Causes of Dementia

• Seizure disorders
  –Retrograde amnesia is most common after a generalized tonic-clonic seizure during the postictal period
  –Some complex partial seizure foci (particularly temporal lobe epilepsy) can also produce “blank” periods of memory

• Toxicologic insults
  –Binge alcohol consumption
  –Benzodiazepine use (e.g., “date rape” drug
  flunitrazepam, also known as Rohypnol)
• Psychogenic causes are relatively common, but should be a diagnosis of exclusion
• Korsakoff's syndrome
• Transient global amnesia
  –A rare, transient, ischemic attack-like condition of proposed vascular etiology
  –Causes abrupt onset of short-term memory loss for minutes to hours
  –Typically occurs in patients older than 50
  –Seen in patients with migraines

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

• Dementia
• Medical etiologies
  –Infections (e.g., UTI, pneumonia, encephalitis, meningitis)
  –Drug toxicity, including alcohol
  –Drug withdrawal (especially benzodiazepines)
  –Fluid, electrolyte, and metabolic disorders (e.g., hyponatremia, hypoglycemia, hypercalcemia, uremia, hypercarbia)
  –CHF
  –Hypoxia (multiple causes, including CHF)
  –Medications (e.g., antiarrhythmics, antidepressants, neuroleptics, analgesics, GI medications)
  –Stroke
  –Cerebral ischemia (multiple causes)
  –Complex partial seizure disorder is associated with an alteration of awareness
  • Psychiatric etiologies
    –Depression
    –Psychotic illness
    –“Sundowning”: Behavioral deterioration occurs during evening hours (typically occurs in demented institutionalized patients)

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

• Delirium
  –Develops over hours to days
  –Fluctuates throughout the day
  –Causes include dehydration, drug-induced, electrolyte imbalance, UTI, URI, hypoglycemia, and alcohol or drug withdrawal
  –Occurs in 10–30% of hospital patients
  –Drug-induced delirium (e.g., cocaine, β-blockers, alcohol, corticosteroids, pseudoephedrine, dopaminergic drugs)
• Alcohol withdrawal (delirium tremens)
  –Often presents in hospitalized patients about 3 days after admission
  –Commonly presents with tactile hallucinations (e.g., formication—the sense of insects crawling over body)
  –May be accompanied by seizure activity
• Hallucinogenic syndromes (e.g., LSD, marijuana, mescaline, phencyclidine, mushrooms, amphetamines)

• Schizophrenia
  –Auditory hallucinations are most frequent; visual hallucinations occur in about 50% of patients, tactile in 20%, olfactory in 6%
  –Progresses to positive psychotic symptoms (e.g., hallucinations, delusions, thought disorder) and/or negative symptoms (e.g., anhedonia, poor concentration, flattened affect, poor social/personal function)
  –1% incidence in the general population, males >females

• Schizophreniform disorder
• Schizoaffective disorder
• Post-traumatic stress disorder
• Dementia
• Systemic lupus erythematosus
  –Auditory hallucinations caused by corticosteroids; visual and tactile by lupus psychosis
• Bipolar disorder
• Psychotic depression
• Postpartum major depression
• Mass lesions
• CNS infections/encephalitis
• Seizures
• Occipital lobe injury
• Heavy metal ingestion
• Lewy body dementia

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

• Alzheimer's disease is the most common cause of dementia
• Lewy body dementia
• Multi-infarct dementia
• Parkinson's disease
• Alcohol/drugs
• Vitamin deficiency (B₁₂, thiamine)
• CNS infections
  –HIV encephalitis
  –Meningitis
  –Herpes encephalitis
  –Creutzfeldt-Jacob disease
  –Cerebral abscess
  –Neurosyphilis
• Depression (pseudodementia)
• Head trauma
• Pick's disease
• Chronic subdural hematoma
• Huntington's disease
• Chronic hydrocephalus
• Paraneoplastic encephalitis
• Hypothyroidism
• Cerebral vasculitis
• Systemic lupus erythematosus (lupus cerebritis)
• Wilson's disease
• Chronic hypoglycemia or hypocalcemia
• Uremic encephalopathy
• Dialysis dementia
• Multiple sclerosis
• Hydrocephalus
• Postanoxic dementia

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

• Acute systemic infection
  –May be viral or bacterial cause
  –Often associated with high fever
• Hypoglycemia, diabetic ketoacidosis
• Central nervous system infection
  –Meningitis, encephalitis, brain abscess

• Drugs
  –Alcohol: Acute intoxication
  –Amphetamines: Also tremors, dry mouth, tachycardia, hyperactivity
  –Hallucinogens (LSD, mescaline, PCB) also tremors, dilated pupils, nausea, and abdominal pain
  –Phencyclidine (a.k.a. Angel Dust) with atxia, nystagmus, hyperreflexia, and hypertension
  –Opiates: Also with pinpoint pupils
  –Antihistamines
  –Phenothiazines
  –Organic solvents
  –Salicylates
  –Glucocorticoids

• Head injury
• Rocky Mountain spotted fever (RMSF)
  –Delirium and hallucinations may precede rash; fever, headache, myalgias, chills
• Malaria
• Rabies
• Syphilis
  –Tertiary syphilis is rare in children
• Hyponatremia
• Uremia
• Migraine
• Hypoxia
• Heat stroke
• Hepatic failure
• Systemic lupus erythematosus
  –Delirium is due to cerebral vasculitis
• Pellagra
  –Due to niacin deficiency
  –Also with diarrhea, dermatitis, dementia
• Hartnup disease
  –Rash, ataxia, psychological disturbance
  –Symptoms may be intermittent
• Porphyria
  –Attacks of abnormal behavior do not begin until late adolescence

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

• Hallucinogenic drugs
  –LSD, “mushrooms,” mescaline, and PCP are primarily hallucinogens
  –Amphetamines, cocaine, inhalants, and marijuana may also produce hallucinations
• CNS acute events
  –Trauma
  –CNS infection
  –Hypoxic events

• Psychosis
  –Defined as a mental state with significant impairment in cognition, interpersonal relations, and reality testing
  –Hallucinations may be a major or minor component
  –Psychosis may be psychiatric or organic (secondary to CNS insult)

• Schizophrenia
  –A disorder of impaired perception, cognition, interpersonal relations, and behavior with illogical and disordered thought content
  –Hallucinations (most often auditory) and delusions are common findings
  –Onset is frequently in adolescence
  –Frequently a positive family history

• Seizure disorders
  –Prominent auras may manifest as perceptual disturbances; visual and olfactory are the most common; tactile may also occur
• Narcolepsy
  –Hypnagogic hallucinations are hallucinations that occur while falling asleep; they may be visual or auditory
• Medications
  –Antipsychotics, anticholinergics, and corticosteroids can rarely cause hallucinations

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

❑ Alzheimer’s disease. Alzheimer’s disease usually begins with retrograde amnesia, which progresses slowly over many months or years to include anterograde amnesia, producing severe and permanent memory loss. Associated findings include agitation, inability to concentrate, disregard for personal hygiene, confusion, irritability, and emotional lability. Later signs include aphasia, dementia, incontinence, and muscle rigidity.

❑ Cerebral hypoxia. After recovery from hypoxia (brought on by such conditions as carbon monoxide poisoning or acute respiratory failure), the patient may experience total amnesia for the event, along with sensory disturbances, such as numbness and tingling.

❑ Head trauma. Depending on the trauma’s severity, amnesia may last for minutes, hours, or longer. Usually, the patient experiences brief retrograde and longer anterograde amnesia as well as persistent amnesia about the traumatic event. Severe head trauma can cause permanent amnesia or difficulty retaining recent memories. Related findings may include altered respirations and LOC; headache; dizziness; confusion; visual disturbances, such as blurred or double vision; and motor and sensory disturbances, such as hemiparesis and paresthesia, on the side of the body opposite the injury.

❑ Herpes simplex encephalitis. Recovery from herpes simplex encephalitis commonly leaves the patient with severe and possibly permanent amnesia. Associated findings include signs and symptoms of meningeal irritation, such as headache, fever, and altered LOC, along with seizures and various motor and sensory disturbances (such as paresis, numbness, and tingling).

❑ Hysteria. Hysterical amnesia, a complete and long-lasting memory loss, begins and ends abruptly and is typically accompanied by confusion.

❑ Seizures. In temporal lobe seizures, amnesia occurs suddenly and lasts for several seconds to minutes. The patient may recall an aura or nothing at all. An irritable focus on the left side of the brain primarily causes amnesia for verbal memories, whereas an irritable focus on the right side of the brain causes graphic and nonverbal amnesia. Associated signs and symptoms may include decreased LOC during the seizure, confusion, abnormal mouth movements, and visual, olfactory, and auditory hallucinations.

❑ Wernicke-Korsakoff syndrome. Retrograde and anterograde amnesia can become permanent without treatment in this syndrome. Accompanying signs and symptoms include apathy, an inability to concentrate or to put events into sequence, and confabulation to fill memory gaps. The syndrome may also cause diplopia, decreased LOC, head-ache, ataxia, and symptoms of peripheral neuropathy, such as numbness and tingling.

Other causes

❑ Drugs. Anterograde amnesia can be precipitated by general anesthetics, especially fentanyl, halothane, and isoflurane; barbiturates, most commonly pentobarbital and thiopental; and certain benzodiazepines, especially triazolam.

❑ Electroconvulsive therapy. The sudden onset of retrograde or anterograde amnesia occurs with electroconvulsive therapy. Typically, the amnesia lasts for several minutes to several hours, but severe, prolonged amnesia occurs with treatments given frequently over a prolonged period.

❑ Temporal lobe surgery. Usually performed on only one lobe, this surgery causes brief, slight amnesia. However, removal of both lobes results in permanent amnesia.

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

Brain tumor.

In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.

Cerebrovascular disorders.

 Cerebrovascular disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.

Decreased cerebral perfusion.

 Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, an irregular pulse, ventricular gallop, edema, and cyanosis.

Fluid and electrolyte imbalance.

The extent of imbalance determines the severity of the patient's confusion. Typically, he'll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.

Head trauma.

 Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, a severe headache, pupillary changes, and sensory and motor deficits are also common.

Heatstroke.

 Heatstroke causes pronounced confusion that gradually worsens as the patient's body temperature rises. Initially, he may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.

Hypothermia.

 Confusion may be an early sign of hypothermia. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, a rapid pulse, and decreased blood pressure and respirations. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.

Hypoxemia.

Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.

Infection.

 Severe generalized infection, such as sepsis, typically produces delirium. Central nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with a headache and nuchal rigidity.

Metabolic encephalopathy.

Hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.

Nutritional deficiencies.

Inadequate dietary intake of thiamine, niacin, or vitamin B₁₂ produces insidious, progressive confusion and possible mental deterioration.

Seizure disorders.

Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.

Other causes

Alcohol.

Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.

Drugs.

Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, a cardiac glycoside, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.

HERB ALERT:Herbal remedies, such as St. John's wort, can cause confusion, especially when taken in conjunction with an antidepressant or other serotonergic drug.

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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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Dissociative amnesia: Causes
(Professional Guide to Diseases (Eighth Edition))

Dissociative amnesia follows severe psychosocial stress, commonly involving a threat of physical injury or death. Amnesia may also occur after thinking about or engaging in unacceptable behavior such as an extramarital affair.

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

Alzheimer’s disease

Alzheimer’s disease usually begins with retrograde amnesia, which progresses slowly over many months or years to include anterograde amnesia and, eventually, severe and permanent memory loss. Associated findings include agitation, inability to concentrate, disregard for personal hygiene, confusion, irritability, and emotional lability. Later signs include aphasia, dementia, incontinence, and muscle rigidity.

Cerebral hypoxia

After recovery from hypoxia (brought on by such conditions as carbon monoxide poisoning or acute respiratory failure), the patient may experience total amnesia for the event along with sensory disturbances such as numbness and tingling.

Head trauma

Depending on the trauma’s severity, amnesia may last for minutes, hours, or longer. Usually, the patient experiences brief retrograde and longer anterograde amnesia as well as persistent amnesia about the traumatic event. Severe head trauma can cause permanent amnesia or difficulty retaining recent memories. Related findings may include altered respirations and LOC; headache; dizziness; confusion; visual disturbances, such as blurred or double vision; and motor and sensory disturbances, such as hemiparesis and paresthesia, on the side of the body opposite the injury.

Herpes simplex encephalitis

Recovery from herpes simplex encephalitis commonly leaves the patient with severe and possibly permanent amnesia. Associated findings include signs and symptoms of meningeal irritation, such as headache, fever, and altered LOC; seizures; and various motor and sensory disturbances, such as paresis, numbness, and tingling.

Hysteria

Hysterical amnesia, a complete and long-lasting memory loss, begins and ends abruptly and is typically accompanied by confusion.

Seizures

In temporal lobe seizures, amnesia occurs suddenly and lasts for several seconds to minutes. The patient may recall an aura or nothing at all. An irritable focus on the left side of the brain primarily causes amnesia for verbal memories, whereas an irritable focus on the right side of the brain causes graphic and nonverbal amnesia. Associated signs and symptoms may include decreased LOC during the seizure, confusion, abnormal mouth movements, and visual, olfactory, and auditory hallucinations.

Vertebrobasilar circulatory disorders

Vertebrobasilar ischemia, infarction, embolus, or hemorrhage may cause complete amnesia that begins abruptly, lasts for several hours, and ends abruptly. Associated findings include dizziness, decreased LOC, ataxia, blurred or double vision, vertigo, nausea, and vomiting.

Wernicke-Korsakoff syndrome

Retrograde and anterograde amnesia can become permanent without treatment in Wernicke-Korsakoff syndrome. Accompanying signs and symptoms include apathy, an inability to concentrate or to put events into sequence, and confabulation to fill memory gaps. The syndrome may also cause diplopia, decreased LOC, headache, ataxia, and symptoms of peripheral neuropathy such as numbness and tingling.

Other causes

Drugs

Anterograde amnesia can be precipitated by general anesthetics, especially fentanyl, halothane, and isoflurane; barbiturates, most commonly pentobarbital; and certain benzodiazepines, especially triazolam.

Electroconvulsive therapy

Sudden onset of retrograde or anterograde amnesia occurs with electroconvulsive therapy. Typically, the amnesia lasts for several minutes to several hours, but severe, prolonged amnesia occurs with treatments given frequently over a prolonged period.

Temporal lobe surgery

Usually performed on only one lobe, this surgery causes brief, mild amnesia. However, removal of both lobes results in permanent amnesia.

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

Alzheimer’s disease

Alzheimer’s disease sometimes causes gradual and irreversible ideomotor apraxia. It can also cause amnesia, anomia, decreased attention span, apathy, aphasia, restlessness, agitation, paranoid delusions, incontinence, social withdrawal, ataxia, and tremors.

Brain abscess

Apraxia occasionally results from a large brain abscess but usually resolves spontaneously after the infection subsides. Depending on the location of the abscess, apraxia may be accompanied by headache, fever, drowsiness, decreased mental acuity, aphasia, dysarthria, hemiparesis, hyperreflexia, incontinence, focal or generalized seizures, and ocular disturbances, such as nystagmus, visual field deficits, and unequal pupils.

Brain tumor

In a brain tumor, progressive apraxia may be preceded by decreased mental acuity, headache, dizziness, and seizures. It may occur with or directly after early signs of increased ICP, such as pupil changes. It may also occur with other localizing signs and symptoms of the tumor, such as aphasia, dysarthria, visual field deficits, weakness, stiffness, and hyperreflexia in the extremities.

Hepatic encephalopathy

Hepatic encephalopathy may cause gradual onset of constructional apraxia, which may be reversible with treatment. Early associated signs and symptoms include disorientation, amnesia, slurred speech, dysarthria, asterixis, and lethargy. Later signs include hyperreflexia, positive Babinski’s reflex, agitation, seizures, fetor hepaticus, stupor, and coma.

Stroke

Stroke commonly causes sudden onset of apraxia, which typically resolves spontaneously but may persist. Associated signs and symptoms vary according to the affected artery but can include headache, confusion, stupor or coma, hemiplegia, unilateral or bilateral visual field deficits, aphasia, agnosia, dysarthria, and urinary incontinence.

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

Brain tumor

In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.

Cerebrovascular disorders

These disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.

Decreased cerebral perfusion

Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, irregular pulse, ventricular gallop, edema, and cyanosis.

Fluid and electrolyte imbalance

The extent of the imbalance determines the severity of the patient’s confusion. Typically, he’ll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.

Head trauma

Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, severe headache, pupillary changes, and sensory and motor deficits are also common.

Heatstroke

This disorder causes pronounced confusion that gradually worsens as body temperature rises. Initially, the patient may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.

Hypothermia

Confusion may be an early sign of this disorder. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, rapid pulse, and decreased blood pressure and respiratory rate. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.

Hypoxemia

Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.

Infection

A severe generalized infection, such as sepsis, commonly produces delirium. Central nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with headache and nuchal rigidity.

Metabolic encephalopathy

Both hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.

Nutritional deficiencies

Inadequate dietary intake of thiamine, niacin, or vitamin B₁₂ produces insidious, progressive confusion and possibly mental deterioration.

Seizure disorders

Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.

Thyroid hormone disorders

Hyperthyroidism produces mild to moderate confusion along with nervousness, inability to concentrate, weight loss, flushed skin, and tachycardia. Hypothyroidism produces mild, insidious confusion and memory loss; weight gain; bradycardia; and fatigue.

Other causes

Alcohol

Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.

Drugs

Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, cardiac glycosides, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.

Heavy metal poisoning

Chronic ingestion or inhalation of heavy metals (such as lead, arsenic, mercury, and manganese) eventually produces confusion and, typically, weakness and drowsiness. The patient may also experience headache, vomiting, seizures, tremors, gait disturbances, and mental deterioration.

Herb Alert

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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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Amnesia: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Concussion

❑ Alzheimer disease

❑ Drugs

❑ Generalized seizure

❑ Migraine

❑ Transient global amnesia

❑ Psychogenic

❑ Herpes simplex encephalitis

❑ Complex partial seizures

❑ Korsakoff syndrome

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Dementia: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Alzheimer disease

❑ Multi-infarct dementia

❑ Depression

❑ Drugs

❑ Parkinson disease

❑ Frontal lobe dementia

❑ Vitamin B₁₂ deficiency

❑ HIV encephalopathy

❑ Korsakoff syndrome

❑ Brain tumor

❑ Normal pressure hydrocephalus

❑ Chronic subdural hematoma

❑ Neurosyphilis

❑ Creutzfeldt-Jakob

❑ Wilson disease

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Delirium/Hallucinations: Differential Overview
(Field Guide to Bedside Diagnosis)

Systemic

❑ Drugs/toxins

❑ Sepsis

❑ Hypoglycemia

❑ Hypercalcemia

❑ Hyponatremia

❑ Shock

❑ Delirium tremens

❑ Vitamin B₁₂ deficiency

❑ Hypoxia

❑ Hypercapnia

❑ Thyrotoxicosis

❑ Uremia

❑ Hepatic encephalopathy

❑ Thiamine deficiency

❑ Heat stroke

❑ Hypothermia

❑ Lead intoxication

❑ Carbon monoxide poisoning

Neurologic

❑ Concussion

❑ Hypertensive encephalopathy

❑ Subdural hematoma

❑ Postictal

❑ Transient global amnesia

❑ Meningitis

❑ Right parietal stroke

❑ Encephalitis

❑ Vasculitis

❑ Carcinomatous meningitis

Hallucinations

❑ Drugs

❑ Schizophrenia

❑ Temporal lobe epilepsy

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

See Apraxia: Causes and associated findings.

Alzheimer’s disease

Brain abscess

Brain tumor

Hepatic encephalopathy

Stroke

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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

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

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.

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 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

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

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. 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

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.

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 vision 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 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

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

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

Alzheimer’s disease

Alzheimer’s disease sometimes causes gradual and irreversible ideomotor apraxia. It can also cause amnesia, anomia, decreased attention span, apathy, aphasia, restlessness, agitation, paranoid delusions, incontinence, social withdrawal, ataxia, and tremors.

Brain abscess

Apraxia occasionally results from a large brain abscess but usually resolves spontaneously after the infection subsides. Depending on the location of the abscess, apraxia may be accompanied by headache, fever, drowsiness, decreased mental acuity, aphasia, dysarthria, hemiparesis, hyperreflexia, incontinence, focal or generalized seizures, and ocular disturbances, such as nystagmus, visual field deficits, and unequal pupils.

Brain tumor

With a brain tumor, progressive apraxia may be preceded by decreased mental acuity, headache, dizziness, and seizures. It may occur with or directly after early signs of increased intracranial pressure, such as pupil changes. It may also occur with other localizing signs and symptoms of the tumor, such as aphasia, dysarthria, visual field deficits, weakness, stiffness, and hyperreflexia in the extremities.

Hepatic encephalopathy

Hepatic encephalopathy may cause gradual onset of constructional apraxia, which may be reversible with treatment. Early associated signs and symptoms include disorientation, amnesia, slurred speech, dysarthria, asterixis, and lethargy. Later signs include hyperreflexia, positive Babinski’s reflex, agitation, seizures, fetor hepaticus, stupor, and coma.

Stroke

Stroke commonly causes sudden onset of apraxia, which usually resolves spontaneously but may persist. Associated signs and symptoms vary according to the affected artery but can include headache, confusion, coma, hemiplegia, unilateral or bilateral visual field deficits, aphasia, agnosia, dysarthria, and urinary incontinence.

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

Brain tumor

In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field defici