Arch Neurol Chicago
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Arch Neurol Chicago · Jan 1985
Vertebrobasilar transient ischemic attacks in internal carotid artery occlusion or tight stenosis.
We studied 12 patients with internal carotid artery (ICA) occlusion or tight stenosis but without vertebrobasilar and subclavian atherosclerosis who suffered vertebrobasilar insufficiency (VBI). The patients with ICA occlusion were compared with a sex- and age-matched control group that had ICA occlusion but no VBI. ⋯ These facts suggested hemodynamic disturbances with "steal VBI." In ICA tight stenosis, VBI symptoms disappeared after endarterectomy but persisted in patients with more than 50% stenosis; this was also suggestive of hemodynamic VBI. Vertebrobasilar insufficiency had a prognostic significance, being associated with an increased occurrence of delayed stroke.
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We reviewed 317 patients with multiple sclerosis (MS) and found that the incidence of clinically significant pain, excluding headache and paresthesia, was 28.8%. Successful treatment requires recognition of the pathophysiology of the pain syndromes encountered in MS. Antidepressant drugs have been of particular value in the treatment of chronic pain in these patients.
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Arch Neurol Chicago · Nov 1984
Trigeminal neuralgia. Current concepts regarding etiology and pathogenesis.
There has long been a controversy over the cause of trigeminal neuralgia. Most clinical data favor a peripheral cause. However, most of the experimental data tend to favor a central mechanism. ⋯ The most plausible hypothesis to reconcile all of these observations is that trigeminal neuralgia has a peripheral cause and a central pathogenesis. Chronic irritation of the trigeminal nerve apparently leads to both a failure of segmental inhibition in the trigeminal nucleus, and ectopic action potentials in the trigeminal nerve. This combination of increased firing and impaired efficiency of inhibitory mechanisms leads to paroxysmal discharges in the trigeminal nucleus, which are perceived as attacks of trigeminal neuralgia when they involve nociceptive trigeminothalamic-relay neurons.
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Arch Neurol Chicago · Oct 1984
Case ReportsAtaxic hemiparesis from small capsular hemorrhage. Computed tomography and somatosensory evoked potentials.
We studied three cases that fit the clinical syndrome of ataxic hemiparesis. Computed tomography revealed small hemorrhages of the posterior limb of the internal capsule in all the cases, and somatosensory evoked potential studies predicted a disturbance of the lemniscal pathway from the thalamus to the parietal sensory cortex without demonstrable sensory loss. These results suggested that ataxia of the contralateral limbs following capsular lesion might result from a disruption of the thalamocortical sensory projection. The site of the lesion, the pathologic cause, and the underlying mechanism of ataxia are not necessarily homogeneous within the syndrome.
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Twenty-one episodes of status epilepticus (SE) were each treated with 1 to 9 mg (mean, 4 mg) of intravenous lorazepam. All patients with generalized tonic-clonic ( GTC ) SE responded within 15 minutes. Nine (82%) of the 11 patients with episodes of partial SE with altered responsiveness responded poorly. ⋯ Generalized tonic-clonic SE was transformed into partial SE with altered responsiveness in three patients. In an additional four patients, marked lethargy developed. Lorazepam appears effective in controlling GTC SE but only occasionally effective in partial SE with altered responsiveness.