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

A 28-year-old woman, with no past medical history, was admitted soon after a motor vehicle accident on March 1, 1990. On admission there were multiple small wounds in the right temporal region, but no wounds around the orbits. She was semicomatose with bilaterally fixed dilated pupils (6mm) and ptosis. The eyes were abducted bilaterally. No other cranial nerve palsy was noted. She moved four limbs spontaneously. No skull fracture was present on X-ray films. Cervical X-ray films revealed straightened cervical vertebral column but no fracture. Pelvic bone X-ray films demonstrated fracture and diastasis of the pubic bone. A computed tomography scan demonstrated a small subdural or subarachnoid hemorrhage in the right ambient cistern. A magnetic resonance imaging (MRI) carried out 12 days after trauma demonstrated bilateral small subdural hematomas under the cerebellar tentorium and contusional lesions of the bilateral medial temporal lobes. There were no abnormalities present in the brain stem. The patient was treated conservatively with diuretics and steroids. Disturbance of consciousness gradually improved until one month after the trauma, when she came close to being alert. Bilateral ptosis cleared after 3 months, and adduction of the eyes recovered after 6 months. Vertical eye movement improved a little in 6 months. Fixed 6mm pupils changed to fixed 4mm pupils in 6 months. Bilateral traumatic oculomotor palsy is a rarely described condition, and its mechanism remains conjectural. We discussed the mechanism of the injury and the site of the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Traumatic bilateral oculomotor nerve palsy: a case report]. 157 79

Six cases of internal ophthalmoplegia due to direct head injury are presented. All six patients had a dilated, nonreactive pupil. Four had no extraocular palsies or ptosis and two had partial extraocular palsies or ptosis. Disturbance of consciousness was absent or very mild, and all patients fully recovered within 1 to 7 days after the traumatic event. No patient had a history that suggested a cause for oculomotor nerve palsy, and emergency CTscans showed no mass lesions. The internal ophthalmoplegia was recognized immediately after trauma. Although minimal oculomotor nerve palsies due to unruptured intracranial aneurysms have been described, none of our patients complained of periorbital or retroorbital pain either before or after the trauma, which rules out intracranial aneurysms as the cause of the internal ophthalmoplegia. Therefore, we concluded that the internal ophthalmoplegia was due to direct head injury. The pathophysiological mechanism of the internal ophthalmoplegia appeared to be slight injury of the pupillomotor fibres on the ventromedial surface of the third nerve at the posterior petroclinoid ligament, which acted as the fulcrum due to the downward displacement of the brainstem at the time of impact.
 ...
PMID:Primary internal ophthalmoplegia due to head injury. 271 3

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)
 ...
PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70