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

A 63-year-old woman experienced two episodes of trismus and painful ophthalmoplegia at an interval of six years. She suffered left visual loss, and enhanced CT scan and MR imaging revealed heterogeneous enlargement of the left extraocular muscles extending to the orbital apex. In addition, the left pterygopalatine fossa was filled with a mass isointense with muscle without evidence of surrounding tissue invasion; 67Ga scintigraphy showed high uptake in this lesion. Steroid administration dramatically resolved the trismus, and the mass in the orbit and extraorbit vanished completely. Orbital pseudotumor is characterized by self-limited, relapsing, steroid-responsive painful ophthalmoplegia, and this case could be a variant of this entity with inflammation extending into the extraorbital area.
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PMID:Recurrent steroid-responsive trismus and painful ophthalmoplegia. 1054 39

Tetanus is a neurologic disorder caused by tetanospasmin, a protein toxin elaborated by Clostridium tetani. Cephalic tetanus is a localized form of the disease causing trismus and dysfunction of cranial nerves. We report the case of a man who presented with facial trauma, complete ophthalmoplegia, exophthalmos, areactive mydriasis, and periorbital hematoma. An orbital CT revealed air bubbles in the right orbital apex. The patient was given a tetanus toxoid booster and antibiotherapy. After extraction of a wooden foreign body, the patient developed right facial nerve palsy, disorders of swallowing, contralateral III cranial nerve palsy, and trismus. Only one case of cephalic tetanus from penetrating orbital wound has been reported in literature 20 years ago. When a patient presents with an orbital wound with ophthalmoplegia and signs of anaerobic infection, cephalic tetanus should be ruled out.
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PMID:Cephalic tetanus from penetrating orbital wound. 1971 Sep 32