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PubMed2003

[Application of diffusion-weighted and perfusion magnetic resonance imaging in definition of the ischemic penumbra in hyperacute cerebral infarction].

OBJECTIVE: To investigate the value of diffusion-weighted imaging (DWI) and perfusion imaging (PI) in definition of the ischemic penumbra in hyperacute cerebral infarction. METHODS: (1) Animal study: Fifty-five SD rats were randomly divided into 5 groups of 10 rats. Nylon monofilament was inserted into the left middle cerebral artery (MCA) and immediately pulled out in 10 rats as controls (sham operation group or group A). The MCA of 40 rats was occluded by nylon monofilament for 30 minutes (group B), 60 minutes (group C), 180 minutes (group D), and 360 minutes (group E). Then all rats were examined by T(1)WI, T(2)WI, DWI, and PI. Apparent diffusion coefficient (ADC), regional cerebral blood volume (rCBV), relative cerebral blood flow (rCBF) and mean transit time (MTT) topographical maps were archived by the Workstation (GE SUN ADW3.0). The relative values of ADC, rCBV, rCBF, and MTT (ratios between the values of the occluded side and the opposite side) were calculated. The rats were killed and the cerebral infarction areas were stained by TTC (C(19)H(15)N(4)CI) and observed by light microscopy and electron microscopy. The results of microscopic examination were compared with the DWI results. (2) Clinical study: Forty-three patients, 24 males and 19 females,aged 68 years on average with acute stroke symptoms underwent MRI examination within 6 hours of symptom onset. T(1)WI, T(2)WI, DWI and PI were performed on all patients at the first MRI examination and T(2)WI was performed for follow up. The relevant parameters, including ADC, rCBV, rCBF and MTT were computed. The values of ADC, rCBV, rCBF and MTT within the lesions were compared to those at the normal sides and the ratio was calculated. The lesion volumes were measured in ADC map (as vDWI), MTT map (as vPI) and follow-up T(2)WI (as vCI). The differences between vDWI and vPI, and between vDWI and vCI were compared. RESULTS: (1) Animal study: In the control group DWI and PI showed no change in the signal intensity and no pathological change was found. Hyper-intensity signal was found in the T(2)WI in groups D and E. No abnormal signal was found in the T(1)WI in all groups. Abnormal signals were found in the MCA-supplying region in the DWI and PI of groups B, C, D, and E. The size of hyper-intensity signal in DWI along with the extension of occlusion time. TTC staining showed that the volume of unstained area was similar to that of hyper-intensity signal area in DWI image (t test, P > 0.05). PI showed a decrease of cerebral perfusion in the MCA-supplying region along with the extension of occlusion time. However, the size enlargement of occluded region was not as severe as shown by DWI along with the extension of occlusion time. The size of region with abnormal perfusion shown by PI was larger than that shown by DWI in groups B, C, and D. PI/DWI mismatch region, indicating the existence of ischemic penumbra zone, became gradually smaller along with the extension of occlusion time and almost disappeared 360 minutes after MCA occlusion. No significant change was found in the PI/DWI mismatch region by light microscope but slight swelling of mitochondrion and Golgi apparatus in neurons were observed by electron microscope. (2) Clinical study: The cases of 38 of the 43 patients were diagnosed as cerebral infarction by clinical and MRI follow-up examinations. The first MRI examination of these 38 cases showed no abnormal signal in T(1)WI and hyper-intensity signal in T(2)WI of 4 cases. The vPI was larger than vDWI in 31 cases and the vPI was equal to or smaller than the vDWI in 7 cases. Follow-up examination showed that vCI was larger than vDWI in 28 cases and vCI almost equaled to vDWI in 10 cases. Spearman correlation analysis showed a positive correlation between the volume of ischemic penumbra zone and that of infarction (r = 0.689, P < 0.001) which suggests that the volume change of ischemic penumbra zone influences the size of final infarction directly. CONCLUSION: Combination of DWI and PI clearly defines the ischemic penumbra in hyperacute stroke patient, thus laying, thus laying a basis for therapeutic intervention plan for stroke patients.

Acute Disease↗
PubMed1989

Confusional state and cerebral infarcts.

Thirteen patients with confusional state and cerebral infarction were studied. Seven patients had optic pathway alterations. On computed tomographic scan, 2 patients had multiple infarctions and 10 had single infarctions, predominantly located in the temporo-occipital associative cortex. One patient had a normal scan. Reduction of 'selective attention', 'release' hallucinations, amnesic syndrome and secondary individual adjustment could explain the confusional state.

Aged↗
PubMed1984

[Regional cerebral blood flow analysis by 133Xe intraarterial injection method. A comparison with cerebral infarction and cerebrovascular dementia].

Nine cases of cerebral infarction (cerebrovascular dementia 4 cases, hemiparesis 4, aphasia 1) were investigated by intraarterial 133Xe injection. Eight of the cases were male and one was female. Ages ranged from 38 to 72, with a mean age of 57.6 years. Two criteria were necessary for a diagnosis of cerebrovascular dementia: the presence of cerebrovascular disease and a score of less than 20 on Hasegawa's dementia scale. Cases of cerebrovascular dementia tended to have a lower mean cerebral blood flow (CBF) value on the white matter by two-compartmental analysis. Two of the five brain areas showed statistically significant differences. These results support the modern theory that cerebrovascular dementia appears as a result of a disturbance of the white matter. Cases of cerebrovascular dementia showed a lower mean CBF value with a coefficient of variance of regional distribution by height over area method. This showed that CBF values in cerebrovascular dementia were generally low and the range of values were narrow. In a comparison of regional CBF and cerebral angiographical findings, cases of cerebrovascular dementia tended to have a lower mean CBF value in proportion to the severity of angiographical findings. In addition, regional CBF showed a tendency to agree closely with angiographical findings.

Adult↗
PubMed2001

Sneddon syndrome with multiple cerebral infarctions 12 years after the onset of livedo vasculitis: a possible involvement of platelet activation.

Sneddon syndrome is characterized by livedo reticularis and multiple cerebral infarctions. Skin and central nervous system symptoms usually have a synchronous onset and at times initial symptoms affect one of them, the other lagging several years behind. We here report a patient with Sneddon syndrome who developed multiple cerebral infarctions more than 10 years after the onset of livedo reticularis. While the neurological symptoms were apparent, the patient did not display active skin manifestations. Laboratory findings excluded collagen diseases, antiphospholipid antibody syndrome, and inherited quantitative deficiency of protein C, protein S and antithrombin III. Abnormal findings included extremely elevated levels of beta-thromboglobulin and platelet factor-4 in the blood, although these acute phase markers of thrombosis were examined several years after the onset of cerebral infarctions. Platelet activation may have caused Sneddon syndrome in the present case.

Adult↗
PubMed2001

Effect of acupuncture on plasmic levels of insulin, glucagon and hypercoagulability in NIDDM complicated by acute cerebral infarction.

Twenty-one cases of acute cerebral infarction secondary to NIDDM were treated with acupuncture and conventional therapy, and compared with 16 cases treated with conventional therapy alone. The results showed that acupuncture was more effective in reducing insulin and glucagon levels (P < 0.001) and improving hypercoagulability (P < 0.05) of blood.

Acupuncture Therapy↗
PubMedDate not supplied

Prevention of cerebral infarction in the monkey by omental transposition to the brain.

The intact omentum of 13 monkeys was lengthened, placed subcutaneously, and laid on the left cerebral hemisphere prior to occluding the left middle cerebral artery. Two of these 13 monkeys developed left cerebral infarct and a right hemiparesis. Nine other monkeys had their left middle cerebral artery occluded without omental protection. All of these 9 developed a left cerebral infarct and 8 of them a right hemiparesis. Intact omentum may prevent a cerebral infarction when placed on the brain prior to MCA occlusion.

Animals↗
PubMed1990

Acute cocaine abuse associated with cerebral infarction.

We present the case of a 29-year-old patient who developed a cerebral infarction, without hemorrhage, after using cocaine. A computed tomography scan of the brain at the time of initial presentation was entirely normal; a repeat CT scan on the fifth hospital day showed a basal ganglion infarction. No evidence of intracranial bleeding was detected. Theories of cocaine-induced cerebral infarction, including promotion of thrombogenesis and vasospasm, are reviewed.

Basal Ganglia↗
PubMed1994

Delayed cerebral infarction after dog bites: case report.

Delayed cerebral infarction occurred after dog bites in the region of the internal carotid artery of a 7-year-old boy. Initial wound exploration and repair did not reveal any signs of vascular trauma. Understanding the dynamics of the bites and relating the wounds topographically to the course of the underlying large vessels are key factors in early diagnosis of occult vascular damage.

Animals↗
PubMed1992

Locations of cerebral infarctions in tuberculous meningitis.

The locations of cerebral infarctions were studied in 14 patients with tuberculous meningitis (TBM) and 173 patients with noninflammatory ischemic stroke (IS). In patients with TBM, 75% of infarctions occurred in the "TB zone" supplied by medial striate and thalamoperforating arteries; only 11% occurred in the "IS zone" supplied by lateral striate, anterior choroidal and thalamogeniculate arteries. In patients with IS, 29% of infarctions occurred in the IS zone, 29% in the subcortical white matter, and 24% in (or involving) the cerebral cortex. Only 11% occurred in the TB zone. Bilaterally symmetrical infarctions of the TB zone were common with TBM (71%) but rare with IS (5%).

Adult↗
PubMed1995

[A case of central retinal artery occlusion followed by cerebral infarction due to internal carotid artery disease].

Reported is a 68-year-old male with left central retinal artery occlusion (CRAO) followed by cerebral infarction due to left internal carotid artery disease. He was referred to our hospital diagnosed as having left CRAO. In view of severe stenosis of ipsilateral internal carotid artery by ultrasound duplex scan, carotid endarterectomy (CEA) was indicated. While waiting for the operation, he suffered from monoparesis in his right lower limb despite the administration of antiplatelet agents. Brain MRI showed cerebral infarction in the left frontal cortex. It was suggested that artery-to-artery embolism from the lesion of the internal carotid artery might be the common mechanism of CRAO and cerebral infarction in this case. According to theses results, CEA should be considered in patients with severe stenosis of the internal carotid artery before it is too late.

Aged↗
PubMed1990

Small deep cerebral infarcts associated with occlusive internal carotid artery disease. A hemodynamic phenomenon?

Small deep cerebral infarcts, often referred to as lacunes, have been traditionally associated with small-vessel disease affecting the deep penetrating arterial system. We describe 10 cases where these infarcts were associated with severe, ipsilateral internal carotid artery occlusive disease. Seven of these patients also had severe occlusive disease of the contralateral internal carotid artery. The clinical and radiologic features, in combination with studies of cerebral blood flow, were consistent with hemodynamically mediated cerebral ischemia. Occlusive internal carotid artery disease may be more commonly associated with hemodynamic cerebral ischemia than previously believed, and small cerebral infarcts in the deep arterial border zone areas are likely to be an important manifestation of this process.

Adult↗
PubMed1983

Why are infant gerbils more resistant than adults to cerebral infarction after carotid ligation?

Younger gerbils have been found to be more resistant than adults to cerebral infarction after carotid ligation. In this study, the perfused cerebral area after bilateral common carotid occlusion was evaluated in infant, young, and adult Mongolian gerbils by the carbon black perfusion method to assess the existence and significance of collateral blood vessels between the vertebrobasilar and carotid circulations. Nineteen gerbils were divided into three groups (i.e., infant, young and adult gerbils aged 3-4, 5-7, and 10-17 weeks, respectively). After bilateral common carotid artery occlusion, carbon black was injected directly into the left ventricle by cardiac puncture through the closed thorax. In five of eight infant gerbils, the whole brain was perfused by carbon black, while in the remaining three, only the cerebellum and brainstem were stained well, and marked bilateral cerebral pallor was observed. On the other hand, carbon black did not perfuse the brain region supplied by the carotid arteries, both in young and adult gerbils (11 animals in total). These results suggest that infant gerbils might have a more highly developed network of collateral blood vessels between the vertebrobasilar and carotid circulations, and the existence of such a significant network might be the basis for the fact that infant gerbils are resistant to cerebral infarction following carotid ligation. We propose that gerbils should be used as a stroke model only when they are 5 weeks old or older.

Aging↗
PubMed1980

Parkinsonism in patients with cerebral infarcts.

From 220 necropsies of patients with cerebral infarcts, 5 were selected, in which the clinical history revealed typical parkinsonian symptoms with a progressive course of the extrapyramidal disorder. No correlation could be found between the location and the size of the infarcts on the one hand and the signs of parkinsonism on the other hand. In the 5 cases presented, the substantia nigra showed patchy areas of neuronal degeneration without any Lewy bodies nor neurofibrillary changes, around a pronounced status cribrosus in areas irrigated by paramedian branches of the mesencephalic arteries. Similar neuropathologic findings were present, but to a minor degree, in 2 of 5 cases of pseudo-bulbar palsy. Some extrapyramidal features were also present. It is proposed that is some rare instances, status cribrosus may be responsible for nigral degeneration and for the occurrence of parkinsonism.

Aged↗
PubMed1995

Contribution of diaschisis to the clinical deficit in human cerebral infarction.

BACKGROUND AND PURPOSE: Regions of decreased cerebral blood flow are often seen on single-photon emission computed tomography (SPECT) after stroke and have been widely reported to add to the clinical deficit. However, such reports have not distinguished between correlation and causation. We analyzed 124 serial SPECT scans performed in 50 patients to assess the role of diaschisis in the clinical deficit after stroke. METHODS: SPECT with the use of 99mTc-hexamethylpropyleneamine oxime (99mTc-HMPAO) was performed in a prospective, unselected series of 50 patients with cerebral infarcts studied at a median of 1.1, 6.8, and 95 days after ictus. Patients were also assessed with the use of the Canadian Neurological Scale, the Barthel Index, a neuropsychological evaluation, and infarct volume measurement. RESULTS: One hundred twenty-four serial SPECT scans were done in 50 patients. Diaschisis was identified at 168 sites. There was insufficient correlation between diaschisis and the clinical measurements to support the suggestion that diaschisis independently causes clinical deficits beyond those due to the infarct itself. Unlike the clinical status, diaschisis showed little tendency to resolve during the 3-month follow-up period of the study. Several of the instances of correlation were shown to be of a noncausal kind, with both the diaschisis and the clinical deficit being due to the lesion directly; there was no known mechanism for the diaschisis to cause the clinical deficit. CONCLUSIONS: Diaschisis does not independently add to the clinical deficit after stroke. It is more likely that it simply represents part of the damage done by the stroke.

Adult↗
PubMed1998

[Effect of cardiac embolism sources on origin of territorial cerebral infarcts].

BACKGROUND AND PURPOSE: To test the association of cardiac sources of embolism with territorial type brain infarcts. METHODS: From a prospective cerebral ischemia data base the 106 consecutive patients with territorial type cerebral infarcts on computerized tomography were analyzed. The 85 consecutive patients with lacunar lesions served as a comparison group. The association of cardiac sources of embolism with territorial types infarcts was assessed using univariate Chi Square tests and logistic regression models. Cardiac sources of embolism were defined as:atrial fibrillation, left cardiac thrombi, valvular vegetations, wall motion and valvular abnormalities, left atrial enlargement, open foramen ovale, septal aneurysm, mitral valve prolaps, and aortic arch atherothrombosis (all findings--except for atrial fibrillation--assessed by echocardiography). RESULTS: Atrial fibrillation was significantly associated with territorial type infarcts (odds ratio 2.2, 95% confidence interval 1.01-4.8). This effect was independent of additional cardiac diseases, other cardiac abnormalities, carotid artery stenosis, and patient age. Most likely due to the small sample size, left cardiac thrombi only showed a non-significant trend towards an association with territorial infarcts (odds ratio 3.0, 95% confidence interval 0.7-12.3). The rate of all other cardiac findings did not differ significantly between the comparison groups. CONCLUSION: Atrial fibrillation and cardiac thrombi showed an association with territorial type infarcts. Other so-called cardiac sources of embolism--except for mechanical valves and bacterial endocarditis which were not represented in our sample--revealed no clinically relevant association with embolic brain infarct pattern.

Adult↗
PubMedDate not supplied

Risk factors for silent cerebral infarction in the elderly.

BACKGROUND: A silent cerebral infarction (SCI) is often found in the elderly. However, studies on SCIs focusing on an elderly population are sparse. Our objective was to evaluate risk factors of SCIs in healthy elderly individuals. METHODS: One hundred seventy-five neurologically normal community-dwelling Japanese people aged >/=65 years (128 men and 47 women; 77.5 +/- 8.7 years) were studied. Among them we assessed the demographic data and detected SCIs on brain magnetic resonance imaging scans. RESULTS: Eighty four subjects had at least one SCI. Hypertension and low body mass index (BMI) were the significant risks for SCIs in multivariate analysis adjusted for age, sex and other risk factors. Mean BMI in subjects with SCIs was significantly lower than those without SCIs (20.8 +/- 3.2 kg/m(2) vs. 22.1 +/- 3.2 kg/m(2)). In the subgroup analysis by age stratum regarding hypertension and BMI, hypertension was a significant risk factor in subjects aged 65-75 years. Lower BMI had a significant risk in subjects aged >/=81 years. CONCLUSIONS: Hypertension and increasing age have been recognized as risk factors for SCIs, and low BMI might be a significant risk especially in superelderly subjects. Further data with a larger sample size is needed to confirm the relationship between BMI and SCIs among the elderly.

Aged↗
PubMed1993

Watershed cerebral infarction associated with perioperative hypotension.

The pathogenesis of perioperative stroke is not clear from the literature. To explore the influence of various risk factors we examined the clinical, Duplex ultrasound and computerised tomography findings of all cases suffering cerebral infarction within 24 hours of surgery in a prospective series of 358 coronary or peripheral vascular reconstructive operations. Four patients (1.1%) had cerebral infarcts within 24 hours of surgery, all associated with perioperative systolic blood pressures of less than 90 mmHg. The other significant risk factor was previous cerebral ischaemic symptoms. Haemodynamic cerebral ischaemia occurred immediately after operation in 2 of 10 cases with severe symptomatic carotid stenosis or occlusion (stroke risk 20%; 95% confidence interval 2.52%-55.61%). Two cases with mild carotid disease had cerebral infarcts in previously asymptomatic hemispheres following coronary artery bypass graft surgery. One of these had clinical and computerised tomographic evidence of cortical watershed infarction. We conclude that cerebral haemodynamics are important in perioperative stroke and that symptomatic patients with severe carotid disease may be at high risk of perioperative watershed infarction.

Blood Pressure↗
PubMed1995

Analysis of plasma fibrinolysis in the patients with acute cerebral infarction.

In the present study, the plasma fibrinolytic activity in 30 cases of cortical artery territory cerebral infarction (CACI) and 32 cases of perforating artery territory cerebral infarction (PACI) within 3 days after ictus, and 30 sex- and age-matched controls without cardio-cerebrovascular diseases were evaluated by a comprehensive panel of assay, including the plasma tPA activity, PAI activity, endothelial capacity of tPA release and PAI/tPA ratio. The results showed that the plasma fibrinolysis and the endothelial potential to release tPA responding to stimulation in both subtypes of the patients were significantly lower than those in the controls, which provide the theoretical basis for carrying out the thrombolytic therapy in the ischemic stroke. And the study also suggested that increased plasma PAI activity could increase the risk of AS thrombotic events with increased serum triglyceride level.

Acute Disease↗