Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.
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PMID:Transient global amnesia -- its clinical and pathophysiological basis and prognosis. 721 Nov 87

Ten patients with transient global amnesia (TGA) associated with symptoms of transient focal cerebral ischemia were seen at the University Department of Neurology, Arhus Kommunehospital in the period 1966-1978. All had either prior to or following the amnesic attack transient ischemic attacks (TIA) in the territory of the posterior cerebral circulation. On admission minor neurological deficits were noted in three and normal findings in the remaining seven. There was no evidence of epilepsy in any case. We studied the course (average, 77 months) and found that three had recurrent amnesic episodes. Four patients had only further transient focal cerebral ischemic attacks, while six developed a completed stroke, in five located in the distribution of the basilar artery. Seven patients had persistent memory impairment. TGA is one manifestation of TIA in the vertebrobasilar arterial system. When TGA appears in connection with other transient cerebral ischemic attacks, the prognosis is apparently grave with a great risk of a subsequent completed stroke or a permanent memory impairment.
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PMID:Transient global amnesia as a manifestation of transient cerebral ischemia. 739 56

In ten patients we treated with distal arch aneurysms exposed through left posterolateral incisions, we induced profound hypothermia and circulatory arrest. Before circulatory arrest, thiopental, nicardipine and glycerol were used to protect the brain. The brain function was objectively evaluated through continuous recording of EEG and PO2 tension of the internal jugular vein. A cardiopulmonary bypass was introduced via the left atrium, pulmonary artery and left femoral artery cannulation. After proximal anastomosis between the graft and transverse aorta, graft cannulation was added. The distal aortic arch was replaced in all patients, with the entire descending thoracic aorta additionally replaced in two. No patients died in hospital. Two suffered neurological deficit, i.e., one having slight memory impairment and the other having a left-sided stroke due to right cerebral infarction, but recovering completely within a week. Our results indicate that profound hypothermia and circulatory arrest can be implemented safely when treating patients with distal arch aneurysm.
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PMID:[The treatment of patients with distal arch aneurysms--hypothermic circulatory arrest and left posterolateral exposure]. 759 44

Global and specific cognitive functions were assessed in 57 patients with ischemic strokes subjected to clinical neuropsychiatric, psychometric, electrophysiological and cranial tomographic evaluation. Patients did significantly worse than normal controls in the Blessed dementia scale, Sandoz clinical assessment geriatric scale but not the Folstein mini-mental state examination. Of the specific cognitive functions, attention and psychomotor performance were significantly impaired in stroke patients when compared to normal controls. The impairment in global cognitive functions, attention and psychomotor performance was more evident in chronic than acute cases. Increasing age correlated positively to the deterioration in psychomotor performance and perception. Cranial tomographic size of infarction was significantly related to global cognitive as well as intentional (sensory) memory impairment. The more marked the conventional electroencephalographic abnormalities, the more impaired were the global cognitive functions. High limit of the theta percent power correlated positively to deterioration in psychomotor performance. All P300 parameters except amplitude correlated significantly with impairment of global cognitive function and psychomotor performance in stroke patients.
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PMID:Cognitive deficits in ischemic strokes: psychometric, electrophysiological and cranial tomographic assessment. 780 62

The effects of the stable prostacyclin analogue TTC-909 on memory impairment in the water maze task and on neuronal damage were studied in rats with cerebral embolism induced by injecting polyvinyl acetate (PVA) into the right internal carotid artery and the ensuing embolism extending out into the right middle cerebral artery. Areas supplied by the lenticulostriate artery were most markedly damaged. In the water maze test, the PVA-embolized rats took longer to reach the platform than did the nontreated control rats. To some extent, repeated administrations of TTC-909 (200 ng/kg, IV) overcame this impairment in water maze learning in the rats. We assume that the vasodilating effects of TTC-909 maintain this blood supply to the ischemic area and that TTC-909 prevents the development of thrombosis around the PVA particles in the arterial capillaries, as a result of antiplatelet aggregative effects. These two mechanisms are likely to be involved in memory improvement. TTC-909 may prove effective for treating subjects with stroke and other cerebrovascular disorders.
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PMID:Prostacyclin analogue TTC-909 reduces memory impairment in rats with cerebral embolism. 854 73

This study aimed to investigate the incidence and nature of memory impairment late after stroke. Out of 193 patients between 12 to 36 months post-cerebrovascular accident contacted in a postal survey, 113 replied that they had experienced memory impairment following the stroke. Seventy of these patients were assessed on an adapted version of the Rivermead Behavioural Memory Test, Warrington's Recognition Memory Test for words and faces, and an every day memory questionnaire. The Token Test and the Benton Facial Recognition Test were also administered as measures of language and visuoperceptual processing. Thirty-five of the patients were impaired on one or more of the memory measures. Of these, 16 showed no evidence of dysphasia or visuoperceptual impairment. The 16 cases of selective memory impairment typically had mild to moderate deficits, and only three were impaired across all three tests. The results suggest that memory impairment following stroke does not necessarily involve general memory impairment. The evidence for material-specific memory deficits was much weaker.
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PMID:The nature and prevalence of memory disorder late after stroke. 888 78

It is widely believed that spontaneous improvements in functioning late after brain damage are due to processes of adaptation to permanent cognitive deficits. Reports of everyday memory and the pattern of performance on memory tests were investigated in 70 patients more than a year after a stroke. Contrary to the adaptation hypothesis, performance on simulations of everyday tasks (Rivermead Behavioural Memory Test) correlated strongly with performance on a test where there was little scope for compensatory strategies (forced-choice recognition memory for words). In 12 cases, initial assessment with the EMQ20 questionnaire suggested few cognitive failures in everyday life despite poor test performance. However, where further investigation was possible, it seemed that unreliability of measures or subtle everyday effects of non-verbal memory impairment could explain the apparent discrepancies. In addition, patients who did poorly on tests were not reported to make frequent use of memory aids. Adaptation to deficit does not therefore appear to be a major influence on everyday memory performance late after stroke, but it may have subtle effects or may be important in other areas of functioning. Implications for clinical memory assessment are discussed.
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PMID:Adaptation to cognitive deficit? An exploration of apparent dissociations between everyday memory and test performance late after stroke. 888 87

To understand central nervous damage after long-term exposure to carbon disulfide (CS2), 10 patients who had polyneuropathy with various neuropsychiatric symptoms in a viscose rayon plant were studied. Clinical and laboratory examinations including electroencephalography (EEG), brain computed tomography (CT), brain magnetic resonance images (MRI), and carotid duplex sonography were carried out. Clinically, headache, unpleasant dreams, memory impairment, fatigue, anorexia and emotional lability were common in these patients while 2 patients had stroke episodes. EEGs were all normal. Brain CT scan showed mild cortical atrophy in 3 and low density lesions in the basal ganglia in 3. Brain MRI studies also disclosed mild cortical atrophy in 4 and multiple lesions involving the basal ganglia and corona radiata in 4. Carotid duplex sonography revealed mild atherosclerosis with plaques (< 20% stenosis) of extracranial vessels in 6. However there was no significant difference in flow velocities and flow volumes in the extracranial carotid arteries between patients and the normal controls. Interestingly, 2 patients had multiple brain lesions in the subcortical white matter but without strokes. In conclusion, encephalopathy with possible strokes may occur after chronic exposure to CS2, as well as polyneuropathy. The lesions usually involve the basal ganglia and subcortical white matter. Furthermore, MRI study may detect brain lesions particularly in the subcortical white matter areas before the occurrence of stroke.
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PMID:Chronic carbon disulfide encephalopathy. 895 4

The side-effects and complications of posteroventral pallidotomy are analysed in 138 consecutive patients who underwent 152 pallidotomies. Transient side-effects, lasting less than three months, appeared in 18% of the patients, that is, 16.5% of the surgical procedures. Long term complications, lasting more than 6 months, were noted in 10% of the patients, that is, 9.2% of the surgical procedures. Sixteen complications occurred alone or in various combinations in 14 patients and included fatigue and sleepiness (2), worsening of memory (4), depression (1), aphonia (1), dysarthria (3), scotoma (1), slight facial and leg paresis (2) and delayed stroke (2). Complications such as dysarthria and paresis could be attributed to MR- or CT-verified pallidal lesions lying too medially and encroaching on the internal capsule. Two of the patients with deterioration in memory had some memory impairment before surgery, and the aphonic patient had dysphonia preoperatively. The study suggests that stereotactic MRI and careful impedance monitoring and macro-stimulation of the posteroventral pallidum area should be sufficient for minimizing the risk of complications; the stereotactic lesion should be centered within the posterior ventral pallidum without involvement of internal capsule. It is concluded that pallidotomy is a safe procedure if performed on cognitively alert patients, and it seems that both the incidence and especially the severity of complications are lower for posteroventral pallidotomy than for thalamotomy.
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PMID:The side-effects and complications of posteroventral pallidotomy. 923 12

Dementia is common among patients with cerebrovascular disease, particularly in a setting of one or more clinically evident strokes. Prior cohort and case studies have suggested that the cognitive syndrome of vascular dementia is characterized by predominant executive dysfunction, in contrast to the deficits in memory and language function that are typical of patients with Alzheimer disease. The course of cognitive decline may also differ between those dementia subtypes, with many, but not all, patients with vascular dementia exhibiting a stepwise course of decline caused by recurrent stroke and most patients with Alzheimer disease exhibiting a gradually progressive course of decline. The findings of prior studies of the cognitive syndrome of vascular dementia must be interpreted with caution, however, because of (1) possible inaccuracies in the determination of the dementia subtype and the loss of precision that might result from pooling heterogeneous subgroups of patients with vascular dementia, (2) difficulties inherent in identifying a pattern of strengths and weaknesses in patients who are required to have memory impairment and other deficits to meet operationalized criteria for dementia, and (3) the use of limited test batteries whose psychometric properties are incompletely understood. Specific questions that should be addressed by future studies are discussed.
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PMID:The cognitive syndrome of vascular dementia: implications for clinical trials. 1060 78


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