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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral cavernous angioma is a rare vascular malformation at any age and is very rare in childhood. In the literature available to us, we have been able to trace only 50 cases, to which we have added the 6 cases from our own series. The incidence in pediatric group is higher at 0-2 years (26.8%) and at 13-16 years (35.7%). The clinical onset shows epilepsy in 45.4% of cases, hemorrhagic syndrome in 27.3%, intracranial hypertension in 16.4%, and focal neurological deficits in 10.9%. Furthermore, we discuss the neuroradiological features (CT, angiography, and MRI) and the therapy of pediatric cavernous angioma.
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PMID:Cerebral cavernous angioma in children. 267 61

Binswanger's disease is the name which has been given to a form of subcortical vascular dementia. These patients have a particular clinical profile which progressively includes strokes, gait disorder, pseudobulbar signs and cognitive impairment suggesting dysfunction of the prefrontal cortex. The radiological pattern of hypodensity of the white matter on CT scan (or an increased MRI signal), albeit much debated, seems to be more closely associated with hypertension, previous strokes and neuropsychological defects. Binswanger's disease probably represents the end stage of a pathological process in which hypertensive arteriolopathy, demyelination of the centra semiovale and deep infarcts all play a role.
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PMID:Binswanger's disease: a review of the literature and a personal contribution. 269 96

We present a rare case of aortitis syndrome associated with dilatation of aorta and coarctation-like effect due to the intraluminal flap formation originated from dissected wall of the aorta. A 31-year-old woman was admitted to our hospital complaining of shortness of breath, palpitation and cough. On admission, her physical status showed congestive heart failure and hypertension of upper extremities and hypotension of lower extremities. Bruits were audible over the neck, the anterior chest and the back. Serological studies showed active inflammation. Chest X-ray film showed upper mediastinal widening, cardiomegaly and pulmonary edema. Aortitis syndrome was strongly suggested by these clinical findings, so that prednisolone therapy was started on 3rd hospital day. Special examinations were performed several days later when inflammatory changes showed a tendency to improve. Chest CT scan, RI angiography and MRI studies showed an aneurysmal dilatation from the ascending aorta to the mid-thoracic aorta. Aortography demonstrated a flap at the terminal portion of this aneurysmal dilatation and grade II (Sellars) aortic regurgitation. There was a pressure difference of 80 mmHg between the parts abutting cranial and caudal sides of the flap. A surgical operation was, then, performed to correct the pressure difference. The dissected wall was extruded toward the aortic lumen creating a flap (2 cm in length). This flap was resected and an artificial graft was inserted. Histologically, the flap consisted of adventitia, media and intima.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of aortitis syndrome which presented coarctation of aorta due to intraluminal flap formation in the middle of the thoracic aorta]. 272 9

Twenty cases of pure sensory deficit of vascular origin are reported in patients aged 36 to 79 years. This type of attack in usually presumed to be due to a thalamic lacuna in the ventro-postero-lateral nucleus. However, other reported cases have shown other causal mechanisms and lesional sites. In the present series, CT scan and MRI in 11 cases demonstrated: infarctions in 9 and hemorrhages in 2 patients. The ventro-postero-lateral nucleus was involved in only 4 cases. An infarct of the posterior limb of the internal capsule (anterior choroidal artery territory) was present in 4 cases. The lesions in the other patients were: a thalamic hemorrhage and a small pontine hemorrhage lesion. The likely cause was embolism of cardiac origin in 4 cases, hypertension in 11 cases and diabetes in 4. One patient had an aneurysm of the posterior cerebral artery.
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PMID:[Cerebral infarct and pure sensory deficit]. 272 35

A patient, 30-year-old man, was admitted to Shinshu University Hospital with gait disturbance and numbness of both arms and legs in June 1985. General physical findings were normal except for facial asymmetry, i.e. mild right facial hemiatrophy. Blood pressure was normal and there were no signs of arteriosclerosis. Neurological examination revealed marked bilateral pyramidal tract signs, muscular weakness of all extremities predominant of the right side, spastic gait and sensory disturbance with impairment of pin prick and light touch sensation in the second and third trigeminal nerve regions and extremities of the left side, and mild loss of vibratory sense and numbness in all extremities. X-ray examination of the cervical spine and the myelogram of the spinal canal were normal. CT scan of the brain performed 3 hours after the myelography showed that the left vertebral artery extended from the left side of the medulla oblongata to the midline and distorted it by compression. MRI confirmed the findings of the CT scan. Vertebral angiography disclosed that the elongated left vertebral artery crossed the ventral aspect of the medulla oblongata. Compression of the medulla oblongata by the vertebral artery was diagnosed and neurovascular decompression was performed. About one month after the operation his spastic gait and muscular weakness were slightly improved, but these symptoms progressed thereafter. One year after operation his spastic gait was more marked than preoperatively. In many cases with dolichoectatic intracranial arteries, hypertension and arteriosclerosis have been reported to be usually associated with this condition. In other opinions dolichoectasia has been suggested to be a congenital disease, because such vessels are occasionally present in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case report of quadriparesis due to compression of the medulla oblongata by the elongated left vertebral artery]. 274 80

There are many reports on the disequilibrium syndrome due to dialysis in patients with chronic renal failure. However, they do not mention the findings of CT cisternography and MRI. We intend to investigate the mechanism of CSF dynamics in a patient with disequilibrium syndrome by means of these radiological examinations. A 31 year-old woman who had suffered from renal failure for 18 years was found to have prominent increase of serum creatinine (18.1 mg/dl) and BUN (127 mg/dl) 3 years ago. At that time, digital marking of the skull was already present by X-ray examination without other destruction in bone survey of the whole body. She was hemodialysed by the hollow fiber kidney three times weekly (dialysis time 4.5 hours, dialysate osmotic pressure 270 mOsm/kg H2O). Three months ago, she began to complain of severe headache, nausea and vomiting 2 hours after the beginning of dialysis, so that she was referred to Kosei Hospital. On admission, she showed exophthalmus, concentric narrowing of the visual field, optic atrophy and hyperreflexia in jaw and four extremities. After admission, she received hemodialysis therapy thrice weekly (dialysis time 5 hours, dialysate osmotic pressure 290 mOsm/kg H2O). At the same time, 200 ml of glycerol (contents of glycerin 10, fructose 5, NaCl 0.9%) was administered intravenously during dialysis, which ameliorated the symptoms of intracranial hypertension. Laboratory studies revealed marked decrease of serum creatinine, BUN and uric acid levels and osmotic pressure, and increase of blood pH at the time of postdialysis compared with predialysis. Manometric CSF pressure increased up to 310 mmH2O at the day without dialysis before the glycerol administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of chronic renal hemodialysis and intracranial hypertension--a study on CSF dynamics]. 276 3

The patient, a man aged 57, was admitted to our clinic on May 1, 1987, because of severe vertigo and unsteadiness in standing. Since the age of 55 he had been suffered from hypertension and atrial fibrillation. In September, 1986, he experienced vertigo but recovered soon without therapy. On April 25, 1987, while working, he noticed severe vertigo, nausea and vomiting. He was admitted to a hospital, and then transferred to our clinic. On admission, he was alert and the mentality was normal. Slight ptosis abducent nerve paresis, hypalgesia on the forehead, nose and cheek, facial paresis of peripheral type and hypacusis were detected on the left side. No anisocoria was observed. Sweating was impaired over the left side of the face. Elevation of the soft palate was limited on the left side and the tongue deviated to the left on protrusion. Dysarthria was detected. Though there was no muscular weakness in the extremities, incoordination and dysmetria were noted in the left arm and leg. He could not stand up because of vertigo and unsteadiness. There was no sensory disturbance in the trunk and extremities. Deep tendon reflexes were well elicited and no pathological reflex was observed. These clinical manifestations, except for the ipsilateral palatal and lingual disturbances, were typical of the lateral inferior pontine syndrome caused by occlusion of anterior inferior cerebellar artery, and the lesion was clearly demonstrated by horizontal and coronal MRI. The palatal and lingual disturbances might be due to the involvements of the corticobulbar tracts of the 10th and 12th nerves after the fibers had decussated.
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PMID:[Lateral inferior pontine syndrome: a case report]. 280 19

Infarction in the territory of the anterior choroidal artery (AchA) has been the subject of several recent reports. To the classical clinical syndrome of hemimotor, hemisensory, and visual field deficit has been added hemiataxia acute pseudobulbar mutism, pure motor and pure sensory syndromes and disorders of higher cortical function. The definition of anatomic and clinical correlates to AchA stroke is aided by CT-MRI findings and reveals an unexpected superior extension of infarct to include the periventricular caudate nucleus and inferior corona radiata. Prognosis depends upon unilaterally, bilateral strokes having often a fatal outcome. Etiology and treatment may be intimately related to hypertension.
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PMID:A new view of anterior choroidal artery territory infarction. 306 61

The terms Binswanger's disease and arteriosclerotic subcortical encephalopathy are often applied to elderly patients with dementia and a diffuse hypodensity of the white matter on CT scan (or increased signal on MRI). Recently, similar white matter abnormalities have been reported in non-hypertensive patients with Alzheimer's disease and in elderly healthy people, casting doubt upon Binswanger's disease as an entity. These findings also suggest that the descriptive term leukoaraiosis meaning rarefied white matter is more appropriate than the term leucoencephalopathy. Nevertheless, within the group of patients with an ischemic stroke, several data suggest that leukoaraiosis is not a fortuitous finding and does not simply reflect ageing. Actually, these patients have a particular clinical profile, with intellectual deterioration, chronic hypertension, usually patent carotid arteries, and a deep location of the presenting infarct. Moreover hypertension seems to be still more strongly associated with leukoaraiosis than with a deep location of the infarct (lacunar infarction).
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PMID:[Leukoencephalopathy, leukoaraiosis and cerebral infarction]. 327 83

Pseudobulbar mutism is rarely attributed to bilateral discrete posterior limb internal capsule-medial globus pallidus infarction. Few cases of bilateral anterior choroidal (AchA) artery territory infarction have been reported. We present 8 patients with ischaemic stroke in this location and vascular distribution who have a characterizable syndrome. All had the abrupt onset of inability to speak, swallow or phonate, accompanied by varying degrees of facial diplegia, hemiparesis, hemisensory loss, lethargy, neglect and change in affect. The appearance of clinical signs depends upon the presence of a new infarct contralateral to an older lesion in mirror position. The pathogenesis and progression of neurological deficit appears to be intimately related to hypertension. The role of intrinsic intracranial vascular pathology related to diabetes mellitus, embolism of cardiac origin and atherosclerosis is currently undefined. The prognosis for recovery is poor. Half of our patients died within a year of onset of symptoms. Capsular pseudobulbar mutism is recognized by the abrupt appearance of neurological deficit consistent with internal capsular pathology and is confirmed by CT scan or MRI.
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PMID:Acute pseudobulbar mutism due to discrete bilateral capsular infarction in the territory of the anterior choroidal artery. 338 10


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