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 10-year-old schoolboy was referred to the Ophthalmic Unit of Ahmadu Bello University Teaching Hospital because of sudden loss of sight following 5 days of severe frontal headache. The child had bilateral ptosis with internal and external ophthalmoplegia and fixed and dilated pupils. There was no papilloedema. Eight days later, a jaw tumour and a rapidly enlarging abdominal tumour appeared. A fine needle aspiration biopsy of the jaw tumour confirmed Burkitt's lymphoma. Combination chemotherapy with cyclophosphamide, vincristine and methotrexate (COM) led to a rapid resolution of the jaw and abdominal tumour but the child never regained his sight. Cerebrospinal fluid examination was not helpful in reaching a diagnosis.
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PMID:Burkitt's lymphoma presenting with blindness: a case report. 170 53

Herpes zoster ophthalmicus was seen in 22 cases out of 195 cases of herpes zoster (11.3% incidence). It was affecting mainly adults (90.9%). Oedema over the lids (81.8%) was invariably present and lead to ptosis. Mucopurulent conjunctivitis, predominantly mucoid (72.7%) was the commonest manifestation associated with vesicles over the lid margins. Sectorial (22.7%) and diffuse (9.1%) episcleritis appeared in later part of first week, while nodular episcleritis was observed in one case only on 12th day of the disease. Nummular keratitis was seen in 31.8% of cases between 8-10 days. Iritis and iridocyclitis was seen in 45.4% of cases out of which 36.3% had secondary ocular hypertension (glaucoma). Neuroparalytic keratitis and internal ophthalmoplegia were detected in one patient each. Postherpetic neuralgia occurred in 22.7% of cases and was uncommon in younger age group (below 40 years, 4.5%). Carbamazepine was effective in relieving the herpetic pain.
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PMID:Clinical profile of herpes zoster ophthalmicus. 174 74

Twelve patients with histologically defined mitochondrial myopathy are described. There were 9 males and 3 females. The age of onset ranged from birth to 35 years with a median of 14 years. The most common clinical picture was that of ophthalmoplegia, ptosis and muscle weakness found in 10 patients. One presented with exercise intolerance due to muscular aches and pains, and the other besides his muscular weakness had mental retardation and an aggressive behavior. The clinical presentation and differential diagnosis of these patients are discussed.
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PMID:[Mitochondrial myopathy: report of 12 cases with histochemical study of the skeletal muscle]. 180 26

A 15 year old patient developed ataxia 2 weeks after an upper respiratory infection. Absent reflexes, external ophthalmoplegia, bilateral ptosis, isochoric mydriasis and week photomotor reflexes (Bell's phenomenon) were noted. A slight increase in protein but not cell content of the CSF was observed. Miller-Fisher syndrome was diagnosed on clinical grounds and visual and auditory evoked potentials were explored and found to be normal. This is in complete agreement to the literature and indicates indemnity of the central nervous system in Miller-Fisher's syndrome. Peripheral nervous system abnormalities that have been identified by pathologic and radiologic studies may explain all of the alterations observed in this syndrome.
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PMID:[Auditory evoked potentials in Fisher's syndrome. A clinical case]. 184 57

Correction of ptosis in patients with chronic progressive ophthalmoplegia is problematic because the ptosis enlarges the palpebral fissure and aggravates the lagophthalmos. Additional lifting of the lower lids, which are often retracted, therefore seems advisable. Experience with various lower lid elongation techniques is reported.
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PMID:[Lower eyelid extension-plasty in patients with ptosis in chronic progressive external ophthalmoplegia]. 188 64

A 9-year-old girl and an 11-year-old boy had ptosis, progressive external ophthalmoplegia, pigmentary retinopathy, and sensorineural hearing loss. The girl had diabetes mellitus and the boy had hypoparathyroidism. Both children also developed recurrent vomiting and cerebral infarcts with lactic acidosis. Muscle biopsy specimens showed ragged-red fibers and Southern analysis demonstrated a distinct heteroplasmic deletion of muscle mitochondrial DNA in each patient but no evidence of the point mutation in the transfer RNALeu(UUR) gene recently identified in mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). These 2 children had combined features of Kearns-Sayre syndrome and MELAS, suggesting that mitochondrial DNA deletions occasionally can have pleomorphic clinical expression.
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PMID:Deletion of mitochondrial DNA in patients with combined features of Kearns-Sayre and MELAS syndromes. 189 71

Traumatic ptosis is most often secondary to a fasciomuscular lesion of the levator system. Less frequently, it results from the paralysis of the levator muscle due to an injury to the third pair of cranial nerves. This ptosis is observed in comminuted orbital fractures or fractures of the base of the skull involving the orbital apex, and it is then associated with oculomotor paralysis. In favorable cases seen early, repairing surgery of the levator system produces excellent results. When associated with ophthalmoplegia or corneal anesthesia, neurogenic ptosis requires a watch and wait policy.
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PMID:[Post-traumatic ptosis]. 189 1

A 42-year-old woman was admitted for complaining of gait disturbance lasting for 2 years. She had a past history of hearing loss and bilateral ocular ptosis since her age of 21 years. Neurological examinations revealed severe external ophthalmoplegia, ptosis and muscular weakness of neck and extremities, but no dementia. Laboratory examinations showed high level of serum CK and slight elevations of CSF protein, lactate and pyruvate. The QT interval on ECG was prolonged. The EEG finding was slightly abnormal. The neurogenic pattern on EMG was noted. Muscle biopsy was performed at the quadriceps muscle. Its specimens demonstrated mixed changes of muscular atrophy and ragged red fibers. From these findings, Kearns-Sayre-Shy syndrome was diagnosed. It was noted in this case that brain MRI (T2-weighted image) revealed bilateral diffuse high signal intensity areas on cerebral white matter and brainstem. It seems that the lesions of central nervous system may progress subclinically for many years in cases of KSS, as our case shows.
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PMID:[A case of Kearns-Sayre-Shy syndrome with abnormal signal intensity on MRI in cerebral white matter and brainstem]. 193 67

A case of Burkitt's type ALL with numb chin syndrome as the initial manifestation is described. A 57-year-old Japanese male was admitted to our hospital in November 14, 1989 because of paresthesia at the chin and lower lip with diplopia and ptosis. Neurological examination revealed oculomotor paralysis of the right side and hypesthesia on the chin, lower lip and buccal mucous membrane. Laboratory findings showed increased leukocyte count. Bone marrow aspirate revealed hypercellular marrow with 92.3% leukemic cells which had vacuoles in the cytoplasm and surface marker of IgM, kappa type. The abnormalities of karyotype included t(8;14). He was treated with chemotherapy and radiation. His conditions were temporarily improved, but relapsed later and died in March 6, 1990. Leukemic infiltrations to the trigeminal nerve were found in autopsy. The relationship between lymphoid malignancies and numb chin syndrome was discussed.
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PMID:[Burkitt's type ALL with numb chin syndrome as an initial manifestation]. 202 41

A 44 year old diabetic woman presented with diplopia and bilateral ptosis and mild exophthalmos. The patient was clinically euthyroid, the baseline thyroid function tests were normal, but the thyroid stimulating hormone response to thyrotrophin releasing hormone was flat. Computed tomographic scan and magnetic resonance imaging of the orbits showed left medial and inferior rectus muscle thickening, more prominent on the left side, consistent with Graves' disease. The tensilon stimulation test resulted in resolution of the ptosis and partial improvement of the ophthalmoplegia. The single fibre electromyography was consistent with a defect in neuromuscular transmission. However, forced duction test was normal and anti-acetylcholine receptor antibodies were undetectable. Significant improvement of the extraocular muscle function and resolution of the right ptosis had resulted from anticholinesterase therapy. These findings and the clinical response to therapy were consistent with concomitant euthyroid Graves' ophthalmopathy and ocular myasthenia gravis. Coexistent isolated ocular myasthenia gravis and Graves' ophthalmopathy is rare and should be considered in patients with findings of ocular myasthenia and extraocular muscle dysfunction.
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PMID:Concomitant euthyroid Graves' ophthalmopathy and isolated ocular myasthenia gravis. 209 29


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