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 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.
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PMID:Neurophysiologic syndromes in stroke as predictors of outcome. 68 54

Pulmonary embolism secondary to deep vein thrombosis is a frequent cause of death in stroke patients. In a multicentre study of deep vein thrombosis prophylaxis, 112 patients with cerebral infarction and leg paresis were given aspirin 300 mg three times a day (t.d.s.) alone or with dipyridamole 100 mg t.d.s. To screen for deep vein thrombosis liquid crystal thermography of the legs was performed daily for 15 days on all patients. Those patients with positive thermography underwent immediate X-ray venography of the appropriate limb as the definitive investigation for venous thrombosis. Twenty-two patients had positive thermograms, of whom 16 had confirmed deep vein thrombosis as demonstrated by X-ray venography. Only 8 of the 22 had clinical signs of deep vein thrombosis and 2 of those had a negative venogram. Of the 14 patients with positive thermography but negative clinical signs 10 had positive venograms. Difference in the incidence of deep vein thrombosis in the two treatment groups was not demonstrated. It is concluded that occult deep venous thrombosis is common after ischaemic stroke and it can occur without clinical signs. Liquid crystal thermography is a simple, rapid and cheap screening test that will allow the detection of clinically unrecognized thrombosis.
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PMID:Liquid crystal thermography as a screening test for deep vein thrombosis in patients with cerebral infarction. 175 94

A 44-year-old woman with a history of cerebral infarction and hypertension developed sudden onset of speech and visual disturbance. On admission, her general physical examinations showed high blood pressure of 210/120 mmHg and Raynaud's phenomena. The neurological examinations revealed right upper quadratic hemianopsia, left oculomotor nerve paresis and left hyperreflexia. Laboratory findings showed that antinuclear and anti-DNA antibodies were positive. The activity of Fletcher factor was reduced to 50%, and the activated partial thromboplastin time (APTT) was prolonged to 82.6 seconds. And a 1:1 dilution with normal plasma failed to correct the prolonged APTT, indicative of circulating anticoagulant to Fletcher factor. Plasma fibrinogen increased to 500 mg/dl but FDP was normal. The CT scan demonstrated the recurrently developed cerebral infarction in the left occipital lobe. Cerebral angiogram revealed mild atherosclerosis of basilar and bilateral posterior cerebral arteries, but any occlusive lesions were not found. Although she had a history of hypertension, this case suggests the possibility that the disturbance in fibrinolytic system may have been caused by the circulating anticoagulant to Fletcher factor, and contributed to her cerebral infarctions.
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PMID:[A case of cerebral infarction with circulating anticoagulant to Fletcher factor]. 191 33

In a prospective study of the incidence of deep vein thrombosis (DVT) after stroke, and the prophylactic effect of dextran, 50 patients, admitted with a diagnosis of cerebral infarction with paresis of the lower extremity within the first 48 hours, were randomly allocated to treatment or non-treatment groups. The treatment group received 500 ml of dextran 40 on admission and on days 1 and 2, and 250 ml on days 4 and 6. Venesection was performed on admission and if necessary on day 1. The control group received no dextran or venesection. DVT was diagnosed with the 125I-fibrinogen test during the first ten days. The incidence of DVT was 54% in the treatment group and 50% in the control group. There were no statistically significant differences between the groups regarding number of DVTs needing treatment, number of positive scanning points or number of days for scan to become positive. Lethal pulmonary emboli occurred in one treated and in three control patients, respectively. Age and progress of neurologic symptoms predisposed for the development of DVT. The high incidence of DVT in stroke patients indicates the need for prophylactic routines.
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PMID:Venous thromboembolism after cerebral infarction and the prophylactic effect of dextran 40. 243 1

There is continuing controversy about the benefits of decompressive craniectomy in the treatment of lesions causing increased intracranial pressure (ICP) and brain edema. Laboratory work has shown a decrease in ICP after craniectomy, but also a paradoxical enhancement in the formation of underlying cerebral edema, which may act to the detriment of the patient. Since Rengachary et al. advocated craniectomy for massive cerebral infarction and reported their group of three patients, we have managed five patients with acute supratentorial cerebral infarction who progressed to uncal herniation and impending death from raised ICP and brain stem compression. All were treated with frontotemporal craniectomy after conventional medical therapy failed to achieve a response. All patients survived and are walking, despite a paresis appropriate to their original stroke. Two have returned to work. Good results with supratentorial craniectomy after infarction show that this procedure is life-saving and can also give acceptable functional recovery.
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PMID:Functional recovery after decompressive craniectomy for cerebral infarction. 318 72

Traumatic dissections of the extracranial internal carotid artery (ICA) in 18 patients aged 19 to 55 years were studied. All had suffered blunt head or neck injury of marked or moderate severity; motor-vehicle accidents were the leading cause of the injury. Delayed focal cerebral ischemic symptoms were the most common presenting symptoms. Less commonly noted was focal unilateral headache associated with oculosympathetic paresis or bruit. Following a head injury, the abrupt onset of focal cerebral symptoms after a lucid interval should raise the suspicion of arterial injury, particularly when computerized tomography fails to show abnormalities that would explain the evolving neurological deficits on the basis of direct trauma to the brain. Unilateral headaches, oculosympathetic palsy, and bruits also help in establishing the diagnosis. Focal cerebral ischemic symptoms may develop months or years after the initial trauma. These delayed symptoms are caused by embolization from a thrombus within a residual dissecting aneurysm. Common angiographic findings, in decreasing order of frequency, are: aneurysm, stenosis of the lumen, occlusion, intimal flap, distal branch occlusion (embolization), and slow ICA-to-middle cerebral artery flow. Although two patients died as the result of massive cerebral infarction and edema and some were left with severe neurological deficits, most made a good recovery. Residual dissecting aneurysms and occlusion seem to occur more frequently with traumatic dissections than with spontaneous dissections of the extracranial ICA.
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PMID:Traumatic dissections of the extracranial internal carotid artery. 333 35

Aneurysm of the extracranial internal carotid artery is a rarely observed condition. Intra-aneurysmatic thrombosis, cerebral embolism with possible neurological consequences, and rupture are the most common complications. Operations were performed on 20 patients for aneurysm of the internal carotid artery. The cases included 14 "genuine" arteriosclerotic aneurysms and seven "false" aneurysms in the wake of shell splinter injuries, tonsillectomy, thrombo-arteriectomy, and blunt traumata. Pulsating tumour was the most important clinical symptom in all aneurysm cases. Arterial continuity was restored by resection of aneurysm in all cases. Sixteen patients were dehospitalised without any complaint. Two patients with preoperative cerebral infarction were left with residual paresis. One patient died of pulmonary embolism, and one patient operated on for rupture died in shock.
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PMID:[Aneurysm of the extracranial internal carotid artery]. 354 7

Thirty (2.5%) of 1200 consecutive patients with a first stroke had a spontaneous dissection with occlusion of the cervical internal carotid artery (ICA). A suggestive picture with ipsilateral headache and oculosympathetic paresis was uncommon (17%), so that diagnosis was uncertain before angiography. Seven patients died within one week. During follow-up (mean, 3.2 years) with sequential Doppler ultrasonographic testing, 12 survivors had a good recovery and early reopening of the occluded ICA, and 11 had a poor recovery usually without reopening of the ICA. Recurrence of a dissection occurred in only one patient. Large infarcts causing death or a severe disability were associated with an ICA thrombus and distal emboli; the organization of this intraluminal thrombosis may explain the absence of reopening in these cases while resorption of the intramural hematoma developed. Early heparin sodium therapy may help prevent intraluminal clotting without carrying an important risk of extending the dissection, but its clinical benefit remains unproven. Contrary to current opinions, ICA dissection with occlusion causing cerebral infarction may often carry a severe prognosis.
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PMID:Spontaneous carotid dissection with acute stroke. 381 30

Three principal diagnostic problems were encountered in a group of 81 elderly patients with epileptic seizures: Post-ictal paresis (Todd's palsy) occurred in 13 patients (16%), of whom seven had evidence of past or present cerebral infarction, and six no such evidence. The paresis lasted up to 4 days, and could be confused with recurrent infarction or a transient ischaemic episode. Ictal and post-ictal confusional states of 24 h or more duration (up to 7-8 days) were noted in 11 patients (14%). They occurred in association with normal intellectual function as well as with pre-existing dementia, and required to be distinguished from other causes of delirium. Two patients presented paroxysmal sensory phenomena of ictal type. The differential diagnosis of episodic pain in hemiplegic limbs is discussed.
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PMID:Epileptic seizures in the elderly: II. Diagnostic problems. 680 29

The validity of a clinical classification system was assessed for subtypes of cerebral infarction for use in clinical trials of putative stroke therapies and clinical decision making in a population based stroke register (n = 536) compiled in Perth, Western Australia in 1989-90. The Perth Community Stroke Project (PCSS) used definitions and methodology similar to the Oxfordshire Community Stroke Project (OCSP) where the classification system was developed. In the PCSS, 421 cases of cerebral infarction and primary intracerebral haemorrhage (PICH), confirmed by brain imaging or necropsy, were classified into the subtypes total anterior circulation syndrome (TACS), partial anterior circulation syndrome (PACS), lacunar syndrome (LACS), and posterior circulation syndrome (POCS). In this relatively unselected population, relying exclusively on LACS for a diagnosis of PICH had a very low sensitivity (6%) and positive predictive value (3%). Comparison of the frequencies and outcomes (at one year after the onset of symptoms) for each subgroup of first ever cerebral infarction in the PCSS (n = 248) with the OCSP (n = 543) registers showed uniformity only for LACI. For example, there were 27% of cases of TACI in the PCSS compared with 17% in the OCSP (difference = 10%; 95% confidence interval (95% CI) 4% to 16%) and 15% of cases in the PCSS compared with 24% in the OCSP were POCI (difference = 9%; 95% CI 3% to 15%). Case fatalities and long-term handicap across the subgroups were not significantly different between studies, but the frequencies of recurrent stroke were significantly greater for POCI in the OCSP compared with the PCSS. Although this classification system defines subtypes of stroke with different outcomes, simple clinical measures-level of consciousness, paresis, disability, and incontinence at onset-are more powerful predictors of death or dependency at one year. It is concluded that simple clinical measures that reflect the severity of the neurological deficit should complement this classification system in clinical trials and practice.
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PMID:Validation of a clinical classification for subtypes of acute cerebral infarction. 793 76


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