Parkinsonian symptoms in a patient with AIDS and cerebral toxoplasmosis.
Explore the source record for details and available documents.
Acquired Immunodeficiency Syndrome↗
Biomedical subjects
M A Samuels
Publications and source records attributed to M A Samuels.
Sensory form of acute polyneuritis.
A patient presented with severe sensory loss and ataxia with total arreflexia, and elevation of CSF protein with pleocytosis. At autopsy there was extensive lymphocytic infiltration of nerves and posterior roots, sparing the anterior roots. Teased fiber preparation of nerve showed a demyelinating lesion. There were no abnormalities in the CNS. The condition appears to be an acute sensory polyneuritis bearing a close relationship to acute Guillain-Barré syndrome.
Acute Disease↗
A misleading cervical bruit in carotid occlusion.
Explore the source record for details and available documents.
Auscultation↗
Neurogenic heart disease: a unifying hypothesis.
Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.
Animals↗
Myocardial contraction band lesions in patients with fatal asthma: possible neurocardiologic mechanisms.
Myocardial contraction band necrosis (MCBN) occurs in catecholamine infusion, central nervous system stimulation, stress, and transient myocardial ischemia with reperfusion. In 4 of 13 children who died with asthma, MCBN was present, suggesting that this cardiac lesion may contribute to the deaths of some asthmatic patients. Two of the 4 patients who had MCBN had not received sympathomimetics intravenously or by an intracardiac route. Therefore, mechanisms other than infusions of large doses of catecholamines are probably involved in production of this cardiac lesion in asthmatics.
Adolescent↗
Multiple simultaneous intracerebral hematomas. Clinical, radiologic, and pathologic findings in two patients.
The simultaneous occurrence of two intracerebral hematomas in different arterial territories of the brain is rare. We report the clinical, radiologic, and post-mortem findings in two such cases. The absence of readily identifiable vascular disease in such patients suggests that a subtle degenerative process may be active in the pathogenesis of this condition.
Aged↗
Clinical exercise trial for stroke patients.
This investigation evaluated the effectiveness of the traditional and facilitation approaches to therapeutic exercise in stroke patients. A total of 42 adults (24 men and 18 women) with a mean age of 61.6 years (SD = 21) were selected from a larger population of hospitalized stroke victims. Stroke patients were classified by CT scan information and judged medically fit to participate in a nonrestrictive program by neurologic examinations and laboratory tests. The Barthel Index and the manual muscle test were administered at admission and discharge. Both facilitation and traditional exercise therapies improved functional and motor performance, but there were no significant differences between these approaches. The lack of differences between the facilitation and traditional exercise therapies may be due to heterogeneity of the stroke population, the small sample size, and the measurements used. The study demonstrates the need for a measurement instrument capable of reliably assessing the facilitation approach. Future investigations should incorporate lesion type, site, and side along with global measurements in evaluating differences among motor remediation approaches.
Activities of Daily Living↗
Diagnosis of stroke by CPK isoenzymes.
Explore the source record for details and available documents.
Cardiovascular Diseases↗
Adverse neurologic effects of glucocorticosteroids.
Explore the source record for details and available documents.
Adolescent↗
A practical approach to coma diagnosis in the unresponsive patient.
Diagnosis of coma in the unresponsive patient can be done in a relatively short time by making key observations that will confirm disease of either the brain stem or the hemispheres, the two locations in which coma originates. Determining the location of the lesion is the primary goal in early assessment of the unresponsive patient. Examination of the patient's eyes is the single most important step in understanding coma.
Brain Stem↗