Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old man presented with a history of dizziness and intermittent vertical oscillopsia after oblique extension of the head and neck, following a neck injury 2 years previously. He had no other symptoms of cerebellar or brainstem dysfunction. On examination, an intermittent downbeat nystagmus lasting about fifty seconds was elicited by head extension and rotation. Radiologic examination showed slight lateral instability of the odontoid on lateral rotation, and computed tomography brain scan with Iopamidol 300 (Niopam) contrast revealed a 5-cm vermian arachnoid cyst in the posterior fossa with obstructive hydrocephalus. Removal of the cyst cured the nystagmus.
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PMID:Intermittent downbeat nystagmus secondary to vermian arachnoid cyst with associated obstructive hydrocephalus. 183 53

Stereotactic radiosurgery is at present being marketed as a reliable alternative to conventional tumor removal in patients with acoustic neuromas. Hearing preservation is possible and treatment modality is presented as being very low. A case history is presented, in which a patient with an 18 mm tumor and normal hearing developed severe hydrocephalus and dizziness 9 months after irradiation, in addition to losing her hearing. Whether the Gamma knife is to be considered a reliable alternative to surgical removal of acoustic neuromas is discussed.
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PMID:Gamma knife: hydrocephalus as a complication of stereotactic radiosurgical treatment of an acoustic neuroma. 224 Jan 75

Prompted by several unsatisfactory outcomes, we reviewed the records of 59 patients with cerebellar metastases (26 solitary) with respect to clinical presentation, diagnosis, and natural history. Eighty-seven percent of patients initially complained of headache, gait disturbance, and/or dizziness. At time of diagnosis, 92% of patients with solitary cerebellar metastases and 74% of the overall series complained of headache and/or difficulty walking. In three of four cases, magnetic resonance imaging (MRI) was superior to x-ray computed tomography (CT) in detecting the cerebellar lesions. Several patients acutely deteriorated during evaluation or at the initiation of radiation therapy. We conclude that a cancer patient presenting with headache and gait difficulty with or without nausea/vomiting and dizziness should promptly undergo head CT scanning, and that MRI is useful even if CT is negative. In addition, we recommend that patients with documented cerebellar metastases receive high-dose glucocorticoid therapy for 48 to 72 hours before beginning radiation therapy. The presence of symptomatic hydrocephalus or failure to respond to glucocorticoids initially are particularly ominous features that may be best managed by early neurosurgical consultation before beginning radiation therapy.
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PMID:Cerebellar metastases: diagnostic and management considerations. 303 34

A series of 12 patients with cerebellar infarcts diagnosed by computerized tomography are reviewed. The clinical features of cerebellar infarctions cover a wide spectrum, mimicking symptoms and signs from an acute labyrinthitis to a rapidly expanding posterior fossa mass lesion with brain stem and cerebral dysfunction. Two patients were asymptomatic and three showed signs of cerebellar dysfunction only. Three patients had evidence of brain stem dysfunction with cranial nerve palsies accompanying the cerebellar deficit. Two presented a pseudovestibular form with sudden onset of nausea, vomiting, rotary dizziness and ataxia. A pseudotumoral form with intracranial hypertension was found in two cases, in which softening tissue acts as a rapidly expanding posterior foss mass lesion. It is difficult to identify the exact artery involved in a cerebellar infarct because of the collateral circulation and connections between the three major arteries. Atherosclerosis and general decrease in blood flow can be regarded as the most likely factors precipitating focal cerebellar infarction. Surveillance is necessary during the first days with anti-edematous therapy. Rapid deterioration of consciousness should be considered a sign of increasing intracranial pressure progressing with the development of hydrocephalus. If necessary, surgical decompression by external drainage or by direct access to the posterior fossa can be carried out.
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PMID:[Cerebellar infarct. Clinical presentation and x-ray computed tomography of the brain]. 394 88

Axial tomograpum (CAT), of 59 patients with dementia and 102 controls suffering from headaches and dizziness were examined. The CAT was normal in 13 demented patients (22%) and in 37 controls (36,3%), and revealed enlarged spaces of the CSF in 46 anoic patients (78%) and 65 controls (63.7%). Multiple areas of subnormal density were observed in 23 anoic patients (39%) and in 6 controls (5.9%). This indicates that the multi infarct syndrome is frequently associated with dementia, while the correlations between Hydrocephalus and dementia is weak.
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PMID:[Cranial computerized tomography in senile dementia]. 716 98

A 28-year old male was admitted to Musashino Red Cross Hospital on June 21, 1975, because of symptoms of increased intracranial pressure and cerebellar dysfunction. Thirteen months prior to admission he had a mild fever, tremor of right arm, headache, nausea and unsteady gait, but made a gradual recovery in about 40 days. A month prior to admission he had unsteady gate again wit dizziness, photophobia and lacrimation. Gait disturbance aggravated and he was admitted to another hospital, where he developed recent memory disturbance and cloudiness of consciousness. Spinal tap revealed initial pressure of 280 mm CSF. So a mass lesion possibly in the posterior fossa was suspected and the patient was referred to the neurosurgical department of musashino Red Cross Hospital. On admission he was moderately disorientated and disturbed in recent memory. Wide based gait, horizontal and vertical nystagmus were also noted. Angiography revealed rounding of the curve of the pericallosal artery but no space occupying lesions. External ventricular drainage was performed on July 25, 1975. After the operation, his orientation improved without change in dizziness, nystagmus and recent memory disturbance. Ventriculography showed hydrocephalus with cisternography revealed a block at the basal cisterns. PPDs was negative and typical sarcoid tubercles were found in the biopsy specimen of the cervical lymphnode. Kveim test was positive. But repeated chest roentgenogram failed to show bilateral hilar lymphadenopathy, or other changes consistent with pulmonary sarcoidosis. Steroid therapy resulted in marked symptomatic improvement.
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PMID:[A case of CNS sarcoidosis -case report of hydrocephalus due to mechanical obstruction secondary to sarcoid granulomata at the outlet of the fourth ventricle (author's transl)]. 723 30

A 55-year-old mildly hypertensive woman died after having developed a subcortical dementia during the past 9 years, with focal neurological signs. She presented at the age of 46 years with short episodes of dizziness and diplopia, suggesting that transient ischemic attacks involved the posterior fossa structures. Over the next 8 years, she developed difficulty in walking, urinary incontinence and seizures. On examination in 1989, she was severely demented. There was tetraparesis, bilateral arm and leg spasticity with hyperreflexia and bilateral Babinski signs. She showed epilepsia partialis continua involving the eyes, left hemiface and limbs. CT showed hypodensity of the white matter and lacunes in the basal ganglia and centrum semiovale, moderate hydrocephalus with cerebellar and cortical atrophy. Clinical and radiological features were similar to those of Binswanger's disease. Similar cases had occurred in the family affecting the patient's grandfather, father and two brothers, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed a Binswanger type of leukoencephalopathy caused by a peculiar microangiopathy characterized by a slightly basophilic small arterial granular degeneration of the medial sheath associated with the presence of ballooned smooth muscle cells with clear cytoplasm. Electron microscopic study revealed degenerative changes in the parietal vessels with notable increase of basal-membrane-type material and electron-dense granular deposits. These lesions could correspond to a specific familial pathology of the small arteries of the brain. They are identical to those reported in some patients with autosomal dominant inheritance. For other patients with similar clinical features and the same familial pattern, reported as "hereditary multi-infarct dementia'' and "chronic familial vascular encephalopathy'', there are no sufficient objective pathological facts to consider that they have the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Small arterial granular degeneration in familial Binswanger's syndrome. 814 Aug 99

Infarction of the cerebellum comprises about 1.5 percent of all strokes. The symptoms are initially very similar to those of benign labyrinthitis, and the diagnosis is easy to miss. There are three major causes of clinical deterioration and death: Expansion of the infarct to the brainstem, swelling of the infarcted cerebellum with compression of the brainstem, and hydrocephalus. Surgical intervention may be lifesaving if hydrocephalus develops. Five patients admitted to our department are described. All described sudden vertigo or dizziness, which in three of them was accompanied by headache. All had ataxia. In four this was ipsilateral to the infarction and in one bilateral. Two had slight hemiparesis and plantar inversion. Two patients developed hydrocephalus. One was operated with external drainage. It is important to have this diagnosis in mind in all patients with acute labyrinthine symptoms. Acute CT scanning should be carried out if the patient becomes less conscious.
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PMID:[Cerebellar infarctions]. 823 75

Arachnoid cysts very rarely occur within the ventricular system, where no arachnoid tissue exists. We present three cases of intraventricular arachnoid cyst with special reference to its origin. The first patient was a 5-year-old boy who complained of headaches and enlargement of his head. A CT scan revealed obstructive hydrocephalus and a large cystic lesion in the right lateral ventricle. The symptoms resolved after fenestration of the cyst and cystoperitoneal shunt. The second patient was a 49-year-old woman who complained of headache and numbness in her left upper extremity. A CT scan and MRI revealed a large cyst in the trigone of the right lateral ventricle. Fenestration of the cyst wall and cystoperitoneal shunt were performed relieving her complaints. The third patient was a 42-year-old man who complained of frequent seizures and dizziness. A CT scan and MRI demonstrated a moderate size cystic mass in the inferior horn of the right lateral ventricle. The symptoms were improved by partial resection of the cyst wall. Immunohistochemical studies and light microscopy confirmed that the cyst walls were composed of arachnoid membrane, implying that the cysts were arachnoid cysts. CT and MRI in these three cases showed widening of the choroidal fissure bordering the cyst wall, occasionally involving a part of the protruding cyst wall. On enhanced CT and MRI, the choroid plexus in the trigone of ipsilateral lateral ventricle was displaced anterolaterally, implying that the cysts had grown from outside the choroid plexus. Postoperative MRI demonstrated the shrunken cyst wall attached to the choroidal fissure. The surgical findings in case 3 also showed that the cyst wall was attached firmly to the choroid plexus. These findings appeared to indicate that the intraventricular arachnoid cyst originated from the arachnoid layer drawn into the choroidal fissure with choroidal vascular mesenchyme.
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PMID:[Intraventricular arachnoid cyst--on the origin of intraventricular arachnoid cysts]. 895 93

Cerebral internal venous thrombosis are rare and diagnosis is difficult. We report three cases in male adults. Clinical data were headaches, vomiting, dizziness and coma, in relation with an intracranial hypertension, or in a case, cardiocirculatory arrest. Cerebral internal veinous thrombosis was diagnosed by a CT scan and cerebral angiography twenty four hours after the admission in neurosurgical intensive care. CT scan showed hemorrhagic and ischemic lesions of thalami in two cases, diffuse cerebral edema in two patients, early or delayed hydrocephaly in two cases. No patient survived despite intensive treatment including heparinotherapy, ventricular CSF drainage, osmotherapy, dehydration, barbiturate, other antiepileptic drugs and mechanical ventilation. In two cases, general or local illness was found, sickle cell disease or radiotherapy for pineal tumor, and in case 3 clinical signs evoked autoimmune disease, not demonstrated by biological samples.
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PMID:[Cerebral deep vein thrombosis: three cases]. 1048 48


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