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PubMed2003

EEG burst recovery is predictive of brain injury after experimental hypothermic circulatory arrest.

OBJECTIVE: To evaluate whether electroencephalography (EEG) recovery could be considered a reliable marker of brain injury after experimental hypothermic circulatory arrest (HCA). DESIGN: Cortical electrical activity was registered before and after a 75-min period of HCA in 27 pigs that survived 7 days after the experiment. The sum of EEG bursts was counted as a percentage of the sum of artifact-free bursts and suppressions, and this percentage was used as a measure of EEG activity in the analysis. RESULTS: Brain infarction developed in 13 animals (48.1%), in 12 cases (44.4%) having involved the cortex, in 1 case the thalamus (3.7%) and in another the hippocampus (3.7%). The mean EEG burst percentage significantly correlated with the total brain histopathological score (rho = -0.588, P = 0.001). EEG burst percentage from the 2 h 20 min to the 7 h 20 min interval correlated with the total brain histopathological score and with the cortex, brainstem and cerebellum scores. The mean EEG burst percentage rate was higher, but not significantly, among the animals without brain infarction (38.5% vs 32.4%), but such a difference was significant at the 3 h 20 min postoperative interval (P = 0.02). The mean EEG burst percentage significantly correlated with brain glucose concentration at the 1 h interval (rho = 0.387; P = 0.046), brain lactate concentration at the 2 h interval (rho = -0.431; P = 0.025), and the brain lactate/glucose ratio at the 1 h 30 min interval from the start of rewarming (rho = -0.433; P = 0.024). CONCLUSION: A decreased EEG burst percentage seems to be associated with an increased risk of developing histologically evident brain ischemic injury in the cortex, brainstem and cerebellum after experimental HCA.

Animals↗
PubMed1993

Decrease in cerebral blood flow with blood pressure reductions in patients with chronic stroke.

BACKGROUND AND PURPOSE: Possible effects of changes in blood pressure on the cerebral circulation were studied in patients with chronic stroke and age-matched nonstroke control subjects at 28 +/- 10 months (mean +/- SD) (range, 18 to 54 months) and 27 +/- 6 months (range, 19 to 44 months), respectively, after the first measurement. METHODS: Cerebral blood flow was measured by the 133Xe inhalation method in 55 patients (mean +/- SD age, 62 +/- 11 years; 39 with brain infarction and 16 with hemorrhage) and 10 control subjects (mean +/- SD age, 61 +/- 9 years). Correlations between changes in cerebral blood flow and blood pressure were evaluated. RESULTS: Among brain infarctions, average cerebral blood flow did not change from the first study; however, changes in cerebral blood flow in each individual were closely related to changes in systolic and mean arterial blood pressures (P < .01 and P < .05, respectively). Of these, in 10 patients with cerebral blood flow decreased more than 15% from the initial levels, systolic and mean arterial blood pressures decreased by 25 +/- 32 mm Hg and 16 +/- 14 mm Hg (P < .05 and P < .005, respectively). In contrast, in 29 patients with unchanged or increased cerebral blood flow, changes in systolic (0 +/- 19 or -2 +/- 12 mm Hg, respectively) and mean arterial blood pressures (3 +/- 22 or -1 +/- 11 mm Hg, respectively) were not significant, and their systolic blood pressure levels were maintained above 110 mm Hg. CONCLUSIONS: Blood pressure importantly correlates with cerebral circulatory changes among patients with chronic brain infarction. Early detection of cerebral hemodynamic changes should be useful for determining the most favorable levels of blood pressure and for selecting appropriate therapy.

Adult↗
PubMed2000

Major histocompatibility complex class II expression by activated microglia caudal to lesions of descending tracts in the human spinal cord is not associated with a T cell response.

Lesion-induced microglial/macrophage responses were investigated in post-mortem human spinal cord tissue of 20 patients who had died at a range of survival times after spinal trauma or brain infarction. Caudal to the spinal cord injury or brain infarction, a strong increase in the number of activated microglial cells was observed within the denervated intermediate grey matter and ventral horn of patients who died shortly after the insult (4-14 days). These cells were positive for the leucocyte common antigen (LCA) and for the major histocompatibility complex class II antigen (MHC II), with only a small proportion staining for the CD68 antigen. After longer survival times (1-4 months), MHC II-immunoreactivity (MHC II-IR) was clearly reduced in the grey matter but abundant in the white matter, specifically within the degenerating corticospinal tract, co-localising with CD68. In this fibre tract, elevated MHC II-IR and CD68-IR were still detectable 1 year after trauma or stroke. It is likely that the subsequent expression of CD68 on MHC II-positive microglia reflects the conversion to a macrophage phenotype, when cells are phagocytosing degenerating presynaptic terminals in grey matter target regions at early survival times and removing axonal and myelin debris in descending tracts at later survival times. No T or B cell invasion or involvement of co-stimulatory B7 molecules (CD80 and CD86) was observed. It is possible that the up-regulation of MHC II on microglia that lack the expression of B7 molecules may be responsible for the prevention of a T cell response, thus protecting the spinal cord from secondary tissue damage.

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PubMed1997

Circadian rhythm of heart rate variability is reversibly abolished in ischemic stroke.

BACKGROUND AND PURPOSE: Acute brain infarction significantly decreases heart rate variability as a result of cardiovascular autonomic dysregulation. However, information regarding circadian rhythms of heart rate and heart rate variability is limited. METHODS: In this prospective study, we analyzed 24-hour circadian rhythm of heart rate and the time and frequency domain measures of heart rate variability in 24 patients with hemispheric brain infarction, 8 patients with medullary brainstem infarction, and 32 age- and sex-matched healthy control subjects. ECG data were obtained from the patients in the acute phase and at 6 months after the infarction. RESULTS: In the acute phase of stroke, all the components of heart rate variability, ie, standard deviation of RR intervals, total power, high-frequency power, low-frequency power, and very-low-frequency power, were similar at night (from midnight to 6 AM) and during the day (from 9 AM to 9 PM), indicating that the circadian oscillation of heart rate variability had been abolished. At 6 months after brain infarction, the circadian rhythm had returned and, as in the control subjects, the values at night were significantly higher than those in the daytime. The values in hemispheric and in brainstem infarction did not differ significantly from each other. CONCLUSIONS: These results suggest that circadian fluctuation of heart rate variability is reversibly abolished in the acute phase of ischemic stroke and that it returns during the subsequent 6 months. The loss of the relative vagal nocturnal dominance may contribute to the incidence of cardiac arrhythmias and other cardiovascular complications after acute stroke.

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PubMed1995

Clinical characteristics of rapidly progressive leuko-araiosis.

INTRODUCTION: 38 patients found to have either pure leuko-araiosis (LA) or LA combined with infarction(s) on computer tomography (CT) in 1989 were re-examined in 1992 in order to evaluate the progression of LA. The follow-up period averaged 3.2 years. MATERIAL AND METHODS: The clinical and radiological data on patients in 1989 were collected from hospital records and re-evaluated. The patients were re-examined clinically (including 24 hour ambulatory blood pressure measurement), and neuroradiologically (CT) in 1992 for this study. RESULTS: 11 (29%) patients were found to have significant (rapid) progression of the extent of LA on CT during the follow-up. At baseline, there was no significant difference in the mean number of brain infarctions between the groups with progressing (prLA) and non-progressing LA (nprLA) or between the number of cortical and central infarctions within these groups. At follow-up, the total number of infarctions had increased significantly in both groups, but it was mostly because of the increase in cortical infarctions in the prLA group (p = 0.043) and, conversely, the central ones in the nprLA group (p = 0.011). prLA was found to be related to heart failure (82% vs 37%, p = 0.029) and atrial fibrillation (55% vs 19%, p = 0.047), whereas nprLA was strongly associated with a sudden onset of symptoms (78% vs prLA 18%, p = 0.001) like a true brain infarction. Other clinical factors, including mean blood pressure and heart rate, did not clearly differentiate between the groups. CONCLUSION: The results suggest that there are different subgroups of patients with LA associated with various vascular factors. The occurrence of LA is not related to the distribution of infarctions. The progression of LA is not related to the number of brain infarctions or to the simultaneous increase of infarctions on CT.

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PubMedDate not supplied

Development of ischemic stroke in normotensive and hypertensive diabetic patients with or without antihypertensive treatment: an 8-year followup study.

Although the impact of hypertension as a risk factor for brain infarction in diabetes mellitus is evident, the beneficial effect of antihypertensive therapy has not been demonstrated. Therefore, we designed a prospective cohort study to elucidate the effects of antihypertensive therapy on the development of ischemic stroke in diabetic outpatients. Two hundred forty patients, 219 non-insulin-dependent diabetes mellitus (NIDDM) and 21 insulin-dependent diabetes mellitus (IDDM), without history of cerebrovascular accident were followed for 8 years, from January 1981 until December 1988, in our diabetic clinic. Forty-eight of 88 hypertensive patients had received antihypertensive drugs. Among 40 untreated hypertensive and 152 initially normotensive diabetics, 14 hypertensives and 11 normotensives required antihypertensive therapy during followup period. Twenty-three patients were dropped out because of the unidentified reasons. Cerebrovascular accident occurred in 24 patients (10%): 18 brain infarctions, 4 transient ischemic attack (TIA), 1 subarachnoidal hemorrhage, and 1 brain hemorrhage. The percent incidence of ischemic strokes in the hypertension-treated patients was 8.9% which was similar to the 8.1% of the normotensives. In contrast, ischemic strokes developed in 29% of the untreated hypertensives, being significantly more frequent than in the former two groups. Multivariate analysis showed that serum total cholesterol and male gender were independent significant precursors of brain infarction in diabetic patients. In conclusion, antihypertensive treatment decreased the incidence of ischemic stroke in diabetics. Serum total cholesterol turned to independent risk factors for ischemic stroke in diabetic patients.

Adult↗
PubMed1976

[Ambulatory treatment with anticoagulents in the prevention of cerebral ischemia].

The degree of effectiveness of preventive therapy with anticoagulants, following brain infarctions and in the stage of transient disorderd brain ciruclation, was studied in comparison with the frequency of repeated ischemic disorders in 166 patients, and in a control group of 138 normals. During permanent administration of anticoagulants repeated ischemic episodes appeared less frequently than with other forms of medication. However, there was an increased amount of ischemic disorders after a discontinuation of the preparations. The most expressed signs of such conditions were in patients with repeated brain infarctions in a low arterial pressure and especially in the stage of transient disorders of brain circulation. In such cases the indications for the use of anticoagulants should be very limited.

Adult↗
PubMed2000

Neuroprotective efficacy and therapeutic window of the high-affinity N-methyl-D-aspartate antagonist conantokin-G: in vitro (primary cerebellar neurons) and in vivo (rat model of transient focal brain ischemia) studies.

Conantokin-G (Con-G), a 17-amino-acid peptide derived from marine snails and a potent N-methyl-D-aspartate (NMDA) antagonist, was evaluated for its neuroprotective properties in vitro and in vivo. In primary cerebellar neurons, Con-G was shown to decrease excitotoxic calcium responses to NMDA and to exhibit differential neuroprotection potencies against hypoxia/hypoglycemia-, NMDA-, glutamate-, or veratridine-induced injury. Using the intraluminal filament method of middle cerebral artery occlusion as an in vivo rat model of transient focal brain ischemia, the neuroprotective dose-response effect of Con-G administration beginning 30 min postocclusion was evaluated after 2 h of ischemia and 22 h of reperfusion. In the core region of injury, an 89% reduction in brain infarction was measured with significant neurological and electroencephalographic recovery at the maximal dose tested (2 nmol), although mild sedation was noted. Lower doses of Con-G (0.001-0.5 nmol) were significantly neuroprotective without causing sedation. Postinjury time course experiments demonstrated a therapeutic window out to at least 4 to 8 h from the start of the injury, providing a 47% reduction in core injury. The neuroprotective effect of Con-G (0. 5 nmol) was also evaluated after 72 h of injury, where a 54% reduction in core brain infarction was measured. Critically, in both recovery models (i.e., 24 and 72 h), the reduction in brain infarction was associated with significant improvements in neurological and electroencephalographic recovery. These data provide evidence for the potent and highly efficacious effect of Con-G as a neuroprotective agent, with an excellent therapeutic window for the potential intervention against ischemic/excitotoxic brain injury.

Animals↗
PubMed1996

The value of routine computed tomography of the brain in the pre-operative assessment of patients for carotid endarterectomy.

OBJECTIVE: To determine the prevalence of brain infarcts and other intracranial pathology on computed tomography (CT) in patients with greater than 50% internal carotid artery stenosis. DESIGN: Descriptive study of CT findings. SETTING: Referral-based cohort at Groote Schuur Hospital. PARTICIPANTS: Sixty-three patients aged 40-82 years who had CT of the head prior to carotid endarterectomy. MAIN OUTCOME MEASURES: Prevalence of brain infarct in patients presenting with transient ischaemic attack (TIA) or stroke, and yield of unsuspected intracranial pathology other than ischaemic necrosis. RESULTS: Brain infarcts were diagnosed in 54% of patients presenting with TIA and in 73% of patients with stroke. True-positive CT scans were present in only 19% and 44% of patients with TIA and stroke, respectively. A single incidental frontal lobe granuloma, unrelated to the patient's clinical presentation, was noted. CONCLUSIONS: In the selected group of patients referred for carotid endarterectomy, routine use of CT of the head is not indicated and can be reserved for cases with extraordinary clinical features.

Adult↗
PubMed2006

Facilitated beam-walking recovery during acute phase by kynurenic acid treatment in a rat model of photochemically induced thrombosis causing focal cerebral ischemia.

We previously demonstrated the presence of activated areas in the non-injured contralateral sensorimotor cortex in addition to the ipsilateral sensorimotor cortex of the area surrounding a brain infarction, using a rat model of focal photochemically induced thrombosis (PIT) and functional magnetic resonance imaging. Using this model, we next applied gene expression profiling to screen key molecules upregulated in the activated area. RNA was extracted from the ipsilateral and contralateral sensorimotor cortex to the focal brain infarction and from the sham controlled cortex, and hybridized to gene-expression profiling arrays containing 1,322 neurology-related genes. Results showed that glycine receptors were upregulated in both the ipsilateral and contralateral cortex to the focal ischemic lesion. To prove the preclinical significance of upregulated glycine receptors, kynurenic acid, an endogenous antagonist to glycine receptors on neuronal cells, was administered intrathecally. As a result, the kynurenic acid significantly improved behavioral recovery within 10 days from paralysis induced by the focal PIT (p < 0.0001), as evaluated with beam walking. These results suggest that intrathecal administration of a glycine receptor antagonist may facilitate behavioral recovery during the acute phase after brain infarction.

Animals↗
PubMed2002

A new reproducible focal cerebral ischemia model by introduction of polyvinylsiloxane into the middle cerebral artery: a comparison study.

A reliable focal cerebral ischemia model is essential in evaluating the efficacy and safety of neuroprotective therapy for stroke. We present a focal embolic ischemic model of rat with reproducible and predictable brain infarction by comparing it with two other most commonly used focal cerebral ischemia models. To produce embolic focal cerebral ischemia, 30 male Wistar rats were subjected to injection of 30 microl hydrophilic polyvinylsiloxane (PVS) or an autologous thrombus or intraluminal filament occlusion in the right middle cerebral artery (MCA) (n = 10 in each group). The percent of brain infarct volume at 48 h after ischemia, neurobehavioral score at 2 h before and after ischemia, intracranial hemorrhagic incidence, and premature reperfusion rate at 3 h after ischemia by MCA angiography were assessed respectively and compared between the focal cerebral models. We found that PVS-induced focal cerebral ischemia had more consistent brain infarct size with less dispersion (32.2+/-7.4%, CV = 0.23) than that with an intraluminal filament occlusion (27.6+/-11.4%, CV = 0.41) or an autologous thrombus embolization (27.2+/-11.8%, CV = 0.43). Injection of PVS also caused more severe neurobehavioral deterioration (3.8+/-0.4) than those produced by two other models (filament, 3.1+/-0.9, P = 0.02; thrombotic, 3.5+/-0.5, P = 0.08). Additionally, animals with PVS-induced focal cerebral ischemia suffered less intracranial hemorrhage (PVS, 0/10, filament, 3/10, thrombotic, 3/10), and less premature reperfusion as determined by MCA angiography (PVS, 0/10, filament, 4/10, thrombotic, 3/10). Our data suggests that permanent focal cerebral ischemia with high reproducibility and low mortality can be achieved by introducing PVS into the right MCA.

Animals↗
PubMed1996

Vascular MR contrast enhancement in cerebrovascular disease.

PURPOSE: To determine the significance of vascular enhancement in stroke patients with and without permanent neurologic deficit. METHODS: We prospectively studied two groups of patients with spin-echo MR imaging before and after injection of gadopentetate dimeglumine. In the patients in group 1 (12 women, 22 men; age range, 32 to 76 years), who had permanent neurologic deficit caused by recent ischemic brain infarction, we obtained 3 to 13 serial MR images during follow-up examination. Group 2 consisted of 26 patients (14 women, 12 men; age range, 54 to 81 years) with transient neurologic deficit caused by angiographically proved high-grade stenosis or occlusion of the internal carotid artery. RESULTS: Vascular enhancement was present in 59% of patients in group 1 and in 65% of patients of group 2. In group 1, the frequency of vascular enhancement declined steadily over several weeks, but it was still present in single cases even after 3 months. Vascular enhancement correlated positively with the extent of brain infarction in group 1 and with the degree of carotid stenosis in group 2. CONCLUSION: Vascular enhancement as shown by MR imaging may herald ischemic brain infarction and could persist over several weeks in areas that show collateral flow after infarction has occurred.

Adult↗
PubMed2005

Evaluation of applied cases of thrombolytic therapy against ultra-acute ischemic stroke. Using the Japanese Standard Stroke Registry Database.

BACKGROUND: A retrospective evaluation was made concerning thrombolytic therapy for ultra-acute ischemic stroke patients, using a recombinant tissue plasminogen activator (rt-PA), which is not yet approved as a drug for brain infarction in Japan. The evaluation was implemented using the database of patients that suffered acute strokes as collected by the Japanese Standard Stroke Registry Study (JSSRS). METHODS: The thrombolytic therapy group, selected from among the registered 6,090 cases of brain infarction patients, was divided into two groups, namely, a group of patients who were admitted in the hospital within 3 hours of the onset (86 cases, average age 69.6) and the other group who were admitted after 3 hours from the onset (28 cases, average age 66.8). Using a Multiple Logistic Regression Analysis adapted for modified Rankin scale (mRS) regarding each group, the clinical effects of thrombolytic therapy for functional outcome and presence or absence of dementia at the time of hospital discharge were examined. Among the 467 cases of patients (average age 74) who were admitted within 3 hours of the onset and for whom the NIH Stroke Scale (NIHSS) was between 6 and 29 at the time of admission, intravenous or intra-arterial thrombolytic therapy was conducted in 88 cases. Then, a case-control study and Multiple Logistic Regression Analysis was implemented for subject groups matched according to the gender, age and severity at the time of admission, and the effects on early-admitted patients were examined. Also, for two rehabilitation patient groups: one whose rehabilitation started within 7 days (216 cases; average age 73) and the other whose rehabilitation started after 7 days (56 cases, average age 76), the effects of early rehabilitation were examined using Multiple Logistic Regression Analysis. Moreover, the effects of thrombolytic therapy on a group of patients who were admitted early and for whom rehabilitation started early (215 cases; average age 73) were examined in the same way. RESULTS: In the comparison between the thrombolytic therapy groups, the functional outcome of the group of patients admitted within 3 hours of the onset at the time of discharge (mRS 0-1) was significantly better compared with that of the group after 3 hours from the onset (OR 2.79, 95% CI: 1.06-7.32). Regarding the comparison between the early admitted patients, the frequency of poor functional outcomes (mRS 2-6) at the time of discharge was significantly lower in the thrombolytic therapy group (OR 0.55, 95% CI 0.31-0.98), and the frequency of dementia was also significantly lower (OR 0.37, 95% CI 0.17-0.86). In the case control study, a significant difference was noted for the presence of dementia. In the group rehabilitation was started early, the frequency of poor functional outcomes was significantly lower (OR 0.33, 95% CI 0.11-0.98), and the frequency of dementia was also significantly lower (OR 0.41, 95% CI 0.19-0.89). As for the comparison of the groups admitted early and for which rehabilitation started early, the frequency of poor functional outcomes at the time of discharge was significantly lower in the thrombolytic therapy group (OR 0.38, 95% CI 0.16-0.86). CONCLUSIONS: From the present analysis, in spite of being a retrospective analysis based on comparatively small number of patient cases from the stroke database, it is concluded that the clinical application of thrombolytic therapy for ultra-acute ischemic strokes was effective. Moreover, it was demonstrated that, if it is possible to start rehabilitation early, a dramatic improvement of the effects might be expected.

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PubMed1996

Stroke subtypes and hypertension. Primary hemorrhage vs infarction, large- vs small-artery disease.

BACKGROUND: Hypertension is the major risk factor for stroke associated with small-artery disease and large-artery disease, but the factors behind the development of a particular stroke subtype in individual patients are not known. METHODS: We determined risk factors potentially predictive of stroke subtype in 822 of 2760 patients consecutively admitted to a primary care stroke center with (1) first-ever stroke, (2) hypertension (blood pressure >160/90 mm Hg at least twice before the stroke), and (3) no cardioembolic source. We used logistic regression analysis to delineate factors associated with ischemic (brain infarct) vs hemorrhagic (primary hemorrhage) stroke and with large- vs small-artery disease. A scoring system was elaborated on the basis of the estimated regression coefficients. Observed proportions and calculated risks were determined. RESULTS: Age greater than 67 years, cigarette smoking, hypercholesterolemia, and a family history of stroke or ischemic heart disease were independent predictors of ischemic vs hemorrhagic stroke. In women, diabetes mellitus was an additional risk factor for ischemic vs hemorrhagic stroke. Only one of 144 patients with primary hemorrhage had an ipsilateral carotid stenosis. In men with brain infarct, cigarette smoking, cardiac ischemia, and a family history of stroke or ischemic heart disease were significantly and independently associated with large- vs small-artery disease. In women with brain infarct, smoking was the only predictive factor for large- vs small-artery disease. CONCLUSION: In patients with stroke and hypertension, associated risk factors influence the subtype of stroke (hemorrhage vs brain ischemia, large- vs small-artery disease).

Adolescent↗
PubMed1994

Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases.

BACKGROUND AND PURPOSE: To investigate the clinical relevance of plasma concentrations of neuron-specific enolase (NSE) in patients with severe cerebrovascular diseases, serial analyses were performed during the first 10 days after the acute event. METHODS: Plasma samples taken from 61 patients (30 with brain infarction, 13 with intracerebral hemorrhage, 11 with cardiogenic hypoxia-ischemia, and 7 with myocardial infarction [as control group]) were analyzed for NSE concentration using an enzyme immunoassay. The time course of plasma NSE was correlated with clinical findings, clinical outcome, cranial computed tomography, intracranial pressure, and other laboratory data. RESULTS: In cases of hypoxia-ischemia there was close correlation between plasma NSE values during the first 72 hours and the clinical outcome. In brain infarction and intracerebral hemorrhage, high plasma NSE mostly indicated an unfavorable outcome, but low values did not permit a reliable prognostic estimation. In cases of cerebral infarction and intracerebral hemorrhage with secondary neuronal destruction (for example, due to malignant edema), increasing NSE concentrations in plasma preceded the change of clinical or other diagnostic parameters. CONCLUSIONS: The course of plasma NSE levels is seen as a relevant parameter for assessing the prognosis of cerebral hypoxia-ischemia. Additionally, it may prove to be a useful tool for monitoring space-occupying brain infarctions and intracerebral hemorrhages and therefore may contribute to improved therapeutic management of severe cerebrovascular diseases.

Adult↗
PubMed1995

Left atrial myxomas. Using gross anatomic tumor types to determine clinical features and coronary angiographic findings.

PURPOSE: To our knowledge, there have been no reports focusing on differences of clinical characteristics according to two gross anatomic types of cardiac myxomas. This study evaluated the differences of clinical features, coronary arteriographic findings, and histopathologic findings. PATIENTS AND METHODS: Twenty-six patients who underwent surgical excisions for left atrial myxomas were analyzed. According to the gross anatomic types, they were divided into two groups: group 1 having solid and ovoid myxomas (n = 14), and group 2 having soft and papillary myxomas (n = 12). Differences of presenting symptoms, prevalence of brain infarction, coronary angiographic findings, and histopathologic findings were analyzed. RESULTS: An incidence of dyspnea was significantly higher in group 1 (78.6% vs 33.3%, p < 0.05) than in group 2. That of neurologic symptoms was higher in group 2 (75% vs 14.3%, p < 0.01) than in group 1. A prevalence of brain infarction was higher in group 2 (75% vs 2.5%, p < 0.05) than in group 1. On coronary angiography, an identification rate of clusters of tortuous vessels was higher in group 1 (81.8% vs 0%, p < 0.01) than in group 2. In histologic findings, most of group 1 tumors displayed many hemorrhages, small vessels, and fibrosis in the stroma, but group 2 had few such structures. CONCLUSIONS: Coronary angiographic findings of tumor-feeding arteries without clusters of tortuous tumor vessels predict a myxoma that is papillary in type. At that time, close attention should be given for the possible existence of silent brain infarction.

Adolescent↗
PubMed1994

Cerebral vasomotor reactivity is significantly reduced in low-flow as compared to thromboembolic infarctions: the key role of the circle of Willis.

To test the hypothesis that cerebral vasomotor reactivity (CVMR) is significantly more reduced in patients with hemispheric low-flow infarctions than in brain infarctions due to arterio-arterial embolism, a series of 64 consecutive patients with internal carotid artery occlusions were studied. CVMR was calculated from relative changes of blood flow velocity within the middle cerebral artery (MCA) measured by transcranial Doppler ultrasonography (TCD) during hypo- and hypercapnia. The configuration of the circle of Willis (COW) was also determined by TCD using common carotid artery compression tests. Anterior, posterior or ophthalmic artery collateral flow, and absence or combinations of these, were differentiated. CT scans were categorized as showing either no infarction (group I; n = 20) or territorial (group II; n = 28), or low-flow infarctions (group III; n = 16). As compared to normal, CVMR was significantly reduced but equal in groups I and II, however, even more reduced in group III. CVMR was lowest, and low-flow infarctions were most frequent in patients whose collateral hemispheric blood supply was from the ophthalmic artery as opposed to patients with a complete or nearly complete COW. Our findings indicate that low-flow infarctions in extracranial ICA occlusions represent brain damage due to a critical reduction in cerebral perfusion pressure, as opposed to thromboembolically induced lesions. The configuration of the COW seems to play the key role. Our findings also support the view that the pattern of hemispheric infarction seen on CT indicates the pathogenesis of stroke.

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