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At least 1,423 records · Page 79Linked to original sources
PubMed1998

Changes in benzodiazepine receptor binding detected with SPECT in patients with cerebral infarction.

SPECT (single photon emission computed tomography) using iomazenil (IMZ) as a ligand for benzodiazepine receptors has recently been developed. Feasibility of the technique for detecting neuronal damage in the cerebral cortex was evaluated in 17 patients with cerebral infarction, specifically, patients with internal carotid artery (ICA) thrombosis (n = 6), middle cerebral artery (MCA) thrombosis (n = 5) and embolism (n = 6). IMZ SPECT was performed 5 to 17 days after stroke. Following the injection of 123I-IMZ 167 or 222 MBq intravenously, images were obtained at 15 minutes (early image) and 180 minutes (late image). In 11 cases, 99mTc-HM-PAO (hexamethyl-propylamine oxime) SPECT was also performed to measure cerebral blood flow (CBF). MRI was performed in all cases to elucidate areas of infarct. Early images from IMZ SPECT correlated well with those from HM-PAO, suggesting that early scans using IMZ SPECT reflect mainly CBF. In late images from IMZ SPECT, observed lesions were consistent with infarcted areas on MRI in most cases. However, in 3 cases of ICA thrombosis, 1 case of MCA thrombosis and 1 case of embolism, late IMZ SPECT imaging showed that the affected area was wider than apparent infarcts on MRI, indicating that the cerebral cortex, which was intact on MRI, was also involved. In these patients, clinical signs of cortical involvement were observed as well. These results suggest that moderately reduced CBF may affect cortical neurons without inducing apparent infarct, and such damage can be detected with IMZ SPECT.

Adult↗
PubMed1989

[Clinical aspects of treatment and preventive treatment with thrombocyte aggregation inhibitors in cerebrovascular diseases].

Inhibitors of thrombocyte aggregation are generally accepted in the therapy and prophylaxis of ischemic cerebrovascular disease. The frequency of re-infarction, morbidity and mortality after TIA, PRIND and minor stroke is influenced favourably. There are controversial opinions, however, about the usefulness for patients suffering from completed strokes. In patients with progressive stroke, cerebral embolism of cardiac source, or non-infective thrombosis of sinuses or cerebral veins, inhibitors of thrombocyte aggregation are used if anticoagulation therapy is not possible. Additionally, they are applied in cases of infective thrombosis of sinuses or cerebral veins, after termination of anticoagulation therapy, after cardiac valve replacement, and after surgical reconstructions of craniocervical vessels. Acetylsalicylic acid is the clinically best examined substance; its effect--especially in males--was proven by numerous prospective trials. A combined treatment with dipyridamole, sulfinpyrazone or other drugs seems to be unnecessary. A daily dose of not more than 300 to 325 mg acetylsalicylic acid is recommended for prophylaxis after ischemic cerebral events; in connection with that dose severe gastrointestinal side effects are hardly to be expected. Whether even lower doses would yield the same prophylactic effects will have to be clarified by further studies.

Aspirin↗
PubMed1993

Diagnosis of prosthetic heart valve thrombosis. The respective values of transthoracic and transoesophageal Doppler echocardiography.

Early diagnosis of acute prosthetic thrombosis remains a challenge. In 20 patients with 23 thrombosed cardiac valves, we evaluated the respective value of transthoracic (TTE) and transoesophageal (TEE) Doppler echocardiography. According to the presence or absence of prosthetic obstruction by continuous-wave Doppler, prostheses were separated into two groups. Group 1 included nine thrombosed prostheses (8 mitral, 1 aortic) with severe obstruction. All patients presented with severe symptoms of heart failure. Transthoracic Doppler echocardiography allowed immediate diagnosis of prosthetic thrombosis, even in critically ill patients, showing (1) eccentric transprosthetic colour flow jets in all eight mitral prostheses, (2) severe obstruction on Doppler examination (mean gradient = 18 to 36 mmHg in eight mitral prostheses, and 69 mmHg in one aortic valve), and (3) direct echocardiographic evidence of thrombosis (i.e. thrombus or abnormal disc or leaflet motion) in four patients. All nine patients were immediately treated by surgery (n = 8) or fibrinolysis (n = 1) on the basis of TTE results only. TEE allowed better visualization of thrombus and restricted leaflet or disc motion, but had little influence on patient management. Group 2 included 14 thrombosed prostheses (10 mitral, 4 aortic) with mild or absent obstruction. In three patients with massive mitral prosthetic thrombosis, an associated minimal thrombosis of a prosthetic aortic valve was found at surgery, but was detected neither by TTE, nor by TEE. The 11 remaining patients with isolated partial mitral (n = 10) or aortic (n = 1) thrombosis. Clinical presentation was fever, cerebral embolism, or mild dyspnoea, but no heart failure. TTE was normal in all.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed1999

Plasma semicarbazide-sensitive amine oxidase in stroke.

Semicarbazide-sensitive amine oxidase (SSAO) has been suggested to be involved in the development of vascular endothelial damage. The source of the soluble form of SSAO found in the blood serum is unknown. However, it has been speculated that it is secreted from cells within the vascular wall where high activity of the enzyme is found. Altered SSAO activity has been reported in atherosclerotic plaques of the human aorta. Stroke is a manifestation of long-term atherosclerotic disease, and in this study, plasma SSAO activities were estimated in 42 patients with cerebral thrombosis and 26 patients with cerebral embolism, and compared to two control groups of 45 individuals in total. No statistically significant differences were found between the patient groups and controls regarding plasma SSAO activity, suggesting that changes in the soluble form of SSAO found in the circulation do not play a major role in this type of acute cerebrovascular event. Furthermore, it does not seem likely that the involvement of vascular tissue occurring in stroke results in release of the enzyme into the circulation. Nevertheless, further studies on tissue-bound SSAO in cerebral vessels would be of great interest.

Aged↗
PubMed1985

Cerebral haemorrhagic infarction in young patients with hereditary protein C deficiency: evidence for "spontaneous" cerebral venous thrombosis.

Among 53 patients with hereditary protein C deficiency belonging to 20 families three women were encountered who, aged 27, 34, and 38 respectively, had had cerebral haemorrhagic infarction, probably due to intracranial venous thrombosis. All three had also had venous thrombosis of the leg and pulmonary embolism either before or after their cerebral infarction. One patient sustained cerebral infarction while receiving an oral contraceptive, but infarction in the two others occurred "spontaneously." One patient also had an intraventricular and subarachnoid haemorrhage during the induction phase of coumarin treatment, which was assumed to have resulted from haemorrhagic infarction of the chorioid plexus, analogous to coumarin provoked haemorrhagic skin necrosis in protein C deficiency. Hereditary protein C deficiency should be considered in young patients with acute or subacute cerebral symptoms, especially if they have a family or personal history of venous thromboembolism.

Adult↗
PubMed2005

Plasma homocysteine is a risk factor for recurrent vascular events in young patients with an ischaemic stroke or TIA.

OBJECTIVES: Young patients with an ischaemic stroke or transient ischaemic attack (TIA) often have no vascular risk factors. Hyper-homocysteinaemia is an established risk factor for stroke in elderly patients but it is uncertain whether it is also important for the prognosis of young ischaemic stroke and TIA patients. We examined the possible effect of the plasma homocysteine level on the risk of recurrent vascular events in patients between 18 and 45 years of age. METHODS: The study population consisted of 161 consecutive patients with a recent cerebral infarction or TIA. Data on the primary event and the homocysteine level were collected retrospectively from hospital records. General practitioners and patients were contacted by telephone to record vascular events and the type of medication used during the follow-up period. Vascular events included cerebral infarction, TIA, pulmonary embolism, venous thrombosis, myocardial infarction and peripheral arterial disease. RESULTS: A Kaplan- Meier curve showed a dose effect relationship between event-free survival time and tertiles of the homocysteine level (Log rank statistic 5.91; p=0.05). The Cox hazard ratio, after adjustment for homocysteine lowering treatment, was 1.7 (95 % CI, 1.1 to 2.8) for any vascular outcome event, 1.9 (95% CI, 1.1 to 3.0) for arterial outcome events and 1.8 (95 % CI, 1.1 to 2.9) for cerebral outcome events. CONCLUSIONS: In spite of our small number of outcome events we found a significant association at the 95% confidence level between homocysteine level and the risk of recurrent vascular events in young patients with an ischaemic stroke or TIA. The association is of the same magnitude as in elderly people.

Adolescent↗
PubMed1983

Cerebrovascular disease in western Australia: an analysis of stroke type and associated risk factors.

The stroke types and major risk factors in 356 patients with cerebrovascular disease were examined. Large artery thrombosis accounted for 53% of strokes, cerebral embolism for 22%, lacunes for 14% and intracerebral hemorrhage for 11%. Hypertension, detected in two-thirds of patients, was the major risk factor. The sex distribution varied with age, the major change being an increase in the number of females affected in older age groups. The extent of systemic vascular disease was greatest in patients with thrombo-embolic infarction.

Adult↗
PubMed1995

[Hemorrhagic cerebral infarction at the old age in a case with familial antithrombin III (ATIII) deficiency].

An old woman had stroke at age 67. Cerebral CT scan disclosed the low-density lesion with high-density area in the left temporal lobe, but no empty delta sign in the superior sagittal sinus. Thereafter, she had sometimes panic attacks. At the age of 70, she was admitted because of loss of consciousness probably caused by the same attack. On admission, Brain CT scan showed no fresh lesions. During the stay in the hospital, she had an episode of deep vein thrombosis of her left leg. The patient was found to have not only reduced biochemical activity but also low immunological level of AT III. Her nephew had also the low plasma AT III antigen concentration. Transesophageal echocardiography showed no abnormality, but atherosclerotic change at the aortic arch. We speculated that hemorrhagic cerebral infarction in the territory of the branch of middle cerebral artery could be induced by the arterial thrombus which was related to the hypercoagulable state associated with familial AT III deficiency, although the possibility of cardiogenic embolic infarction or of cerebral vein thrombosis could not be ruled out. Familial AT III deficiency is one of the causes of cerebral infarction even in the elderly.

Aged↗