Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of generalized choreic movement associated with subarachnoid hemorrhage is reported. A 71 year-old hypertensive woman suddenly developed severe headache 14 days before admission. Consciousness disturbance and involuntary movement involving the face and upper extremities appeared about 8 days after onset. The involuntary motion was diagnosed as generalized choreic movement. CT scans showed subarachnoid hemorrhage with ventricular dilatation and periventricular lucency involving bilateral caudate nuclei. On admission the patient was stuporous with Hunt & Kosnik Grade 4. She showed involuntary choreic movement in both arms, trunk and face; hemiparenis and hyperreflexia were absent. An angiography revealed a right internal carotid-anterior choroidal artery aneurysm with vasospasm. After clipping the aneurysm in the following day, the consciousness disturbance and choreic movement gradually improved. By eight days after operation, the choreic movement completely disappeared. An MRI showed lacunar infarcts in the bilateral basal ganglia, predominantly in the caudate nuclei. In our case, the choreic movement is supposed to have been caused by impaired circulation in the bilateral corpora striata due to vasospasm and hydrocephalus after subarachnoid hemorrhage, in addition to the preexisting lacunar infarcts in the basal ganglia. This is claimed to be the first reported case of generalized choreic movement in associated with subarachnoid hemorrhage, which improved after surgery.
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PMID:[Generalized choreic movement associated with subarachnoid hemorrhage]. 174 95

Two cases of disproportionately large communicating fourth ventricle (DLCFV) accompanied by consciousness disturbance and bilateral exotropia are reported. Case #1 was a 21-year-old male who suffered from consciousness disturbance and bilateral exotropia due to malfunction of the ventriculoperitoneal shunt (VPS) which had previously been operated on twice for a left parietal arteriovenous malformation, which had caused ventricular hemorrhage several times. The last hemorrhage was massive and made ventricular casting, including the fourth ventricle. Both bilateral exotropia and the fourth ventricular dilatation were well controlled by the reconstruction of the VPS. Case #2 was a 66-year-old female, semicomatous because of massive subarachnoid hemorrhage with ventricular casting hematoma due to rupture of the right middle cerebral aneurysm. Though an improvement of the consciousness disturbance was obtained by continuous ventricular drainage (CVD), bilateral exotropia and consciousness deterioration appeared after lumboperitoneal shunt followed by the removal of the CVD. Another CVD was then carried out and some improvement was obtained again. However, the same symptoms appeared again after the VPS, followed by the removal of the CVD. The patient finally died despite a third CVD. Autopsy revealed a markedly dilated fourth ventricle and massive subarachnoid clots particularly around the foramen of Magendie and Luschka. The pathogenesis of DLCFV and bilateral exotropia are also discussed.
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PMID:[Disproportionately large communicating fourth ventricle with bilateral exotropia: report of two cases]. 223

We report a 85-year-old woman who died after one year history of convulsion, dementia, and consciousness disturbance. She was apparently well until January 6, 1995 when she was 85 year old; on that evening, she suddenly stated that some one was in her room and she became confused. A local MD gave her diazepam and she fell into sleep. At 3 o'clock in the following morning, she developed tonic-clonic convulsion in her right lower extremity which showed a march to her right upper extremity and the left lower extremity. She was admitted to our hospital. On admission, she was comatose with respiratory acidosis. She was intubated and placed on a ventilator. She was treated with intravenous phenytoin. She gradually gained consciousness and became alert. Respiration became normal. Her MRI revealed ventricular dilatation, fronto-parietal cortical atrophy, and a T1-low and T2-high signal intensity lesion in the left occipital lobe. She was discharged for out patient follow-up on February 4, 1995. Since then, she noted loss of memory and small step gait. A follow-up CT scan revealed a mass lesion which showed a ring-shaped enhancement in the left occipital lobe and was admitted again. On admission, she was alert but markedly demented. The optic fundi was unremarkable, but she appeared to have right homonymous hemianopsia. No motor weakness was noted. In Gd-DTPA enhanced MRI, the above tumor showed a ring enhancement. The diagnosis of glioblastoma was entertained, however, considering her age, she was treated with intravenous glycerol and intramuscular steroid. She was discharged for out-patient follow-up on July 15, 1995. Her gait disturbance had progressively become worse and she developed nausea and vomiting and was admitted again on October 2, 1995. On admission, she was somnolent and markedly demented. Brain stem responses were retained normally. She was unable to stand or walk. Deep tendon reflexes were slightly increased in the right upper extremity and the plantar response was extensor on the right. Her hospital course was complicated by respiratory tract infection and respiratory acidosis. She expired on November 2, 1995. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that she had a glioblastoma involving the left occipital lobe and the adjacent areas. Post-mortem examination revealed an infiltrating tumor in the left occipital lobe. On microscopic examination, the tumor was very cellular; nuclear atypism was marked and tumor cells undergoing mitosis were seen. In some areas, capillary proliferation was seen. Histologic characteristics were consistent with glioblastoma.
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PMID:[A 85-year-old woman with one year history of convulsion, dementia, and consciousness disturbance]. 936 96

We present a case of isolated adrenocorticotropic hormone (ACTH) deficiency complicated by acute adrenal crisis and severe myocardial dysfunction. A 54-year-old woman developed consciousness disturbance, hypoglycemia, hyponatremia, and rhabdomyolysis. Initial echocardiographic examinations on the sixth hospital day revealed marked right-sided atrial and ventricular dilatation and severe tricuspid regurgitation. A computed tomography scan for pulmonary embolism was negative. On the 14th hospital day, she became dyspneic and hypotensive. Repeated echocardiographic examinations demonstrated diffuse and severe hypokinesis of the left ventricle. The previous right-sided chamber dilatation became less apparent. Congestive heart failure and severe hypotension were refractory to catecholamines, while she was eventually diagnosed as having acute adrenal crisis due to isolated ACTH deficiency. Hydrocortisone replacement therapy was started, and echocardiographic examinations revealed that the left ventricular dysfunction completely returned to normal in the following eight days. Severe myocardial dysfunction is an uncommon but serious complication of acute adrenal insufficiency. The present case was unique in that diffuse left ventricular dysfunction was preceded by right ventricular dysfunction.
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PMID:Isolated ACTH deficiency presenting with severe myocardial dysfunction. 3054 10