Causes of Epilepsy

List of causes of Epilepsy

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Epilepsy) that could possibly cause Epilepsy includes:

• Brain injury
• Brain tumor
• Brain infection
• Brain hemorrhage (see Brain symptoms)
• Meningitis
• Encephalitis
• Hypoglycemia
• Childbirth trauma
• Certain poisons

More causes: see full list of causes for Epilepsy

Causes of Epilepsy: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review the full text of medical books online, free, without registration, for more information about the causes of Epilepsy.

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)
  • Physiologic nonepileptic seizures
    –Usually due to an underlying physiologic cause (e.g., fever, hypoglycemia, hypo- or hyperthyroidism, renal failure, cerebral anoxia)
  • Absence seizures (petit mal seizure) only rarely have an aura

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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

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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

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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
  • Inherited choreas
    –Benign familial chorea
    –Juvenile Huntington chorea (usually presents with rigidity)
    –Familial paroxysmal choreoathetosis
  • 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)
  • Acquired brain disorders
    –Multiple sclerosis, basal ganglia stroke, hypoxic ischemic encephalopathy, neoplasm
  • Abetalipoproteinemia
  • Glutaric aciduria type I
  • Neuroacanthocytosis
  • Systemic lupus erythematosus
  • Kernicterus
  • Antiphospholipid antibody syndrome
  • Mitochondrial encephalopathies

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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

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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

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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.

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

Amyotrophic lateral sclerosis

Coarse fasciculations usually begin in the small muscles of the hands and feet, and then spread to the forearms and legs. Widespread, symmetrical muscle atrophy and weakness may result in dysarthria; difficulty chewing, swallowing, and breathing; and, occasionally, choking and drooling.

Bulbar palsy

Fasciculations of the face and tongue commonly appear early. Progressive signs and symptoms include dysarthria, dysphagia, hoarseness, and drooling. Eventually, weakness spreads to the respiratory muscles.

Poliomyelitis (spinal paralytic)

Coarse fasciculations, usually transient but occasionally persistent, accompany progressive muscle weakness, spasms, and atrophy. The patient may also exhibit decreased reflexes, paresthesia, coldness and cyanosis in the affected limbs, bladder paralysis, dyspnea, elevated blood pressure, and tachycardia.

Spinal cord tumors

Fasciculations may develop along with muscle atrophy and cramps, asymmetrically at first and then bilaterally as cord compression progresses. Motor and sensory changes distal to the tumor include weakness or paralysis, areflexia, paresthesia, and a tightening band of pain. Bowel and bladder control may be lost.

Other causes

Pesticide poisoning

Ingestion of organophosphate or carbamate pesticides commonly produces an acute onset of long, wavelike fasciculations and muscle weakness that rapidly progresses to flaccid paralysis. Other common effects include nausea, vomiting, diarrhea, loss of bowel and bladder control, hyperactive bowel sounds, and abdominal cramping. Cardiopulmonary findings include bradycardia, dyspnea or bradypnea, and pallor or cyanosis. Seizures, visual disturbances (pupillary constriction or blurred vision), and increased secretions (tearing, salivation, pulmonary secretions, or diaphoresis) may also occur.

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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.

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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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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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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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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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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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Epilepsy: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

In about half the cases of epilepsy, the cause is unknown. However, some possible causes of epilepsy include:

❑birth trauma (inadequate oxygen supply to the brain, blood incompatibility, or hemorrhage)

❑perinatal infection

❑anoxia (after respiratory or cardiac arrest)

❑infectious diseases (meningitis, encephalitis, or brain abscess)

❑ingestion of toxins (mercury, lead, or carbon monoxide)

❑tumors of the brain

❑inherited disorders or degenerative disease, such as phenylketonuria or tuberous sclerosis

❑head injury or trauma

❑metabolic disorders, such as hypoglycemia or hypoparathyroidism

❑stroke (hemorrhage, thrombosis, or embolism).

Alcohol withdrawal can cause nonep-ileptic seizures.

Epilepsy affects 1% to 2% of the population. However, 80% of patients have good seizure control if they strictly adhere to the prescribed treatment regimen.

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

Amyotrophic lateral sclerosis

In this progressive motor neuron disease, coarse fasciculations usually begin in the small muscles of the hands and feet, and then spread to the forearms and legs. Widespread, symmetrical muscle atrophy and weakness may result in dysarthria; difficulty chewing, swallowing, and breathing; and, occasionally, choking and drooling.

Bulbar palsy

Fasciculations of the face and tongue commonly appear early in bulbar palsy. Progressive signs and symptoms include dysarthria, dysphagia, hoarseness, and drooling. Eventually, weakness spreads to the respiratory muscles.

Guillain-Barré syndrome

Fasciculations may occur in Gullain-Barré syndrome, but the cardinal neurologic symptom is muscle weakness, which typically begins in the legs and spreads quickly to the arms and face. Other findings include paresthesia, incontinence, footdrop, tachycardia, dysphagia, and respiratory insufficiency.

Herniated disk

Fasciculations of the muscles innervated by compressed nerve roots may be widespread and profound, but the hallmark of a herniated disk is severe low back pain that may radiate unilaterally to the leg. Coughing, sneezing, bending, and straining exacerbate the pain. Related effects include muscle weakness, atrophy, and spasms; paresthesia; footdrop; steppage gait; and hypoactive deep tendon reflexes in the leg.

Poliomyelitis (spinal paralytic)

Coarse fasciculations, usually transient but occasionally persistent, accompany progressive muscle weakness, spasms, and atrophy in this disorder. The patient may also exhibit decreased reflexes, paresthesia, coldness and cyanosis in the affected limbs, bladder paralysis, dyspnea, elevated blood pressure, and tachycardia.

Spinal cord tumor

Fasciculations, muscle atrophy, and cramps may develop asymmetrically at first and then bilaterally as cord compression progresses. Motor and sensory changes distal to the tumor include weakness or paralysis, areflexia, paresthesia, and a tightening band of pain. Bowel and bladder control may be lost.

Syringomyelia

In this disorder, fasciculations may occur along with Charcot’s joints, areflexia, muscle atrophy, and deep, aching pain. Additional findings include thoracic scoliosis and loss of pain and temperature sensation over the neck, shoulders, and arms.

Other causes

Pesticide poisoning

Ingestion of organophosphate or carbamate pesticides commonly produces acute onset of long, wavelike fasciculations and muscle weakness that rapidly progresses to flaccid paralysis. Other common effects include nausea, vomiting, diarrhea, loss of bowel and bladder control, hyperactive bowel sounds, and abdominal cramping. Cardiopulmonary findings include bradycardia, dyspnea or bradypnea, and pallor or cyanosis. Seizures, vision disturbances (pupillary constriction or blurred vision), and increased secretions (tearing, salivation, pulmonary secretions, or diaphoresis) may also occur.

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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 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.

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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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

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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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

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 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

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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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

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.

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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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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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

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 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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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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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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Epilepsy: Causes
(Handbook of Diseases)

In about one-half of all epilepsy cases, the cause is unknown. Possible causes include:

❑ birth trauma (inadequate oxygen supply to the brain, blood incompatibility, or hemorrhage)

❑ perinatal infection

❑ anoxia

❑ infectious diseases (meningitis, encephalitis, or brain abscess)

❑ ingestion of toxins (mercury, lead, or carbon monoxide)

❑ brain tumors

❑ inherited disorders or degenerative disease, such as phenylketonuria or tuberous sclerosis

❑ head injury or trauma

❑ metabolic disorders, such as hypoglycemia and hypoparathyroidism

❑ stroke (hemorrhage, thrombosis, or embolism).

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

Amyotrophic lateral sclerosis

Coarse fasciculations usually begin in the small muscles of the hands and feet, and then spread to the forearms and legs. Widespread, symmetrical muscle atrophy and weakness may result in dysarthria; difficulty chewing, swallowing, and breathing; and, occasionally, choking and drooling.

Bulbar palsy

Fasciculations of the face and tongue commonly appear early. Progressive signs and symptoms include dysarthria, dysphagia, hoarseness, and drooling. Eventually, weakness spreads to the respiratory muscles.

Guillain-Barré syndrome

Fasciculations may occur, but the dominant neurologic symptom is muscle weakness, which typically begins in the legs and spreads quickly to the arms and face. Other findings include paresthesia, incontinence, footdrop, tachycardia, dysphagia, and respiratory insufficiency.

Herniated disk

Fasciculations of the muscles innervated by compressed nerve roots may be widespread and profound, but the overriding symptom is severe low back pain that may radiate unilaterally to the leg. Coughing, sneezing, bending, and straining exacerbate the pain. Related effects include muscle weakness, atrophy, and spasms; paresthesia; footdrop; steppage gait; and hypoactive deep tendon reflexes in the leg.

Poliomyelitis (spinal paralytic)

Coarse fasciculations, usually transient but occasionally persistent, accompany progressive muscle weakness, spasms, and atrophy. The patient may also exhibit decreased reflexes, paresthesia, coldness and cyanosis in the affected limbs, bladder paralysis, dyspnea, elevated blood pressure, and tachycardia.

Spinal cord tumors

Fasciculations may develop along with muscle atrophy and cramps, asymmetrically at first and then bilaterally as cord compression progresses. Motor and sensory changes distal to the tumor include weakness or paralysis, areflexia, paresthesia, and a tightening band of pain. Bowel and bladder control may be lost.

Syringomyelia

Fasciculations may occur along with Charcot’s joints, areflexia, muscle atrophy, and deep, aching pain. Additional findings include thoracic scoliosis and loss of pain and temperature sensation over the neck, shoulders, and arms.

Other causes

Pesticide poisoning

Ingestion of organophosphate or carbamate pesticides commonly produces acute onset of long, wavelike fasciculations and muscle weakness that rapidly progresses to flaccid paralysis. Other common effects include nausea, vomiting, diarrhea, loss of bowel and bladder control, hyperactive bowel sounds, and abdominal cramping. Cardiopulmonary findings include bradycardia, dyspnea or bradypnea, and pallor or cyanosis. Seizures, vision disturbances (pupillary constriction or blurred vision), and increased secretions (tearing, salivation, pulmonary secretions, or diaphoresis) may also occur.

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

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

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

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)

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 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.

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.

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; 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)

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

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 in