Proton magnetic resonance spectroscopy during transient global amnesia.

There is uncertainty about the etiology of transient global amnesia and none of the pathogenetic hypotheses proposed so far, i.e. transient ischemia, epileptic discharge and spreading depression of cortical electrical activity, is completely satisfactory. Using water suppressed proton magnetic resonance spectroscopy we studied one patient during a typical episode of transient global amnesia and 2 weeks thereafter in order to investigate the metabolic changes in the hippocampal region. In both hippocampi, spectra of N-acetyl-aspartate, creatine-phosphocreatine, compounds containing choline and lactate failed to show changes consistent with cerebral ischemia, both in the acute phase and in the follow-up. Spreading depression in response to emotional stress seems a likely explanation in this patient, who suffered from migraine in the past.

Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions.

BACKGROUND AND PURPOSE: The purpose of the present study was to make an attempt to ascertain the etiology of transient global amnesia (TGA), which is still disputed more than 30 years after the first description of this clinical entity. METHODS: In a case-control study, we compared the prevalence of vascular risk factors in 64 TGA patients with 64 first-ever transient ischemic attack (TIA) control subjects and 108 normal community-based control subjects matched for age and sex. We prospectively studied the vascular events and mortality rates of the TGA cases and of the TIA control subjects. Then we compared the outcome of the two groups using actuarial analysis based on survival curves. RESULTS: We did not find evidence of an increased risk of TGA associated with any vascular risk factor. In contrast to TIA control subjects, no TGA patient suffered stroke, myocardial infarction, or TIA during the follow-up period. Migraine was more common in TGA patients than in both normal and TIA control subjects. In three patients (4.5%), the TGA was eventually considered to be of epileptic origin. CONCLUSIONS: The results of our case-control and longitudinal studies point to the conclusion that TGA and TIA do not share the same etiology. Since half of our patients had a precipitating event in their history, it is reasonable to hypothesize that spreading depression may play a role in TGA. The significant positive association between migraine and TGA may support this hypothesis. Epilepsy may mimic TGA in a minority of cases.

Acute encephalopathy and polyneuropathy after disulfiram intoxication.

A chronic alcoholic who had ingested a very high dose of disulfiram (29 g over a 1-week period) without simultaneous alcohol intake developed an acute encephalopathy and a severe flaccid tetraparesis that worsened over the course of several days, even after the intake of the drug had stopped. Recovery was both slow and incomplete. One year after intoxication, the patient still had distal weakness in the arms and legs, and hypesthesia in the hands and feet.

Immediate prognosis of primary intracerebral hemorrhage using an easy model for the prediction of survival.

We reviewed the medical records and CT scans of 138 patients hospitalized for spontaneous supratentorial hemorrhage and conservatively treated. Seventeen clinico-anamnestic variables and five CT desumed findings were collected. Using univariate analysis we found eight significant predictors of 30-day mortality: intraventricular spread (IVS) of blood, volume of the hemorrhage, Glasgow Coma Scale (GCS) score, midline shift, hyperglycemia, pupillary abnormalities, limb paresis and gaze deviation. With multivariate logistic regression analysis we found three independent predictors of 30-day mortality: IVS of blood, volume of the hemorrhage and GCS score. Using these three independent variables we developed an easy model which allows an immediate estimate of the probability of survival with a high degree of sensitivity and specificity.