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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ptosis occurs in a variety of disorders including myasthenia gravis, oculomotor palsy, Horner's syndrome and brain stem disorders. There are also supranuclear lesions causing blepharoptosis. The latter disorders are reflex blepharospasm, apraxia of eyelid opening and Meige's syndrome. Since the total number of bilateral ptosis associated with cerebral hemispheric lesions is very few, whether the responsible lesions are located in the nondominant hemisphere or bilateral hemispheres are still controversial. We report here a case of bilateral cerebral ptosis that occurred in association with cerebral infarction of the nondominant hemisphere.
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PMID:A case of bilateral ptosis associated with cerebral hemispheric lesions. 207 18

A healthy 28 year old housewife presented with sudden right hemiplegia and aphasia. No predisposing factors could be ascertained apart from posterior cusp mitral value prolapse on two dimensional echocardiography. Extensive investigations confirmed the presence of cerebral infarction and persistent occlusion of the left internal carotid artery near its origin.
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PMID:Internal carotid artery occlusion in a young female with mitral valve prolapse. 365 49

All patients 20 years old or older referred for echocardiographic examination and found to have mitral valve prolapse during the period January 1975 through December 1979 were included in the study. Of the 1,138 patients, two-thirds were women and one-third were men. Their average age was 48.4 years. Forty patients (3.5%) had histories of prior focal cerebrovascular ischemic events. In 26 of the 40 patients, no responsible mechanism other than mitra valve prolapse was identified, and in 4, the ischemic event occurred during an episode of bacterial endocarditis, a known complication of mitral valve prolapse. In 10 of the 26 patients, there was clinical information to suggest an embolic mechanism for the ischemic. A conservative estimate of the prevalence rate for cerebral infarction in this group of patients is four times greater than the rate expected in a normal population. This difference is likely due to the contribution of mitral valve prolapse in the pathogenesis of cerebral infarction.
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PMID:Cerebral ischemic events in patients with mitral valve prolapse. 710 43

Between January 1978 and September 1992, 127 patients with isolated mitral regurgitation due to prolapse underwent mitral valve reconstruction. There were 74 men and 53 women whose mean age was 49.7 years, ranging from 16 to 74 years. Follow up was 99.2% complete and totaled 483.0 patient-years (mean: 3.8 years). One hundred and forty-eight procedures were carried out to repair the prolapses using four types of techniques: (1) leaflet plication in 97 patients; (2) artificial chordal replacement with polytetrafluoroethylene sutures in 30 patients; (3) chordal shortening in 16 patients; and (4) commissural imbrication in five patients. In order to repair the annular dilation, commissural plications were done in 75 and ring prostheses were implanted in 15 patients. There were one hospital and eight late deaths. One (cerebral infarction) of all deaths was related to the reconstructed mitral valve. There were 14 reoperations (11.0%) for recurrent mitral incompetence with a freedom from reoperation of 89.0% at five, and 81.1% at 10 years. There were four cases of thromboembolism (one fatal, three non-fatal) with freedom from thromboembolism of 96.7% at five, and 93.3% at 10 years. No endocarditis or hemorrhagic complications were noted. Linearized incidence of recurrent mitral regurgitation according to repair technique for the prolapse was 1.44%/pty in the leaflet plication series, 1.45%/pty with chordal replacement, 4.37%/pty after chordal shortening and 8.67%/pty following commissural imbrication. The linearized rate of failure in annuloplasty was 2.91%/pty after commissural plication and 1.74%/pty after ring annuloplasty. Statistically significant difference was confirmed only between leaflet plication and chordal shortening.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of repair techniques for mitral valve prolapse. 795 19

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

Stroke mortality represents the third leading cause of death worldwide, after coronary artery disease and cancer. It has been demonstrated that in Mongolian gerbils, a unilateral hemispheric cerebral infarction can be produced following unilateral occlusion of the carotid artery because of the absence of connecting arteries between the basilar and carotid systems in these animals. The objective of this study was to comprehensively characterize the model of cerebral infarction in gerbil, clinically, biochemically and especially morphologically for prospective use in testing new therapeutic agents. Cerebral infarction was produced by ligation of the left common carotid artery in experimental gerbils. The control animals were sham-operated. One hour after surgery, 0.5 ml of 1% trypan blue was administered intraperitoneally to all animals. Initial clinical evaluations were made 8 h after surgery and every day thereafter for 30 days. On each of days 10 and 30, 4 animals were sacrificed. The degree of cerebral infarction was evaluated on the basis of clinical response, electrolyte and enzyme changes, vascular permeability of blood-brain barrier and morphological alterations. The total post-infarction mortality rate was 50%. The clinical symptoms presented as ipsilateral hemiparesis, ptosis of the eyelid, circling behavior, decreased breathing rate, decreased blood pressure and increased heart rate. Such symptoms developed within 8 h of ligation and persisted to sacrifice at day 30. Creatine kinase increased significantly on the 10th day and remained high to day 30. Increased potassium from the damaged cells and breakdown of the blood-brain barrier were first detected 72 h post-infarction. The morphological data showed evidence of brain cell necrosis, autolysis and phagocytosis 10 and 30 days post-ligation in left hemispheres. Minor intercellular edema and some cell shrinkage was evident in the right brain. Areas of focal necrosis in the vicinity of blood vessels, especially in the left brain suggested a reperfusion injury as a consequence of minimal collateral reflow from the right brain into the left brain microvasculature. Experimental infarction in gerbil recreates the ischemic conditions causing stroke in humans. The animal model may be used for evaluating the efficacy of therapeutic agents that may ameliorate the condition in man.
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PMID:Mongolian gerbil (Meriones unguiculatus) as a model of cerebral infarction for testing new therapeutic agents. 1093 31

A 79-year-old woman, with no immune deficit, had presented progressive visual disturbance, diplopia and ptosis of her left eye over 2 weeks. T1-weighted MR images with gadolinium showed a heterogeneously enhanced lesion extending from the left orbital apex along the optic nerve to the cavernous sinus. Although we could not detect fungus by a transsphenoidal biopsy, we suspected fungal infection because of high level of galactomanan antigen in serum. Despite antifungal chemotherapy, her symptoms did not improve. CT image on day 40 showed an aneurysm in the left internal carotid artery, on day 43 cerebral infarction in the left internal carotid artery distribution and on day 45 she died. Autopsy disclosed that aspergillus hyphae invaded the left sphenoid sinus, cavernous sinus and wall of the aneurysm. In this case, fungal infection in the frontal skull base including orbital apex caused mycotic aneurysm in the intracavernous portion of the left internal carotid artery. Skull base aspergillosis presenting orbital apex syndrome is itself rare and in addition, the occurrence of cerebral infarction in the mycotic aneurysm has hardly been reported. We should have cerebrovascular disease in mind as a complication of CNS aspergillosis.
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PMID:[A case of CNS aspergillosis developing orbital apex syndrome and causing mycotic aneurysm and the subsequent cerebral infarction]. 1270 Dec 24

A 29-year-old man presented with lethargy, headache, high fever, and visual disturbance. Neurological examination showed mydriatic pupil, ptosis, diminished light reflex, and ophthalmoplegia on the left. Magnetic resonance (MR) imaging showed the typical findings of pituitary apoplexy, and cerebral angiography disclosed mild narrowing of the A1 segment of the left anterior cerebral artery (ACA). Transsphenoidal tumor resection was performed. Transient severe right hemiparesis occurred directly after the operation. Computed tomography demonstrated cerebral infarction in the territory of the left Heubner's and medial lenticulostriate arteries. Pituitary apoplexy followed by cerebral infarction is very rare. Vasospasm of the perforating arteries of the ACA probably caused the cerebral infarction. Subarachnoid blood or vasoactive agents released from the tumor were the most likely cause of the vasospasm. MR imaging findings of contrast enhancement around the vessels may indicate reactive processes around the vessels.
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PMID:Cerebral infarction following pituitary apoplexy--case report. 1560 Feb 83

A 42-year-old woman suddenly developed weakness in her left extremities when stretching her neck two days after the onset of a nuchal pain. Because computed tomography (CT) of the brain did not show any apparent lesion, the patient had initially been treated as having a cerebral infarction until magnetic resonance imaging (MRI) of the cervical spine revealed a presence of a cervical epidural hematoma the next day. She was therefore transferred to our hospital, and a neurological examination showed moderate left hemiparesis, dissociated sensory loss under C6 on the right side, urinary incontinence, and left miosis and ptosis. A CT of the cervical spine demonstrated an anteriorly located left-sided epidural hematoma extending from C4 to C7. The T2-weighted MRI revealed hyperintense lesions around the gray matter on the left side that were compressed by the epidural hematoma. The patient underwent an emergent laminoplasty from C3 to C7. Although her neurological signs were consistent with Brown-Sequard syndrome, which was associated with left-sided Homer's sign, they gradually and completely subsided following surgery. The authors therefore emphasize that cervical lesions should be considered in the differential diagnosis in patients with acute onset of hemiparesis.
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PMID:[Spontaneous cervical epidural hematoma presenting with hemiparesis following neck extension: a case report]. 1870 May 37

Isolated oculomotor nerve palsy is well known as a symptom of microvascular infarction and intracranial aneurysm, but unilateral oculomotor nerve palsy as an initial manifestation of chronic subdural hematoma (CSDH) is a rare clinical condition. We report a rare case of an 84-year-old woman with bilateral CSDH who presented with unilateral oculomotor nerve palsy as the initial symptom. The patient, who had a medical history of minor head injury 3 weeks prior, presented with left ptosis, diplopia, and vomiting. She had taken an antiplatelet drug for lacunar cerebral infarction. Computed tomography (CT) of the head showed bilateral CSDH with a slight midline shift to the left side. She underwent an urgent evacuation through bilateral frontal burr holes. Magnetic resonance angiography (MRA) after evacuation revealed no intracranial aneurysms, but constructive interference in steady-state (CISS) magnetic resonance imaging (MRI) revealed that the left posterior cerebral artery (PCA) ran much more anteriorly and inferiorly compared with the right PCA and the left oculomotor nerve passed very closely between the left PCA and the left superior cerebellar artery (SCA). There is the possibility that the strong compression to the left uncus, the left PCA, and the left SCA due to the bilateral CSDH resulted in left oculomotor nerve palsy with an initial manifestation without unconsciousness. Unilateral oculomotor nerve palsy as an initial presentation caused by bilateral CSDH without unconsciousness is a rare clinical condition, but this situation is very important as a differential diagnosis of unilateral oculomotor nerve palsy.
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PMID:Unilateral oculomotor nerve palsy as an initial presentation of bilateral chronic subdural hematoma: case report. 2406 74


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