Hindbrain stroke in children caused by extracranial vertebral artery trauma. (49/698)

Hindbrain transient ischemic attacks (TIAs) culminating in posterior circulation stroke are described in five children. Atlanto-axial subluxation and angiographical documentation of C1 to C2 level arterial pathology are documented in one patient. Four additional patients with nearly identical clinical presentations, posterior fossa TIAs, stroke and basilar angiographical pathology are reviewed. A mechanical traumatic etiology is suggested. Unexplained transient repeated brain stem and/or cerebellar sympotomatology may be due to extracranial vetebral artery stenosis or occlusion by atlanto-axial instability. After appropriate documentation, stabilization may prevent further TIAs or strokes.  (+info)

Spontaneous thrombosis of deep cerebral veins: a complication of arteriovenous malformation. (50/698)

An uncommon type of stroke in children is presented. An intracranial arteriovenous malformation in a 13-year-old boy spontaneously occluded about 22 months after surgical intervention. Precipitating factors, such as bacterial infections, could not be demonstrated in this patient, who had been attending school since the time of the craniotomy. The histological features of venous encephalomalacia in the galenic territory are contrasted with hemorrhagic encephalomalacia as seen after arterial occlusions: in the former, hemorrhages are more widespread and edema is more pronounced.  (+info)

An unusual case of recurrent left atrial myxoma. (51/698)

In a patient who had a calcified left atrial myxoma resected, recurrence developed 31 months later. Although complete radical resection of the recurrent tumour presented a special problem, the patient survived the second operation. The tumour recurred again and the patient had two episodes of cerebral embolism 1 1/2 and 2 years later, respectively, and died 3 1/2 years after the second operation. The erythrocyte sedimentation rate correlated with the size of the tumor, and the recurrent tumour seemed to grow more rapidly than the primary tumour. Experience with this case and a review of the nine reported cases of recurrent left atrial myxoma suggest that a radical approach is necessary at the primary operation.  (+info)

Serial changes in cerebral blood flow and flow-metabolism uncoupling in primates with acute thromboembolic stroke. (52/698)

The authors recently developed a primate thromboembolic stroke model. To characterize the primate model, the authors determined serial changes in cerebral blood flow (CBF) and the relation between CBF and cerebral metabolic rate of glucose (CMRglc) using high-resolution positron emission tomography. Thromboembolic stroke was produced in male cynomolgus monkeys (n = 4). Acute obstruction of the left middle cerebral artery was achieved by injecting an autologous blood clot into the left internal carotid artery. Cerebral blood flow was measured with [15O]H2O before and 1, 2, 4, 6, and 24 hours after embolization. CMRglc was measured with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) 24 hours after embolization. Lesion size and location 24 hours after embolization was determined by the 2,3,5-triphenyltetrazolium chloride (TTC) staining method. The results are summarized as follows: (1) 1 hour after embolization, CBF in the temporal cortex and the basal ganglia decreased to < 40% of the contralateral values. In these regions, regarded as an ischemic core, CBF decreased further with time and CMRglc at 24 hours also decreased. Infarcted lesions as indicated by being unstained with TTC were consistently observed in these regions. (2) In the parietal cortex and several regions surrounding the ischemic core, CBF was > 40% of the contralateral values 1 hour after embolization and recovered gradually with time (ischemic penumbra). In these regions, CMRglc at 24 hours increased compared with that in the contralateral regions, indicating an uncoupling of CBF and CMRglc. No obvious TTC-unstained lesions were detected in these regions. The authors demonstrated a gradual recovery of reduced CBF, an elevated CMRglc and a CBF-CMRglc uncoupling in the penumbra regions of the primate model. Positron emission tomography investigations using this model will provide better understanding of the pathophysiology of thromboembolic stroke in humans.  (+info)

Massive haemorrhagic transformation in cardioembolic stroke: the role of arterial wall trauma and dissection. (53/698)

The pathogenesis of massive haemorrhagic transformation is not well established. Fatal haemorrhagic transformation associated with in situ dissection after acute middle cerebral artery (MCA) occlusion in a patient with atrial fibrillation is reported. An 80 year old woman with atrial fibrillation developed mild hemiparesis and aphasia. Brain CT and MRI at 4 and 5 hours, respectively, of symptom onset showed proximal MCA trunk occlusion with developing striatocapsular infarct and hypoperfusion in the superficial MCA territory. A few hours later, she developed massive bleeding into the ischaemic area and died. Pathological examination showed MCA trunk dissection, surrounded by a subarachnoid clot which communicated with the cerebral haematoma. It is suggested that direct arterial wall trauma as a result of cardioembolic MCA occlusion caused bleeding into the infarct. Secondary in situ dissection may be an overlooked mechanism of haemorrhagic transformation.  (+info)

Predicting the outcome of stroke: acute stage after cerebral infarction. (54/698)

On admission to hospital during the acute phase of a stroke presumed due to ischaemic infarction in one cerebral hemisphere 93 patients were examined to determine the factors associated with a poor prognosis for immediate survival. The patients particularly at risk were those who were overtly unconscious and those with any combination of impaired consciousness, dense hemiplegia, and failure of conjugate ocular gaze towards the side of the limb weakness. Necropsy evidence suggested that these signs usually indicate infarction of the whole of one middle cerebral artery territory which is often secondary to internal carotid artery occlusion and commonly produces fatal cerebral oedema.  (+info)

Stroke from carotid endarterectomy: when and how to reduce perioperative stroke rate? (55/698)

OBJECTIVES: To analyse four years of CEA with respect to the underlying mechanisms of perioperative stroke and the role of intraoperative monitoring in the prevention of stroke. PATIENTS AND METHODS: From January 1996 through December 1999, 599 CEAs were performed in 404 men and 195 women (mean age: 65 years, range: 39-88). All operations were performed under general anaesthesia using computerised electroencephalography (EEG) and transcranial Doppler (TCD). Any new or any extension of an existing focal cerebral deficit, as well as stroke-related death were registered. Perioperative strokes were classified by time of onset (intraoperative or postoperative), outcome (minor or major stroke), and side (ipsilateral or contralateral). Stroke aetiology was assessed intraoperatively by means of EEG, TCD, completion arteriography or immediate re-exploration, and postoperatively by duplex sonography, computerised tomography (CT) or magnetic resonance imaging (MRI) of the head. RESULTS: Perioperative stroke or death occurred in 20 (3.3%) patients. In four operations stroke was apparent immediately after surgery. Mechanisms of these strokes were ipsilateral carotid artery occlusion (1) and embolisation (3). In 16 patients stroke developed after a symptom-free interval (2-72 h, mean 18 h) due to occlusion of the internal carotid artery on the side of surgery (9). Other mechanisms were: contralateral occlusion of the internal carotid artery (1), postoperative hyperperfusion syndrome (1), intracerebral haemorrhage (1), and contralateral ischaemia due to prolonged clamping (1). In three procedures the cause was unknown. CONCLUSIONS: In our experience most strokes from CEA developed after a symptom-free interval and mainly due to thromboembolism of the operated artery. We suggest the introduction of additional TCD monitoring during the immediate postoperative phase.  (+info)

Polymorphism of the lipoprotein lipase gene and risk of atherothrombotic cerebral infarction in the Japanese. (56/698)

BACKGROUND AND PURPOSE: Lipid and lipoprotein abnormalities have been implicated in the pathogenesis of ischemic cerebrovascular disease and atherosclerosis. Lipoprotein lipase (LPL) plays an important role in plasma lipoprotein metabolism. Several studies have recently reported the presence of a relationship between Ser447Stop mutation of LPL and coronary artery disease. Other polymorphisms (HindIII and PvuII) of the LPL gene have already been shown to correlate significantly with dyslipidemia. We investigated whether these polymorphisms are associated with increased risk of ischemic cerebrovascular disease (CVD). METHODS: We recruited 177 CVD patients (atherothrombotic infarction, n=71; cardioembolic infarction, n=30; lacunar infarction, n=76) and 177 healthy control subjects. Subjects were genotyped for the Ser447Stop mutation and for HindIII/PvuII restriction fragment length polymorphisms of the LPL gene, and the findings were investigated for associations with the clinical subtypes of CVD and with lipid levels. RESULTS: The Ser447Stop mutation correlated significantly with CVD (0.107 versus 0.158; P=0.035). For the CG+GG versus CC genotype, the odds ratio between control subjects and CVD patients with atherothrombotic infarction was 0.42 (95% CI, 0.18 to 0.99) (P=0.046). Serum HDL cholesterol and triglyceride levels did not correlate significantly with the Ser447Stop genotype. HindIII polymorphism correlated significantly with CVD (0.234 versus 0.169; P=0.031), but the frequency of PvuII polymorphism was not significantly different between groups. CONCLUSIONS: Our results suggest that the Ser447Stop mutation of the LPL gene is a novel genetic marker for low risk of atherothrombotic cerebral infarction.  (+info)