Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied three patients with spontaneous dorsal mesencephalic hemorrhages. One patient had Parinaud's syndrome with a unilateral hemorrhage confined to the rostral tectal plate. The second patient had vertical gaze palsy, skew deviation, and bilateral Horner's syndrome due to a unilateral hemorrhage that involved the superior colliculus and extended anteriorly into the midbrain tegmentum and inferiorly to the rostral dorsal pons. The third patient had a hemorrhage in the caudal tectal plate, with bilateral fourth cranial nerve palsies, unilateral Horner's syndrome, and ataxia. There was hydrocephalus due to obstruction of the aqueduct in two patients. The patients recovered, but with some degree of disability.
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PMID:Partial dorsal mesencephalic hemorrhages: report of three cases. 396 Mar 28

After reviewing the literature, a personal series of 10 adult patients with cerebellar infarction diagnosed by CT scan is described. The clinical picture in young adult men is characterized by rapid onset of headache, vomiting, vertigo, ataxia and blurred vision. After this sudden onset the patients may present a stable course or a rapid or delayed onset of brain stem compression, revealed by impairment of consciousness. CT scan is the diagnostic method of choice. The correlation between angiographic and CT localization of the infarction is not good. For therapy the following policy is suggested: in alert and clinically stable patients: medical treatment (mannitol, glycerol, dexamethason), ICP and serial CT monitoring; in alert patients with hydrocephalus or mass effect: medical treatment and monitoring as mentioned before; ventricular drainage if ICP surpasses 350 mm H2O; in patients with impaired consciousness and hydrocephalus or mass effect: immediate ventricular drainage. If it is not followed by prompt improvement of the level of consciousness, an emergency suboccipital craniectomy with removal of the infarcted tissue should be done.
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PMID:Surgical management of acute cerebellar infarction. 398 89

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

Animal studies have indicated a "vomiting center" situated in the dorsal portion of the lateral reticular formation of the medulla at the level of the dorsal nucleus of the vagus. There is also a chemoreceptor trigger zone in the floor of the fourth ventricle in the area postrema which influences the vomiting center. A 63 year old man with a three year history of metastatic malignant melanoma presented with nausea, projectile vomiting, gait ataxia and diplopia associated with horizontal and vertical nystagmus. CT scan showed a solitary brainstem metastasis without hydrocephalus and he was treated with radiotherapy with resolution of his vomiting after four weeks. At post mortem three months later a metastasis was found in the right middle cerebellar peduncle and lateral tegmentum of the pons; there was no pathological change in the area of the vomiting center or area postrema. It is postulated that this lesion caused projectile vomiting because of involvement of either afferent projections to the vomiting center. The neuroanatomy of vomiting is discussed.
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PMID:The neuroanatomy of vomiting in man: association of projectile vomiting with a solitary metastasis in the lateral tegmentum of the pons and the middle cerebellar peduncle. 407 83

The case reported here is that of a woman, without any significant pathological antecedent. At age 54, she developed signs of thalamic dementia and died 5 years later. The prominent symptoms were massive anterograde amnesia, apathia, apragmatism, ataxia and a frontal syndrome. She never showed aphasia, apraxia, agnosia or disorders of ocular motility. The C. T. Scan showed lacunar low densities in the mesencephalon and both thalami, mainly on the left side, as well as hydrocephalus caused by a stenosis of the aqueduct as shown by other neuroradiological procedures. The neuropathological examination showed space-occupying lacunae, bulging in the third ventricle, squeezing the aqueduct and protruding into the fourth ventricle. These lacunae were situated in the territory of the paramedian mesencephalo-thalamic arterial pedicle. They were perivascular spaces distensions, probably caused by disorder of the permeability of the arterial wall. This hypothesis is supported by the presence of severe lesions of segmental necrotizing angeitis on a paramedian mesencephalic artery. The etiology of this angeitis is unknown. As far as we know, such neuropathological lesions have never been reported previously. Therefore the pathology and etiopathogeny of cerebral lacunae should be reconsidered.
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PMID:[Thalamic dementia. Expansive lacunae of the thalamo-paramedian mesencephalic area. Hydrocephalus caused by stenosis of the aqueduct of Sylvius]. 613 53

Six years after apparent complete recovery from intestinal Whipple's disease, a 56 year old man developed insidious progressive somnolence and gait ataxia. Studies showed hydrocephalus with obstruction of the aqueduct and CSF leukocytosis and elevated protein. Arachnoid biopsy during craniotomy revealed chronic inflammatory infiltration with PAS-positive macrophages. The patient died 5 years later despite two courses of antibiotic therapy. This is the first report of histologically confirmed cerebral Whipple's disease during life. Whipple's disease is a systemic infectious disorder. Cerebral involvement even in neurologically asymptomatic patients should be sought with periodic CSF cytologic studies and a search for hydrocephalus. The possibility of cerebral Whipple's disease should be considered in the presence of unexplained hydrocephalus and/or chronic inflammatory changes in the spinal fluid, especially in those with past or active intestinal disease.
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PMID:Meningo-ependymitis in Whipple's disease. 615 64

Dementia, a syndrome of acquired intellectual deterioration, is an etiologically nonspecific condition that can be permanent or reversible. When evaluating demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. Physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistence of dementia and a peripheral neuropathy usually indicates the existence of a toxic or metabolic disorder. Depressed mood, sleep disturbance, anorexia, impotence, constipation, and psychomotor retardation indicate the presence of a depressive syndrome. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, whereas resting tremor, choreoathetosis, or rigidity occur in progressive extrapyramidal disorder. EEG is focally abnormal in cases of cerebral mass lesions and shows generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid function tests, serum calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia may be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be sought in all demented patients.
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PMID:Treatable dementias. 635 58

Basilar impression was found in three members of one family. The mother showed an asymptomatic deformity, her eldest son complained of headache, drop-attacks, nystagmus, unilateral ophthalmoplegia, and ataxia; the middle son presented with headache, nystagmus, and hemiparesis. Magnetic resonance (MR) imaging demonstrated convexobasia of various degrees with elevation of the upper spine and malformation of the occipital bone. The medulla oblongata and the pons were flattened and dislocated backward in two cases. Chiari malformation was present in one case and mild hydrocephalus in another. A comparison of MR with CT imaging demonstrates some advantages of the former method in the assessment of the neural structures directly involved in basilar impression.
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PMID:MR imaging of familial basilar impression. 647 Feb 65

A term of 'disproportionately large, communicating fourth ventricle' (DLCFV) was first proposed by in Harwood-Nash in 1980. It is somewhat different from the well known clinical entity of 'isolated or trapped fourth ventricle', because of apparent patency of aqueductal canal. Two cases of typical DLCFV encountered in our clinic were described. First patient was a 24 year old man in whom this condition developed following operations for lumber disc and second patient was 22 year old woman in whom the disease developed after subarachnoid hemorrhage. In both cases, main symptoms were attributable to hydrocephalus but three posterior fossa symptoms, nystagmus, Parinaud' sign and truncal ataxia were also characteristic. On the CT scan, the fourth ventricle was extraordinarily enlarged. Patency of the aqueductal canal was demonstrated by air study or Conray and Metrizamide ventriculography. On the other hand, occlusion was demonstrated or highly suspected in or near the foramina Magendie and Luschka. After a routine ventriculo-peritoneal shunt operation, the fourth ventricle decreased in size and the symptoms were immediately relieved. Plausible explanation for mechanism involved in occurrence of DLCFV were (1) occlusion process in or near the fourth ventricle outlets seems to be crucial in this pathologic condition. Collision of CSF pulse waves against the obstruction may yield a water hammer effect on the fourth ventricle. (2) abnormal weakness of the brain stem parenchyma around the fourth ventricle to CSF pressure may be another contributory factor.
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PMID:[Disproportionately large communicating fourth ventricle--report of 2 cases]. 660 22

The case of a 16-year-old boy with occipital headache, diplopia, ataxia, and weakness in the lower extremities of 1-month duration is reported. Slowness of mentation, speech, and motor action was also present. Massive chronic hydrocephalus was indicated by an enlarged head. The prominent clinical features suggested involvement of the brainstem, and contrast studies showed compression of the brainstem and a filling defect posteriorly at C1-2. Brainstem auditory evoked potential latency suggested bilateral lesions of the brainstem. Posterior fossa decompression confirmed the presence of an Arnold-Chiari malformation, with the cerebellar tonsils as low as C-3. The fourth ventricle was microdissected and opened. Remarkable clinical and evoked potential recovery ensued over several months. Clinical-anatomic and anatomic-physiologic correlations in Arnold-Chiari malformation are discussed.
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PMID:Clinical and electrophysiologic recovery in Arnold-Chiari malformation. 662 43


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