Alcohol Intoxication

Encephalopathy due to sepsis, multiple organ failure, or burns may arise within a few hours, manifesting itself as impaired concentration, disorientation, confusion, and psychomotor agitation in addition to the already severe systemic disturbances. In severe cases, there may be delirium, stupor or coma. Focal neurological signs are absent; meningismus may be present, and CSF studies do not show signs of meningoencephalitis. There are nonspecific EEG changes (generalized delta and theta wave activity). The pathogenesis of these syndromes is unclear. Their prognosis is poor if the underlying disease does not respond rapidly to treatment. Paraneoplastic encephalopathy occurs as a complication of neoplasms outside the central nervous system. It can only be diagnosed after the exclusion of local tumor invasion or metastasis, complications of tumor treatment, or other complications of the primary disease. For paraneoplastic encephalopathy, see Table 51, p. 388; for paraneoplastic disorders affecting the PNS, neuromuscular junction, and muscle, see p. 406.

Wernicke-Korsakoff syndrome. Wernicke encephalopathy is characterized by gaze-evoked nystagmus or dissociated nystagmus, ophthal-moplegia (abducens palsy, conjugate gaze palsy or, rarely, miosis), postural and gait ataxia, and impairment of consciousness (p. 116; apathy, indifference, somnolence). Korsakoff syndrome is characterized by confabulatory amnesia (p. 134), disorientation, and decreased cognitive flexibility. Most patients have a combination of these two syndromes, which is then called Wernicke-Korsakoff syndrome. Polyneuropathy, au-tonomic dysfunction (orthostatic hypotension, tachycardia, exercise dyspnea), and anosmia may also be present. These syndromes are caused by a deficiency of thiamin (vitamin B1) due to alcoholism or malnutrition (malignant tumors, gastroenterologic disease, thiamin-free parenteral nutrition). This, in turn, causes dysfunction of thiamin-dependent enzymes (increase in transketolase, pyruvate decarboxylase, a-ketoglutarate dehydrogenase, and serum py-ruvate and lactate; decrease in transketolase activity in erythrocytes). MRI reveals lesions in paraventricular areas (thalamus, hypothalamus, mamillary bodies) and periaqueductal areas (mid brain, motor nucleus of X, vestibular nu clei, superior cerebellar vermis). Treatment: Immediate intravenous infusion of thiamin (50100 mg) in glucose solution. Note: glucose infusion without thiamin in a patient with latent or unrecognized thiamin deficiency may provoke or exacerbate Wernicke encephalopathy.

Encephalopathies Due to Substance Abuse

Alcohol. Acute alcohol intoxication (drunkenness, inebriation) may be mild (blood alcohol 0.1-1.5% ^ dysarthria, incoordination, disinhibition, increased self-confidence, uncritical self-assessment), moderate (blood alcohol 1.5-2.5% ^ ataxia, nystagmus, explosive reactions, aggressiveness, euphoria, suggestibility), or severe (blood alcohol > 2.5% ^ loss of judgment, severe ataxia, impairment of consciousness, au-tonomic symptoms such as hypothermia, hypotension, or respiratory arrest). Concomitant intoxication with other substances (sedatives, hypnotics, illicit drugs) is not uncommon. The possibility of a traumatic brain injury (subdural or epidural hematoma, intracerebral hemorrhage) must also be considered. Pathological intoxication after the intake of relatively small quantities of alcohol is a rare disorder characterized by intense outbursts of emotion and destructive behavior, followed by deep sleep. The patient has no memory of these events. Alcohol withdrawal syndrome. Reduction of alcohol intake or total abstinence from alcohol after chronic alcohol abuse causes acute auton-omic disturbances (sweating, tachycardia, insomnia, nausea, vomiting), tremor, impairment of concentration, and behavioral changes. This initial stage of predelirium is followed by a stage of delirium (delirium tremens), in which all of the disturbances listed worsen and are accompanied by visual hallucinations. Epileptic seizures may occur. The course of delirium tre-mens can be complicated by systemic diseases that are themselves complications of alcoholism (hepatic and pancreatic disease, pneumonia, sepsis, electrolyte imbalances). Auditory alcoholic hallucinosis without autonomic symptoms or disorientation is an unusual form of alcohol withdrawal syndrome.

Microemboli in a patient with bacteremia (Staphylococcus aureus)

Microemboli in a patient with bacteremia (Staphylococcus aureus)

Acute Alcohol Withdrawal Symptoms
Acute alcohol intoxication (uncritical self-assessment, disinhibition)

» Decline of general health

> Loss of appetite, weight loss Gastrointestinal disturbances Behavioral changes

> Wernicke-Korsakoff syndrome Brain atrophy

Head trauma

Polyneuropathy

Myopathy

Additional intoxication with hypnotics or other substances

1 Epileptic seizures Predelirium/delirium Alcoholic hallucinosis

Alcoholic Hallucinosis

1 Epileptic seizures Predelirium/delirium Alcoholic hallucinosis

Alcoholic Dementia

Alcohol withdrawal syndrome

Chronic alcoholism

Alcoholism

Alcohol withdrawal syndrome

Late complications of alcoholism. Various disorders are associated with chronic alcohol abuse, though alcohol abuse may not be their only causative factor. Brain atrophy is often seen in CT or MRI scans and seems to be reversible by abstinence. In alcoholic dementia, brain atrophy is accompanied by cognitive impairment; most cases are probably due to Wernicke-Korsakoff syndrome (p. 312). Cerebellar atrophy predominantly affects the anterosuperior vermis (o postural and gait ataxia). Central pontine myelinoly-

sis (p. 310) and tobacco-alcohol amblyopia (bilateral impairment of visual acuity and visual defects, probably due to a combined deficiency of vitamins B1, B6, and B12) are other late complications of alcoholism. Fetal alcohol syndrome (congenital malformations, hyperactivity, attention deficit, impaired fine motor control) is seen in the children of alcoholic mothers. Substance abuse. Neurological signs of substance abuse are described in the table below.

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