Metabolic acidosis in cerebral ischemia is considered deleterious to cell function. Amelioration of systemic and focal cerebral acidosis by an alkalizing agent could reduce ischemic brain damage. We investigated the effect of tromethamine (TRAM) on focal cerebral ischemia by temporary middle cerebral artery occlusion in rats. 45 male Wistar rats were intubated and ventilated with 0.8% halothane and a mixture of 70% NO2 and 30% O2. The animals were subjected to middle cerebral artery (MCA) occlusion by inserting a 4-0 nylon monofilament into the proximal MCA. Recirculation was performed by removal of the thread from the internal carotid artery. All rats were subjected to 2 hours of MCA occlusion followed by 2 hours of reperfusion. In the control group, physiological saline was continuously infused. The THAM group received continuous administration of 0.3 M THAM (2 ml/kg/hr). The brain water content was measured by the specific gravimetric method. The regional changes in brain tissue pH and infarction volume were estimated by the umbelliferone method and TTC staining, respectively. In the control group, the brain water content of the infarct area was significantly increased. However, in the THAM group, the water content showed no significant change in one part of the parietal cortex on the lesion side. The brain regional pH in the control group was significantly decreased in the infarct area. In the THAM group, the regional pH was markedly increased in the peripheral lesion of the ischemic area, although the regional pH was decreased in the center of the ischemic lesion. The volume of acidotic lesion was significantly reduced in the THAM group. The size of the infarct area was significantly decreased from 16.29 ± 16.19% in the control group to 0.78 ± 1.03% in the TRAM group. These findings suggest that THAM can improve intracellular acidosis in the periinfarct area at the acute phase of MCA occlusion, leading to improvement of brain edema. Normalization of systemic acidosis with THAM was effective for reducing brain edema and infarct size at the early stage of temporary cerebral ischemia.

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To visualize the vascular anatomy of the brain, we have developed a system for producing threedimensional (3D) color Doppler images from a series of two-dimensional color Doppler images. Twodimensional images of cerebral vessels were obtained through the temporal bone or foramen magnum in 5 healthy volunteers by acquiring color Doppler and power Doppler, and specially designed software was used to reconstruct the 3D volumes and display volume-rendered images of the cerebral vessels. 3D images of color Doppler represented as cerebral vessels were successfully obtained in all volunteers. We discuss the possibility of applying ultrasound 3D imaging to patients with neurosurgical disorders.

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We examined 95 patients with pontine ischemic lesions documented by MRI. Of 137 infarcts, 62 were asymptomatic and all of them were lacunar infarctions. Compared with symptomatic infarctions, asymptomatic infarctions were found to be significantly smaller in average size, and located mainly in the paramedian arterial territory of the middle part of the pons. As underlying risk factors for stroke, only heart disease and hypercholesterolemia were less prevalent in the patients with asymptomatic infarction than in the symptomatic infarction group.

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We conducted MRI and MR angiography to evaluate the relationship between causes and symptom in cases of paramedian thalamic infarction. All symptomatic cases were similar to those reported previously in which thalamic lesions were identified on either the left or both sides. Of the 14 cases, 9 had permanent neuropsychologic disturbances, and in severe cases, cardiogenic embolism was thought to be the major cause. Hypotension or orthostatic blood pressure fall was often confirmed in cases of mild neuropsychologic disturbances, and in cases of vertical gaze palsy or those withiout any symptoms. In such cases, MRI could detect negligible complications of ischemic lesions in other intracranial regions, and MR angiography frequently revealed hypoplasia of the circle of Willis (P1 hypoplasia). From these findings, it appears that the causes of paramedian thalamic infarction are varied, and accordingly the treatment used should differ.

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To investigate the effects of carotid artery stenosis and carotid endarterectomy (CEA) on the cerebral circulation, we measured the internal carotid artery (ICA) flow, regional cerebral blood flow of the middle cerebral artery territory (rCBF), stump perssure of the ICA, somatosensory evoked potential (SEP), and cerebral oxygenation. A linear relationship existed between the degree of stenosis and ICA, flow, but no relationship was noted between stenosis and the rCBF. Most patients demonstrated normal rCBFs which may have been compensated by the collateral circulation and vasodilatation of the cerebral vasculature. Six patients with a low rCBF on the stenotic side demonstrated improvement of rCBF after CEA. One patient with a remarkable increase in ICA flow after CEA developed permanent neurologic deficits which may have been caused by postoperative hyperperfusion. Ischemia after cross-clamping of the ICA during CEA was detected by SEP with greatest reliability. For the prevention of cerebral ischemic injury, a multi-modality monitoring system is considered necessary.

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A patient (51-year-old man) with bilateral medullary infarction wore an ambulatory blood pressure monitoring device in the chronic phase to observe his circadian variations of blood pressure. The decline in blood pressure normally observed during sleep disappeared, but his heart rate fell during sleep. The diminished nocturnal blood pressure decline could be explained by assuming that the information from higher centers governing the sleep-wakefulness rhythm did not reach the primary circulatory center in the medulla as a result of medullary damage. These findings suggest that vasomotor integration with the sleep mechanism in the lower brainstem may be responsible for the nocturnal blood pressure decline.

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We report two cases of dissecting aneurysm (DA) of the posterior inferior cerebellar artery (PICA) presenting with Wallenberg syndrome. A 34-year-old man was hospitalized due to sudden onset of headache, vertigo, left facial dysesthesia, nausea, and vomiting. A few days later, he complained of right hemi-dysesthesia. A T2-weighted MRI image revealed a high intensity area at the left lateral medulla. An angiogram showed an aneurysm on the lateral medullary segment and dilatation of the posterior medullary segment of the PICA. The proximal portion of the PICA was clipped. The medullary segment was dilated and purplish-red in color. This patient was discharged after 2 months with disappearance of Wallenberg syndrome. The second patient was a 49-year-old man, who complained of sudden onset of vertigo and gait disturbance. An MRI demonstrated infarctions of the right lateral medulla and cerebellum. An angiogram displayed typical findings of DA: the so-called "peral and string sign" at the anterior lateral medullary segment of the left PICA, associated with a fusiform aneurysm of the right VA. The neurological signs improved and the patient was discharged. A follow-up angiogram at 6 months after the onset revealed no findings of DA.

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We report a case of upper pontine infarction with ipsilateral adduction palsy, convergence paralysis and alternating exotropia. A 77-year-old man revealed vomiting, diplopia, gait disturbance, numbness of the right face and palm, impaired adduction of the left eye, convergence paralysis, and alternating exotropia. MRI of the brain demonstrated a high intensity area in the left paramedian tegmentum of the upper pons, which was recognized as a new lesion. On the 7th day, the exotropia of the right eye improved in frontal gaze, in upper gaze and lower gaze. On the 12th day, the alternating exotropia disappeared. On the 16th day, at the time of discharge, exotropia was still evident. The adduction palsy, convergence paralysis and alternating exotropia could have been due to hyperactivity of the PPRF because of severe MLF damage.

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A 59-year-old right-handed woman was admitted to our hospital because of left hemiparesis. On the second day brain CT revealed right striatocapsular infarction and bilateral temporoocipital infarction. Electrocardiography, and transthoracic and transesophageal echocardiography showed no abnormalities. On the second day, cerebral angiography disclosed stenosis of the bilateral middle cerebral arteries. Antithrombotic therapy was started under a diagnosis of cerebral infarction associated with essential thrombocythemia. Follow-up cerebral angiography on the 9th day revealed disappearance of the stenotic lesions of the bilateral middle cerebral arteries This patient represents a rare case with disappearance of thrombotic stenosis of the bilateral middle cerebral arteries associated with essential thrombocythemia following antithrombotic therapy.

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We report the case of a 26-year-old woman who was suffering from cerebral infarction concurrent with nephrotic syndrome caused by membranous nephropathy. MRI of the brain and angiography revealed cerebral infarction in the area of the right middle cerebral artery. The onset of her nephrotic syndrome was inferred to be contemporaneous with the cerebral infarction. Oral administration of prednisolone was effective for the nephrotic syndrome, and the patient was discharged from our hospital with mild hemiparesis at 2 months after the onset. In this case, we considered that vasculitis with collagen disease and intravascular dehydration associated with membranous nephropathy had caused the cerebral infarction.

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