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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with progressive signs and symptoms suggestive of a pontine lesion is described. Intracranial investigations, CAT scan, vertebral angiography, and lumbar pneumoencephalogram revealed a space-occupying lesion of the pons and midbrain. The exact nature of the lesion was not established before the operation. A posterior fossa exploration was performed and a pontine haematoma was discovered and evacuated. The pathological specimen was designated as a cryptic arteriovenous malformation. Preoperative neurological deficits disappeared except for minimal left sixth nerve palsy and mild truncal ataxia.
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PMID:Successful removal of an intrapontine haematoma. 50 71

A 39-year-old male was admitted because of slowly progressive disturbance of consciousness, diplopia, and ataxia after laparotomy. Ventriculoperitoneal shunting and removal of an arteriovenous malformation had been performed previously. Neurological examination on admission revealed drowsiness, rotatory nystagmus, Parinaud's sign, and truncal ataxia. Computed tomography scan revealed extraordinary dilatation of the fourth ventricle compared with other dilated ventricles, and old low-density areas in the cerebellar hemispheres. After an external ventricular drainage (EVD) was inserted, all the ventricles decreased in size and the symptoms disappeared. The authors confirmed the patency of the aqueductal canal. One week later, the EVD was replaced by a ventriculoperitoneal shunt. A disproportionately large, communicating fourth ventricle (DLCFV) should be differentiated from an isolated fourth ventricle, which consists of marked enlargement of the fourth ventricle with obstruction of both the inlet and outlet of the fourth ventricle. The authors propose the importance of the fragility to pressure of the brain parenchyma and cerebellar hemispheres around the fourth ventricle as the mechanism of producing DLCFV.
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PMID:[Disproportionately large, communicating fourth ventricle. Case report]. 172 33

Nontraumatic intracerebellar hemorrhage is rare during childhood. We report such a case due to rupture of arteriovenous malformation, in which surgery was able to bring about satisfactory recovery from deep coma without spontaneous respiration. This case shows that operative treatment should not be abandoned even though neurological deficits are very serious. This 6-year-old boy suddenly complained of headache while playing in a nursery and became restless. Because of deterioration of consciousness level followed by loss of respiration, he was transferred from a local physician to our clinic 4 hours after the onset. Computerized tomography scan disclosed a hematoma in the cerebellar hemisphere. Emergency suboccipital craniectomy was carried out 1 hour later. Immediately after operation, respiration was restored. Vertebral arteriography was performed 1 month after the operation, when the patient had recovered but could barely communicate with his family. The study revealed a small arteriovenous malformation supplied by the anterior inferior cerebellar artery. The malformation was removed 3 months after admission. The postoperative course was uneventful and the patient attended a primary school without neurological deficits except for slight ataxia 6 months after the onset.
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PMID:[A case of intracerebellar hemorrhage in infancy]. 189 25

Two patients had paresis of the trochlear nerve contralateral to the site of lesions in the brainstem. Both patients had ipsilateral blepharoptosis and miosis suggesting oculosympathetic paresis from involvement of the descending sympathetic tract, adjacent to the fourth cranial nerve nucleus and its fascicles, in the caudal mesencephalon. Cerebral antiography documented an arteriovenous malformation of the brainstem in Case 1. Magnetic resonance imaging disclosed a lesion of high signal intensity on T2-weighted images involving the dorsal mesencephalon in Case 2. Involvement of the superior cerebellar peduncle produced ipsilateral dysmetria and ataxia. Lesions involving the fourth cranial nerve nucleus or its fascicles, before decussation in the superior medullary velum, and adjacent sympathetic fibers may produce an ipsilateral Horner's syndrome and contralateral superior oblique muscle paresis.
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PMID:Contralateral trochlear nerve paresis and ipsilateral Horner's syndrome. 291 20

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

The case of a man with a large arteriovenous malformation, fed by meningeal arteries and draining into the Galenic system is reported. Mental deterioration and gait ataxia were attributed to an associated noncommunicating hydrocephalus. The symptoms recurred two months after successful ventriculoatrial shunting.
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PMID:Dural arteriovenous malformation involving the Galenic system and producing hydrocephalus. 405 Mar 14

We report a case of congestive venous necrosis involving the diencephalon symmetrically, presumably precipitated by a dural arteriovenous malformation (AVM). The patient presented with a 1-month history of intermittent confusion and gait ataxia. The initial radiological work-up revealed a dural AVM. The patient's subsequent deterioration was accompanied by computed tomographic findings of diencephalic congestion. Pathological examination showed subacute necrosis of the diencephalon. We discuss the pathogenesis of this case of subacute diencephalic necorsis and its possible relationship to the entity of subacute diencephalic angioencephalopathy.
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PMID:Subacute diencephalic necrosis and dural arteriovenous malformation. 405 2

One week after chiropractic manipulations, a 60-year-old normotensive man suffered acute onset of vertigo, ataxia, and dysarthria. CT disclosed an isodense mass of the posterior fossa. Vertebral arteriography showed that the avascular mass arose from the right cerebellar hemisphere. Hydrocephalus developed, and suboccipital craniotomy revealed a large cerebellar hematoma due to a small arteriovenous malformation. A similar episode occurred 2 months later. CT isodense cerebellar hematomas should be considered before giving anticoagulant therapy.
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PMID:Isodense cerebellar hematoma. 668 55

The authors report 3 cases in which, in addition to venous angioma, other types of vascular malformations coexisted. They discussed the pathological significance of this coexistence, and the treatment to be given in these conditions. Case 1: A 38-year-old man was admitted to the hospital because of progressive headaches of 3 days' duration. X-ray CT revealed a large hematoma in the left cerebellar hemisphere. Vertebral angiogram showed a caput medusae in the venous phase, which is a typical picture of venous angioma. The hematoma was surgically removed and careful inspection of the cavity wall was made. A thick vein and many thin walled dilated venules draining to the vein were observed in the cavity wall. These abnormal vessels were completely removed. Because of reaccumulation of the hematoma and massive edema of the hemisphere, reoperation was performed. On removing a part of the cerebellar hemisphere, a small mass of vascular network was found and removed together with the hematoma. Histologically, the first specimen was a typical venous angioma, and the second one was a arteriovenous malformation. Case 2: A girl 9 years of age was admitted because of headache and left sided ataxia. CT and MRI revealed a multi staged hematoma in the left cerebellar hemisphere. Vertebral angiography, however, failed to demonstrate any kind of vascular malformations. The hematoma was removed with its wall. The histological appearance was compatible with venous angioma. 4 years later she bled again, and reoperation was performed. Histological examination this time revealed a cavernous angioma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Venous angioma coexisting with other types of cerebrovascular malformations]. 807

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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