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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A psychogenic voice disorder co-occurred or evolved with the symptoms and signs of unilateral superior laryngeal nerve paresis. We speculated that the former was a manifestation of a musculoskeletal tension or conversion reaction disorder, whereas the latter was a sequela to a self-limiting inflammatory process. Voice therapy proved effective for alleviating the psychogenic dysphonia after the signs of the neuropathy had resolved, whereas psychotherapy offered strategies for stress management. A multidisciplinary approach to this patient provided for differential diagnosis and efficacious treatment.
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PMID:A case of superior laryngeal nerve paresis and psychogenic dysphonia. 268 99

A number of different therapies have been used in the management of spasmodic dysphonia. None are curative, and the results of the most widely used surgical procedure (resection of the recurrent laryngeal nerve) are not universally good, with a high recurrence rate in some series. Furthermore, the procedure is not reversible. Using a special electromyographic hypodermic needle, we injected botulinum A toxin into one of the vocal folds of two patients with severe spasmodic dysphonia. Both had significant improvement without any complications. Although the resultant paresis is not permanent, the injection can be repeated as needed as an outpatient procedure.
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PMID:Botulinum toxin injection of the vocal fold for spasmodic dysphonia. A preliminary report. 356 40

Eleven cases presenting a syndrome of the medulla oblongata are discussed with reference to the findings of clinical and angiographic investigation. The diagnosis of Wallenberg's syndrome is justified when the classic symptoms are apparent (Horner's syndrome, nystagmus, dysphonia and dysphagia, ataxia, ipsilateral sensory impairment of the face and contralateral elsewhere, and accompanying vegetative disturbances). If additional symptoms such as a facial or extra-ocular muscle paresis, especially hemiparesis, exist, another, more lateral or medial, syndrome of the oblongata should be considered. Angiographic findings vary considerably, ranging from a normal vertebral artery or posterior inferior cerebellar artery (PICA) to an occlusion of these arteries (in three and two of the 11 cases respectively). Modification are often seen in the anterior inferior cerebellar artery (AICA). A kind of complementary supply in the PICA-AICA region must occasionally exist. Localised processes affecting these vessels rather than diffuse multifocal vascular processes would lead to Wallenberg's syndrome. It is difficult to conclude from the clinical picture where a possible responsible vascular narrowing or obliteration may lie, even if pareses of the limb were present.
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PMID:[Clinical and angiographic findings in vascular medullary syndromes (author's transl)]. 731 26

Ten patients with atrophy of the tongue, from a group of 752 with generalized acquired myasthenia gravis (MG), were studied. Tongue atrophy developed late in the majority of patients and was accompanied by tongue paresis (70% of the cases) and eventually associated to atrophy of other muscles of the palate, especially the uvula. All the patients exhibited severe forms of MG with bulbar involvement, mainly persistent dysphonia and dysphagia, almost always refractory to treatment. There is no correlation among atrophy of the tongue, sex, and thymus pathology. There is correlation between severeness of symptoms and early, persistent and treatment refractory dysphonia and dysphagia.
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PMID:Atrophy of the tongue with persistent articulation disorder in myasthenia gravis: report of 10 patients. 777 22

The current treatment of choice of adductor spasmodic dysphonia due to focal dystonia is thyroarytenoid-vocalis injection of botulinum toxin type A (Botox). Botox exerts its effect by presynaptic motor endplate blockade, preventing the release of acetylcholine and causing muscle paresis. Botox treatment protocols vary. Some centres perform unilateral injections, whereas others treat both cords. Our hypothesis is that unilateral injections may reduce the severity of whisper voice and aspiration side effects in the early two to three weeks after treatment. The purpose of this study, therefore, is to compare the efficacy of unilateral versus bilateral Botox injections in the treatment of adductor spasmodic dysphonia in terms of duration of effect versus the side effects of breathing and swallowing difficulties. This study presents data from a retrospective chart review and a prospective telephone interview of all patients receiving bilateral and unilateral Botox injections.
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PMID:A comparison of the efficacy of unilateral versus bilateral botulinum toxin injections in the treatment of adductor spasmodic dysphonia. 806 52

Chemodenervation by injection of botulinum toxin type A into the vocal fold(s) has become the preferred treatment for patients with adductor spasmodic dysphonia. Injection may be done either perorally or transcutaneously; each method has its advocates and advantages. The authors have used the transcutaneous transcricothyroid membrane route exclusively with satisfactory results in more than 50 patients. Temporary breathliness and aspiration are common. The preferred injection site should be as close as possible to the motor end plates of the affected muscle. The thyroarytenoid muscle end plates are distributed throughout the muscle, whereas in the lateral cricoarytenoid muscle they are located in band in the center of the muscle. The transcutaneous injection site is below and posterior to the midpoint of the vibrating vocal fold as visualized by indirect laryngoscopy. The proximity of this site to the lateral cricoarytenoid muscle suggests that postinjection breathiness and aspiration may be related to spread of botulinum toxin type A to the lateral cricoarytenoid muscle. However, it is likely that thyroarytenoid muscle paresis is mainly responsible for this side effect and that the rapid clearing of the breathy dysphonia in the face of prolonged relief of spasmodic dysphonia symptoms suggests the action of an adaptive neural response, such as axonal sprouting. Further research of this subject is warranted.
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PMID:Anatomic considerations in botulinum toxin type A therapy for spasmodic dysphonia. 819 38

The side-effects and complications of posteroventral pallidotomy are analysed in 138 consecutive patients who underwent 152 pallidotomies. Transient side-effects, lasting less than three months, appeared in 18% of the patients, that is, 16.5% of the surgical procedures. Long term complications, lasting more than 6 months, were noted in 10% of the patients, that is, 9.2% of the surgical procedures. Sixteen complications occurred alone or in various combinations in 14 patients and included fatigue and sleepiness (2), worsening of memory (4), depression (1), aphonia (1), dysarthria (3), scotoma (1), slight facial and leg paresis (2) and delayed stroke (2). Complications such as dysarthria and paresis could be attributed to MR- or CT-verified pallidal lesions lying too medially and encroaching on the internal capsule. Two of the patients with deterioration in memory had some memory impairment before surgery, and the aphonic patient had dysphonia preoperatively. The study suggests that stereotactic MRI and careful impedance monitoring and macro-stimulation of the posteroventral pallidum area should be sufficient for minimizing the risk of complications; the stereotactic lesion should be centered within the posterior ventral pallidum without involvement of internal capsule. It is concluded that pallidotomy is a safe procedure if performed on cognitively alert patients, and it seems that both the incidence and especially the severity of complications are lower for posteroventral pallidotomy than for thalamotomy.
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PMID:The side-effects and complications of posteroventral pallidotomy. 923 12

We report our clinical experience in managing a 59-year-old Italian male with Churg-Strauss syndrome (CSS) whose first clinical manifestation was a persistent dysphonia; the patient worked as a mechanic. Video-laryngostroboscopic examination revealed paresis of the right vocal fold with a reduction in adduction together with incomplete glottal closure. Spectrographic and spirometric tests both showed abnormal changes. Laryngeal electromyography revealed neurogenic damage of the right thyroarytenoid and crycoarytenoid muscles. Due to the appearance of typical signs of systemic involvement of CSS as a necrotizing vasculitis, the patient was admitted to the Rheumatology Unit of the University of Pisa. Histologic analysis of a skin lesion on the patient's foot confirmed the diagnosis. Treatment with 6-methylprednisolone quickly brought remission from systemic and laryngeal symptoms, as well as improvement in the results of video-laryngostroboscopic, spectrographic and laryngeal myographic tests.
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PMID:Neuro-laryngeal involvement in Churg-Strauss syndrome. 969 26

Usually dysphonia is the result of a functional disorder of the larynx. It can also result from paresis or paralysis of a hemilarynx. Four patients, men aged 57, 41, 42 and 18 years, had a neurological cause of paralysis of a hemilarynx. Processes responsible for this kind of pathology can appear at three different levels: central, nuclear and peripheral. Each of the four patients had a disorder at the peripheral level: two had a tumour, in one the vagus nerve was severed during lobectomy for squamous cell carcinoma (iatrogenic), and in the last one an upper respiratory viral infection was the probable cause. Other causes of these peripheral lesions are toxicological, traumatic or idiopathic. When dysphonia does not improve within three weeks, inspection of the larynx and palpation of the neck, including examination of the aspect and mobility of the vocal folds by an otorhinolaryngologist should be performed. If paresis of a hemilarynx is seen, an orientation examination of the cranial nerves and selective additional examination is necessary, as paresis of a hemilarynx is a symptom, not a diagnosis.
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PMID:[The immobile vocal cord]. 985 73

We prospectively determined the frequency of vocal cord paresis (VCP) among first-ever acute ischemic stroke patients. Vocal cords were examined endoscopically within 48 h of stroke onset, at 1 week and 1 month. Of the 54 study patients, 64.8% had lacunar (group 1), 22.2% cortical/large subcortical (group 2), 9.3% lateral medulla (group 3) and 3.7% other brainstem (group 4) infarcts. VCP was found in 11 (20.4%): 11.4% of group 1, 16.4% of group 2, 100% of group 3 and 0% of group 4. VCP was contralateral to the brain lesion in groups 1 and 2, and ipsilateral in 80% of group 3. VCP was strongly correlated with dysphonia (p < 0.0001) and resolved in 2/11 patients after 1 week and in 5/11 after 1 month. Our finding of VCP among acute ischemic stroke patients questions the belief that the nucleus ambiguous is invariably bilaterally innervated by supranuclear centers.
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PMID:Vocal cord paresis in acute ischemic stroke. 1020 8


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