Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0262471 (ENT)
 5,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemifacial weakness, or palsy, results from disruption of communication between cortical motor centres and the facial musculature along the course of the facial nerve. Bell's palsy has a typical presentation of sudden onset, mild otalgia, altered facial sensation and/or taste, with no obvious prodrome. It represents over half of hemifacial weakness cases in primary care. However, as a diagnosis of exclusion, there are a number of key clinical features of more sinister diagnoses that must be considered. Acute hemifacial weakness secondary to isolated facial nerve palsy must be differentiated from acute cerebrovascular accident. The latter results in sparing of the brow musculature due to the bilateral innervation of the frontalis. Altered facial sensation and mild otalgia are common in Bell's palsy, however severe pain is suggestive of Ramsay Hunt syndrome. Recent facial or head trauma and surgery should also be excluded in causation. Patients with the following conditions should be referred: lagophthalmos if the weakness persists beyond a few days or ocular damage is suspected; Ramsay Hunt syndrome (immunocompromised patients, those with significant pain, and where intraoral vesicles prohibit oral intake); and palsy secondary to trauma or surgery. A parotid mass with facial palsy implies malignant change and must be referred within the two-week wait pathway. A history of progressive hearing loss and tinnitus with palsy also requires urgent referral to neuro-otology for assessment of cerebellopontine angle tumours. All cases of facial palsy associated with infective otological symptoms should be discussed with ENT.
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PMID:A case of persistent hemifacial weakness. 2419 32

In ophthalmology, there have been few reports of botulinum toxin type-A (BTX-A) injection into the lacrimal gland to treat epiphora. In ENT, adductor and abductor (ABSD) spasmodic dysphonia are often treated with BTX-A injections into the respective overacting vocal cord muscles. We describe a 53-year old male with Parkinson's disease who did not respond to BTX-A injections to either the lacrimal gland, for epiphora secondary to Parkinsonian-related blink lagophthalmos, or posterior cricoarytenoid (PCA) muscles for ABSD. Subsequent BTX type-B (BTX-B) injections into the lacrimal gland remarkably improved his epiphora. BTX-B injections into the PCA muscle also greatly improved his dysphonia. We describe the first reported case of (1) BTX-B injection into the lacrimal gland for epiphora, (2) use of Botox in treating epiphora due to blink lagophthalmos/reduced blink frequency secondary to Parkinson's disease, (3) BTX-B use in treating ABSD, and (4) association between ABSD and Parkinson's disease.
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PMID:Botulinum toxin-B injection into the lacrimal gland and posterior cricoarytenoid muscle for the treatment of epiphora and abductor spasmodic dysphonia secondary to Parkinson's disease. 2993 26