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 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of spontaneous occlusion of an arteriovenous malformation (AVM) verified by the second angiography performed 3 days after the initial one. This 65-year-old man had a sudden attack of headache, nausea, and vomiting and was admitted to our hospital next day. On admission, CT scan showed subcortical hemorrhage in the right temporo-parietal area and right CAG showed a small AVM in the same area. The main feeder was a MCA distal branch and the drainer joined Labbe's vein. Repeated angiography 3 days after initial one failed to demonstrate the AVM. Craniotomy was performed and thrombosed AVM was totally removed. Mechanism for disappearance of the malformation is assumed to be acute thrombosis due to intracranial hemorrhage and arteriosclerotic change. The literature is reviewed.
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PMID:[Spontaneous occlusion of a cerebral arteriovenous malformation--report of a case]. 332 Aug 5

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70

A 59-year-old man was admitted because of frequent vomiting and obtundation in February 1982. Neurological examination on admission revealed only slight impairment of consciousness. Papilledema, meningeal irritation sign and paralysis were not elicited. The plain CT scan was normal, but the CT scan with contrast material showed patchy enhancement in the left temporal lobe and around the third ventricle. Cerebral angiography showed a dural arteriovenous malformation (dural AVM) in the left transverse sinus fed by the left occipital artery, and the retrograde flow into the straight sinus. By the third day following admission, the level of consciousness became alert. The patient did not complain of headache, bruit and visual disturbance. He showed mild disorientation and memory disturbance. But his ordinary daily-living was independent. In August 1982, the patient gradually became inactive and apathetic. At times he lay in bed with moving his eyes, swallowing foods. At other times, he lay in bed with closing his eyes, immobile, and unresponsive except to strong painful stimuli. The patient was incontinent and required nursing care. During three month periods, the patient progressively became somnolent, speechless and immobile. Eventually, he was in a state of akinetic mutism. The patient became unresponsive. The state of consciousness fluctuated within a narrow range. The pupils were isocoric and did not react to light. He sometimes moved his eyes horizontally, but the vertical eye movement was limited. Deep tendon reflexes were hyperactive with Babinski reflex bilaterally. Passive mobilization of extremities revealed hypertonic. The CT scan disclosed the bilateral symmetrical infarction of the thalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of dural arteriovenous malformation with bilateral thalamic infarction]. 381 31

A 49-year-old man who had been suffering from disturbance of hearing for 5 years suddenly developed severe headache, nausea, and vomiting. Computed tomography (CT) scans both with and without contrast medium enhancement, performed on the day of admission, showed a nearly round high-density area in the left cerebellopontine angle. A left transaxillary vertebral angiogram showed no aneurysm or arteriovenous malformation. Hemorrhage from a tumor in the left cerebellopontine angle was suspected. CT scan without contrast medium enhancement, performed on the 17th day after onset, showed only a small, ill-defined high-density area in the cerebellopontine angle. An operation was performed on the 20th day after onset. The tumor was totally extirpated together with a clot. Histologically the tumor was an acoustic neurinoma with hemorrhage and necrosis. The postoperative course was favorable. Massive hemorrhage from primary intracranial tumors, especially acoustic neurinomas, is discussed. Radical operation on the tumor should be performed as soon as possible.
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PMID:Acoustic neurinoma presenting as subarachnoid hemorrhage. 660 70

The authors described a case of arteriovenous malformation (AVM) of the choroid plexus, and presented a review of literature. This 40-year-old male experienced a sudden onset of severe headache and vomiting on February 5th 1982. At the other hospital, CT scans revealed marked intraventricular hemorrhage, however his general condition was relatively good without a loss of consciousness, motor weakness and sensory disturbance. After about a month of conservative treatment, he was transferred to the Kochi Medical School Hospital. On admission, he had shown no neurological deficit except for slight occipital headache. Transfemoral cerebral angiography revealed an angioma of the choroid plexus, which was fed by the anterior and medial posterior choroidal arteries and drained into the internal cerebral vein. CT scans showed a small high density area due to the nidus of angioma at the interspace of bilateral frontal horns of the lateral ventricles. On March 25th 1982, using an anterior transcallosal approach, the angioma was totally removed. The histological diagnosis was AVM. The post-operative course was uneventful and the patient discharged without adding neurological deficit on April 12th 1982. Review of literature revealed 27 documented cases of angioma of the choroid plexus; 12 cases of AVM, 5 of cavernous angioma, 2 of telangiectasia, 1 of venous angioma and the other 7 of undefined description. Almost all cases were initiated with an episode of variable intracranial hemorrhage, particularly of intraventricular hemorrhage. Clinical course of them, however, were variable. On the contrast to male prevalence of AVM located in the other sites, the ratio of female to male was 2:1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arteriovenous malformations of the choroid plexus--a case report]. 663 12

Arteriovenous malformation ruptured in the neonatal period is rare. The authors report a case of arteriovenous malformation showed onset of symptoms on the late neonatal period. A female Japanese baby was born at full term. Neonatal history was uneventful until she had bad temper, pallor and vomiting on 23th day. Her head size increased abnormally until it was 42.5 cm when she was admitted to Shizuoka Children's Hospital with a diagnosis of possible hydrocephalus at 2 months old. CT scan showed a large cystic cavity communicated with the dilated lateral ventricles. The ventriculo-peritoneal shunt was performed, but unfortunately the shunt was removed for the suspicion of abdominal complication. At the age of 4 months, right retrograde brachial angiography showed a tangle of abnormal vascular channels in the right fronto-lateral basal region (15X13X8 mm in size), which was fed a frontopolar artery and drained to superior saggital sinus. Frontal osteoplastic craniotomy was performed and total arteriovenous malformation with a partial frontal lobe was excised. Ventriculo-peritoneal shunt was reinserted for the post-hemorrhagic hydrocephalus. She was healthy on 3 years old with mild motor deficit.
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PMID:[A case of arteriovenous malformation showed onset of symptoms on the late neonatal period]. 713 11

A 29 year old woman suffered sudden hemiplegia, vomiting and headache during the 28th week of her first pregnancy. She was diagnosed as the intracranial hemorrhage due to the ruptured arteriovenous malformation, and emergency operation was performed. Anesthesia was induced with crush induction using thiamylal, fentanyl, pancuronium and suxamethonium, and maintained with fentanyl, isoflurane and nitrous oxide in oxygen. During and after surgery, fetal heart rate and uterine contraction were monitored continuously. Intense hypotension was not chosen because it may place a fetus at risk of intrauterine asphyxia. Ventilation was controlled to maintain PaCO2 between 30 and 35 mmHg. During surgery, D-mannitol 60 g was infused slowly to prevent fetal dehydration, and after surgery no osmotic diuretics were used. Ritodrine hydrochloride, which prevented premature delivery, was continuously infused after surgery. Her neurological symptom was improved and her baby was delivered vaginally at 41st gestational week.
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PMID:[Anesthesia for a pregnant patient with ruptured cerebral arterio-venous malformation]. 796 29

A case of dural arteriovenous malformation (AVM) in the posterior cranial fossa detected after STA-MCA anastomosis surgery. A 52-year-old male consulted a neighbourhood hospital for sudden headache and vomiting. He was diagnosed as having intraventricular hemorrhage on CT scan. Though the obstruction of the right internal carotid artery was revealed angiographically, his symptoms improved after conservative therapy. Two weeks after onset, his consciousness deteriorated and he developed left hemiparesis. Thereafter, he was transferred to our hospital. After thorough examination, right STA-MCA anastomosis surgery was performed. Approximately 2 months after surgery, right tinnitus developed and gradually exacerbated. Since it was thought to be due to increased blood flow in the right superficial temporal artery, it was kept under observation. On angiogram, 8 months after surgery, good blood flow supplied from the right superficial temporal artery to the territory of the right middle cerebral artery was shown, and a dural AVM fed by the right occipital artery was found. Fourteen months after the surgery, an enlarged dural AVM with backflow to the superficial cerebral veins fed by the enlarged right occipital artery and right ascending pharyngeal artery was revealed. Embolization therapy to the right occipital and ascending pharyngeal artery was performed using coils and ivalon, and irradiation of 30 Gy was added. After this treatment, right tinnitus improved. On angiography 2 years later, transverse sinus was slightly visible via the right occipital artery and ascending pharyngeal artery, but the dural AVM was significantly reduced. The origin of dural AVMs remains controversial. In our case, dural AVM was not found before the STA-MCA anastomosis surgery, and sinus thrombosis was not found throughout the course of observation. It is thought that the occult dural AVM was disclosed and enlarged by the increased blood flow through the external carotid artery via the STA-MCA anastomosis. Therefore, the dural AVM seemed to be congenital in origin.
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PMID:[A case of dural AVM detected after STA-MCA anastomosis]. 855 71

The nucleus caudatus is not a common location of spontaneous intracerebral hemorrhage. Twelve patients (8 men and 4 women) aged 38-76 years who had caudate hemorrhage between November 1, 1992 and March 31, 1994 were evaluated. These cases represented 2.1% of intracerebral hemorrhage cases at Neurological Institute, Veterans General Hospital-Taipei, Taiwan. Cerebral angiography was performed on eight patients. Six patients were evaluated by an extensive neuropsychological battery. The most frequent symptoms of caudate hemorrhage were headache and/or vomiting, and decreased consciousness. Clinical features were similar to those of subarachnoid hemorrhage. Angiography showed characteristic moyamoya disease in one patient but did not show an aneurysm or arteriovenous malformation in any patient. The etiology in most patients was hypertension. Neuropsychological assessments showed significant impairment in tasks of short-term and long-term memory and in verbal fluency as well as trends of impairment of orientation rather than of controls. Neurobehavioral symptoms probably resulted from interruption of the cortical-subcortical loops between the caudate nucleus and prefrontal cortex.
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PMID:Caudate hemorrhage: clinical features, neuropsychological assessments and radiological findings. 859 95

We report a 32-year-old man who developed cerebellar ataxia and a posterior fossa mass 12 years after the radiation therapy for a cerebellar arteriovenous malformation (AVM). The patient was well until 19 years of the age when he had an acute onset of vertigo and vomiting. A spinal tap was performed and the CSF was bloody. He was admitted to another hospital where an arteriovenous malformation was found in the cerebellum by angiography. Four years after the onset, he developed tingling sensation in the distribution of the second division of the right trigeminal nerve. He was admitted to the neurosurgery service of our hospital where the cerebellar AVM was confirmed. He was transferred to University of California where Bragg peak stereotaxic radiotherapy was successfully performed; this utilizes high energy alpha-ray produced by a cyclotron. Three years after the radiotherapy, marked reduction in the size of the AVM was confirmed by angiography. Twelve years after the onset of his initial symptom, he noted unsteadiness of gait. He was readmitted to our neurosurgery service where obstructive hydrocephalus was found. He was treated by ventriculoperitoneal shunting and placement of a Ommaya reservoir. After these therapy, he noted marked improvement in his gait and ataxia. However, in 1993, his unsteadiness of gait recurred, and he was again admitted to our neurosurgery service on June 20, 1993. On admission, T1-weighted MRI revealed a slightly low signal intensity mass lesion in the right cerebellar hemisphere compressing the brain stem; a spotty high signal intensity lesion and another small low intensity lesion were seen within the mass. Vertebro-basilar angiograms revealed upward displacement of the superior cerebellar arteries. No arteriovenous nidus was visualized. On July, 3rd, the cyst was surgically drained and the Ommaya reservoir was removed. Post-operative course was uneventful, however, he developed head tremor after the surgery. Neurologic examination on July 20, 1993 revealed an alert and well oriented man in no acute distress. General physical examination was unremarkable. Neurologic examination revealed no dementia; higher cerebral functions appeared intact. The optic discs were flat, and visual fields were intact. Ocular movements were full but convergence was restricted. Horizontal gaze nystagmus was noted more in the right lateral gaze. Pupils were intact. Facial sensation and facial muscles were intact. Hearing was normal. His voice was of nasal quality. Pharyngeal reflex was diminished. The tongue showed deviation to the left without atrophy. Head tremor at 5 c/s was noted. He was able to stand with support but was unable to walk. No muscle atrophy or weakness was noted. The finger-to-nose and the heel-to-knee tests showed dysmetria and decomposition more on the right. Rapid alternating movements were ataxic on the right. Muscle tone was diminished on the right. Muscle stretch reflexes were normally elicited and were symmetric. The plantar response was flexor bilaterally. Sensation was intact. On July 21, a posterior fossa exploration was performed. After the surgery, he was treated with 30 mg/day of alotinolol which showed no effect on his head tremor. He was then treated with gradually increasing doses of clonazepam; when he received 8 mg/day of clonazepam, his tremor showed marked improvement. He was discussed in a neurologic CPC on the nature of the posterior fossa lesion and his tremor. Opinions were divided between delayed radiation necrosis and a radiation-induced brain tumor. The chief discussant arrived at the conclusion that the patient had delayed radiation necrosis compressing the brain stem and cerebellar hemispheres. Regarding the nature of his tremor, he thought that his head tremor was of cerebellar type of postural tremor. Histologic examination of the biopsied specimen revealed accumulation of relatively fresh blood constituents in the deep area of the cerebellum forming a mass. Most of the
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PMID:[A 32-year-old man who developed a posterior fossa mass 12 years after the radiation therapy for cerebellar arteriovenous malformation]. 867 25


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