphasia, a sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

Syringomyelia, a degenerative spinal cord disease, produces segmental paresis, leading to flaccid paralysis of the hands and arms. Reflexes are absent, and loss of pain and temperature sensation is distributed over the neck, shoulders, and arms in a capelike pattern.

Thoracic aortic aneurysm

Occlusion of spinal arteries by a ruptured thoracic aortic aneurysm may cause the sudden onset of transient bilateral paralysis. Severe chest pain radiating to the neck, shoulders, back, and abdomen and a sensation of tearing in the thorax are prominent symptoms. Related findings include syncope, pallor, diaphoresis, dyspnea, tachycardia, cyanosis, diastolic heart murmur, and abrupt loss of radial and femoral pulses or wide variations in pulses and blood pressure between the arms and legs. Paradoxically, however, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.

Transient ischemic attack (TIA)

West Nile encephalitis

A brain infection, West Nile encephalitis is caused by West Nile virus, a mosquito-borne flavivirus endemic to Africa, the Middle East, western Asia, and the United States. Mild infections are common and include fever, headache, and body aches, which are sometimes accompanied by a skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Drugs

Therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.

Electroconvulsive therapy (ECT)

ECT can produce acute, but transient, paralysis.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Seizures, generalized tonic-clonic: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Alcohol withdrawal syndrome

Seizures as well as status epilepticus may develop 7 to 48 hours after abrupt cessation of alcohol consumption by the individual with alcohol dependency. Restlessness, hallucinations, profuse diaphoresis, and tachycardia may also occur.

Brain abscess

Generalized seizures may occur in the acute stage of abscess formation or after the abscess disappears. Decreased level of consciousness (LOC) varies from drowsiness to deep stupor according to the size and location of the abscess. Early signs and symptoms reflect increased intracranial pressure (ICP) and include constant headache, nausea, vomiting, and focal seizures. Typical later features include ocular disturbances, such as nystagmus, impaired vision, and unequal pupils. Other findings vary with the abscess site, but may include aphasia, hemiparesis, abnormal behavior, and personality changes.

Brain tumor

Cerebral aneurysm

Occasionally, generalized seizures may occur with an aneurysm rupture. Premonitory signs and symptoms may last several days, but the onset is typically abrupt with severe headache, nausea, vomiting, and a decreased LOC. Related signs and symptoms vary according to the site and amount of bleeding, but may include nuchal rigidity, irritability, hemiparesis, hemisensory defects, dysphagia, photophobia, diplopia, ptosis, and unilateral pupil dilation.

Chronic renal failure

End-stage renal failure produces the rapid onset of twitching, trembling, myoclonic jerks, and generalized seizures. Related signs and symptoms include anuria or oliguria, fatigue, malaise, irritability, decreased mental acuity, muscle cramps, peripheral neuropathies, anorexia, and constipation or diarrhea. Integumentary effects include skin color changes (yellow, brown, or bronze), pruritus, and uremic frost. Other effects include ammonia breath odor, nausea and vomiting, ecchymoses, petechiae, GI bleeding, mouth and gum ulcers, hypertension, and Kussmaul’s respirations.

Eclampsia

Generalized seizures are a hallmark of eclampsia. Related findings include severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, fever of up to 104° (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and a decreased LOC.

Encephalitis

Seizures are an early sign of encephalitis, indicating a poor prognosis; they may also occur after recovery as a result of residual damage. Other findings include fever, headache, photophobia, nuchal rigidity, neck pain, vomiting, aphasia, ataxia, hemiparesis, nystagmus, irritability, cranial nerve palsies (causing facial weakness, ptosis, and dysphagia), and myoclonic jerks.

Epilepsy (idiopathic)

In most cases, the cause of recurrent seizures is unknown.

Head trauma

In severe cases, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause a decreased LOC, leading to coma. Other signs and symptoms may include soft-tissue injury of the face, head, or neck as well as facial edema and clear or bloody drainage from the mouth, nose, or ears. The patient may also exhibit Battle’s sign, lack of response to oculocephalic and oculovestibular stimulation, and bony deformity of the face, head, or neck. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit visual deficits, behavioral changes, and headache.

Hepatic encephalopathy

Hypertensive encephalopathy

A life-threatening disorder, hypertensive encephalopathy may cause seizures along with severely increased blood pressure, a decreased LOC, intense headache, vomiting, transient blindness, paralysis and, eventually, Cheyne-Stokes respirations.

Hypoglycemia

Hyponatremia

Seizures develop when serum sodium levels fall below 125 mEq/L, especially if the decrease is rapid. Hyponatremia also causes orthostatic hypotension, headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.

Hypoparathyroidism

Worsening tetany causes generalized seizures. Chronic hypoparathyroidism produces neuromuscular irritability and hyperactive DTRs.

Hypoxic encephalopathy

Besides generalized seizures, hypoxic encephalopathy may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.

Multiple sclerosis (MS)

MS rarely produces generalized seizures. Characteristic findings include vision deficits, paresthesia, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, ataxic gait, dysphagia, dysarthria, impotence, and emotional lability. Urinary frequency, urgency, and incontinence may also occur.

Neurofibromatosis

Porphyria (intermittent acute)

Generalized seizures are a late sign of porphyria, indicating severe CNS involvement. Acute porphyria also causes severe abdominal pain, tachycardia, psychotic behavior, muscle weakness, and sensory loss in the trunk.

Sarcoidosis

Stroke

Seizures (focal more common than generalized) may occur within 6 months of an ischemic stroke. Associated signs and symptoms vary with the location and extent of brain damage. They include a decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. The patient may also develop visual deficits, memory loss, poor judgment, personality changes, emotional lability, urine retention or urinary incontinence, constipation, headache, and vomiting.

Other causes

Arsenic poisoning

Besides generalized seizures, arsenic poisoning may cause a garlicky breath odor, increased salivation, and generalized pruritus. GI effects include diarrhea, nausea, vomiting, and severe abdominal pain. Related effects include diffuse hyperpigmentation, paresthesia of the extremities, alopecia, irritated mucous membranes, weakness, muscle aches, peripheral neuropathy, and sharply defined edema of the eyelids, face, and ankles.

Barbiturate withdrawal

In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.

Diagnostic tests

Contrast agents used in radiologic tests may cause generalized seizures.

Drugs

Toxic blood levels of some drugs, such as theophylline, lidocaine, Indocin, meperidine, penicillins, and cimetidine, may cause generalized seizures. Phenothiazines, tricyclic antidepressants, amphetamines, isoniazid, and vincristine may cause seizures in patients with preexisting epilepsy.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Aura: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Classic migraine headache

A migraine headache is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic

A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase); then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Carpopedal spasm: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Hypocalcemia

Chronic hypocalcemia may be accompanied by mental status changes; cramps; dry, scaly skin; brittle nails; and thin, patchy hair and eyebrows.

Tetanus

With tetanus, an infectious disease caused by Clostridium tetani, the patient develops muscle spasms and painful seizures. Difficulty swallowing and a low-grade fever are also present. If the patient isn’t treated or treatment is delayed, the mortality rate is very high.

Other causes

Treatments

Multiple blood transfusions and parathyroidectomy may cause hypocalcemia, resulting in carpopedal spasm.

Surgical procedures

Surgical procedures that impair calcium absorption, such as ileostomy formation and gastric resection with gastrojejunostomy, may also cause hypocalcemia.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Chorea: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Carbon monoxide poisoning

Cerebral infarction

A cerebral infarction that involves the thalamic area produces unilateral or bilateral chorea. The patient may also experience dysarthria, tremors, rigidity, weakness, and sensory disturbances such as paresthesia.

Encephalitis

Chorea may occur in the recovery phase of encephalitis. Low-grade fever and athetosis may also be present, in addition to such focal neurologic signs as hemiparesis, hemiplegia, and facial droop. Other signs and symptoms include headache, vomiting, photophobia, stiff neck, confusion, and drowsiness.

Huntington’s disease

In Huntington’s disease, an inherited disease, chorea may be the first sign or may occur with the intellectual decline that leads to emotional disturbances and dementia. The patient’s movements tend to be choreoathetotic and may be accompanied by dysarthria, dystonia, prancing gait, dysphagia, and facial grimacing.

Lead poisoning

In the later stages of lead poisoning, chorea occurs in addition to seizures, headache, memory lapses, and severe mental impairment. The patient may also develop masklike facies, footdrop, wristdrop, dizziness, ataxia, weakness, lethargy, abdominal pain, anorexia, nausea, vomiting, constipation, lead line on his gums, and a metallic taste in his mouth.

Manganese poisoning

In miners who have been exposed to manganese dioxide for prolonged periods, chorea characteristically occurs with propulsive gait, dystonia, and rigidity. Initially, the patient may have masklike facies, a resting tremor, and personality changes; later, extreme muscle weakness and lethargy occur.

Other causes

Drugs

Such drugs as phenothiazines (especially the piperazine derivatives), haloperidol, thiothixene, and loxapine commonly produce chorea. Metoclopramide, metyrosine, hormonal contraceptives, levodopa, and phenytoin may also cause this sign.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Level of consciousness, decreased: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Adrenal crisis

Decreased LOC, ranging from lethargy to coma, may develop within 12 hours of adrenal crisis onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms — constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

In patients with brain tumors, LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset of a ruptured cerebral aneurysm is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Cerebral contusion

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in LOC that ranges from lethargy to coma. It’s commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 48 hours of onset, the patient with encephalitis may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babin-ski’s reflex; absent doll’s eye sign; and fixed pupils.

Epidural hemorrhage (acute)

Acute epidural hemorrhage, a life-threatening posttraumatic disorder, produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms of heatstroke include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.6° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia

Hypernatremia, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma in hyperosmolar hyperglycemic nonketotic syndrome (HHNS). Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia

With hypokalemia, LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, polyuria, weakness, decreased reflexes, malaise, dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hypothermia

Intracerebral hemorrhage

Intracerebral hemorrhage, a life-threatening disorder, produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Meningitis

Myxedema crisis

The patient experiencing myxedema crisis may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.

Pontine hemorrhage

With pontine hemorrhage, a sudden, rapid decrease in LOC to the point of coma occurs within minutes; death occurs within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock

Decreased LOC — lethargy progressing to stupor and coma — occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

With stroke, LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

CULTURAL CUE:The incidence of stroke is higher in Blacks than Whites. In fact, Blacks have a 60% higher risk for stroke than Whites or Hispanics of the same age. This is believed to be the result of an increased prevalence of hypertension in Blacks.

Subdural hematoma (chronic)

LOC deteriorates slowly in patients with chronic subdural hematomas. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.

Subdural hemorrhage (acute)

With acute subdural hemorrhage, a potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms of a thyroid storm include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.6°C).

TIA

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours of a TIA. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

Signs and symptoms of this brain infection caused by the West Nile virus include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Myoclonus: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Alzheimer’s disease

Generalized myoclonus may occur in advanced stages of this slowly progressive dementia. Other late findings in Alzheimer’s disease include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence, delusions, and hallucinations.

Creutzfeldt-Jakob disease

Diffuse myoclonic jerks appear early in Creutzfeldt-Jakob disease — a rapidly progressive dementia. Initially random, they gradually become more rhythmic and symmetrical, typically occurring in response to sensory stimuli. Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and vision disturbances or, possibly, blindness.

Encephalitis (viral)

With viral encephalitis, myoclonus is usually intermittent and either localized or generalized. Associated findings vary but may include rapidly decreasing LOC, fever, headache, irritability, nuchal rigidity, vomiting, seizures, aphasia, ataxia, hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.

Encephalopathy

Hepatic encephalopathy occasionally produces myoclonic jerks in association with asterixis and focal or generalized seizures.

Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual intention myoclonus.

Uremic encephalopathy commonly produces myoclonic jerks and seizures. Other signs and symptoms include apathy, fatigue, irritability, headache, confusion, gradually decreasing LOC, nausea, vomiting, oliguria, edema, and papilledema. The patient may also exhibit elevated blood pressure, dyspnea, arrhythmias, and abnormal respirations.

Epilepsy

Other causes

Drug withdrawal

Myoclonus may be seen in patients with alcohol, opioid, or sedative withdrawal, or delirium tremens.

Poisoning

Acute intoxication with methyl bromide, bismuth, or strychnine may produce an acute onset of myoclonus and confusion.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Paralysis: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is an invariably fatal disorder that produces spastic or flaccid paralysis in the body’s major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and, possibly, respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagial drooling, choking, and difficulty chewing.

Bell’s palsy

Bell’s palsy, a disease of cranial nerve VII, causes transient, unilateral facial muscle paralysis. The affected muscles sag, and eyelid closure is impossible. Other signs include increased tearing, drooling, and a diminished or absent corneal reflex.

Brain tumor

Conversion disorder

Encephalitis

Guillain-Barré syndrome

Head trauma

Migraine headache

Hemiparesis, scotomas, paresthesia, confusion, dizziness, photophobia, or other transient symptoms may precede the onset of a throbbing unilateral headache and may persist after it subsides. The patient may also experience nausea and vomiting.

Multiple sclerosis

With multiple sclerosis, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis

Myasthenia gravis is a neuromuscular disease that causes profound muscle weakness and abnormal fatigability that may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages but becomes more persistent as the disease progresses. Associated findings in myasthenia gravis depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient’s jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress — dyspnea, shallow respirations, and cyanosis.

Neurosyphilis

Irreversible hemiplegia may occur in the late stages of neurosyphilis. Dementia, cranial nerve palsies, meningitis, personality changes, tremors, and abnormal reflexes are other late findings.

Parkinson’s disease

Peripheral nerve trauma

Peripheral neuropathy

Typically, peripheral neuropathy produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, loss of vibration sensation, hypoactive or absent deep tendon reflexes, neuralgia, and skin changes such as anhidrosis.

Rabies

Rabies produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms — fever; headache; hyperesthesia; paresthesia, coldness, and itching at the bite site; photophobia; tachycardia; shallow respirations; and excessive salivation, lacrimation, and perspiration — develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupil changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, high fever, urine retention, drooling, and hydrophobia.

Seizure disorders

Spinal cord injury

Spinal cord tumor

With a spinal cord tumor, paresis, pain, paresthesia, and variable sensory loss may occur along the nerve distribution pathway served by the affected cord segment. Eventually, these symptoms may progress to spastic paralysis with hyperactive deep tendon reflexes (unless the tumor is in the cauda equina, which produces hyporeflexia) and, perhaps, bladder and bowel incontinence. Paralysis is permanent without treatment.

Stroke

Subarachnoid hemorrhage

A subarachnoid hemorrhage is a potentially life-threatening disorder that can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are severe headache, mydriasis, photophobia, aphasia, sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

Thoracic aortic aneurysm

Occlusion of spinal arteries by a ruptured thoracic aortic aneurysm may cause sudden onset of transient bilateral paralysis. Severe chest pain radiating to the neck, shoulders, back, and abdomen and a sensation of tearing in the thorax are prominent symptoms. Related findings include syncope, pallor, diaphoresis, dyspnea, tachycardia, cyanosis, diastolic heart murmur, and abrupt loss of radial and femoral pulses or wide variations in pulses and blood pressure between arms and legs. Paradoxically, however, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.

Transient ischemic attack

Episodic transient ischemic attacks (TIA) may cause transient unilateral paresis or paralysis accompanied by paresthesia, blurred or double vision, dizziness, aphasia, dysarthria, decreased LOC, and other site-dependent effects.

West Nile encephalitis

Mild infections of West Nile encephalitis, a mosquito-borne flavivirus, are common and include fever, headache, and body aches, which are sometimes accompanied by skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Drugs

Therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.

Electroconvulsive therapy

Electroconvulsive therapy can produce acute, but transient, paralysis.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Seizures, complex partial: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Brain abscess

Head trauma

Temporal lobe tumor

Complex partial seizures may be the first sign of a tumor in the temporal lobe. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Seizures, generalized tonic-clonic: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Alcohol withdrawal syndrome

Sudden withdrawal from alcohol dependence may cause seizures 7 to 48 hours later as well as status epilepticus. The patient may also be restless and exhibit hallucinations, profuse diaphoresis, and tachycardia.

Arsenic poisoning

Brain abscess

Brain tumor

Cerebral aneurysm

Eclampsia

Generalized seizures are a hallmark of eclampsia. Related findings include severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, fever of up to 104° F (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and decreased LOC.

Encephalitis

Head trauma

In severe cases, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause a decreased LOC, leading to coma; soft-tissue injury of the face, head, or neck; clear or bloody drainage from the mouth, nose, or ears; facial edema; bony deformity of the face, head, or neck; Battle’s sign; and lack of response to oculocephalic and oculovestibular stimulation. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit vision deficits, behavioral changes, and headache.

Hepatic encephalopathy

Hypertensive encephalopathy

Hypertensive encephalopathy, a life-threatening disorder, may cause seizures along with severely increased blood pressure, decreased LOC, intense headache, vomiting, transient blindness, paralysis, and (eventually) Cheyne-Stokes respirations.

Hypoglycemia

Hyponatremia

Seizures develop when serum sodium levels fall below 125 mEq/L, especially if the decrease is rapid. Hyponatremia also causes orthostatic hypotension, headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.

Hypoparathyroidism

Worsening tetany causes generalized seizures. Chronic hypoparathyroidism produces neuromuscular irritability, Chvostek’s sign, dysphagia, tetany, and hyperactive DTRs.

Hypoxic encephalopathy

Besides generalized seizures, hypoxic encephalopathy may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.

Neurofibromatosis

Renal failure (chronic)

Stroke

Other causes

Barbiturate withdrawal

In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.

Diagnostic tests

Contrast agents used in radiologic tests may cause generalized seizures.

Drugs

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Seizures, simple partial: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Brain abscess

Brain tumor

Head trauma

Multiple sclerosis

Focal or generalized seizures may occur with multiple sclerosis, usually during the late stages. Other findings include visual deficits, paresthesia, constipation, muscle weakness, spasticity, paralysis, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, emotional lability, impotence, and urinary frequency, urgency, and incontinence.

Neurofibromatosis

With neurofibromatosis, multiple brain lesions cause focal seizures and, at times, generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, progressive monocular blindness, nystagmus, and endocrine abnormalities.

Stroke

A major cause of seizures in patients older than age 50, a stroke may induce focal seizures up to 6 months after its onset. Related effects depend on the type and extent of the stroke but may include decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. A stroke may also cause vision deficits, memory loss, poor judgment, personality changes, emotional lability, headache, urinary incontinence or retention, and vomiting. It may result in generalized seizures.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Seizures: Principal Causes of Seizures
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Febrileseizures
Hypoxic-ischemic encephalopathy
Brain disorders
1. Cerebralmalformations
2. Intracranial infection
3. Intracranial hemorrhage
4. Other
Hypertensive encephalopathy
Drugs and toxins
Metabolic disorders
1. Hypoglycemia
2. Hypocalcemia
3. Hypomagnesemia
4. Hyponatremia
5. Hypernatremia
6. Uremia
7. Bilirubin encephalopathy (kernicterus)
8. Pyridoxine dependency
9. Inborn errors of metabolism
Selected epileptic syndromes
1. Neonatalseizures
2. Benign neonatal epilepsy
3. Infantile spasms (West syndrome)
4. Lennox-Gastaut syndrome
5. Benign focal epilepsy with centrotemporalspikes
6. Temporal lobe epilepsy
7. Juvenile myoclonic epilepsy
8. Posttraumatic epilepsy
9. Childhood absence epilepsy
Unknown

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Aura: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Classic migraine headache.A migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient's vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic.A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase), and then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Carpopedal spasm: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Hypocalcemia.Carpopedal spasm is an early sign of hypocalcemia. It's usually accompanied by paresthesia of the fingers, toes, and perioral area; muscle weakness, twitching, and cramping; hyperreflexia; chorea; fatigue; and palpitations. Positive Chvostek's and Trousseau's signs can be elicited. Laryngospasm, stridor, and seizures may appear in severe hypocalcemia.

Chronic hypocalcemia may be accompanied by mental status changes; cramps; dry, scaly skin; brittle nails; and thin, patchy hair and eyebrows.

Tetanus.With tetanus, the patient develops muscle spasms and painful seizures. Difficulty swallowing and a low-grade fever are also present. If the patient isn't treated or treatment is delayed, the mortality rate is very high.

Other causes

Treatments.Multiple blood transfusions and parathyroidectomy may cause hypocalcemia, resulting in carpopedal spasm. Surgical procedures that impair calcium absorption, such as ileostomy formation and gastric resection with gastrojejunostomy, may also cause hypocalcemia.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Level of consciousness, decreased: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Adrenal crisis.A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of the onset of adrenal crisis. Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess.With a brain abscess, decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site. Early signs and symptoms—a constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor.With a brain tumor, the patient's LOC decreases slowly, from lethargy to coma. He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured).Somnolence, confusion and, at times, stupor characterize a moderate cerebral bleed; deep coma occurs with severe bleeding, which can be fatal. The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Diabetic ketoacidosis.Diabetic ketoacidosis produces a rapid decrease in the patient's LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul's respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis.Within 24 to 48 hours after onset of encephalitis, the patient may develop changes in his LOC ranging from lethargy to coma. Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal).Postvaccinal encephalomyelitis is a life-threatening disorder that produces rapid deterioration in the patient's LOC, from drowsiness to coma. He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy.With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski's reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, the patient's LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in the LOC, leading to coma and brain death. Initially, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski's reflex; an absent doll's eye sign; and fixed pupils.

With uremic encephalopathy, the LOC decreases gradually from lethargy to coma. Initially, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul's and Cheyne-Stokes respirations.

Heatstroke.With heatstroke, as body temperature increases, the patient's LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient's skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia.Hypernatremia, life-threatening if acute, causes the patient's LOC to deteriorate from lethargy to coma. He's irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome (HHNS).LOC decreases rapidly from lethargy to coma with HHNS. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia.LOC gradually decreases to lethargy with hypokalemia; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia.Hyponatremia, life-threatening if acute, produces a decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia.With severe hypothermia (temperature below 90° F [32.2° C]), the patient's LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage.Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski's reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis.If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity. Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.

Meningitis.Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis. A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig's and Brudzinski's signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Pontine hemorrhage.A sudden, rapid decrease in the patient's LOC to the point of coma occurs within minutes and death within hours of pontine hemorrhage. The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski's reflex, an absent doll's eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders.A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in the patient's LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock.A decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Stroke.When a stroke occurs, changes in the patient's LOC vary in degree and onset, depending on the lesion's size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs) or an episode of atrial fibrillation. Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Subdural hemorrhage (acute).Acute subdural hemorrhage is a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma. The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski's reflex.

Thyroid storm.The patient's LOC decreases suddenly with thyroid storm and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105º F (40.5º C).

TIA.When a TIA occurs, the patient's LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis.Signs and symptoms of West Nile encephalitis include fever, headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol.Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs.Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Myoclonus: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Alzheimer's disease.Generalized myoclonus may occur in advanced stages of Alzheimer's disease, a slowly progressive dementia. Other late findings include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence, delusions, and hallucinations.

Creutzfeldt-Jakob disease.Diffuse myoclonic jerks appear early in Creutzfeldt-Jakob disease. Initially random, they gradually become more rhythmic and symmetrical, usually occurring in response to sensory stimuli. Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and vision disturbances, or possibly, blindness.

Encephalitis (viral).With viral encephalitis, myoclonus is usually intermittent and either localized or generalized. Associated findings vary, but may include rapidlydecreasing LOC, fever, headache, irritability, nuchal rigidity, vomiting, seizures, aphasia, ataxia, hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.

Encephalopathy.Hepatic encephalopathy occasionally produces myoclonic jerks in association with asterixis and focal or generalized seizures.

Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual intention myoclonus.

Uremic encephalopathy commonly produces myoclonic jerks and seizures. Other signs and symptoms include apathy, fatigue, irritability, headache, confusion, gradually decreasing LOC, nausea, vomiting, oliguria, edema, and papilledema. The patient may also exhibit elevated blood pressure, dyspnea, arrhythmias, and abnormal respirations.

Epilepsy.With idiopathic epilepsy, localized myoclonus is usually confined to an arm or leg and occurs singly or in short bursts, usually upon awakening. It's usually more frequent and severe during the prodromal stage of a major generalized seizure, after which it diminishes in frequency and intensity.

Other causes

Drug withdrawal.Myoclonus may be seen in patients with alcohol, opioid, or sedative withdrawal or delirium tremens.

Poisoning.Acute intoxication with methyl bromide, bismuth, or strychnine may produce an acute onset of myoclonus and confusion.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Paralysis: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Amyotrophic lateral sclerosis (ALS).ALS produces spastic or flaccid paralysis in the body's major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and possibly respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagial drooling, choking, and difficulty chewing.

Bell's palsy.Bell's palsy causes transient, unilateral facial muscle paralysis. The affected muscles sag, and eyelid closure is impossible. Other signs include increased tearing, drooling, and a diminished or absent corneal reflex.

Botulism.Botulism can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after the ingestion of contaminated food. Respiratory muscle paralysis leads to dyspnea and respiratory arrest. Nausea, vomiting, diarrhea, blurred or double vision, bilateral mydriasis, dysarthria, and dysphagia are some early findings.

Brain abscess.Advanced abscess in the frontal or temporal lobe can cause hemiplegia accompanied by other late findings, such as ocular disturbances, unequal pupils, decreased LOC, ataxia, tremors, and signs of infection.

Brain tumor.A tumor affecting the motor cortex of the frontal lobe may cause contralateral hemiparesis that progresses to hemiplegia. The onset is gradual, but paralysis is permanent without treatment. In early stages, a frontal headache and behavioral changes may be the only indicators. Eventually, seizures, aphasia, and signs of increased ICP (decreased LOC and vomiting) develop.

Conversion disorder.Hysterical paralysis, a classic symptom of conversion disorder, is characterized by the loss of voluntary movement with no obvious physical cause. It can affect any muscle group, appears and disappears unpredictably, and may occur with histrionic behavior (manipulative, dramatic, vain, irrational) or a strange indifference.

Encephalitis.Variable paralysis develops in the late stages of encephalitis. Earlier signs and symptoms include rapidly decreasing LOC (possibly coma), fever, headache, photophobia, vomiting, signs of meningeal irritation (nuchal rigidity, positive Kernig's and Brudzinski's signs), aphasia, ataxia, nystagmus, ocular palsies, myoclonus, and seizures.

Guillain-Barré syndrome.Guillain-Barré syndrome is characterized by a rapidly developing, but reversible, ascending paralysis. It commonly begins as leg muscle weakness and progresses symmetrically, sometimes affecting even the cranial nerves, producing dysphagia, nasal speech, and dysarthria. Respiratory muscle paralysis may be life-threatening. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.

Head trauma.Cerebral injury can cause paralysis due to cerebral edema and increased ICP. The onset is usually sudden. The location and extent vary, depending on the injury. Associated findings vary, but include decreased LOC; sensory disturbances, such as paresthesia and loss of sensation; headache; blurred or double vision; nausea and vomiting; and focal neurologic disturbances.

Multiple sclerosis (MS).With MS, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, an intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis.With myasthenia gravis, profound muscle weakness and abnormal fatigability may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages, but becomes more persistent as the disease progresses. Associated findings depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient's jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress—dyspnea, shallow respirations, and cyanosis.

Parkinson's disease.Tremors, bradykinesia, and lead-pipe or cogwheel rigidity are the classic signs of Parkinson's disease. Extreme rigidity can progress to paralysis, particularly in the extremities. In most cases, paralysis resolves with prompt treatment of the disease.

Peripheral neuropathy.Typically, peripheral neuropathy produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, a loss of vibration sensation, hypoactive or absent DTRs, neuralgia, and skin changes such as anhidrosis.

Rabies.Rabies produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms—fever; headache; hyperesthesia; paresthesia, coldness, and itching at the bite site; photophobia; tachycardia; shallow respirations; and excessive salivation, lacrimation, and perspiration—develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupil changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, a high fever, urine retention, drooling, and hydrophobia.

Seizure disorders.Seizures, particularly focal seizures, can cause transient local paralysis (Todd's paralysis). Any part of the body may be affected, although paralysis tends to occur contralateral to the side of the irritable focus.

Spinal cord injury.Complete spinal cord transection results in permanent spastic paralysis below the level of injury. Reflexes may return after spinal shock resolves. Partial transection causes variable paralysis and paresthesia, depending on the location and extent of injury. (see Understanding spinal cord syndromes.)

Spinal cord tumors.With a spinal cord tumor, paresis, pain, paresthesia, and variable sensory loss may occur along the nerve distribution pathway served by the affected cord segment. Eventually, these symptoms may progress to spastic paralysis with hyperactive DTRs (unless the tumor is in the cauda equina, which produces hyporeflexia) and, perhaps, bladder and bowel incontinence. Paralysis is permanent without treatment.

Stroke.A stroke involving the motor cortex can produce contralateral paresis or paralysis. The onset may be sudden or gradual, and paralysis may be transient or permanent. Associated signs and symptoms vary widely and may include headache, vomiting, seizures, decreased LOC and mental acuity, dysarthria, dysphagia, ataxia, contralateral paresthesia or sensory loss, apraxia, agnosia, aphasia, vision disturbances, emotional lability, and bowel and bladder dysfunction.

Subarachnoid hemorrhage.Subarachnoid hemorrhage is a potentially life-threatening disorder that can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are severe headache, mydriasis, photophobia, aphasia, sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia.Syringomyelia produces segmental paresis, leading to flaccid paralysis of the hands and arms. Reflexes are absent, and loss of pain and temperature sensation is distributed over the neck, shoulders, and arms in a capelike pattern.

Transient ischemic attack (TIA).Episodic TIAs may cause transient unilateral paresis or paralysis accompanied by paresthesia, blurred or double vision, dizziness, aphasia, dysarthria, decreased LOC, and other site-dependent effects.

West Nile encephalitis.Symptoms of West Nile encephalitis include fever, headache, and body aches, which are sometimes accompanied by a skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Drugs.The therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.

Electroconvulsive therapy (ECT).ECT can produce acute, but transient, paralysis.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Seizures, complex partial: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Brain abscess.If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include headache, nausea, vomiting, generalized seizures, and decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.

Head trauma.Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.

Herpes simplex encephalitis.Herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include fever, headache, coma, and generalized seizures.

Temporal lobe tumor.Complex partial seizures may be the first sign of a temporal lobe tumor. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause decreased LOC, vomiting and, possibly, papilledema.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Seizures, generalized tonic-clonic: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Brain abscess.Generalized seizures may occur in the acute stage of a brain abscess formation or after the abscess disappears. Depending on the size and location of the abscess, a decreased LOC varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure (ICP) and include a constant headache, nausea, vomiting, and focal seizures. Typical later features include ocular disturbances, such as nystagmus, impaired vision, and unequal pupils. Other findings vary with the abscess site but may include aphasia, hemiparesis, abnormal behavior, and personality changes.

Brain tumor.Generalized seizures may occur with a brain tumor, depending on it's location and type. Other findings include a slowly decreasing LOC, a morning headache, dizziness, confusion, focal seizures, vision loss, motor and sensory disturbances, aphasia, and ataxia. Later findings include papilledema, vomiting, increased systolic blood pressure, widening pulse pressure and, eventually, a decorticate posture.

Chronic renal failure.End-stage renal failure produces the rapid onset of twitching, trembling, myoclonic jerks, and generalized seizures. Related signs and symptoms include anuria or oliguria, fatigue, malaise, irritability, decreased mental acuity, muscle cramps, peripheral neuropathies, anorexia, and constipation or diarrhea. Integumentary effects include skin color changes (yellow, brown, or bronze), pruritus, and uremic frost. Other effects include an ammonia breath odor, nausea and vomiting, ecchymoses, petechiae, GI bleeding, mouth and gum ulcers, hypertension, and Kussmaul's respirations.

Eclampsia.Generalized seizures are a hallmark of eclampsia. Related findings include a severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, a fever of up to 104° F (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and decreased LOC.

Encephalitis.Seizures are an early sign of encephalitis, indicating a poor prognosis; they may also occur after recovery as a result of residual damage. Other findings include fever, headache, photophobia, nuchal rigidity, neck pain, vomiting, aphasia, ataxia, hemiparesis, nystagmus, irritability, cranial nerve palsies (causing facial weakness, ptosis, and dysphagia), and myoclonic jerks.

Epilepsy (idiopathic).In most cases, the cause of recurrent seizures is unknown.

Head trauma.With severe head trauma, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause decreased LOC, leading to coma; soft-tissue injury of the face, head, or neck; clear or bloody drainage from the mouth, nose, or ears; facial edema; bony deformity of the face, head, or neck; Battle's sign; and a lack of response to oculocephalic and oculovestibular stimulation. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as a decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit visual deficits, behavioral changes, and headache.

Hepatic encephalopathy.Generalized seizures may occur latein hepatic encephalopathy. Associated late-stage findings in the comatose patient include fetor hepaticus, asterixis, hyperactive DTRs, and a positive Babinski's sign.

Hypoglycemia.Generalized seizures usually occur with severe hypoglycemia, accompanied by blurred or double vision, motor weakness, hemiplegia, trembling, excessive diaphoresis, tachycardia, myoclonic twitching, and decreased LOC.

Hyponatremia.Seizures may develop when the serum sodium level falls below 125 mEq/L, especially if the sodium loss is rapid. Hyponatremia also causes orthostatic hypotension, headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.

Hypoparathyroidism.Chronic hypoparathyroidism produces neuromuscular irritability and hyperactive DTRs. Worsening tetany causes generalized seizures.

Hypoxic encephalopathy.Besidesgeneralized seizures, hypoxic encephalopathy may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.

Neurofibromatosis.Multiple brain lesions from neurofibromatosis cause focal and generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, monocular blindness, and nystagmus.

Stroke.Seizures (focal more commonly than generalized) may occur within 6 months of an ischemic stroke. Associated signs and symptoms vary with the location and extent of brain damage. They include decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. The patient may also develop visual deficits, memory loss, poor judgment, personality changes, emotional lability, urine retention or urinary incontinence, constipation, headache, and vomiting.

Other causes

Arsenic poisoning.Besides generalized seizures, arsenic poisoning may cause a garlicky breath odor, increased salivation, and generalized pruritus. GI effects include diarrhea, nausea, vomiting, and severe abdominal pain. Related effects include diffuse hyperpigmentation; sharply defined edema of the eyelids, face, and ankles; paresthesia of the extremities; alopecia; irritated mucous membranes; weakness; muscle aches; and peripheral neuropathy.

Barbiturate withdrawal.In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.

Diagnostic tests.Contrast agents used in radiologic tests may cause generalized seizures.

Drugs.Toxic blood levels of some drugs, such as theophylline, lidocaine, meperidine, penicillins, and cimetidine, may cause generalized seizures. Phenothiazines, tricyclic antidepressants, amphetamines, isoniazid, and vincristine may cause seizures in patients with preexisting epilepsy.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Seizures, simple partial: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Brain abscess.Seizures can occur in the acute stage of a brain abscess formation or after resolution of the abscess. A decreased LOC varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure and include a constant, intractable headache; nausea; and vomiting. Later signs and symptoms include ocular disturbances, such as nystagmus, decreased visual acuity, and unequal pupils. Other findings vary according to the abscess site and may include aphasia, hemiparesis, and personality changes.

Brain tumor.Focal seizures are commonly the earliest indicators of a brain tumor. The patient may report a morning headache, dizziness, confusion, vision loss, and motor and sensory disturbances. He may also develop aphasia, generalized seizures, ataxia, decreased LOC, papilledema, vomiting, increased systolic blood pressure, and widening pulse pressure. Eventually, he may assume a decorticate posture.

Head trauma.Any head injury can cause seizures, but penetrating wounds are characteristically associated with focal seizures. The seizures usually begin 3 to 15 months after injury, decrease in frequency after several years, and eventually stop. The patient may develop generalized seizures and decreased LOC that may progress to coma.

Stroke.A major cause of seizures, a stroke may induce focal seizures up to 6 months after its onset. Related effects depend on the type and extent of the stroke, but may include decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. A stroke may also cause visual deficits, memory loss, poor judgment, personality changes, emotional lability, headache, urinary incontinence or urine retention, and vomiting. It may result in generalized seizures.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Seizures, absence: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Idiopathic epilepsy.Some forms of absence seizure are accompanied by learning disabilities.

Other causes

Drugs.Drugs that lower the threshold for seizures, such as alcohol, cocaine, penicillin in high doses, isoniazid, and phenothiazines may trigger seizures in patients with preexisting epilepsy.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Seizures - Case 19-3: 8-Month-Old Boy: I. Differential Diagnosis
(Pediatric Complaints and Diagnostic Dilemmas)

This infant had seizures related to hypoglycemia. Hypoglycemia in an infant, defined as a blood glucose concentration of 40 mg/dL or less, warrants immediate treatment followed by appropriate investigation. Many inborn errors of metabolism responsible for hypoglycemia manifest during the first year of life, whereas milder defects of glycogen degradation and gluconeogenesis manifest in childhood only after prolonged periods of fasting. Causes of hypoglycemia in an infant include hyperinsulinism, hormone deficiency, and defects in branched-chain amino acid metabolism, fatty acid oxidation, and hepatic enzymes.

Urinary ketones are absent or low in children with hyperinsulinism and fatty acid oxidation defects who present with hypoglycemia. Hypoglycemia secondary to hyperinsulism most commonly appears during the first year of life. It is usually associated with islet-cell dysplasia and rarely with islet-cell adenomas. Insulin is elevated (greater than 5 µU/mL), and injection of glucagon elicits a rapid rise in blood glucose levels. Children with disorders of fatty acid metabolism can present with hypoglycemia and profound disturbance of consciousness that may not improve when the plasma glucose is normalized. In addition to hypoketonemia, they have high plasma free fatty acid concentrations, elevated ALT and AST, rhabdomyolysis, cardiomyopathy, and cerebral edema.

The presence of urinary ketones usually suggests hormone deficiency, glycogen storage disease (GSD), or defects in gluconeogenesis. Hypoglycemia is a common presentation for infants with panhypopituitarism, isolated growth hormone deficiency, and absolute (adrenal hypoplasia, Addison 's disease, adrenal leukodystrophy) or relative (congenital adrenal hyperplasia) glucocorticoid deficiency. Midline defects such as cleft lip or palate, optic dysplasia, and microphallus suggest anterior pituitary hormone deficiency. Hyperpigmentation associated with Addison 's disease rarely occurs in young children. Addison's disease is occasionally associated with hypoparathyroidism (hypocalcemia). Severely compromised adrenal function, as in congenital adrenal hyperplasia, may lead to serum electrolyte disturbances or ambiguous genitalia.

Children with branched-chain ketonuria (maple syrup urine disease) excrete urinary ketoacids that impart the characteristic odor of maple syrup. Clinically, these infants have frequent hypoglycemic episodes, lethargy, vomiting, and muscular hypertonia. GSDs are inherited autosomal recessive defects that are characterized by either deficient or abnormally functioning enzymes involved in the formation or degradation of glycogen. Hepatomegaly, growth failure, hyperlipidemia, and hyperuricemia are common clinical features. Other disorders to consider include galactosemia, especially in children with hepatosplenomegaly, jaundice, and mental retardation; and fructose-1,6-diphosphatase deficiency, in children with hepatomegaly due to lipid storage but only mildly abnormal liver function studies.

» READ BOOK EXCERPT ONLINE »

Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

» Next page: Symptoms of Grand mal seizures

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Causes of Grand mal seizures

Grand mal seizures Causes: Book Excerpts

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Related information on causes of Grand mal seizures:

Causes of Grand mal seizures: Online Medical Books

Aura: Differential Diagnosis (In a Page: Signs and Symptoms)

Chorea: Differential Diagnosis (In a Page: Signs and Symptoms)

Seizures/Convulsions: Differential Diagnosis (In a Page: Signs and Symptoms)

Facial Paralysis & Bell's Palsy: Differential Diagnosis (In a Page: Signs and Symptoms)

Chorea: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Facial Paralysis: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Seizures – Childhood: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Seizures – Neonatal: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Aura: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Carpopedal spasm: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Hypocalcemia.

Tetanus.

Other causes

Treatments.

Level of consciousness, decreased: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Adrenal crisis

Brain abscess

Brain tumor

Cerebral aneurysm (ruptured)

Diabetic ketoacidosis

Encephalitis

Encephalomyelitis (postvaccinal)

Encephalopathy

Heatstroke

Hypernatremia

Hyperosmolar hyperglycemic nonketotic syndrome

Hypokalemia

Hyponatremia

Hypothermia

Intracerebral hemorrhage

Listeriosis

Gender cue

Meningitis

Pontine hemorrhage

Seizure disorders

Shock

Stroke

Subdural hemorrhage (acute)

Thyroid storm

TIA

West Nile encephalitis

Other causes

Alcohol

Drugs

Myoclonus: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Alzheimer’s disease

Creutzfeldt-Jakob disease

Encephalitis (viral)

Encephalopathy

Epilepsy

Other causes

Drug withdrawal

Poisoning

Paralysis: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

Bell’s palsy

Botulism

Brain abscess

Brain tumor

Conversion disorder

Encephalitis

Guillain-Barré syndrome

Head trauma

Multiple sclerosis (MS)

Myasthenia gravis

Parkinson’s disease

Peripheral neuropathy

Rabies

Seizure Disorders

Spinal cord injury

Spinal cord tumors

TREATMENTS &
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Dr. Huntley's
Diagnosis
Checklist

Aura: Differential Diagnosis
(In a Page: Signs and Symptoms)

Chorea: Differential Diagnosis
(In a Page: Signs and Symptoms)

Seizures/Convulsions: Differential Diagnosis
(In a Page: Signs and Symptoms)

Facial Paralysis & Bell's Palsy: Differential Diagnosis
(In a Page: Signs and Symptoms)

Chorea: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Facial Paralysis: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Seizures – Childhood: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Seizures – Neonatal: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Aura: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Carpopedal spasm: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Level of consciousness, decreased: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Myoclonus: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Paralysis: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Seizures, complex partial: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Seizures, generalized tonic-clonic: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Seizures, simple partial: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Seizures, absence: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Vocal cord paralysis: Causes
(Professional Guide to Diseases (Eighth Edition))

Aura: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Carpopedal spasm: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Level of consciousness, decreased: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))