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)

Thirty-seven patients with retinoblastoma were evaluated prospectively by clinical examination, lumbar puncture, and CT. Eight (22%) of the 37 were found to have meningeal dissemination. The tumor was bilateral in three patients. Two cases showed no CT signs of local recurrence. Headache, nausea/vomiting, and restlessness were the most common symptoms. CT scans in these patients showed diffuse meningeal contrast enhancement, nodular masses, ependymal-subependymal enhancement, and ventricular dilatation. Our series of eight patients with meningeal spread illustrates a considerable range of dissemination patterns referable to retinoblastoma. One case illustrated the CT finding of multiple epidural metastases.
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PMID:Meningeal dissemination of retinoblastoma: CT findings in eight patients. 212 Oct 4

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25

A Japanese male showed gradually progressing dementia with psychiatric symptoms including abnormal behavior, night and day reversal, nocturnal delirium, loud shouting, agitation, resistance to care, and loud soliloquy. The patient had a history of right cerebral embolism due to atrial fibrillation 1 month before the onset of dementia. Head CT revealed widespread cerebral infarction in the right cerebral hemisphere with bilateral lateral ventricular dilatation. The patient died at the age of 83, 10 months after the onset of cerebral embolism. The clinical diagnosis was mixed-type dementia. On autopsy the brain weighed 1,160 g. Widespread cerebral amyloid angiopathy (CAA) was observed, with distribution most severe in the cerebral cortical vessels and slightly milder in the leptomeningial and subarachnoid vessels. The artery, arteriole, and capillary walls were thickened by the deposition of amorphous, eosinophilic and beta-protein immunopositive amyloid. Abeta-deposition was more severe in capillaries and CAA tended to be more severe in the occipital regions. Multiple cortical microinfarcts were found, particularly in the crests of the cerebral gyri of watershed zones. Cerebral white matter, basal ganglia, thalamus, brainstem and spinal cord were relatively preserved from CAA. Infarction was not apparent, except for an embolic lesion in the right cerebral hemisphere and the cortical microinfarcts. We did not observe fibrinoid necrosis, granulomatous angiitis or giant cell reaction associated with CAA-vasculopathies. Rare instances were observed of neurofibrillary tangles and senile plaques corresponding to Braak stages II and A, respectively. We thought the multiple cortical microinfarcts occurred due to chronic hypoperfusion associated with CAA-associated vasculopathies of capillaries in the cerebral cortex. We suspected that the dementia was influenced by the CAA with multiple cortical microinfarcts. Pathologic findings of the patient suggest that CAA without AD-related Abeta-deposition might exist and that capillary Abeta-deposition might be an important factor of hemodynamic perturbation.
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PMID:[An autopsy case of senile dementia suspected to be influenced by cerebral amyloid angiopathy with multiple cortical microinfarcts]. 2096 Sep 31