Two hundred and twenty nine patients with generalised tonic-clonic seizures were prospectively evaluated. Fourteen were identified who had transient focal neurological deficits thought to be Todd's post-epileptic paralysis (PEP). Eight of these 14 patients had underlying focal brain lesions associated with the postictal deficits. All patients with PEP were weak, but there was wide variation in the pattern (any combination of face, arm, leg), severity (plegia to mild), tone (spastic, flaccid, or normal), and reflexes (increased, decreased, or normal). Significant sensory loss occurred in only one patient. The only other signs of PEP were aphasia (in five patients all with underlying lesions) and gaze palsy (in four patients). Post-epileptic paralysis persisted from halfan hour to 36 hours (mean of 15 hours). Post-epileptic paralysis may occur with the first seizure or after many years of seizures and does not appear after every seizure. The clinical features of PEP are thus heterogeneous.
We found Cop 1 to be effective and relatively safe in a previous (exacerbating-remitting) clinical trial. This current trial involves 106 chronic-progressive patients. The major end point, confirmed progression of 1.0 or 1.5 units (depending on baseline disability) on the Kurtzke Expanded Disability Status Scale, was observed in nine (17.6%) treated and 14 (25.5%) control patients. The differences between the overall survival curves were not significant. Progression rates at 12 and 24 months were higher for the placebo group (p = 0.088) with 2-year probabilities of progressing of 20.4% for Cop 1 and 29.5% for placebo. We found a significant difference at 24 months between placebo and Cop 1 at one but not the other center. Two-year progression rates for two secondary end points, unconfirmed progression, and progression of 0.5 EDSS units, (p = 0.03) are significant.
Coronary artery disease is the cause of death in most patients who have transient ischemic attacks or stroke. Evaluation for this condition is not routinely performed in such patients, and no prospective studies have been reported. We prospectively examined 50 consecutive patients with transient ischemic attacks or mild stroke to determine the prevalence and importance of coronary artery disease. All patients were examined by a cardiologist and underwent both exercise thallium-201 scintigraphy and exercise radionuclide ventriculography. Sixteen patients were suspected to have coronary artery disease on the basis of clinical evaluation. In 15 of these the was confirmed by the nuclear scans. The remaining 34 patients had no clinical evidence of heart disease, yet 14 had abnormal cardiac scans. Twenty of 22 patients with abnormal scans who underwent cardiac catheterization had significant coronary artery disease or a cardiomyopathy. The discovery of heart disease altered clinical management in 13 patients. Overall, 29 of 50 patients had significant coronary artery disease, compared with a 7% prevalence of the condition in other patients of similar age at the same institution.
Whether multiple sclerosis (MS) can cause headaches is controversial. To clarify the association between headaches and MS we prospectively analyzed 104 consecutive MS patients using detailed headache evaluations. Fifty-four patients (52%) reported headaches, compared with 5 of 35 (14%) patients initially suspected to have MS but subsequently proven to have other disorders, and 18 of 100 (18%) matched general neurology patients. The MS patients had tension headaches or vascular headaches of the migraine type; there was no distinctive "MS headache." Seven of these patients had headaches with their first MS symptoms, but in only one did headaches recur with disease activity. Headaches did not correlate with any clinical features of MS. We conclude that an association between headaches and MS may exist.
Multiple sclerosis (MS), the most common disabling neurologic disease of young people, afflicts approximately a quarter of a million Americans. The symptoms of MS result from recurrent attacks of inflammation in the central nervous system, which probably occur through an autoimmune mechanism. The target of the immune attack is myelin, the lipoprotein sheath that surrounds the axons and insulates them, and enhances nerve conduction. The white matter of the brain takes its name from the glistening white appearance of this lipid wrapping, which contains most of the pathways, tracts and axonal projections of the central nervous system. (The gray matter contains primarily the cell bodies of the neurons themselves.) Myelin is made by cells called oligodendrocytes and when it is inflamed and damaged, nerve conduction is disrupted and nerves thus lose function, thereby producing the neurologic symptoms of MS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.