Patients with acute behavior, mood, or thought disturbances must be medically evaluated for the presence of dementia or delirium. Dementia is a chronic, progressive alteration in memory associated with cognitive decline, agnosia (inability to recognize familiar objects), apraxia (inability to perform tasks), and aphasia (defective language function). Alzheimer's disease is the classic type of dementia. However, infections, such as HIV, and other neurologic conditions, such as stroke, can also cause dementia.
Delirium, by contrast, is an acute disturbance in consciousness. It may also involve cognitive decline, but the patient's level of consciousness is decreased, unlike in dementia. Delirium has a short onset and usually a fluctuating course.
Alzheimer's disease is the most common type of dementia. It starts with memory loss affecting recent memory. Long-term memory is usually preserved. As the disease progresses, more cognitive deficits become apparent until the patient is no longer able to function. History and physical examination are the most important contributors to the diagnosis. Magnetic resonance imaging (MRI) is an important adjunct.
Acetylcholinesterase inhibitors (eg, tacrine, donepezil) are used to increase central nervous system (CNS) levels of acetylcholine. This treatment helps to delay the progression of disease in some patients. However, no agent is currently available that can prevent the ultimate progression of Alzheimer's disease.
Multiple medical problems can cause a delirious state, which may be confused with psychosis. Drug intoxication or withdrawal; infection; and endocrine, metabolic, neurologic, and cardiopulmonary disturbances are most often implicated.
Drug Intoxication and Withdrawal
The stimulant drugs such as cocaine and amphetamines, including MDMA (Ectasy), can cause symptoms of behavioral and personality disturbance. These drugs can also induce someone with a compensated psychiatric illness such as schizophrenia to decompensate. Therefore, when evaluating a patient with mental status changes and bizarre behavior, the physician should determine whether stimulant drugs are present. The diagnosis is based on history of substance abuse, characteristic signs, and a positive drug screen.
Cocaine and amphetamines both cause a sympathetic hyperactivity. They cause hypertension, tachycardia, dilated pupils, and diaphoresis. MDMA causes less sympathetic hyperactivity and has more hallucinogenic properties. Psychological manifestations of stimulants include dysphoria, paranoid psychosis, and potentially a delirious state. Stimulants also cause a disinhibition leading to poor impulse control. As a result, patients with acute intoxication are more likely to be violent, homicidal, or suicidal. This property is seen especially in patients taking amphetamines.
Management of patients with acute toxicity is supportive. Benzodiazepines are the treatment of choice for the acutely agitated and violent person taking cocaine or amphetamines.
Withdrawal from stimulants initially involves anxiety, anhedonia, depression, fatigue, and severe craving for the drug of abuse. Withdrawal does not cause a significant risk for death from cardiac or pulmonary disturbances. The withdrawal state may be a risk factor, however, for suicide. Patients receive supportive measures, usually lasting 1–2 weeks until improvement in the anxiety and lethargy is seen. However, the anhedonia and cravings may continue for weeks.
Alcohol and benzodiazepines are the classic depressants. The diagnosis is based on clinical findings coupled with a positive drug level. They cause a decrease in sensorium, lethargy, ataxic gait, nystagmus, and respiratory depression. Individuals presenting with symptoms of intoxication and lethargy warrant evaluation for depressant use. These chemicals, however, can inhibit impulse control, and some people have a paradoxical excitation using depressants. Monitoring of airway and breathing status is crucial. Searching for any other cause of the behavior (eg, head injury) is also important.
Alcohol withdrawal is noteworthy due to the continued morbidity and even mortality that occurs from such a widely used substance. Delirium tremens can cause a clinical picture very similar to that of an acute psychotic break. Patients with delirium tremens have stopped drinking for as little as a few hours to days. Patients clinically show signs of sympathetic overload, including hypertension and tachycardia. They are usually diaphoretic and, by definition, tremulous. This delirious state can be differentiated from functional psychosis on the basis of the history, autonomic dysfunction, and visual hallucinations. Treatment is with benzodiazepines. A titrated lorazepam infusion may be needed to decrease the hypertension, tachycardia, and CNS symptoms.
All narcotic substances, such as morphine and heroin, can cause the classic triad of respiratory depression, miosis, and decreased mental status. Diagnosis is based on the clinical picture, positive drug screen, or response to naloxone. Usually the patient abusing narcotics presents with lethargy and not bizarre behavior. However, if these chemicals are mixed with stimulants (eg, cocaine or amphetamines), the result may be any type of delirium that can mimic functional psychosis or mood disorder.
Lysergic acid diethylamide (LSD) and phencyclidine (PCP) are the traditional hallucinogenic drugs. LSD is absorbed through the oral mucosa and binds to post-synaptic serotonergic receptors. The patient may report kaleidoscopic hallucinations. However, the drug may also cause violence, suicidal ideation, and bizarre memories or flashbacks.
PCP is a dissociative anesthetic. Patients are awake but exhibit bizarre behavior that can become suddenly violent. Patients may be hypertensive and tachycardic. Patients may also experience a host of behavioral and neurologic changes such as loss of concentration or the presence of illogical speech, nystagmus, or ataxia. Diagnosis is based on the history of use, clinical findings, and drug screen results. Treatment for hallucinogens includes ruling out any other associated acute medical problem and providing supportive care in a calm, quiet environment. Benzodiazepines may be used in acutely agitated patients.
Many patients with systemic infections, especially the elderly, present with delirium. Sometimes the delirious state involves behavioral changes. Any elderly patient with acute mental status changes should be evaluated for systemic infection. Diagnosis is based on the clinical picture coupled with the source of infection detected on urinalysis, chest X-ray, or from cultures.
Encephalitis is an infectious process that causes inflammation around the brain. The etiology often is viral (eg, herpes). Clinical manifestations usually involve fever and headache. If the infection affects the limbic area of the brain, personality and behavioral changes may occur, including floridly psychotic behavior and aggression. Meningitis, likewise, may cause delirium and altered mental status. Therefore, if an infectious cause is suspected, especially in a patient with fever, the patient should undergo a head CT scan and lumbar puncture. Diagnosis is based on these two tests in the appropriate clinical setting. Treatment is aimed at the underlying infectious or inflammatory process. If infection is suspected, initiate acyclovir and antibiotics as soon as possible.
Endocrine and Metabolic Disorders
(See Chapter 37) Patients with stigmata of liver failure routinely present with altered mental status. These patients may be delirious. At times they may be violent or aggressive. In the context of liver failure, an elevated ammonia level may be helpful in narrowing down the differential diagnosis to hepatic encephalopathy. Treatment is usually supportive along with lactulose to enterally eliminate toxins usually cleared by the liver.
(See Chapter 44) Hypercalcemia and alterations in sodium, either hyponatremia or hypernatremia, are the most common electrolyte causes of altered mental status. Personality and behavioral changes are much less common than lethargy. Seizures, coma, and death are possible if the electrolyte abnormality is not corrected appropriately. Fortunately, the diagnosis is easily made with routine electrolyte panels.
(See Chapter 43) The brain requires glucose to function. A low blood glucose level can mimic any type of CNS event. Patients may present with decreased consciousness or focal neurologic findings similar to a stroke. Blood glucose level should be checked as soon as possible in any patient with behavioral changes. Rapid correction of hypoglycemia can itself cause behavioral changes. Violence and aggression from the rapid correction are usually short in duration. However, if a patient continues to have symptoms after the glucose level has been corrected, further investigation into the cause is warranted.
(See Chapter 43) Hyperthyroidism and hypothyroidism have been implicated in acute behavioral changes mimicking functional disorders. Hyperthyroidism may cause anxiety and tremor. These patients usually present with mild to moderate hypertension and tachycardia along with weight loss and heat intolerance. Patients with hypothyroidism can present with symptoms of fatigue all the way to delirium or coma. Other symptoms include gastrointestinal complaints such as constipation, cold intolerance, weight gain, and menstrual irregularities. Diagnosis can be reliably made based on laboratory levels of thyroid hormones.
(See Chapter 19) Patients who have had a seizure may present with a normal mental status or may have decreased consciousness from a postictal state. A history of seizure or witnessed seizure activity may guide the workup. Nonconvulsive status epilepticus is much more difficult to determine. These patients may present with decreased consciousness or may be awake and alert. Patients may even have behavioral changes from blank stare to aggression depending on the location of the seizure focus. Nonconvulsive status epilepticus should be considered in patients with behavioral or neurologic changes, especially if a history of epilepsy is present. If necessary, neurologic consultation and an electroencephalogram would be appropriate to confirm the diagnosis.
Cerebral Vascular Accident
(See Chapter 37.) Cerebral vascular accidents (CVAs) are usually associated with focal weakness and a variable level of consciousness. Depending on the area of the brain affected, patients may have significant cognitive deficits. Patients may present with bizarre behavior secondary to aphasia or neglect. Therefore, a CVA should be considered in patients with risk factors for vascular disease or cardioembolic phenomenon. CT scanning and MRI can be helpful in the diagnosis.
Wernicke's encephalopathy, a clinical diagnosis, is due to thiamine deficiency and occurs mostly in alcoholic patients. The main features clinically are ataxia, ophthal-moplegia (either nystagmus or gaze palsy), and mental status changes. The mental status change involves anything from confusion to delirium or even coma. Thus, this entity should be considered in anyone with a history of alcohol abuse, eye changes, and mental status changes. The development of Korsakoff's psychosis can accompany these findings. Altered patients with malnutrition and alcohol abuse should be given thiamine.
Diseases of the cardiopulmonary system can cause significant behavioral changes. Myocardial infarction, pulmonary edema, and pulmonary embolism can cause anxiety secondary to pain, shortness of breath, and a possible sense of doom. These disorders may elicit significant fear in patients, which may manifest itself as panic attack or even aggression.
Patients may also be hypoxic or hypotensive, which may cause decreased consciousness and cognitive dysfunction. Diagnosis is based on clinical suspicion coupled with basic cardiac function evaluation (EGG, cardiac enzymes, pulse oximetry, and chest X-ray).