Search

Introduction: Botulism is a potentially fatal infectious disease induced by a neurotoxin secreted by Clostridium botulinum, a sporulated species of obligate anaerobic bacteria. This neurotoxin inhibits the normal release of acetylcholine in the synaptic cleft, inducing presynaptic neuromuscular blockade. The diagnosis is often difficult because of the range and the lack of specificity of the symptoms., Case: We report two cases of human botulism. The first case was easy to diagnose, with dysphagia, dysphonia, blurred vision, and xerostomia, associated with potentiation on electromyogram and B botulinum toxin in the serum. Symptoms in the second case included diplopia, blurred vision, dysphagia, dysphonia, with potentiation on electromyogram but no botulinum toxin., Discussion: These two cases remind us of the necessity to keep botulism in mind when systemic atropinic symptoms are found together with generalized, progressive and extensive paralysis. The diagnosis is confirmed by electromyogram and serology. There is no specific treatment for botulism; only intensive care surveillance and symptomatic treatment improve survival.

The development of several population stroke registries has improved our knowledge of the epidemiology of strokes, their natural history, and their trends over time and place. In Europe, stroke incidence decreases from east to west and from north to south. Incidence and mortality have also been decreasing regularly over time. The diagnostic tools created with the arrival of computed tomography (CT), magnetic resonance imaging (MRI), and other forms of vascular and cardiac imaging have improved the identification of risk factors for stroke according to its mechanism--hemorrhagic or ischemic--and according to the subtype of ischemic stroke. Hypertension is the leading risk factor for both ischemic and hemorrhagic strokes. New independent stroke risk factors have been confirmed, including elevated cholesterol and homocysteine levels. The regular decline of the incidence of some types of stroke and of mortality is partly due to the positive effects of prevention and confirms the usefulness of screening and early treatment of stroke risk factors. Development of new treatments during the acute phase and in the field of primary and secondary stroke prevention (such as statins) is necessary to improve prognosis, which remains too serious, especially in women.

Little is known about 5-hydroxyindolacetic acid (5-HIAA) and homovanillic acid (HVA) levels in cerebrospinal fluid of patients with Delirium Tremens revealed at onset by seizures. The aim of the study is to understand the biochemical abnormalities induced by seizures in the cerebrospinal fluid of patients involved by Delirium Tremens. Nine patients 42-62 years of age, who had experienced a Delirium Tremens after alcohol withdrawal, with one or two seizures at onset, were included in this study. The lumbar puncture (and a CT scan) were performed after the last seizure. Nine patients with neither Delirium Tremens nor seizure, needing a lumbar puncture for their medical problem, were matched by sex and by age. For the measures of 5-HIAA and HVA, we systematically took the first cm3. The mean value of 5-HIAA levels were 12.70 ng ml(-1) in the group of nine patients with Delirium Tremens versus 13.45 ng ml(-1) in the control group. The mean value of HVA levels were 19.81 ng ml(-1) in the group of nine patients with Delirium Tremens versus 25.25 ng ml(-1) in the control group. The differences were not statistically significant. During a Delirium Tremens with seizure at onset, there are no statistically significant changes in 5-HIAA and HVA levels in the cerebrospinal fluid. Our work raises the question of the role of Delirium Tremens in the normalization of the levels of neuro-mediators that usually decrease soon after seizures.