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A 14-year-old girl developed transient disturbance of consciousness, dysarthria, and clumsiness of the right upper limb 4 months after herpes zoster ophthalmicus. Brain MRI showed acute cerebral infarction in the left middle cerebral artery (MCA) territory. CT angiography demonstrated mild stenosis in the top of the left internal carotid artery and the proximal side of the MCA. Cerebrospinal fluid (CSF) examination showed slightly mononuclear pleocytosis (6/μl). Titer of the anti-varicella zoster virus (VZV) IgG antibodies in CSF was increased, and gadolinium-enhanced brain MRI (T 1 -weighted imaging) revealed enhancement of the vessel walls at the stenotic lesions. Based on the diagnosis of VZV vasculopathy, methylprednisolone and valacicrovir were administered, followed by acyclovir, in addition to antithrombotic therapy using aspirin and warfarin. After these treatment, her right upper clumsiness was resolved and gadolinium-enhancement of the vessel walls was disappeared on MRI. VZV vasculopathy may cause ischemic stroke in young patients, especially in children. A careful history-taking about herpes is necessary to detect the disease as a potential cause in young stroke patients.

We reported 2 patients with top of the basilar syndrome manifested by onset seizure. Patient 1 was a 76-year-old man. When he was sleeping, suddenly he gave a loud cry and went into convulsions. So he was brought to our hospital by ambulance. On admission, he had unconsciousness and left hemiplegia. Patient 2 was a 70-year-old man. When he was bathing, he lost his consciousness and brought to our hospital by ambulance. On admission, he had convulsion and tetraplegia. Both patients had convulsions and palsy when they had brain infarctions. Brain diffusion weighted MR image showed high intensity area in bilateral internal thalamus, brainstem and cerebellum and no high intensity area in cerebral cortex. We know well that Todd's palsy is palsy after convulsion, but vertebro-basilar occlusion also shows convulsion and palsy. Therefore attention should be paid in the case of the patients who had convulsion and palsy.

We reported a 61-year old man with cardioembolic stroke manifested by isolated tonic seizure of the left upper limb. He had a history of chronic atrial fibrillation and transient ischemic attack. He was brought to our hospital by ambulance, when he suddenly had isolated tonic seizure of left upper limb. On admission, he had no neurological symptoms and signs. Brain diffusion weighted MR image disclosed high intensity area in the right parietal lobe, although T2-weighted image did not show any abnormalities. On 8th day, a high intensity area was observed both on the diffusion-weighted and T2-weighted MR images. In case of isolated tonic seizure of left upper limb, careful examination of stroke is required especially if the patient had a high risk of stroke.

We report here a 50-year-old man on maintenance hemodialysis who presents right hemiparesis, aphasia. MRI diffusion weighted image showed an increased signal intensity in the area of the left middle cerebral artery. Transthoracic and transesophageal echocardiography revealed a mitral annular calcification (MAC) with a mobile component. After treated with heparin, follow-up echocardiography demonstrated a decrease in the size of the mobile component, but not disappeared. Intraoperative findings showed calcified attachment on the posterior mitral valve. This patient was diagnosed as having cardioembolic stroke due to a MAC with a mobile component.

We reported a 77-year-old woman with atrial fibrillation. She was admitted to our hospital because of bradycardia and disturbance of consciousness. She regained consciousness soon after the admission, however on the 3rd day of admission, she abruptly fell into a coma. Neurological examination revealed decerebrate rigidity, conjugate eye deviation to the right, and bilateral Babinski signs, but remaining oculocephalic reflex in both vertical and horizontal directions. Diffusion-weighed MR image of the brain on the same day demonstrated extensive hyperintense lesions in the bilateral hemispheres, sparing the brainstem. On the duplex carotid ultrasonography just after the MR study, oscillating intraluminal thrombi occluded the right common carotid and the left internal carotid artery. We diagnosed the patient as having bilateral carotid occlusions by cardioembolic mechanism.

We here report two patients (58-year-old, 77-year-old women) who presented themselves with generalized convulsion, impaired consciousness and hypertension several days after cancer surgery and transfusion. MRI T2 weighted images show an extensive area of increased signal intensity along the occipital cortex, but the underlying white matter revealed slight high signal intensity on diffusion weighted images. Despite similarities of those two cases to posterior leukoencephalopathy syndrome, they differ since the neuroimaging abnormalities are mostly in the occipital cortex. It is likely that the posterior cerebral cortex and white matter are vulnerable to circulatory, vascular and metabolic/toxic impairments. Depending on the abnormalities of many physiological variables, either the subcortical white matter, cortical gray or both might become a major target of this syndrome.

A 47-year-old man lost his consciousness and brought to our hospital by ambulance. On admission, he had aphasia and upper right limb paresis. Diffusion weighted MR image of the brain on admission showed multiple high intensity areas in the left middle cerebral artery (MCA) territory. Brain angiography performed on the 2nd hospital day revealed the left MCA severe stenosis. We started intravenous antithrombotic therapy on the 1st day. The left carotid angiography on 12th day demonstrated that the left MCA stenosis was improved. He had medical history of hypertension, diabetes mellitus and gout. But he had only slight atherosclerosis, and had no arrhythmia and patent foramen ovale. Blood chemistry test showed marked hypoproteinemia and hyperlipidemia, and urine examination showed proteinuria. He was diagnosed as nephrotic syndrome for the first time. Nephrotic syndrome brought hypercoagulability, so we suspected that nephrotic syndrome concerned with brain infarction.

A 21 year-old female college student with a history of Turner syndrome at age 9, and 6-year growth hormone replacement therapy noticed weakness of right extremities when she got up on March 26, 2001. On admission, she showed right hemiparesis (4+/5) and hypesthesia on the right of body. The hemiparesis progressed (3-/5) in spite of antithrombotic therapy. Brain MRI revealed a high intensity lesion with a diameter of 1.5 cm in the posterior limb of the left internal capsule and putamen on DWI and T2WI. MR angiography and TC-CFI revealed no stenosis in her left middle cerebral artery, but > 50% stenosis in the horizontal portion (M1) of her right middle cerebral artery. Branch lesions were presumed to exist in the left M1. Non-atherosclerotic angiopathy, coagulopathy, and other conventional risk factors of brain infarction were not found. Pathogenesis of Turner syndrome might have played a role in the development of brain infarction in this patient.