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

Twenty post-stroke depressive patients who obtained more than 11 points on Self-Rating Questionnaire for Depression, were treated with 0.075 mg/day lisuride maleate for 12 weeks. The drug effect on depression was evaluated quantitatively by the Hamilton Rating Scale for Depression. The relationships between brain CT or MRI and SRQ-D score were investigated in 24 subjects. More than 80% of post-stroke depressive patients improved after lisuride maleate treatment for 8 or 12 weeks. In particular, depressed mood, hypobulia, sleep disturbance, anxiety, etc. were significantly improved compared to the baseline condition. As for the relationships with CT and/or MRI findings, the group with moderate to severe brain atrophy had a significantly higher grade of depressive state than those without.
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PMID:[Therapeutic effect of lisuride maleate on post-stroke depression]. 815 72

Despite recent advances in understanding the pathophysiology of poststroke depression, major questions remain. They include the relative importance of lesion location and size and the confounding effects of time since stroke, age, prior history of depression, and cerebral atrophy. To evaluate these issues, we systematically assessed depressive features, functional status, and brain structure with computer tomography scans in 91 men undergoing stroke rehabilitation. Forty percent met DSM-III criteria for major depressive disorder. Mood disturbance was more severe for patients with right than with left hemisphere lesions, correlated with functional disability and lesion size, and was associated with previous history of depression. Age, time since stroke, and atrophy did not correlate with mood. Depression is common in delayed stroke recovery, regardless of lesion location. Because there are no demographic or anatomic features that predict the absence of depression, depression screening should be part of the assessment of all patients undergoing stroke rehabilitation.
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PMID:Depression in stroke rehabilitation. 835 64

To document the occurrence, time course, and predictors of global cognitive impairment following a supratentorial stroke, we prospectively studied 41 consecutive patients with acute cerebral ischemia and no evidence of pre-existing intellectual disturbances. The Graded Neurologic Scale and Mattis Dementia Rating Scale were used to assess neurologic and cognitive deficits within the first week, 3 weeks and 6 months after the onset of symptoms. CT was performed at each examination and semiquantitative measurements of infarct volumes and brain atrophy were obtained. Sixty-one percent of patients were found to be cognitively impaired within the first week. After 6 months this deficit had resolved in 24%, but was still present in 37% of individuals. Initial findings associated with a high risk of long-term intellectual dysfunction were: 1. moderately severe cognitive impairment, 2. diminished alertness in the acute stroke stage, 3. infarction involving the temporal lobe, 4. evidence of multiple brain infarcts and 5. pronounced ventricular enlargement. Logistic regression analysis revealed temporal infarcts and evidence of multiple ischemic lesions as the most powerful predictors of persistent cognitive impairment. By these two factors alone, 85.4% of study participants could be correctly classified regarding their cognitive outcome. These results suggest cognitive dysfunction to be a frequent sequela of supratentorial stroke. Its long-term persistence may be predicted on the basis of certain features.
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PMID:Cognitive impairment after acute supratentorial stroke: a 6-month follow-up clinical and computed tomographic study. 839 5

Headaches are one of the most common symptoms that neurologists evaluate. Although most are caused by primary disorders, the list differential diagnoses is one of the longest in all of medicine, with over 300 different types and causes. The cause or type of most headaches can be determined by a careful history supplemented by a general and neurologic examination. Reasons for obtaining neuroimaging include medical indications as well as anxiety of patients and families and medico-legal concerns. In the era of managed care, concerns over deselection and negative capitation may dissuade the physician from ordering even a medically indicated scan. The yield of neuroimaging in the evaluation of patients with headache and a normal neurologic examination is quite low. Combining the results of multiple studies performed since 1977 for a total of 3026 scans reveals the overall percentages of various pathologies as: brain tumors, 0.8%; arteriovenous malformations, 0.2%; hydrocephalus, 0.3%; aneurysm, 0.1%; subdural hematoma, 0.2%; and strokes, including chronic ischemic processes, 1.2%. EEG is not useful in the routine evaluation of patients with headache. Similarly, the yield of neuroimaging in the evaluation of migraine is quite low. Combining the results of multiple studies performed since 1976 for a total of 1440 scans of patients with various types of migraine, the overall percentages of various pathologies are: brain tumor, 0.3%; arteriovenous malformation, 0.07%; and saccular aneurysm, 0.07%. WMA have been reported on MRI studies of patients with all types of migraine, with a range from 12% to 46%. The cause of WMA in migraine is not certain. Cerebral atrophy has been variable reported as more frequent and no more frequent in migraineurs compared with controls. The "first or worst" headache has a long list of possible causes and always includes the possibility of acute subarachnoid hemorrhage. Headaches--especially the sentinel type caused by SAH--often are misdiagnosed. The probability of detecting an aneurysmal hemorrhage of CT scans performed at various intervals after the ictus is: day 0.95%; day 3, 74%; 1 week, 50%; 2 weeks, 30%; and 3 weeks, almost nil. The location of a ruptured saccular aneurysm often is suggested by the predominant site of the SAH. The probability of detecting xanthochromia with spectrophotometry in the CSF at various times after a subarachnoid hemorrhage is: 12 hours, 100%; 1 week, 100%; 2 weeks, 100%; 3 weeks, more than 70%; and 4 weeks, more than 40%. The management of thunderclap headaches with normal CT scan and CSF examinations is controversial. Most patients have a benign course but an unruptured saccular aneurysm occasionally may be responsible for the headache. MR angiography may be a reasonable test to obtain instead of a cerebral arteriogram in many of these cases. About 30% to 90% of patients have headaches of various types and causes after mild head injury. Although most headaches are relatively benign, perhaps 1% to 3% of these patients have life-threatening pathology, including subdural and epidural hematomas, that are detected on CT and MRI scans. Headaches caused by subdural hematomas can be nonspecific. When new-onset headaches begin in patients over the age of 50 years, the physician always should consider whether it may be a secondary headache disorder requiring specific diagnostic testing and treatment. Up to 15% of patients 65 years and over who present to neurologists with new-onset headaches may have serious pathology such as stroke, TA, neoplasm, and subdural hematoma. Headaches are the most common symptom of TA, reported by 60% to 90%. The only over the temple. The diagnosis of TA is based on a high index of clinical suspicion that usually but not always is confirmed by laboratory testing. The erythrocyte sedimentation rate can be normal in 10% to 36% of patients with TA. A superficial temporal artery biopsy can give a false-negative result in 5% to 44% of patients.
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PMID:Diagnostic testing for the evaluation of headaches. 867 38

Cerebral atrophy (CA) in stroke patients is associated with poststroke dementia and may reflect underlying neurodegenerative pathology. Therefore, regional CA may be valuable to study in patients who develop poststroke dementia. The aim of this study was to test the reproducibility of a qualitative rating scale of CA on MRI. MRI scans were performed in 50 consecutive patients (age range 19-81) admitted for an acute hemispheric ischemic stroke. CA was assessed on 2 occasions 24 h apart, on axial T2-weighted sequences by 4 independent observers. We evaluated CA in 13 regions on a 0-3 scale. The sum of the subscores was called the CA score (range: 0-39). The level of agreement was expressed by kappa statistics as well as by analysis of variance for interexaminer reproducibility studies. The mean CA scores ranged from 2.8 to 11.0, indicating the low prevalence of CA in this sample. Complete agreement was reached in 41.7% during the first assessment and in 44.1% in the second assessment. The interobserver agreement was moderate in the first session (mean overall kappa: 0.48) and substantial in the second (mean overall kappa: 0.67). The intraobserver agreement was good for all raters (mean kappa: 0.65). Standardized to the range of the scale, standard deviations of the differences between CA scores of the 4 raters in the 2 sessions were 11.1 and 11.2%; within raters it was 4.4%. We conclude that the assessment of CA using this rating scale is possible in stroke patients. It provides regional atrophy measurements and is reproducible when performed by 1 rater.
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PMID:Inter- and intraobserver reproducibility of cerebral atrophy assessment on MRI scans with hemispheric infarcts. 886 6

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

The clinical data and the magnetic resonance imaging (MRI) findings of 41 patients with clinically diagnosed dementia of the Alzheimer type (DAT) and 20 age-matched healthy controls were evaluated with the aim of determining the value of MRI in the diagnosis and differential diagnosis of dementia. Patients and controls with cerebrovascular risk factors, including a history of stroke, were excluded from the analysis. The MRI findings of patients with dementia revealed pathological changes, in particular cerebral atrophy (p < 0.0005), significantly more frequently than did those of controls (p < 0.005). Periventricular demyelinisation and lesions of the white matter were found in 23 (56%) patients, and in 6 (30%) of the controls. MRI revealed one case each of subdural hematoma, hydrocephalus and cerebral amyloid angiopathy. In 14 patients, the detection MRI scans of cerebral infarctions or hematomas suggested a major vascular component of the dementia. In contrast, lesions of the white matter can not reliably by ascribed to a vascular etiology. On the basis of our findings, it is concluded that cranial MRI is of great value for the differential diagnosis of dementia, even when the clinical diagnosis of Alzheimer's dementia is probable and cerebrovascular risk factors are absent.
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PMID:[Cranial magnetic resonance tomography--value in diagnosis of dementia. Important additional information for differential diagnosis]. 908 92

The purpose of our study was to define the neuroimaging features of the cardiolipin antibody syndrome. Thirty-eight patients with elevated anticardiolipin antibody titers were studied with magnetic resonance imaging or computed tomography or both. Two patients underwent cerebral angiography. All patients had recurrent transient ischemic attacks, amaurosis, or strokes. One patient had normal imaging findings. The remaining patients had a combination of infarction and atrophy. Focal infarcts, the most common finding, were seen in 32 patients. Cerebral atrophy was seen in 26 patients and was the only radiographic finding in 5. Angiography demonstrated dramatic abnormalities in the distal portions of the anterior and posterior circulations, with multiple stenosis and occlusions and extensive pial and transdural collateral networks. The cardiolipin antibody syndrome should be suspected in young patients with transient ischemic attacks or strokes in the absence of the usual risk factors for cerebrovascular disease. The presence of raised anticardiolipin antibody titers or the cardiolipin antibody syndrome in patients with lupus, in those with other connective tissue diseases, and in patients without overt manifestations of an autoimmune disorder should be viewed as a risk factor for future ischemic cerebrovascular events. Further understanding of the precise role of these antibodies in the pathogenesis of vascular thrombosis may lead to a better understanding of the mechanisms underlying certain forms of stroke.
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PMID:The neuroimaging features of the cardiolipin antibody syndrome. 911 34

Clinical course has been studied and tomographic examination has been performed in 50 patients with diabetes mellitus and cerebral stroke. 46 patients were thought to have a clinically ischaemic stroke, 2 ones were thought to have a haemorrhagic stroke and two were TIA cases in the first diagnosis. Among 50 patients with clinically focal neurologic deficits cortico-subcortical ischaemic focus was the most frequent CT finding (28%) with or without concomitant cortico-subcortical atrophy. There were 2 haemorrhagic pictures (4%). 13 CT scans (26%) were without any focal changes. CT cerebral atrophy was found in 34 patients (68%).
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PMID:[Clinical-tomographic correlation in patients with neurologic deficits of the brain due to diabetes mellitus]. 946 46

Stroke patients were assessed by brain CT scan, accompanied by demographic and clinical factors to predict the development of dementia following an ischemic episode. Vascular dementia was defined by NINDS-AIREN criteria. From 50 demented and 50 non-demented stroke patients, we analyzed the location of lesion, counted the numbers of lacunae, and semiquantitatively assessed the size of infarction, severity of overall white matter lesions (WML), and degree of brain atrophy. Compared to the non-demented patients, the demented patients: 1) encountered more stroke episodes (p < 0.001); 2) had more lacunae at bilateral basal ganglion (p < 0.001) or thalamus (p < 0.01); and 3) tended to have lesions in left cortex (p < 0.001), particularly a large infarct at the parietal (p < 0.001) or temporal lobe (p < 0.001). Periventricular changes (p < 0.001), subcortical WML (p < 0.001), overall WML (p < 0.001), and brain atrophy (p < 0.05) were also more severe in the demented group. However, no difference existed in demographic factors between the two groups. We concluded that several factors were important in developing dementia following an ischemic stroke, and the order by logistic regression would be: the severity of overall WML, left parietal infarct, and numbers of thalamic lacunae.
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PMID:Cranial computed tomography in ischemic stroke patients with and without dementia--a prospective study. 958 13


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