Acute withdrawal: diagnosis and treatment.

Symptoms of alcohol withdrawal range in severity from mild "hangover" to fatal delirium tremens (DTs). Tremor, hallucinosis, and seizures usually occur within 48 hours of abstinence. Seizures tend to be generalized without focality, occurring singly or in a brief cluster, but status epilepticus is not unusual. DTs usually appears after 48 hours of abstinence and consists of marked inattentiveness, agitation, hallucinations, fluctuating level of alertness, marked tremulousness, and sympathetic overactivity. The mainstay of treatment for alcohol withdrawal is benzodiazepine pharmacotherapy, which can be used to control mild early symptoms, to prevent progression to DTs, or to treat DTs itself. Alternative less evidence-based pharmacotherapies include phenobarbital, anticonvulsants, baclofen, gamma-hydroxybutyric acid, beta-blockers, alpha-2-agonists, and N-methyl-d-aspartate receptor blockers. Treatment of DTs is a medical emergency requiring heavy sedation in an intensive care unit, with close attention to autonomic instability, fever, fluid loss, and electrolyte imbalance. Frequent comorbid disorders include hypoglycemia, liver failure, pancreatitis, sepsis, meningitis, intracranial hemorrhage, and Wernicke-Korsakoff syndrome.

Neurologic complications of illicit drug abuse.

PURPOSE OF REVIEW: This review familiarizes clinicians with the symptoms of overdose and withdrawal, as well as neurologic complications, associated with particular illicit drugs. RECENT FINDINGS: Recent arrivals on the recreational drug scene include synthetic cathinone analogs, synthetic cannabinoid agonists, and a variety of novel hallucinogens. SUMMARY: Clinicians need to be aware of neurologic disorders associated with particular illicit drugs and should consider drug abuse in any patient with unexplained symptoms and signs.In addition to tobacco and alcohol, a large number of substances, legal and illegal, are used recreationally. Broad categories include opioids, psychostimulants, marijuana and related agents, sedatives, hallucinogens, inhalants, phencyclidine and related agents, and anticholinergics. Each type of agent has its own characteristic symptoms of overdose and withdrawal, and many agents are associated with trauma, infection, seizures, stroke, cognitive impairment, and teratogenicity. Some drugs have unique neurologic complications not encountered with other agents. A history of recreational drug use should be sought in any neurologic patient regardless of age or socioeconomic status.

Systematic review: efficacy and safety of medical marijuana in selected neurologic disorders: report of the Guideline Development Subcommittee of the American Academy of Neurology.

OBJECTIVE: To determine the efficacy of medical marijuana in several neurologic conditions. METHODS: We performed a systematic review of medical marijuana (1948-November 2013) to address treatment of symptoms of multiple sclerosis (MS), epilepsy, and movement disorders. We graded the studies according to the American Academy of Neurology classification scheme for therapeutic articles. RESULTS: Thirty-four studies met inclusion criteria; 8 were rated as Class I. CONCLUSIONS: The following were studied in patients with MS: (1) Spasticity: oral cannabis extract (OCE) is effective, and nabiximols and tetrahydrocannabinol (THC) are probably effective, for reducing patient-centered measures; it is possible both OCE and THC are effective for reducing both patient-centered and objective measures at 1 year. (2) Central pain or painful spasms (including spasticity-related pain, excluding neuropathic pain): OCE is effective; THC and nabiximols are probably effective. (3) Urinary dysfunction: nabiximols is probably effective for reducing bladder voids/day; THC and OCE are probably ineffective for reducing bladder complaints. (4) Tremor: THC and OCE are probably ineffective; nabiximols is possibly ineffective. (5) Other neurologic conditions: OCE is probably ineffective for treating levodopa-induced dyskinesias in patients with Parkinson disease. Oral cannabinoids are of unknown efficacy in non-chorea-related symptoms of Huntington disease, Tourette syndrome, cervical dystonia, and epilepsy. The risks and benefits of medical marijuana should be weighed carefully. Risk of serious adverse psychopathologic effects was nearly 1%. Comparative effectiveness of medical marijuana vs other therapies is unknown for these indications.

Spice, pot, and stroke.

The endocannabinoid system includes 2 types of G-protein coupled receptors: CB1 (mostly in the brain) and CB2 (in peripheral lymphoid tissue). The major cannabinoid ligands are arachidonylethanolamine ("anandamide," the Sanskrit word for bliss) and 2-arachidonylglycerol ("2AG"). It is by binding to CB1 receptors that δ-9-tetrahydrocannabinol (THC), the principal psychoactive ingredient in marijuana ("pot"), produces its intended subjective effects.

Substance abuse and movement disorders.

An array of movement disorders is associated with ethanol, illicit drugs, and tobacco. Heavy ethanol users experience withdrawal tremor and, less often, withdrawal parkinsonism, chorea, and myoclonus. Asterixis is a feature of hepatic failure. On the other hand, ethanol can ameliorate essential tremor and myoclonus-dystonia. Among opioid drugs, meperidine can precipitate myoclonus. Severe parkinsonism affected users of a synthetic meperidine analog contaminated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Spongiform leukoencephalopathy, sometimes with chorea and myoclonus, occurred in inhalers of heroin vapor (chasing the dragon). Psychostimulants including cocaine acutely cause stereotypies and dyskinesias. Phencyclidine toxicity causes myoclonus. Tobacco use, on the other hand, protects against Parkinson's disease. Clinicians need to consider substance abuse in patients with unexplained movement disorders.

Ethanol and cognition: indirect effects, neurotoxicity and neuroprotection: a review.

Ethanol affects cognition in a number of ways. Indirect effects include intoxication, withdrawal, brain trauma, central nervous system infection, hypoglycemia, hepatic failure, and Marchiafava-Bignami disease. Nutritional deficiency can cause pellagra and Wernicke-Korsakoff disorder. Additionally, ethanol is a direct neurotoxin and in sufficient dosage can cause lasting dementia. However, ethanol also has neuroprotectant properties and in low-to-moderate dosage reduces the risk of dementia, including Alzheimer type. In fetuses ethanol is teratogenic, and whether there exists a safe dose during pregnancy is uncertain and controversial.

Seizures, illicit drugs, and ethanol.

Recreational substance users are at risk for seizures by indirect mechanisms, including cerebral trauma, central nervous system infection, ischemic and hemorrhagic stroke, and metabolic derangements such as hypoglycemia, hypocalcemia, and renal failure. Drugs and ethanol can also cause seizures more directly, either as a feature of intoxication (eg, psychostimulants) or of withdrawal (eg, sedatives, including ethanol). In any patient with a seizure, clinicians should consider illicit drug or ethanol use. Seizures in known alcoholics or illicit drug users require workup to exclude treatable coexisting conditions.

The association of race and sex with the underuse of stroke prevention measures.

BACKGROUND: Underuse of effective stroke prevention measures has been demonstrated in the general population. Blacks and Hispanics are at increased risk of recurrent stroke relative to white non-Hispanics. More profound underuse of prevention measures may contribute to this disparity. In this study we attempted to compare the degree of underuse of diagnostic and treatment strategies in patients of these racial/ethnic groups with recent ischemic stroke. METHODS: At 4 participating urban hospitals, patient charts were reviewed with regard to the completeness of the diagnostic evaluation, discharge treatment regimen, and stroke risk factor and antithrombotic medication use at 6 months postdischarge. RESULTS: Of 501 patients hospitalized with acute ischemic stroke, almost all received electrocardiograms and brain imaging, 75% had carotid artery evaluations, and 70% had serum lipid determinations. Blacks and women were less likely to have complete evaluations. At discharge, 88% of patients received antithrombotic medications and 89% of patients were prescribed antihypertensive medications appropriately, but only 65% were prescribed lipid-lowering medications appropriately, with blacks least likely to receive appropriate prescriptions. At 6 months poststroke, of the 200 patients with data available for evaluation, 72% exhibited underuse of at least one stroke prevention measure. Blacks (81.6%) were more likely to experience underuse than Hispanics (62.5%) or whites (66.7%). Women were more likely to receive incomplete inhospital evaluations and discharge regimens. CONCLUSIONS: There is clinically important underuse of effective diagnostic and prevention measures in each of the groups studied, especially among blacks.

A 74-year-old man with memory loss and neuropathy who enjoys alcoholic beverages.

Adverse effects of alcohol on the peripheral and central nervous system can be direct (ie, neurotoxicity) or indirect (eg, nutritional deficiency). Using the case of Mr E, an older, moderate to heavy drinker experiencing memory difficulty, the diagnostic considerations, which include mild cognitive impairment, early Alzheimer dementia, Wernicke-Korsakoff syndrome, and "alcoholic dementia," are discussed. These disorders are not mutually exclusive, and in a patient with either mild cognitive impairment or dementia, the contributory role of alcohol can be difficult to determine. In fact, epidemiological studies suggest that mild to moderate intake of alcohol actually reduces the risk of developing mild cognitive impairment or dementia, including Alzheimer dementia. Appropriate management includes measures to reduce alcohol dependence (eg, behavioral or pharmacological therapy) and to delay progression of the cognitive impairment (eg, engaging in healthy behaviors such as cognitive leisure activities).

Seizures and substance abuse: treatment considerations.

Seizures often occur in substance abusers. The mechanism may be indirect (CNS infection, cerebral trauma, stroke, metabolic derangement) or direct (intoxication or withdrawal). These mechanisms are not mutually exclusive. A patient with obvious overdose or abstinence symptoms might also have meningitis or an acute subdural hematoma, and a polydrug abuser might be simultaneously intoxicated by one drug while withdrawing from another. Management of such patients often requires much more than simple administration of an anticonvulsant medication. Medical and surgical emergencies must be identified and nonconvulsive signs of intoxication and withdrawal must be addressed. A basic principle in treating drug withdrawal is to use an agent from the same pharmacologic class or one with a degree of cross-tolerance. Long-term anticonvulsant prophylaxis is usually not indicated when drug intoxication or withdrawal is the sole cause of a seizure.