BACKGROUND: The obstruction of intracranial arteries causes cerebral hemodynamic impairment. It is now evident that patients with cerebral hemodynamic compromise have a higher risk of stroke than those with normal cerebral blood flow. The purpose of this study is to investigate the changes of cerebral blood flow and vascular reactivity after extra-intracranial arterial bypass (EIAB) surgery in patients with cerebral hemodynamic compromise. METHODS: We enrolled 16 consecutive patients (8 female and 8 male patients) with transient ischemic attack or cerebral infarction resulted from the occlusion of distal internal carotid artery (ICA) or middle cerebral artery (MCA). We measured the relative regional cerebral blood flow (rrCBF) at rest and after Diamox infusion, and vasomotor reactivity by using single photon emission computed tomography (SPECT). We performed extra-intracranial arterial bypass (EIAB) surgery in patients with impaired vasomotor reactivity. Follow-up brain SPECT was done at 3months after EIAB. We compared the rrCBF and vasomotor reactivity before and after EIAB, and evaluated the effect of collateral vessels on the cerebral hemodynamic after surgery. RESULTS: EIAB increases the vasomotor reactivity significantly (-19.6+/-10 before EIAB, 11.2+/-27 after EIAB, p=0.003) but does not increase the cerebral blood flow at rest (70.5% before EIAB, 70.9% after EIAB). The degree of collateral vessel development did not influence on the restoration of vasomotor reactivity. CONCLUSIONS: These results demonstrate that EIAB increases the vasomotor reactivity of the distal part on the occluded ICA or MCA, but does not increase the cerebral blood flow at rest.
Acetazolamide ; Arteries ; Brain ; Carotid Artery, Internal ; Cerebral Infarction ; Female ; Follow-Up Studies ; Hemodynamics* ; Humans ; Ischemic Attack, Transient ; Male ; Middle Cerebral Artery ; Stroke ; Tomography, Emission-Computed, Single-Photon

No abstract available.
Arterial Pressure* ; Aspirin ; Erythromelalgia* ; Thrombocytosis

Deep cerebral venous thrombosis is a rare condition associated with edema, infarction or hemorrhage in basal ganglia, thalamus and periventricular white matter. It presents nonspecific clinical manifestations such as altered consciousness, headache, focal neurological deficit, nausea and vomiting. Extrapyramidal signs are very rare in deep cerebral venous thrombosis. We report a patient who presented micrographia, hypophonia and bradykinesia as an early manifestation of deep cerebral venous thrombosis.
Basal Ganglia ; Consciousness ; Edema ; Headache ; Hemorrhage ; Humans ; Hypokinesia* ; Infarction ; Nausea ; Parkinsonian Disorders* ; Thalamus ; Venous Thrombosis* ; Vomiting

BACKGROUND: Chronic subclinical ischemia has been considered as one of major causes of leukoaraiosis, although its trigger is unknown. The vascular endothelium plays a major role in maintaining cerebral perfusion through autoregulation. In this study we evaluated the endothelial bioavailability of nitric oxide (NO) in patients with leukoaraiosis. METHODS: We enrolled consecutive patients with lacunar syndrome or transient ischemic attack; the control group comprised age- and sex-matched patients with hypertension but with no neurological abnormality. All participants underwent flow-mediated dilatation of the brachial artery (FMD) to evaluate endothelial function. Leukoaraiosis was defined as ill-defined patches with high signal intensities on FLAIR and low signal intensities on T1-weighted images. Patients were defined as having ischemic leukoaraiosis if they presented with leukoaraiosis and lacunar infarction. Leukoaraiosis only was defined when patient had leukoaraiosis without lacunar infarction leukoaraiosis without lacunar infarction. RESULTS: In total, 75 patients (37 with leukoaraiosis and 38 controls) were enrolled in this study. The demographic and clinical characteristics were similar in the two groups. FMD was lower in patients with leukoaraiosis than in controls (p<0.05), and lower in patients with only leukoaraiosis and in those who also had ischemic leukoaraiosis than in the controls (p<0.05). However, FMD did not differ significantly between patients with leukoaraiosis only and those who also had ischemic leukoaraiosis (p>0.05). CONCLUSIONS: The bioavailability of NO in the vascular endothelium is decreased in patients with leukoaraiosis only and in those who also have ischemic leukoaraiosis compared to controls. These results are suggestive of a causative role of endothelial dysfunction in the pathomechanism of leukoaraiosis.
Biological Availability ; Brachial Artery ; Dilatation ; Endothelium ; Endothelium, Vascular ; Homeostasis ; Humans ; Hypertension ; Ischemia ; Leukoaraiosis ; Nitric Oxide ; Perfusion ; Stroke, Lacunar ; Vasodilation

A thirty-nine year old woman was consulted because of personality change, agitation and memory disturbance. She received chemotherapy and oral steroids because of carcinoma within the bronchus. She had a high serum osmolarity caused by hyperglycemia and hypernatremia, and it was corrected rapidly. Her brain MRI showed EPM (extrapontine myelinolysis). Brain SPECT showed hypoperfusion in the bilateral orbitofrontal regions. We report a patient with EPM with typical frontal lobe dysfunction as an initial manifestation and bilateral orbitofrontal hypoperfusion.
Brain ; Bronchi ; Dihydroergotamine ; Drug Therapy ; Female ; Frontal Lobe* ; Humans ; Hyperglycemia ; Hypernatremia ; Magnetic Resonance Imaging ; Memory ; Myelinolysis, Central Pontine* ; Osmolar Concentration ; Perfusion* ; Steroids ; Tomography, Emission-Computed, Single-Photon*