Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 14-year-old girl who presented with yearly attacks of bilateral internal ophthalmoplegia, nausea and headache, since the age of nine. The episodic isolated bilateral mydriasis in this child is believed to be a migraine equivalent.
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PMID:Bilateral episodic mydriasis as a migraine equivalent in childhood: a case report. 188 77

A 59 year-old female with hypercereatinekinasemia associated with pituitary apoplexy was presented. The patient showed headache, nausea, vomiting and pyrexia. On admission, slight nuchal rigidity and photophobia were observed. However all the cranial nerves were intact; neither ophthalmoplegia nor visual defect were observed. Cerebrospinal fluid analysis revealed an elevated protein concentration of 164 mg/dl. There were 157 cells/mm2 (30% neutrophils). Skull X-P disclosed the ballooning of the sella turcica. CT scan, endocrinological examination and angiography lead us to the diagnosis of pituitary apoplexy. By the sphenoidal approach necrotic tissue with a little chromophobe adenoma were removed. No haematoma was detected. The isozyme pattern of serum CK showed 100 percent MM type. Serum CK concentration reached as high as 2502 IU/l on the fifth day from the onset of the symptom and then normalized in 12 days. Though the cause of the hypercreatinekinasemia uncertain, the similar pattern of hypercreatinekinasemia is known in the acute stage of cerebrovascular accident, and it is more often observed in thalamic hemorrhage. We assumed that the hypercreatinekinasemia in our case was caused by hypothalamic irritation, which lead hyperpermeability of sarcolemma and leakage of the enzymes of muscle origin.
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PMID:[Pituitary apoplexy with hypercreatinekinasemia]. 235 Sep 34

Hypophysis apoplexy is a clinical syndrome characterized by the sudden development of headache, visual disturbance, associated with nausea, vomiting, signs of meningeal irritation and ophthalmoplegia. The symptoms are caused by the hemorrhage of a hypophyseal adenoma. This leads to the swelling of the tumor and compression of the perisellar structures. The authors processed the clinical and pathological characteristics of 28 cases occurring among the patient material of the National Institute of Neurosurgery of the past 10 years. According to the experiences the most important factor of a successful treatment of hypophyseal apoplexy is an early diagnosis and quick admittance to an institute of neurosurgery of satisfactory conditions. Thereafter a steroid hormone therapy of large doses and decompression operation performed by transnasal-transsphenoidal approach leads in the majority of cases to recovery.
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PMID:[Surgical treatment of pituitary apoplexy]. 264 84

A 7-year-old girl presented with bilaterally dilated pupils, nausea, and vomiting 2 days after head trauma. Pilocarpine pupil testing led to the correct diagnosis of pharmacologic pupillary dilation from an unexpected and unusual source of plant poisoning, Solanum dulcamara (blue nightshade). In patients with internal ophthalmoplegia, awareness of the possibility of pharmacologic mydriasis and correct use of topical pilocarpine testing can preclude the necessity for neuroradiologic and invasive diagnostic studies, even in cases with atypical or complex presentations.
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PMID:Accidental mydriasis from blue nightshade "lipstick". 295 78

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70

Pain characteristics of the Tolosa-Hunt syndrome were abstracted from the observations of five patients with repeated incidents of painful ophthalmoplegia. The pain was experienced either as pressure behind the ophthalmoplegic eye or as boring pain in one orbital region, fluctuating in intensity, sometimes worsening to knife stab-like pain in the eye. The unilateral pain did not shift side during a solitary incident of painful ophthalmoplegia and was never completely absent. The pain was increased when the eyes were strained, when cold wind blew against the face, and when a change in the weather took place. It was accompanied by a feeling of swelling in the affected region, but not by nausea nor vomiting. Conventional headache drugs provided little relief. All cases experienced tenderness when pressure was applied to the ipsilateral supraorbital foramen. The pain was suggested to be related to an increased load on the impaired venous blood flow in the region of the superior orbital fissure.
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PMID:Pain characteristics of painful ophthalmoplegia (the Tolosa-Hunt syndrome). 401 17

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

The author presented a case of a girl, aged 10, with total ophthalmoplegia of the right eye, recurring 4 times. The onset of the disease was preceded by nausea, vomits and headache. The symptoms of the palsy released spontaneously after 2-3 weeks.
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PMID:[A case of recurrent total ophthalmoplegia]. 789 86

Unexpected autopsy findings are presented of a patient who died suddenly after a 6-month history of progressive headaches, nausea, and vomiting. A ruptured Rathke's cleft cyst (RCC) was identified within the adenohypophysis, with a chronic inflammatory reaction in surrounding pituitary and overlying hypothalamus. A brisk lymphoplasmacytic response was also seen in the cavernous sinuses bilaterally, identical to the pathology reported for idiopathic painful ophthalmoplegia, also called Tolosa-Hunt syndrome (THS). The pathogenesis of THS has not been elucidated; based on the findings in this report, it is suggested that some THS cases may result from a hyperimmune response to RCC rupture with extension into one or both cavernous sinuses. Although prompt alleviation of symptoms with corticosteroid treatment is generally encountered with THS, recurrence of symptoms is not uncommon. A careful search for a ruptured RCC should be undertaken in atypical cases of THS, with possible consideration of surgical intervention.
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PMID:Ruptured Rathke's cleft cyst: a possible cause of Tolosa-Hunt syndrome. 910 Nov 12

We report a 56-year old female with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), presenting with protein-losing gastroenteropathy and serum copper deficiency. There was no neuromuscular disease in her family members. Three years prior to admission, she developed severe gastrointestinal symptoms including diarrhea, nausea, vomiting and ascites, and was diagnosed as having protein-losing gastroenteropathy based on alpha(1)-antitrypsin clearance and other tests. She was referred to our department when neurological symptoms were apparent. Neurological examinations revealed bilateral ptosis, ophthalmoplegia, hearing loss, facial and limb muscle weakness, mild sensory deficit of vibration on her feet and hypoactive deep tendon reflexes. Pigmentary retinopathy, cerebellar ataxia and heart block were not seen. Serum copper level was decreased to 45 micrograms/dl (normal: 83-155). Chronic intestinal pseudo-obstruction was proven by X-ray studies, and diffuse leukoencephalopathy demonstrated on brain MRI. On EMG, motor nerve conduction velocities were prolonged with temporal dispersion. Her muscle biopsy from biceps brachii muscle showed both neuropathic and myopathic changes, scattered ragged-red fibers and focal cytochrome c oxidase deficiency. Southern blot and polymerase chain reaction analysis on mitochondrial DNA showed no deletions nor point mutations. The clinical and pathologic findings of the present patient fulfilled the diagnostic criteria of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) proposed by Hirano et al. There are few reported patients with MNGIE in Japan, but none presented with protein-losing gastroenteropathy and serum copper deficiency. Since the copper is a cofactor of cytochrome c oxidase, decreased serum copper level may aggravate the respiratory chain enzyme metabolism in mitochondria. Therefore, treatment for gastrointestinal tract disturbance and copper administration may be necessary to prevent disease progression.
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PMID:[Mitochondrial neurogastrointestinal encephalomyopathy presenting with protein-losing gastroenteropathy and serum copper deficiency: a case report]. 949 Sep 4


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