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Over a 24-month period we evaluated 14 patients with neurologic disease associated with cocaine abuse. Five patients developed previously unreported complications: anterior spinal artery syndrome, lateral medullary syndrome, transient ischemic attacks in the middle cerebral artery and vertebrobasilar artery territories, and partial motor seizures. The recent availability of crack has led to a great increase in neurologic problems associated with the use of this drug.

This article has emphasized a basic approach to coma. First, the patient must have airway, breathing, and circulation protected. If the etiology of coma is in doubt, a broad metabolic screen is necessary. Table 5 demonstrates the major differences between structural and metabolic coma. Usually, history alone is sufficient to make an accurate diagnosis. If history or neurologic examination suggests a structural cause for the coma, then a cranial CT scan is mandatory. An electroencephalogram is often helpful, particularly in metabolic coma, and at times may even show structural abnormalities not demonstrated by CT scan. Rapid assessment and treatment is critical because coma is the clinical manifestation of brain failure, and often irreversible injury will occur if treatment is slow or incorrect.

A case presenting with headaches, organic dysfunction with visual hallucinations, and incontinence of urine, all of two days' duration is described here. EEG obtained on the fourth hospital day showed right-sided PLEDS and on the fifth hospital day a generalized seizure occurred. The other clinical and laboratory data led to a diagnosis of bilateral subdural hematomas. The patient recovered following surgical treatment. No etiologic factor other than the subdural hematomas was found to explain the PLEDS. Possible mechanisms of pathophysiology are discussed.

Gas chromatography-mass spectrometry (GC-MS) is a technique especially suitable for the analysis and characterization of steroids, and its power has been extensively demonstrated. The efficacy of GC-MS is limited, nevertheless, by the fact that steroid mixtures - whether of natural origin only, or augmented by synthetic analogs - often contain similar components that are poorly distinquished. The fortuitous overlap of gas chromatographic peaks from disparate compounds also impairs the definition of retention data. Controlled modification of the sample by means of selective reactions is therefore a valuable adjunct to the application of GC-MS. Two examples are discussed: (a) the enzyme cholesterol oxidase, isolated from various microorganisms, catalyzes the oxidation of many 3 beta-hydroxy-5-enes (with concomitant isomerization) to 4-en-3-ones; 3 beta-hydroxy-5 alpha-steroids are also oxidized to the corresponding 3-ones, but other steroids (3 alpha-hydroxy- or 5 beta-isomers, etc.) are unaffected. The mild conditions required (pH 7, 30 C) are advantageous for the analysis of sensitive steroids, and the retention index increments, as well as the mass spectra of the ketones, are characteristic. The enzyme accepts as substrates a wide range of 3 beta-hydroxysteroids, tolerating oxygenation in ring B and even catalyzing the oxidation of 2-oxacholesterol to the expected lactone; and (b) Steroids possessing 1,2-diol or 1,3-diol groupings include estriols, 2-hydroxyestrone, 20,22-dihydroxycholesterols, ecdysones, brassinolide and many corticosteroids. The selective formation of cyclic derivatives can provide several analytically useful features, such as convenient retention times, moderate mass increments (24 amu for a methaneboronate), distinctive mass spectra and usually abundant molecular ions. These are exemplified for 5-pregnene-3 beta, 20,21-triols and for 20,22-dihydroxycholesterol as well as its enzymic oxidation product.

If cerebellar Purkinje cells function in a manner so as to terminate at least some types of seizures or to prevent their clinical development then loss of Purkinje cells should predispose to the prolonged or continuous occurance of these seizures. This study presents clinical data that may document such an instance and cites the supporting experimental data.

This article discusses identification of different types of seizures seen in all age groups, their differential diagnosis, clinical features and management. Guidelines for anticonvulsant therapy are included.

Electroencephalographic (EEG) frequency analysis and evoked potentials (EPs) of 27 hyperactive children were examined to determine which, if any, of these electrophysiological parameters might be useful for the selection of those children likely to respond to stimulant medication. The children were treated with placebo, d-amphetamine, and l-amphetamine in double-blind fashion and in random order. EEGs for frequency analysis, visual EPs, and auditory EPs were obtained before and during treatment. Off medication, hyperactive responders to amphetamine had higher predominant beta frequency and shorter latencies of some EP waves than did nonresponders. Although the findings reported here would not select all responders, they would allow the exclusion of most nonresponders.

Six New Zealand White rabbits (5 females and 1 male) were anesthetized with a combination of xylazine (4.3 mg/kg of body weight) and ketamine (29.1 mg/kg) administered IM. The rabbits were then attached to instruments that continuously monitored blood pressure and electrocardiographic and electroencephalographic values. Each rabbit was then administered a lethal dose of ketamine (600 mg, IV). Within 90 seconds after injection of the ketamine, brain death developed and the heart rate and blood pressure decreased greatly. Circulatory activity persisted for a maximum of 240 seconds. This method of euthanasia did not result in histopathologic changes in tissue specimens evaluated. Although death occurred rapidly, extensive muscle contractions made euthanasia of rabbits with ketamine aesthetically unacceptable. Therefore, this method would not be a suitable means of euthanasia for routine use in rabbits.