Neurotoxicology

Published on 14/05/2017 by admin

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Last modified 14/05/2017

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E. Lee Murray, MD

OVERVIEW

Toxin exposure is a common reason for a ED visit, and although most of these are managed by emergency physicians and internists, neurologists are sometimes called on to assist with selected toxin exposures. Prescription medications and household chemicals are common causes of toxic neurologic symptoms, some acute, some insidious. Here, we focus on some of the most important toxic exposures, selected by virtue of frequency or severity.

PRESCRIPTION MEDICATIONS

A list of medications with potential neurologic toxicity is far beyond the scope of this book, but a brief synopsis of some of the most important is discussed. It is sometimes difficult to distinguish between idiosyncratic effect, hypersensitivity, allergy, and dose-dependent toxicity, so some of these are blended in this discussion. The neurologic toxicity of some common medications includes:

Anticonvulsants

Sedation: Many

Exacerbation of seizures: Several, especially carbamazepine.1

Hyponatremia: especially carbamazepine and oxcarbazepine.

Neuroleptics

Acute dystonic reaction: Many

Tardive dyskinesia: Many, less for atypical neuroleptics

Neuroleptic malignant syndrome: Many

Parkinsonism: Especially typical neuroleptics

Antidepressants

Seizures

Headaches

Orthostatic hypotension

Confusion

Amiodarone

Tremor: Most common neurological complication, postural and intention2

Parkinsonism: Uncommon3

Baclofen

Encephalopathy: Can be profound

Antidepressants are associated with a variety of neurologic complications; however, they are overrepresented even in patients who are not treated.4

ETHANOL AND OTHER ALCOHOLS

Alcohol intoxication is usually presumed to be ethanol, but this term includes others, especially isopropanol, methanol, and ethylene glycol. This section will focus on ethanol with subsequent brief discussions of the other alcohols.

Ethanol

Hospital neurologists see the spectrum of ethanol effects from acute intoxication to chronic neuronal degeneration to neurologic manifestations of liver failure. The list presents some of the important syndromes resulting in neurologic consultation:

Acute intoxication

Hepatic failure: Chapter 11

Wernicke-Korsakoff syndrome: Chapter 29

Ethanol withdrawal

Cerebellar degeneration

Optic neuropathy

Central pontine myelinolysis (CPM): Chapter 13

Optic neuropathy

Neuropathy

Myopathy

Ethanol Intoxication

Ethanol intoxication manifests a range of symptoms that depend on individual susceptibilities and metabolism. Levels that are well-tolerated by some may produce severe intoxication in others. Chronic ethanol use can produce neuronal degeneration directly and/or manifest neurologic symptoms through coexistent nutritional deficiency.

PRESENTATION may be excitatory or depressive. Patients may have agitation, excitement, and enhanced loquaciousness. Alternatively, they may be lethargic or somnolent. There may be cognitive dysfunction with disinhibition progressing to confusion, stupor, and even coma. Motor manifestations are most commonly dysarthria and gait ataxia. Rare complications are acute psychosis and “blackouts”—epochs for which the patient is amnestic.

DIAGNOSIS is suspected with the clinical presentation of cognitive and behavioral deficits with ataxia and dysarthria. Clinicians usually notice the typical breath of ethanol intoxication. Confirmation is by documentation of elevated ethanol levels. Note that identification of ethanol intoxication does not rule out coexistent disorder so computed tomography (CT) should be performed if the symptoms are out of proportion to the ethanol level or if there are clinical signs of head injury, mental status changes, focal deficits, or seizures.

MANAGEMENT begins with supportive care for most patients. Hemodialysis is considered for refractory patients and those with extremely high ethanol levels.

Ethanol Withdrawal

Ethanol withdrawal can cause an array of neurologic manifestations. Timing of onset depends on the manifestation. Persistent intake and abrupt withdrawal can begin to produce symptoms within 6 hours, whereas delirium tremens (DTs) has an onset 48–72 hours later.

PRESENTATION begins in about 6 hours with mild tremor, the “morning shakes.” With progressive time and severity, progression through delirium to DTs can occur. Symptoms of ethanol withdrawal are summarized here:

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