Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 38-year-old female presented with a left-sided peripheral N. VI-paresis and negative neuroradiologic work-up. After one year she developed an incomplete N. III paresis, numbness of her face correlating to N. V1 and V2, reduced lacrimal secretion as well as a palpable mass at the lateral orbital rim. Magnetic resonance imaging revealed an orbital tumor extending into the cavernous sinus. Biopsy disclosed an adenoid cystic carcinoma of the lacrimal gland with basaloid, cribriform and tubular pattern. Therefore, an exenteration with postoperative radiation therapy was performed. Immunohistochemical findings included positive reactions for keratin (KL-1 and AE 1 + 3), Vimentin and Egp 34. By determination of Ki 67 the proliferative activity of the tumor was found to be 15%. Our case report demonstrates that even in absence of an exophthalmus or pain a malignant orbital tumor may be assumed as the underlying cause for a combined monolateral oculomotor and trigeminal paresis. Immunohistochemical results support the notion, that the adenoid cystic carcinoma of the lacrimal gland may arise from precursor cells of the terminal duct system.
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PMID:[Adenoid cystic carcinoma of the lacrimal gland]. 132 11

Over a 49-month period, 121 orbital wall fractures were treated and 92 were followed for a median of 6.5 months (minimum, 3 months). Associated injuries included a 17% incidence of serious globe or optic nerve injuries and 13% incidence of lacrimal drainage disruption. Diplopia occurred in 23% and dystopia in 11%. Management was by observation alone in 14% and exploration in the remainder, with layered gelfilm for defects smaller than 4 cm2, alloplastic sheeting for defects to 6 cm2, and outer cortex of parietal bone for larger dehiscences. There were no decrements in vision from operation, dystopias were corrected to within 2 mm of normal, and diplopia persisted only in those with extraocular muscle paresis. There was no benefit to exploration of orbital wall defects smaller than 2.5 cm2 or with reduction of other midfacial fractures (e.g., malar) when neither dystopia nor entrapment was present, because defects not obturated in such cases had no sequelae.
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PMID:Orbital wall fractures: evaluation and management. 175 54

Work-up of 120 patients with peripheral facial paresis included evaluation of spontaneous and reflex lacrimal secretion, electrogustometry, impedance, tonal and supraliminal tonal audiometry. Symptom complexes for different by severity nerve lesions are specified. In patients with basilar skull fractures 3 types of postdenervation syndromes were observed: atropine salivary paradox, paradoxical facial hyperemia, crocodile tears. A scheme of topical diagnosis is presented.
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PMID:[Diagnosis of peripheral diseases of the facial nerve]. 787 58

Impairment of the peripheral or central part of the facial nerve causes an ipsilateral peripheral facial nerve paresis. It is quite a common syndrome and affects 20-35 persons per 100,000 per year in Western Europe and the United States. A possible complication of facial palsy is paralytic lagophthalmos with aesthetic and functional impairment for the patient. Beside primary nerve reconstructive procedures plastic-reconstructive procedures play a major role in correcting paralytic lagophthalmos. The eyebrow, upper and lower lids, medial and lateral lid angle as well as the lacrimal system need to be seen as functional units and can be corrected with local surgical procedures. Restoration of eye closure is the most important goal in treating the affected eye. Due to the significant aesthetic limitations and resultant psychological stress for the patient cosmetic aspects must be included in the surgical concept.
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PMID:[Surgical treatment of paralytic lagophthalmos]. 2011 5

Ramsay Hunt syndrome is defined as herpes zoster oticus associated with an acute peripheral facial nerve paresis and quite often with other cranial nerve lesions. The combination of motor, sensory and autonomic involvement leads to a variety of neurological damage patterns, i. e. facial muscle paresis, hearing and balance disorders, sensory problems and disturbances of taste as well as lacrimal and nasal secretion. Additional variability of the clinical picture of Ramsay Hunt syndrome is produced by varying patterns of skin involvement explained by individual anastomoses between cranial and cervical nerves. Knowledge of these findings and an early diagnosis of Ramsay Hunt syndrome are important as prognosis of cranial nerve damage depends on the time at which acyclovir-corticosteroid therapy is started.
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PMID:Ramsay Hunt syndrome. 2242 45

Lattice corneal dystrophy gelsolin type was first described in 1969 by Jouko Meretoja, a Finnish ophthalmologist. It is caused by an autosomal dominant mutation in gelsolin gene resulting in unstable protein fragments and amyloid deposition in various organs. The age of onset is usually after the third decade of life and typical diagnostic triad includes progressive bilateral facial paralysis, loose skin, and lattice corneal dystrophy. We report a case of a 53-year-old female patient referred to our Department of Ophthalmology by severe dry eye and incomplete eyelid closure. She had severe bilateral facial paresis, significant orbicularis, and perioral sagging as well as hypoesthesia of extremities and was diagnosed with Meretoja's syndrome at the age of 50, confirmed by the presence of gelsolin mutation. At our observation she had bilateral diminished tear film break-up time and Schirmer test, diffuse keratitis, corneal opacification, and neovascularization in the left eye. She was treated with preservative-free lubricants and topical cyclosporine, associated with nocturnal complete occlusion of both eyes, and underwent placement of lacrimal punctal plugs. Ocular symptoms are the first to appear and our role as ophthalmologists is essential for the diagnosis, treatment, and monitoring of ocular alterations in these patients.
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PMID:Meretoja's Syndrome: Lattice Corneal Dystrophy, Gelsolin Type. 2825 Jul 73

Trigeminal schwannomas are benign lesions arising from the Schwann cells of the trigeminal nerve. This is an unusual tumor that accounts for less than 0.4% of intracranial pathologies, even though they are the second most frequent schwannoma after the vestibular schwannoma. The tumor spreads along the natural course of the V nerve at its cisternal portion, along the ganglion inside Meckel's cave or through its peripheral division. Even though the tumor can reach great size and become multicompartmental. We present a 51-yr-old woman, with an history of 3 mo of incapacitating facial pain, that was found on examination to be on the territory of the third division of the trigeminal nerve on the right side. The MRI depicted a large homogeneous enhancing lesion at the base of the right middle fossa with extension through the petrous apex to the most superior and medial part of the posterior fossa. The patient was operated by the senior author, through a middle fossa approach, dissecting between the two layers of the middle fossa dura (the apparent inner and the true outer layer of the cavernous sinus), the so called middle fossa "peeling". We achieved total resection of the tumor, but the patient presented after surgery with facial nerve paresis. This is thought to be related to geniculate ganglion manipulation, as it was unprotect by bone at the middle fossa and the patient maintained lacrimal function (post-geniculate alteration). It resolved completely after 6 mo. The patient consented to publication of her images.
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PMID:Microsurgical Resection of Trigeminal Schwannomas: 3-Dimensional Operative Video. 3112 Jan 16