Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of acute laryngeal dystonia (laryngospasm), a rarely reported extrapyramidal reaction to neuroleptics, occurred in a public psychiatric hospital. A review of the literature revealed only seven well-documented case reports. This article discusses the clinical significance of this rare, alarming, and probably underreported phenomenon. Factors related to recognition, prediction, and management are also discussed. The review strongly advocates immediate intravenous administration of anticholinergic drugs to relieve dystonia.
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PMID:Acute laryngeal dystonic reactions to neuroleptics. 233 Apr 7

Episodic paroxysmal laryngospasm (EPL) is a sign of laryngeal dysfunction, often without a specific organic etiology, which can masquerade as asthma, vocal fold paralysis, or a functional voice disorder. The intermittent respiratory distress of EPL may precipitate an apparent upper airway obstructive emergency, resulting in unnecessary endotracheal intubation, cardiopulmonary resuscitation, or tracheostomy. During 27 months, seven women and three men, age 30-76 years, were assessed by a high diagnostic index of suspicion, an intensive history including psychosocial factors, physical examination of the airways, provocative asthma testing, and swallowing studies. Videolaryngoscopy, stroboscopy, and pulmonary flow-volume loop testing were definitive. The classic appearance was paradoxic inspiratory adduction of the anterior vocal folds with a posterior diamond-shaped glottic gap. During an attack of stridor or wheezing, attenuation of the inspiratory flow rate as depicted by the flow-volume loop suggested partial extrathoracic upper airway obstruction. Swallowing evaluation by videolaryngoscopy and videosophagography may uncover gastroesophageal reflux disease. Hallmarks of management include patient and family education by observation of laryngoscopic videos, a specific speech therapy program, psychotherapy, and medical treatment of associated disorders. Electromyography may become a valuable future adjunct. Unlike laryngeal dystonia, patients with EPL do not benefit from botulinum toxin type A.
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PMID:Episodic paroxysmal laryngospasm: voice and pulmonary function assessment and management. 865 82

Muscular tension dysphonia, episodic laryngospasm, globus, and cough may be considered to be hyperfunctional laryngeal symptoms. Suggested etiological factors for these symptoms include gastroesophageal reflux, psychological problems, and/or dystonia. We propose a unifying hypothesis that involves neural plastic change to brainstem laryngeal control networks through which each of the above etiologies, plus central nervous system viral illness, can play a role. We suggest that controlling neurons are held in a "spasm-ready" state and that symptoms may be triggered by various stimuli. Inclusion criteria for the irritable larynx syndrome are episodic laryngospasm and/or dysphonia with or without globus or chronic cough; visible or palpable evidence of tension or tenderness in laryngeal muscles; and a definite symptom-triggering stimulus. thirty-nine patients with irritable larynx syndrome were studied. Gastroesophageal reflux was felt or proven to play a major role in a large number of the group (>90%), and about one third were deemed to have psychological causative factors. Viral illness seemed quite prevalent, with one third of patients able to relate the onset of symptoms to a viral illness that we feel might lead to central nervous system changes. Our proposed hypothesis includes a mechanism whereby acquired plastic change to central brainstem nuclei may lead to this form of hyperkinetic laryngeal dysfunction. It gives structure and reason to an array of therapy measures and suggests direction for basic research.
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PMID:The irritable larynx syndrome. 1049 60

We identified the IgG autoantibody ANNA-2 ("anti-Ri") in 34 patients in a 12-year period by immunofluorescence screening of sera from approximately 75000 patients with subacute neurological disorders that were suspected to be paraneoplastic. Detailed clinical information was available for 28 patients (10 men, 18 women). Cancer was diagnosed in 24 patients (86%); 21 had histologically proven carcinoma (10 lung, 9 breast, 1 cervical, 1 bladder), and 3 had an intrathoracic imaging abnormality. Cancer anteceded neurological symptoms in 4 of 28 patients. Cancer detection frequency increased with continued surveillance. Neurological disorders, in decreasing frequency, were brainstem syndrome (including opsoclonus, myoclonus, or both), cerebellar syndrome, myelopathy, peripheral neuropathy, cranial neuropathy, movement disorder, encephalopathy, Lambert-Eaton syndrome, and seizures. Four patients had laryngospasm and four had jaw opening dystonia (two with neck dystonia). Nine (32%) were wheelchair-bound 1 month after neurological symptom onset. Most improved neurologically after immunomodulatory or tumor-directed therapy. Accompanying autoantibodies, found in 73% of sera, included ANNA-1, ANNA-3, CRMP-5-IgG, P/Q-type and N-type Ca(2+) channel antibodies, and muscle-type acetylcholine receptor antibody. Some neurological accompaniments of ANNA-2 may reflect potentially pathogenic humoral or cell-mediated responses to coimmunogenic tumor antigens, for example, Lambert-Eaton syndrome (P/Q-type Ca(2+) channel antibody) and peripheral neuropathy (ANNA-1 effector T cells).
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PMID:Anti-neuronal nuclear autoantibody type 2: paraneoplastic accompaniments. 1273 Sep 91

Tardive dystonia was identified in 25 patients: involvement of the face and neck was most common; truncal and limb dystonia were also observed. There were 3 cases of laryngospasm and 2 of spasmodic dysphonia. The latter has not been previously reported as a manifestation of tardive dystonia. In all cases, movements typical of classic tardive dyskinesia could be demonstrated. This group illustrates the variety of dystonic disorders that may occur in conjunction with tardive dyskinesia.
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PMID:Tardive dystonia: clinical spectrum and novel manifestations. 2448

Laryngeal stridor is recognized as a characteristic clinical manifestation in patients with multiple system atrophy (MSA). However, the pathogenic mechanisms underlying this symptom are controversial. Neurogenic atrophy of the posterior cricoarytenoid muscle has been identified in cases of MSA, suggesting that laryngeal abductor weakness contributes to laryngeal stridor. However, dystonia in the laryngeal adductor muscles has also been reported to cause laryngeal stridor. Depletion of serotonergic neurons in the medullary raphe nuclei, which exert tonic drive to activate the posterior cricoarytenoid muscle, has recently been identified in MSA cases. This adds weight to the possibility that laryngeal abductor weakness underlies laryngeal stridor in MSA. Continuous positive airway pressure therapy is currently used in the treatment of laryngeal stridor, but should be used with caution in patients showing contraindications. Current knowledge of the clinical and neuropathological features of laryngeal stridor is summarized in this paper, and the hypothesized causes and possible therapeutic options for this symptom are discussed.
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PMID:Laryngeal stridor in multiple system atrophy: Clinicopathological features and causal hypotheses. 2681 May 50