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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1898, Alzheimer wrote an exhaustive update on psychogeriatric issues. He discussed paralytic dementia, involutional melancholia, senile dementia, presenile dementia, arteriosclerotic dementia, Binswanger disease, stroke-induced dementia, and other dementias of vascular origin. In this paper, he appeared to describe his very first case of Alzheimer disease, he anticipated the ischemic score, and outlined his opinion about numerous issues of dementia research that are of current interest.
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PMID:Recent studies on dementia senilis and brain disorders caused by atheromatous vascular disease: by A. Alzheimer, 1898. 178 68

During a three-year period, 337 CT or MR scans were ordered for psychiatric patients in a teaching hospital. Scans were normal in 185 instances, equivocal in 34, and abnormal in 118 instances. When a history of neurologic disorder and/or the presence of abnormal neurologic/organic mental signs was positive, scans were abnormal in 74% of cases; when these indicators were negative, scans were normal in 72% of cases. In all, only 4 new diagnoses were made. Two patients, both with markedly abnormal neurological findings, were shown to have brain tumors, which changed their management. Two others showed abnormalities which would have been missed, both of which were of no clinical consequence. The following are suggested as sound indications for ordering CT or MR brain imaging among psychiatric patients: 1) positive history of head injury, stroke or other neurologic disease, as well as suspected Alzheimer disease or multi-infarct dementia; 2) presence of abnormal neurologic signs or organic mental signs, such as confusion or cognitive decline; and, 3) a first psychotic break or personality change after the age of 50 years.
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PMID:Clinical use of CT and MR scans in psychiatric patients. 178 61

The plasma distribution of gallium (as an analogue of aluminium) was investigated in patients with Alzheimer disease, Down syndrome, or stroke dementia, in subjects on haemodialysis for chronic renal failure, and in healthy controls. Gallium-transferrin binding was significantly lower in the Alzheimer (mean [SEM] 7.9 [1.1]%) and Down syndrome groups (6.9 [0.7]%) than in the controls (17.1 [1.6]%), whereas stroke dementia and haemodialysis patients had normal binding. There were no differences among the groups in plasma citrate concentration. The plasma transferrin concentration was slightly lower in the Alzheimer and Down syndrome groups than in the controls, but even lower in stroke dementia patients (1.74 [0.14] g/l vs 2.98 [0.18] g/l in controls). Transferrin iron saturation was higher in the Alzheimer (58.9%) and Down syndrome groups (81.6%) than in the controls (39.0%) or stroke dementia patients (33.4%). This deficiency of gallium/aluminium binding would leave more unbound aluminium which could move readily into the brain, where it has neurotoxic effects.
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PMID:Defective gallium-transferrin binding in Alzheimer disease and Down syndrome: possible mechanism for accumulation of aluminium in brain. 197 9

We present a practical set of guidelines for assessing competency in patients with cognitive deficits due to neurologic disorders such as stroke, head injury, Alzheimer disease, and multi-infarct dementia. Our focus is the evaluation of cognitive processes underlying the ability to make competent decisions, with an emphasis on the identification of areas of preserved function that may be used to bypass intellectual deficits. The assessment of the cognitive processes underlying competency involves a series of steps designed to evaluate attention, language, memory, and frontal lobe function. The examiner must first show that the patient has an adequate level of attention for participation in the further testing of specific cognitive functions; second, that the patient is able to comprehend relevant instructions, retain information long enough to evaluate it in relation to relevant recent and remote experiences, and express his or her wishes; and finally, that the patient has sufficiently intact judgment and awareness. The examiner must determine whether the patient's preserved cognitive abilities are sufficient for him or her to make an adequate judgment in relation to the specific question being asked. If cognitive function is found to be significantly impaired, the examiner should do a detailed assessment for the presence of compensatory abilities that can be used to bypass the deficits. For example, the examiner should assess whether patients who cannot speak are still able to express their wishes by pointing, using gesture, or even by drawing pictures. Unless such an assessment has been done, patients should not be considered incompetent.
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PMID:Assessment of competency: the role of neurobehavioral deficits. 205 75

It is widely held that a glutamate-like toxin that resembles N-methyl-D-aspartate may be responsible for the death of nerve cells seen after severe neurological insults including stroke, seizures, and degenerative disorders, such as Huntington disease, Alzheimer disease, and the amyotrophic lateral sclerosis-parkinsonism-dementia complex found on Guam. One puzzling fact about these maladies is the differential vulnerability of specific groups of neurons peculiar to each condition. We report here that an identified population of central neurons, rat retinal ganglion cells, are resistant to the neurotoxic effects of millimolar concentrations of glutamate under otherwise normal culture conditions. Patch-clamp experiments show that this resistance is associated with a very small ionic current response to N-methyl-D-aspartate. Varying the ionic milieu by increasing the extracellular Ca2+ concentration, however, results in a striking increase in glutamate-induced cell death in this population. Under these conditions, Mg2+ or the amino acid antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo-(alpha,gamma)-cyclohepten-5 ,10-imine maleate], blockers of N-methyl-D-aspartate receptor-coupled ion channels, completely abrogate the lethal effects of glutamate. These findings strongly suggest that Ca2+ entry through N-methyl-D-aspartate-activated channels is responsible for this type of neuronal death and suggest strategies that may be clinically useful in the treatment of various neurological disorders.
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PMID:Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801. 290 Nov 1

Positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) was used to map local cerebral glucose utilization in the study of local cerebral function. This information differs fundamentally from structural assessment by means of computed tomography (CT). In normal human volunteers, the FDG scan was used to determine the cerebral metabolic response to controlled sensory stimulation and the effects of aging. After stroke, regional brain dysfunction is more extensive than had been suspected on the basis of CT scans. Cerebral metabolic patterns are distinctive among depressed and demented elderly patients. The FDG scan appears normal in the depressed patient, studded with multiple metabolic defects in patients with multiple infarct dementia, and in the patients with Alzheimer disease, metabolism is particularly reduced in the parietal cortex, but only slightly reduced in the caudate and thalamus. The caudate is markedly hypometabolic in Huntington disease, even in the absence of caudate atrophy, and possibly may be mildly hypometabolic even before the appearance of symptoms. The interictal FDG scan effectively detects hypometabolic brain zones that are sites of onset for seizures in patients with partial epilepsy, even though these zones usually appear normal on CT scans. The future prospects of PET are discussed.
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PMID:Imaging local brain function with emission computed tomography. 660 81

We studied the frequency of oligoclonal immunoglobulin G bands in the cerebrospinal fluid (CSF) of patients with various neurological diseases. We used a micromethod employing sodium dodecyl sulfate polyacrylamide gel electrophoresis that required only 50 microliters of unconcentrated CSF. Oligoclonal bands were detected in the CSF of 95% of the patients with multiple sclerosis, 90% with subacute sclerosing panencephalitis, and 100% with herpes simplex encephalitis, but less frequently in other central nervous system infections. No oligoclonal bands were detected in the CSF of patients with Parkinson, Huntington, Creutzfeldt-Jakob, or herniated disc diseases. Bands were detected in some patients with Alzheimer disease, cerebrovascular accident, idiopathic vertigo, idiopathic seizures, amyotrophic lateral sclerosis, polyneuropathy, and central nervous system glioma. Patients with other conditions infrequently had positive bands. The determination of oligoclonal bands is a useful aid in the diagnosis of multiple sclerosis, subacute sclerosing panencephalitis, and herpes simplex encephalitis. The presence of oligoclonal bands indicates an immunological response but is not diagnostic for a particular condition.
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PMID:Oligoclonal IgG bands in cerebrospinal fluid in various neurological diseases. 683 75

Discussions about Paragraph 218 of the German federal abortion law have spawned antithetical opinions: on the one hand, the full right of the mother or parents to decide about the incipient human life; and on the other hand, under the dogma of abortion is murder, providing abortion is rejected even when the pregnancy is the result of rape and it is unwanted. Two questions are closely related to this issue: 1) what makes human beings human and 2) when does human life begin. From a medical point of view the function of the brain is fundamentally linked to being human. The brain controls almost all functions of the body and determines its psychological makeup, such as intellect and, in a theological sense, the soul. Without the brain such functioning is not possible, since brain death means the death of human life. Children born with anencephaly and microencephaly can never live a human life. At the end of life various diseases (stroke, Alzheimer disease) can severely damage the brain. In these cases normal living is also no longer possible. Yet ethically it is untenable to actively kill these human beings. But when one considers that life-threatening diseases can require life-support intervention, then often the pragmatic intervention is not far removed from active euthanasia. The other question related to the beginning of human life is even more difficult to answer. It is the fertilization of the egg cells; but a conglomeration of cells in the early phase of pregnancy can hardly be characterized as a human person. The human identity, personality, and worth is associated with the functioning of the brain, so only when the brain is fully developed can there be any talk about an unborn human being.
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PMID:[Is abortion murder?]. 747 58

Gelatinase A is an enzyme capable of cleaving soluble beta-amyloid protein (beta AP), and may function as an alpha-secretase to produce secretory forms of amyloid precursor protein. We examined gelatinase A immunoreactivity in the brains and posterior roots of neurologically normal, lacunar stroke, Alzheimer disease (AD), amyotrophic lateral sclerosis, progressive supranuclear palsy and myasthenia gravis cases. The gelatinase A antibody stained only microglial cells in the white matter in all the brain tissues. In AD brain, the reactive microglia located in the center of classical senile plaques, as well as in other microglial cells in the gray matter, showed no immunoreactivity. Gelatinase A in white matter microglial cells may play a role in preventing local deposition of beta AP. In the posterior root, Schwann cells had positive immunoreactivity. As with other metalloproteases, gelatinase A in Schwann cells may play an antiproliferative role.
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PMID:Selective localization of gelatinase A, an enzyme degrading beta-amyloid protein, in white matter microglia and in Schwann cells. 753 20

Establishing the basic defect in Canavan disease has led to reliable biochemical methods for the diagnosis of this disease. The isolation of the gene and identification of mutations causing Canavan disease have led to the possibility of using DNA methods for the diagnosis of Canavan disease and for carrier detection. A surprising finding is the high carrier frequency of this gene defect among Ashkenazi Jewish people. Analysis for two mutations leads to the identification of 97% of Jewish patients with Canavan disease, and screening of Ashkenazi Jews is possible. N-Acetylaspartic acid has been considered to be an inert compound. The pathophysiology of Canavan disease links lack of NAA hydrolysis to a severe, debilitating white matter disease. Currently, NAA is being studied in many other brain disorders, such as Alzheimer disease, Huntington disease, and stroke. However, the only disease with a specific defect in the metabolism of NAA is Canavan disease. An animal model for Canavan disease is needed to study some of the questions regarding the role of NAA in brain tissue, and for the study of therapeutic modalities, including gene therapy.
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PMID:Canavan disease: from spongy degeneration to molecular analysis. 756 69


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