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)

The eradication of basicranial meningiomas by traditional surgical techniques is often hindered by neoplastic entanglement with critical neurovascular structures. Apparent, complete tumor resection is frequently followed by extensive, yet clinically silent, recurrent disease with local infiltration of bone, cranial nerves, and brain. Fifty-five cases of sphenoid wing or parasellar meningioma were analyzed to identify clinical manifestations suggestive of early tumor recurrence. Regrowth patterns were then defined according to preoperative radiographic and intraoperative surgical findings. Medial tumor regrowth, involving the cavernous sinus, caused neurapraxia of cranial nerves III, IV, or VI, with associated diplopia or ophthalmoplegia. Inferior (caudal) regrowth of disease involved the infratemporal fossa, pterygomaxillary space, or paranasal sinuses by bony erosion of the middle cranial fossa floor or through natural anatomic foramina and fissures. Such inferior extension was manifested clinically by facial hypesthesia, trismus, and referred otalgia caused by trigeminal nerve involvement and by autophony or serous otitis media related to eustachian tube obstruction. Posterior tumor regrowth occurred along the petrous bone and horizontal carotid canal, resulting in internal auditory meatus erosion and cerebellopontine angle extension with associated tinnitus, hearing loss, unsteadiness, and occasional facial twitching. While the clinical and radiographic evaluations of any patient with a suspected recurrent basicranial meningioma are critical in planning the method and magnitude of reoperation, an understanding of potential recurrence patterns can be used in devising more extensive, combined approaches that may allow complete tumor extirpation at the initial surgical intervention.
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PMID:Meningiomas of the lateral skull base: neurotologic manifestations and patterns of recurrence. 212 32

Miller-Fisher syndrome (MFS) typically presents with ophthalmoplegia, ataxia, and areflexia. Atypical MFS additionally includes bulbar impairment, affection of the limbs, or abortive presentations. Mostly, MFS follows an infection with Campylobacter jejunii. Aspergilloma has not been reported to trigger MFS. In a 48-year-old male tiredness, tinnitus, otalgia, parietal hyperaesthesia, coughing, plugged nose, hypoacusis, globus sensation, epipharyngeal pain, dysarthria, hypogeusia, arthralgia, lid cloni, facial hypaesthesia and tooth ache consecutively developed. There were occasional lid cloni, left-sided facial hypaesthesia, reduced gag reflex, divesting soft palate, and absent tendon reflexes. CSF investigations revealed normal cell-count but increased protein. Antibodies against GM1 and GQ1b were negative. Atypical MFS was diagnosed. Otolaryngological examinations revealed chronic sinusitis maxillaris from an aspergilloma. After immunoglobulins and resectioning of the aspergilloma, neurological abnormalities disappeared within 19d. MFS may manifest as unilateral lower cranial nerve lesions without affection of the upper cranial nerves or ataxia. Atypical MFS may be triggered by parasinusoidal aspergilloma.
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PMID:Anti-GQ1b-negative Miller-Fisher syndrome with lower cranial nerve involvement from parasinusoidal aspergilloma. 1608 Nov 59

We report the case of a 40-year-old female who presented to us with earache and a rapidly progressive painful ophthalmoplegia involving the right eye with right temporal swelling. A clinical and radiological assessment revealed it to be temporal cellulitis with orbital apex syndrome secondary to acute otitis media. In spite of prompt initiation of treatment, the patient died within 30 hr of presentation. The case is discussed in detail with a brief review of medical literature.
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PMID:Acute suppurative otitis media: an unusual cause of orbital apex syndrome. 1908 5