Alan J. Tuchman

Central nervous system involvement in patients with acquired immune deficiency syndrome (AIDS)

ABSTRACT – Central nervous system involvement occurred in 28 of 121 patients with acquired immune deficiency syndrome (AIDS). The major risk factor in this AIDS population was intravenous drug abuse (64%). A neurologic symptom or disability was the principal reason for hospitalization in 16 cases (57%). Three patients had primary lymphoma of the brain and the remainder had opportunistic infections. Patients with focal neurological features usually had toxoplasmosis. Progressive headache and meningeal signs occurred with cryptococcosis. A progressive subacute dementia was probably due to cytomegalovirus. Other infections included atypical mycobacteria, candida, herpes zoster and possible progressive multifocal leukoencephalopathy.

Neurovascular complications of cocaine

Use of cocaine in the USA, has reached epidemic proportions since 1983, when “crack” was introduced, its higher potency compared with cocaine HCl has been associated with a tremendous increase in the incidence of strokes. This study reports our experience with 55 cases of neurovascular events (25 ischemic and 30 hemorrhagic) related to cocaine use in 54 patients. Only 15 patients had other risk factors for stroke. Twenty six patients smoked “crack”, 10 snorted cocaine and 12 injected it intravenously. Strokes occurred within 3 h of cocaine use in 15 patients with infarcts and 17 with hemorrhages. Ten infarcts occurred after an overnight binge. Of the hemorrhage group 9 were subarachnoid, 16 intracerebral (8 basal ganglia, 7 hemispheric and one brain stem) and 5 intraventricular. Computerized tomography (CT) showed an aneurysm of the anterior communicating artery, as well as one of the vein of Galen. Four aneurysms and 3 AVMs were identified on angiography. CT revealed 15 infarcts; it was normal in 7 patients with pure motor hemiparesis and in 3 with findings consistent with anterior spinal artery infarction. Several mechanisms may be responsible for the cerebrovascular complications. A sudden rise in systemic arterial pressure may cause hemorrhages, frequently in association with an underlying aneurysm or AVM. Vasospasm, arteritis, myocardial infarction with cardiac arrhythmias and increased platelet aggregation may provoke infarcts.

Central nervous system infarction related to cocaine abuse.

Background Cocaine use in the United States has reached epidemic proportions, and increased availability of “crack” since 1983 has noticeably increased the incidence of neurovascular complications. In this report, we examine the relationship between cocaine use and ischemic infarct. Summary of Comment This study reports 18 cases of ischemic cerebrovascular events, which occurred among 15 men and three women aged 21-47 years who were evaluated in a 2-year period. Clinical presentations include thirteen cases with hemispheric infarcts, two brain stem strokes, two anterior spinal artery infarcts, and one with both hemispheric and cerebellar infarcts. Nine patients smoked crack, four snorted cocaine, and three injected it intravenously. In two cases, the route of administration could not be determined. Two patients died, but the others survived with various degrees of neurological deficit. Conclusions Traditional risk factors for strokes were identified in only six patients, suggesting that these factors are not necessary for the occurrence of a cocaine-related infarct. Multiple overlapping mechanisms may be responsible, including vasospasm, sudden onset of hypertension, myocardial infarction with cardiac arrhythmias, increased platelet aggregation, and vasculitis.

Cocaine-related intracranial hemorrhage. Report of nine cases and review.

ABSTRACT— Nine cases of intracranial hemorrhages related to cocaine usage are presented. Another 5 cases from the literature are reviewed. The relationship between severe cocaine‐induced hypertension, and the development of subarachnoid or intracerebral hemorrhages is noted, and apparently is related to sudden transient increases of blood pressure related to cocaine use.

Amelioration of refractory dysesthetic limb pain in multiple sclerosis by gabapentin

Pain is a well-recognized and disabling symptom in patients with MS. In one large clinical series, 55% of MS patients experienced acute or chronic pain at some time during their illness.1 Chronic neuropathic pain syndromes, which include dysesthetic extremity pain (DEP), painful spasms due to spasticity, and paroxysmal tonic spasms, occur in as many as 48% of patients with MS.1 DEP in MS is particularly difficult to treat. Therapies for chronic DEP include amitriptyline, carbamazepine, phenytoin, and opiates; however, many patients do not receive complete pain relief or cannot tolerate these medications because of adverse effects.1 There is a need for more effective and better tolerated treatment for DEP in patients with MS. Gabapentin is a novel anticonvulsant agent that is effective as adjunctive therapy for partial seizures.2 There is anecdotal evidence that gabapentin may be helpful in the treatment of …

Rhabdomyolysis and hyperthermia after cocaine abuse: a variant of the neuroleptic malignant syndrome?

Rhabomyolysis with myoglobinuria has been added relatively recently to the neurologic complications associated with the increased use of cocaine and the introduction of its alkaloid form (crack). This retrospective study reports our experience with 14 patients who presented with rhabdomyolysis after cocaine use in a municipal hospital over a 3‐year period. Seven patients used “crack”, 2 intravenous and 3 nasal insufflation. All patients but one had hyperthermia, 11 altered mental status, 8 tachycardia, and 4 muscle rigidity. Nine developed renal failure; 3 of these patients died. Two other patients died of cardiorespiratory arrest. Cocaine‐related rhabdomyolysis has a high mortality. The observed association with hyperthermia and other central neurologic features resembles the neuroleptic malignant syndrome. Since chronic cocaine use may alter the availability of dopamine either through transmitter depletion or decrease in the number of dopamine receptors, a common pathogenetic mechanism is possible. However, other mechanisms, which are not mutually exclusive but rather frequently overlapping, may play an important role. These include agitation, hyperthermia, adrenergic overstimulation leading to vasoconstriction and ischemia or calcium release from the sarcoplasmic reticulum resulting in increased entry into the muscle cell leading to cell death; in addition, cocaine has direct toxic effect on the muscles.

Combination valproate—carbamazepine therapy in partial epilepsies resistant to carbamazepine monotherapy

Eighteen patients with poorly controlled partial epilepsy on carbamazepine monotherapy at maximum tolerated doses were treated with valproate adjunctive therapy. Both medications were maintained for at least 3 months at the highest tolerated doses. Three patients had >50% decrease in seizure frequency on bitherapy; six patients were moderately improved, with a 22–44% decrease in seizure frequency; the remaining nine patients were unchanged or worsened; with up to a 49% increase in seizure frequency. Five of six patients with more than four seizures per month improved on bitherapy. Four patients had a shift of predominant seizure type from tonic—clonic to complex partial; two of these patients were moderately improved and two had an overall increase in seizures. Clinical toxicity was common on bitherapy, managed by a reduction in carbamazepine dose in most patients. We conclude that valproate—carbamazepine bitherapy may be beneficial in approximately half of patients who have failed high-dose carbamazepine monotherapy; however, marked improvement is infrequent. Valproate—carbamazepine bitherapy is also frequently associated with clinical anticonvulsant toxicity at the beginning of bitherapy, but this is generally easily managed with medication adjustment.

Low amplitude EEGs in demented AIDS patients

We have observed an unusual low amplitude, slow and featureless electroencephalogram (EEG) pattern in some human immunodeficiency virus (HIV) infected patients without focal lesions on computerized tomography (CT scan) of the head. Out of 17 cases, 13 with AIDS and 4 with HIV positive status, 6 had low amplitude EEGs with slowing, all in the AIDS group. Nine of the 13 AIDS patients were demented, and 4 of these demented patients had slow verbal responses and mutism, indicating advanced HIV-related dementia. All 4 had low amplitude, slow EEGs. The patients with low amplitude, slow EEGs also had atrophy on CT scan by visual assessment and by measurement of ventricular indices. Of 17 age-matched controls referred for non-specific complaints such as headache and dizziness or for psychiatric disorders, 3 had EEGs read as low amplitude with slowing; two had normal mental status and one was psychotic. Although this EEG pattern is not etiologically specific, it may correlate with advanced dementia and atrophy on CT scan in AIDS patients.

Cocaine Causing Convulsions in a Large Municipal Hospital Population

We reviewed all cases with a diagnosis of convulsions admitted to a large municipal hospital in 1 year and determined which of these patients had an additional diagnosis of ongoing cocaine use. Of 795 patients with convulsions, 29 also had a diagnosis of active cocaine use (4%). On review of these cases, only 4 (0.5%) were determined by history to possibly show a causal relationship between cocaine use and convulsions. On review of 22 cases of convulsions related to cocaine use over the past 4 years, 9 were found to have multiple convulsive episodes related to cocaine. Our findings suggest that cocaine is an infrequent cause of seizures in a city hospital population. However, there is a small number of patients in whom cocaine is apparently highly proconvulsant.

Recurring Strokes with Repeated Cocaine Use

Cerebral infarctions or subarachnoid hemorrhages have been described in association with cocaine use. We describe a patient who initially developed a subarachnoid hemorrhage following cocaine use, due