Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old white male with a 25-year history of hypertension experienced the onset of intermittent diplopia and gait disturbance 24 hours after a change in antihypertensive medication from atenolol 50 mg/d to enalapril 5 mg bid. Three weeks later, the patient was admitted with a worsening of symptoms. Cerebral arteriography revealed significant bilateral vertebral artery stenosis. Symptoms continued to progress in the hospital, and at the time of posterior circulation revascularization the patient had a persistent bilateral internuclear ophthalmoplegia and right ptosis. The need for a neurovascular workup and adjustment of therapy in patients with antihypertensive-associated cerebral ischemia is discussed.
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PMID:Hemodynamic vertebrobasilar insufficiency as an adverse effect of antihypertensive therapy. 254 68

In 51 consecutive patients with acute transitory cerebral ischaemia cross-sectional echocardiograms, 24-hour electrocardiograms (ECG) and exercise ECGs were recorded. The subsequent observation period averaged 13 (3-30) months. The echocardiogram was abnormal in 27 of 46 patients (58%). A holosystolic mitral-valve prolapse was found in eight: cerebral ischaemia recurred in five. There was no correlation between arrhythmias in the 24-hour ECG and renewed cerebral ischaemia. In addition to the 14 patients who--according to history and resting ECG--had already had a myocardial infarction, the exercise ECG revealed probably coronary heart disease in a further 11, i.e. half of the patients had coronary heart disease. Renewed attacks of cerebral ischaemia occurred in 13 patients during the follow-up period; four patients died, all of them also having had coronary heart disease. Because of the high prevalence of coronary heart disease (often previously undiagnosed) in the whole group, routine exercise ECGs are recommended for patients with transitory ischaemic attacks, protracted ischaemic neurological deficit or "minimal stroke", while 24-hour ECG monitoring does not seem essential. Randomized trials are needed to determine whether patients with cerebral ischaemia and echocardiographic evidence of mitral-valve prolapse should be treated prophylactically.
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PMID:[Patients with transient ischemic attacks. Their cardiac status and its prognostic significance]. 335 33

The etiology of cerebrovascular disease (CDV) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an age- and sex-matched control group. The mean plasma beta-thromboglobulin (beta-TG) level of the patients (mean = 54.9 +/- 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 /- 6.9 ng/ml, p less than 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p less than 0.01). However, the beta-T levels of patients with MVP (n = 13, 52.9 +/- 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 +/- 33.7 ng/ml) significantly (p less than 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma beta-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between beta-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.
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PMID:Cerebral ischemia in young patients: it is associated with mitral valve prolapse and abnormal platelet activity in vivo? 621 70

One hundred and eighty-two patients (100 females, 82 males) with mitral valve prolapse (MVP) confirmed by echocardiography are described. Their ages range from 12 to 87 years (mean 48 years). The symptoms of breathlessness, pain in the chest and palpitations were analysed. They were associated with left ventricular failure, co-existing ischaemic heart disease and arrhythmias in some, but in a proportion the symptoms were thought to be due to psychoneurosis. Seventy-two patients (40 per cent) were referred because of complications of MVP. In 67 patients (37 per cent) the condition was discovered by chance and in 43 patients (24 per cent) neurotic symptoms had led to referral to hospital. A systolic click was heard in 117 patients (54 per cent); 41 patients (23 per cent) had a late systolic murmur and 30 patients (16 per cent) had a pansystolic murmur. The incidence of murmurs rose with increasing age, and pansystolic murmurs were more frequent in males. Thirty-two patients (18 per cent) had neither a click nor a murmur. Twenty-four patients (13 per cent) had associated supraventricular tachycardia and 22 (12 per cent) atrial fibrillation. Twelve patients (7 per cent) had severe mitral incompetence and eight (4 per cent) developed bacterial endocarditis. Only three patients had symptoms suggesting cerebral ischaemia. Twelve patients (7 per cent) had associated aortic incompetence. Twenty-two patients had had an inguinal hernia, the incidence in males over 50 being 26 per cent. Twenty-six patients (14 per cent) had non-specific T wave changes in the electrocardiogram. Echocardiography showed that 112 patients (62 per cent) had mid-systolic buckling of the posterior leaflet and 70 patients (38 per cent) had holosystolic prolapse. In view of the high incidence of complications it is felt that the long-term prognosis not as good as has been generally believed.
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PMID:Mitral valve prolapse: an assessment of clinical features, associated conditions and prognosis. 661 38

The effects of naloxone or thyrotropin releasing hormone (TRH) upon neurologic outcome were evaluated in gerbil models of cerebral ischemia. Following temporary bilateral carotid occlusion, hypotension was transiently reversed by these endorphin antagonists. However, neither drug altered time to awaken, time to death, or the severity of neurologic signs (ptosis, movement, retracted paws, circling, righting reflexes, seizures, or opisthotonus) when evaluated by a blinded rater. Hot plate escape and roto-rod performance were also unaltered by naloxone or TRH; TRH, but not naloxone, increased respiratory rates. Thus, the transient improvement of cardiorespiratory function produced by these drugs is unrelated to the morbidity and mortality associated with temporary cerebral ischemia in the gerbil. Additional studies evaluating the effects of naloxone or TRH upon neurologic outcome following permanent unilateral carotid occlusion also failed to show any therapeutic effects of these drugs. Both morphine and TRH exacerbated the effects of ischemia. Of gerbils which developed neurologic impairment, the deficit was usually ipsilateral to the occluded carotid. Collectively, these results indicate that neither naloxone nor TRH prevents ischemic deficits in the gerbil. Further studies with different cerebral ischemia models in other species are required to clarify the possible therapeutic effects of these drugs in experimental stroke.
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PMID:Naloxone or TRH fails to improve neurologic deficits in gerbil models of "stroke". 681

Echocardiography demonstrates prolapse of the mitral valve in at least 5 per cent of the population. Since some observations have linked this condition to stroke, we studied its incidence in two groups of patients with cerebral ischemia. The older group contained 141 patients over 45 years of age (mean, 64.7 years) who had transient ischemia or partial stroke. Prolapse was found in eight (5.7 per cent) of these patients and in 10 (7.1 per cent) of 141 age-matched controls. The second group contained 60 patients who had transient ischemia or partial stroke and were under 45 years old (mean 33.9 years). Prolapse was detected in 24 patients (40 per cent) but in only five (6.8 per cent) of 60 age-matched controls (mean age, 33.7 years). The odds ratio, 9.33, was highly significant (P less than 0.001). In six of the 24 patients there were other potential causes for cerebral ischemia leaving 18 whom the only recognizable potential cause was a prolapsing mitral valve (odds ratio, 7.00; P less than 0.001). This study suggests that this entity has a role in cerebral ischemia, at least in younger patients. (N Engl J Med 302:139-144, 1980).
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PMID:Further evidence relating mitral-valve prolapse to cerebral ischemic events. 735 Apr 39

A cerebral injury was induced by the bilateral common carotid artery occlusion and recirculation in spontaneously hypertensive rats (SHRs). Employing this ischemia-recirculation rat model, the effects of beraprost sodium (beraprost) on (1) lipid peroxide formation, (2) the increase in the brain water content and (3) neurological signs were examined. In a dosage of 25 micrograms kg-1 or higher, beraprost, administered orally, significantly inhibited the formation of lipid peroxides in the brain and serum induced by cerebral ischemia and subsequent recirculation in a dose-dependent manner. Beraprost also alleviated ptosis and markedly inhibited abnormal running behaviour caused by the ischemia and subsequent recirculation. In addition, although administration of beraprost did not cause marked inhibition of the increase in the brain water content (used as an index of cerebral oedema) during the first 3 h after recirculation, it restored the normal brain water content within 24 h after recirculation. Therefore, this effect was observed evidently later than the effect of inhibition of lipid peroxide formation. Moreover, administration of beraprost resulted in improvement in the symptoms accompanying the ischemic treatment. These results suggest that beraprost is potentially useful for or treatment of the pathological state accompanying cerebral infarction.
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PMID:Inhibitory effect of beraprost sodium on formation of lipid peroxides in ischemia and recirculation-induced cerebral injury. 810 15

Emotional disturbances, such as lack of motivation or depression, are common after stroke. The drugs mainly used to treat these syndromes in Japan are the cerebral metabolic enhancers whose biochemical and pharmacological profiles are similar to those of antidepressant drugs. In order to examine the possible therapeutic effect of T-794 [(5R)-3-(6-(cyclopropylmethoxy) 2-naphthalenyl)-5-(methoxymethyl) 2-oxazolidone], a new reversible inhibitor of monoamine oxidase (MAO) type A, on those emotional disturbances, its antidepressant activity was compared with those of major cerebral metabolic enhancers in rodents with or without treatment of cerebral ischemia. Oral administration of T-794 potently prevented reserpine-induced ptosis (ED50 = 4.41 mg/kg), akinesia (ED50 = 3.29 mg/kg), and hypothermia (minimum effective dose = 3 mg/kg) in mice. It was at least 3.7, 13.0, and 3.3 times more potent than cerebral metabolic enhancers tested (indeloxazine, bifemelane, amantadine and idebenone) in antagonism of the ptosis, the akinesia, and the hypothermia, respectively. Effect of T-794 was also examined in the behavioral despair test in rats subjected to forebrain ischemia. The ischemia was induced by a combination of bilateral common carotid artery occlusion (15 min) and systemic hypotension (sodium nitroprusside 5 mg/kg, s.c). From 13 d after the surgery, drugs were orally administered twice daily 7 times, and following the last administration rats were assessed for their behavior. T-794 reduced the duration of immobility in the behavioral despair test at 30 mg/kg without affecting spontaneous motor activity, whereas indeloxazine showed no significant effect. Antidepressant-like activity of T-794 was suggested in rodents with as well as those without cerebral ischemia. The results suggest that T-794 may make an important contribution to the treatment of emotional disturbances following stroke.
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PMID:Possible therapeutic effect of T-794, a novel reversible inhibitor of monoamine oxidase-A, on post-stroke emotional disturbances, assessed in animal models of depression. 914 8

Mitral valve prolapse shows a wide spectrum from a benign anatomic variant to a progressive disease with severe cardiovascular morbidity and mortality. Echocardiography is the most important tool for diagnosis and risk stratification. Predictors for high risk are significant thickening of mitral leaflet of > 5 mm ("classic" prolapse), moderate to severe mitral regurgitation and reduced left ventricular function. These patients have an increased risk of infective endocarditis, cerebral ischemia and sudden cardiac death. Because of the risk for the development of severe mitral regurgitation requiring surgery short follow-up intervals are necessary. In mitral prolapse syndrome cardiac clinical signs (palpitation, rhythm disorders, syncope, etc.) are associated with a prolapse that can be treated symptomatically with drugs after exclusion of other causes and significant mitral regurgitation requiring surgery.
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PMID:[Mitral valve prolapse: identification of high-risk patients and therapeutic management]. 1650 68

A 50-year-old man presented with pituitary apoplexy resulting in internal carotid artery occlusion manifesting as sudden onset of severe headache, right ptosis, and left hemiparesis, associated with visual impairment. Computed tomography showed a nodular mass, located in the sellar and suprasellar regions with early signs of acute cerebral ischemia. Magnetic resonance (MR) imaging indicated that the mass compressed the bilateral cavernous sinuses, resulting in obliteration of the cavernous portion of the right internal carotid artery. Right middle cerebral artery territory infarction was also found. Conservative therapy with steroids was given in the acute stage and repeated MR imaging showed recanalization of the internal carotid artery with reduction of the tumor size. The tumor was removed through the transsphenoidal approach to obtain a definitive diagnosis in the chronic stage. The histological diagnosis was consistent with non-functioning pituitary adenoma. Eye movement of this patient showed full recovery after the operation. Pituitary apoplexy resulting in internal carotid artery occlusion is rare. Surgical decompression through the transsphenoidal approach is appropriate, but the optimal timing should consider severe disturbance of visual acuity and visual field in the acute stage.
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PMID:Pituitary apoplexy causing internal carotid artery occlusion--case report. 2127 45


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