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)

The aim of this study was to determine whether the percentage of akinesia on echocardiography during the acute phase of transmural anterior myocardial infarction could predict secondary left ventricular dilatation. The study group comprised 24 patients (18 men and 6 women) with an average age of 59 years. The patients underwent two echocardiographic examinations, the first during the acute (< 72 hours) phase and the second, 6 months later. Ventricular volumes were calculated by the ellipse monoplane method in the apical 4 chamber view. The percentage of akinesia was defined as the ratio between the length of the akinetic segment and the left ventricular end diastolic perimeter in the apical 4 chamber view. An increase in end diastolic volume (83 +/- 25 vs 62 +/- 18 ml/m2; p < 0.01) and in end systolic volume (51 +/- 27 vs 34 +/- 11 ml/m2; p < 0.01) was observed 6 months after infarction without a significant change in ejection fractions (42 +/- 17% vs 44 +/- 10%). The percentage of akinesia in the acute phase was > 30% in 15 patients (Group I) and < 30% in 9 patients (Group II). The increase in ventricular volumes at 6 months after infarction was significant in Group I (p < 0.02) but not in Group II. At 6 months after infarction, the end systolic volumes were greater (60 +/- 27 vs 37 +/- 22 ml/m2, p < 0.5) and the ejection fractions were lower (35 +/- 13% vs 53 +/- 18%, p < 0.01) in Group I than in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Left ventricular dilatation after primary transmural anterior myocardial infarction. Influence of the percentage of akinesia on echocardiography]. 129 91

This report describes a case of cerebrotendinous xanthomatosis (CTX) accompanied by clinical manifestations of parkinsonism, including oily and masked face, marked akinesia, muscle rigidity and resting hand tremor. Magnetic resonance imaging (MRI) of the brain showed high intensity areas on T2 weighted imaging, and slightly low intensity areas on T1 weighted imaging in the right globus pallidus and the left putamen. Cerebral cortical atrophy with slight ventricular dilatation and cerebellar atrophy were present as well. This is a case report of CTX which manifested parkinsonism. Parkinsonism may not be a coincidental manifestation in CTX, but rather represent a symptom of the same underlying diathesis.
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PMID:Parkinsonism in cerebrotendinous xanthomatosis. 186 93

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 51-year-old man with early onset parkinsonism]. 760 92