Nimodipine is a 1,4-dihydropyridine derivative that shows a preferential cerebrovascular activity in experimental animals. Clinical data suggest that nimodipine has a beneficial effect on the neurologic outcome of patients suffering an acute ischemic stroke. Our double-blind placebo-controlled multicenter trial was designed to assess the effects of oral nimodipine on the mortality rate and neurologic outcome of patients with an acute ischemic stroke. One hundred sixty-four patients were randomly allocated to receive either nimodipine tablets (30 mg q.i.d.) or identical placebo tablets for 28 days. Treatment was always started <48 hours after the acute event. The Mathew Scale, slightly modified by Gelmers et al, was used for neurologic assessment. Mortality rate and neurologic outcome after 28 days were used as evaluation criteria. We considered 123 patients to be valid for the analysis of efficacy. Mortality rates did not differ significantly between groups. Neurologic outcome after 28 days of therapy did not differ between groups. However, when only those patients most likely to benefit from any intervention (Mathew Scale sum score of <65 at baseline) were analyzed separately in post hoc-defined subgroups, the nimodipine-treated subgroup showed a significantly better neurologic outcome. This result suggests that some patients with acute ischemic stroke will benefit from treatment with nimodipine tablets.
The three volumes (38, 28, and 20 ml) of mepivacaine 10 mg x ml(-1) ensured a similar and high percentage of complete sensory blocks in axillary brachial plexus anaesthesia with nerve stimulation involving the location of four motor responses.
Meningovascular neurosyphilis (MN) is an unusual cause of stroke in young adults. The clinical manifestations include prodromal symptoms weeks or months before definitive stroke. The diagnosis is based on clinical findings and examination of the serum and cerebrospinal fluid. We report a case of MN with basilar artery irregularities demonstrated by magnetic resonance angiography.
Ataxic hemiparesis with cerebellar-like features has been reported following infarction or hemorrhage of the thalamus. We describe five patients with incoordination and corticospinal tract signs in the limbs opposite a dorsolateral thalamic hemorrhage. In four patients the hemorrhage extended superiorly into the lateral ventricle, the adjacent paraventncular region, and the upper and medial parts of the posterior limb of the internal capsule. Instead of cerebellar dysfunction, these patients exhibited directional errors of movement that improved distinctly when performed under visual guidance. We explain the incoordination on the basis of conscious deep sensory loss in the involved limbs. Perception of light touch, painful pinprick, and temperature were preserved in all patients. We use the term "sensory ataxic hemiparesis" to distinguish these patients from those with "classic" ataxic hemiparesis and cerebellar-like features, a distinction that may be important when planning functional rehabilitation. (Stroke 1990;21:1749-1753)
A previously healthy man developed an acute encephalopathy with coma after a single wasp sting on his chin. Brain CT showed bilateral pallidostriatal radiolucencies. He died 72 hours after the sting with no evidence of primary cardiorespiratory failure or allergic reaction. Pathological findings were bilateral pallidostriatal necrosis and diffuse neuronal damage in the frontal, temporal, and parietal cortex. The neurotoxic effect of the poison, together with a hypersensitivity are the most likely explanations for this unusual encephalopathy. eral decerebrate rigidity. Tendon jerks were brisk and symmetric. The rest of the physical examination was normal except for an axillary temperature of 38°C. The blood count and electrolytes, blood clotting tests, and serum creatinine, glucose, creatine phosphokinase, lactic acid, pyruvic acid, transaminases, and variables in urine were within normal limits. An ECG chest radiograph, cerebral CT, and CSF were all normal. Repeated CT 48 hours after the sting showed low density of both lenticular nuclei, most pronounced in the left globus pallidus ( figure, A). The patient died suddenly 72 hours after the sting with no signs at any time of cardiorespiratory failure or metabolic derangements.A full necropsy was carried out immediately after death. The abnormal pathological findings were confined to the cerebrum. No other organ showed lesions that could indicate a hypersensitivity reaction, such as oedema, collections of eosinophils, or mastocytes in the skin and lungs, or bronchospasm. The brain weighed 1430 g and had been fixed in 10% formaldehyde for several weeks before detailed examination. Tonsillar hemiation was found. Before dissection it was noted that the brain had a softer consistency than normal. Macroscopically there were bilateral cavitations of the globus pallidus and softening of the putamen and caudate nuclei (figure, B). Histologically the globus pallidus was completely destroyed. The neurons of the putamen, caudate nucleus and frontal, parietal and temporal cortex were shrunken, with eosinophilic cytoplasm and pyknotic nuclei. The frontal, parietal, and temporal cortex showed vacuolation, spongiform changes, and eosinophilic shrunken neurons. The subcortical white matter underlying the damaged areas of the cortex showed pallor of the myelin. Capillaries were congested in the damaged areas and contained numerous polymorphonuclear leucocytes in Virchow Robin's space, which also invaded the neighbouring parenchyma at some points. There were no capillary proliferations or lymphoplasmocytic infiltrates. The occipital cortex and the hippocampus were undamaged, as were the thalamus, midbrain, pons, medulla oblongata, cerebellum, mamillary bodies,
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