Stroke: 30 years of progress: 1987-1991.
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Biomedical subjects
Publications and source records attributed to O M Reinmuth.
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This case study involves the differential diagnosis of aphasia versus dementia. However, the case of Dr. JJ is instructive from a number of aspects, presented here as "cautionary notes" which are intended to remind clinicians of sometimes-forgotten interpersonal issues in the diagnosis of disorders of speech and language. This case also is intended to illustrate that merely distinguishing between dementia and aphasia is sometimes inadequate, particularly when potentially transmittable (and in some cases, curable) dementias might be involved.
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BACKGROUND AND PURPOSE: In this study we sought to evaluate the clinical significance of serum autoantibodies to dementing processes. METHODS: We assessed 40 age-matched subjects: 10 patients with probable Alzheimer's disease, 10 with possible Alzheimer's disease with cerebrovascular disease, 10 with vascular dementia, and 10 nondemented control subjects. Serum from each subject was tested for the presence of antithyroglobulin antibody, thyroid antimicrosomal antibody, gastric anti-parietal cell antibody, anti-smooth muscle antibody, antinuclear antibody, rheumatoid factor, antineuronal antibody, and anticardiolipin antibody. In addition, we investigated the sera of these patients for the presence of an antivascular antibody directed against the vascular basement membrane proteoglycan antigen and for circulating immune complexes. RESULTS: Autoantibodies were present in 100% of the patients with possible Alzheimer's disease with cerebrovascular disease, 80% of those with vascular dementia, 40% of those with probable Alzheimer's disease, and 30% of the nondemented control subjects. The highest number of autoantibodies was observed in patients with vascular dementia and possible Alzheimer's disease with cerebrovascular disease. Antinuclear antibody was present in 60% of vascular dementia patients and antineuronal antibody in 50% of these patients. However, no individual autoantibody could differentiate Alzheimer's disease from cerebrovascular disorders. Immune complexes were detected in the serum of 20-30% of each patient group. Neither the patient nor the control sera was found to contain antiendothelial antibody. CONCLUSIONS: Despite the relatively small number of individuals examined in each category, the elevated number of autoantibodies associated with possible Alzheimer's disease with cerebrovascular disease and vascular dementia indicates a possible link between the presence of autoantibodies and cerebrovascular disorders in dementia.
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We report a 52-year-old woman with episodes of vertigo accompanied by right beating nystagmus and left posterior temporoparietal sharp waves and spikes on electroencephalogram without change in level of consciousness. Electrooculography demonstrated that the episodes of nystagmus were not preceded by gaze deviation and that nystagmus slow component velocities were linear. This patient's epileptic nystagmus may have been the result of excitation of cerebral ocular pursuit pathways.
Although the NINCDS-ADRDA Work Group has recently developed uniform clinical criteria for the diagnosis of Alzheimer's disease (AD), inter-rater reliability studies of these criteria are few. We report a study in which 2 neurologists and 2 psychiatrists independently reviewed clinical data abstracted from the records of 30 demented subjects and 10 nondemented control subjects participating in a longitudinal study of AD at the University of Pittsburgh. We recorded the clinical data on a standardized form; the subjects' identity and clinical and pathologic diagnoses were omitted. Each physician diagnosed each case according to the NINCDS-ADRDA criteria. We calculated the inter-rater agreement for all possible 2-way combinations of clinicians with the Kappa statistic, which ranged from 0.36 (fair agreement) to 0.65 (substantial agreement). We conclude that current NINCDS-ADRDA criteria enable moderate levels of agreement among clinicians in general.
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We reviewed the clinical features of 12 patients with fat embolism seen in 10 years. Based on neurologic manifestations, patients were grouped into those with focal cerebral syndromes and those with diffuse encephalopathy. Patients with focal signs tended to present earlier with neurologic findings alone, did not have fever, and had less risk of pulmonary disorder than patients with encephalopathy.
Minimal neck injury produced vertebral artery damage in two women and three men, 20 to 57 years of age. Serious neurologic deterioration occurred in two patients when positioned for roentgenographic procedures. Dissection or thrombosis of one or both vertebral arteries while in the transverse foramina occurred in three, one at the site of an osteophyte. The arteriogram of one patient showed a traumatic aneurysm at C-7, and a second patient had segmental arterial stenosis with bilateral traumatic aneurysms at C-5. The location of the arterial injury is not restricted to the occipitoatlantoaxial level but includes the course through the transverse foramina. The use of anticoagulation appears to be important in the immediate management of this process.
Sixteen consecutive cases of subcortical stroke were studied prospectively and systematically. Behavioral and neurological manifestations of different sides, sites, and causes of lesion were evaluated by means of daily, standard observations during the patient's hospitalization and formal testing at monthly intervals thereafter. Language and cognitive impairments were observed following hemorrhagic and nonhemorrhagic strokes to both the left and right thalami and basal ganglia. The patterns were unlike those characteristic of traditional aphasia syndromes. One patient was asymptomatic; four demonstrated only dysarthria or dysarthria with abnormal affect; and 11 displayed a combination of speech, language, and cognitive deficits. Language skills recovered more rapidly and completely than did cognitive skills. Recovery was most dramatic within the first six to eight weeks after onset.
This paper is a detailed retrospective history of a patient who began to have difficulty with speaking and comprehension in 1967, and whose neuropathological examination at time of death 12 1/2 years later was consistent with a diagnosis of Pick's disease, complicated by neurofibrillary tangles. It follows the deteriorating course of his language abilities in the context of relatively less-impaired general cognitive abilities, using two sources of information. The first is his own written record of his deteriorating abilities, shown in letters and notes he wrote over this period. The second is through an oral history obtained from the patient's family. The purpose of this report is to illustrate in detail the course of a degenerative condition and to suggest the utility of such descriptional records in increasing understanding of language deterioration in dementia.
The paper presents a daily analysis of the language recovery of a patient who was globally aphasic at the time of her first observation and who had recovered language, as measured by the Western Aphasia Battery, at the time of her discharge 14 days later. The paper emphasizes the relatively regular growth of normal syntactic, lexical, and pragmatic features coupled with similar regular decreases in aphasic features. Observations of both phenomena are necessary to describe language recovery.
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Fifteen patients with chronic subdural hematomas had transient neurological deficits. The important clinical features were aphasia in 9 patients, absence of headache in 8, and head injury in 8. Computed tomographic scan correctly identified all 15 cases of chronic subdural hematoma and should be considered mandatory before initiating anticoagulation in patients with transient ischemic attacks.
Anesthetized ventilated rats were subjected to insulin-induced hypoglycemia (50 units/kg i.v.) while EEG, ECG, mean arterial pressure, blood gases, arterial pH and rectal temperature were controlled. Animals were sacrificed by rapid transcalvarial freezing of the brain in situ. Glucose, pyruvate and lactate were measured in blood, CSF and cortical tissue, in which additionally glycogen, phosphocreatine, ATP, ADP, AMP, aketoglutarate (aKG), glutamate, oxalacetate, aspartate, ammonia and water content were estimated. ATP/ADP ratio, energy charge (ECh) energy reserve, NADH/NAD+ quotient and intracellular pH were calculated. ECh does not correlate with either dysfunction of carbohydrate depletion, but declines in a threshold fashion when tissue glucose has fallen by over 97% and glycogen by over 60%. The EEG correlates with the degree and duration of carbohydrate depletion in cortical tissue. An isoelectric EEG occurs pari passu with the fall of the ECh. Increase in ammonia and decrease in aKG and Glut are supportive evidence of intrinsic substrate. Lactate decrease during hypoglymecia is not reversed by super-imposed hyqoxia.
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