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Argentina is facing an increase in cocaine use by adolescents and young adults from every socioeconomic background. It is calculated that up to 10% of all cocaine passing through this country is locally sold and consumed. Nevertheless, local information describing common cocaine-related neurological events is scarce. From August 1988 to March 1993, 13 patients were evaluated with neurological disease associated with cocaine abuse. Among these 13 patients (Table 1), the mean age was 29; 70% were men. Patients most commonly used the nasal route (snorting). Concomitant abuse of other intoxicants, especially alcohol, was frequent (85%). The major neurological complications included one or more seizures (n = 7), ischemic stroke (n = 2) (Fig. 1-2), hemorrhagic stroke (n = 2) associated with arteriovenous malformation (Fig. 3a-b), memory disturbances (n = 1) and paroxysmal dystonia (n = 1). Psychiatric complaints were present in all patients. Mortality was not observed. There was no correlation between the appearance of complications and the amount of cocaine used, or prior experience with this drug. Only one of the 7 patients with seizures had a previous history of seizures. All had generalized tonic-clonic seizures, and one had concomitant absence episodes. Cocaine modulates central neurotransmitters and has direct cerebrovascular effects. The neurological complications appear to be related to cocaine hyperadrenergic effects, striatal dopaminergic receptor hypersensitivity and perhaps vasculitis. Structural changes in the brain of long-term cocaine abusers could explain the persistence of neurologic symptoms after drug withdrawl.

A 39 year old man presenting multifocal demyelinating neuropathy (MFDN) is reported. Fifteen days before onset he had been vaccinated with 75 IU of tetanus toxoid. Although recent histories of vaccination or viral infection support the immunological hypothesis proposed for chronic acquired demyelinating neuropathies (CADN) it is reported for the first time in MFDN, suggesting that MFDN and CADN may share common pathophysiological mechanisms.

Clinical and neurophysiological examination was performed in 35 normal aged subjects (72 +/- 6.4; range 65-86 years). Seventeen showed abnormal ankle reflex (48.6%), one case had patellar areflexia as well (2.9%), six had malleolar appalesthesia (17%), and five revealed both areflexia and apallesthesia (14%). Electromyography and motor conduction were normal in every case. Sural nerve conduction velocity and the amplitude of the sensory evoked potential showed no differences between subjects with and without clinical abnormalities. It is concluded that a) reflex and vibration sensibility changes in the elderly are not consequence of peripheral nerve involvement and b) there is no reason to believe there is an "aging neuropathy".