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Vocal cord paralysis

MedGen UID:
53047
Concept ID:
C0042928
Disease or Syndrome
Synonyms: Palsies, Vocal Cord; Palsies, Vocal Fold; Palsy, Vocal Cord; Palsy, Vocal Fold; Paralyses, Vocal Cord; Paralysis, Vocal Cord; Total Vocal Cord Paralysis; Vocal Cord Palsies; Vocal Cord Palsy; Vocal Cord Paralyses; Vocal Cord Paralysis; Vocal Fold Palsies; Vocal Fold Palsy
SNOMED CT: Vocal cord palsy (302912005); Vocal cord paralysis (302912005); VCP - Vocal cord palsy (302912005); Paralysis of vocal cords (302912005); Vocal fold palsy (302912005)
 
HPO: HP:0001605

Definition

A loss of the ability to move the vocal folds. [from HPO]

Conditions with this feature

Williams syndrome
MedGen UID:
59799
Concept ID:
C0175702
Disease or Syndrome
Williams syndrome (WS) is characterized by cardiovascular disease (elastin arteriopathy, peripheral pulmonary stenosis, supravalvar aortic stenosis, hypertension), distinctive facies, connective tissue abnormalities, intellectual disability (usually mild), a specific cognitive profile, unique personality characteristics, growth abnormalities, and endocrine abnormalities (hypercalcemia, hypercalciuria, hypothyroidism, and early puberty). Feeding difficulties often lead to poor weight gain in infancy. Hypotonia and hyperextensible joints can result in delayed attainment of motor milestones.
Hereditary liability to pressure palsies
MedGen UID:
98291
Concept ID:
C0393814
Disease or Syndrome
Hereditary neuropathy with liability to pressure palsies (HNPP) is characterized by recurrent acute sensory and motor neuropathy in a single or multiple nerves. The most common initial manifestation is the acute onset of a non-painful focal sensory and motor neuropathy in a single nerve (mononeuropathy). The first attack usually occurs in the second or third decade but earlier onset is possible. Neuropathic pain is increasingly recognized as a common manifestation. Recovery from acute neuropathy is usually complete; when recovery is not complete, the resulting disability is mild. Some affected individuals also demonstrate a mild-to-moderate peripheral neuropathy.
Congenital laryngeal abductor palsy
MedGen UID:
96004
Concept ID:
C0396059
Congenital Abnormality
Laryngeal abductor paralysis is an autosomal dominant condition characterized by variable penetrance and expressivity ranging from mild symptoms to neonatal asphyxia. (summary by Morelli et al., 1982; Manaligod and Smith, 1998).
Brown-Vialetto-van Laere syndrome 1
MedGen UID:
163239
Concept ID:
C0796274
Disease or Syndrome
Brown-Vialetto-Van Laere syndrome is a rare autosomal recessive neurologic disorder characterized by sensorineural hearing loss and a variety of cranial nerve palsies, usually involving the motor components of the seventh and ninth to twelfth (more rarely the third, fifth, and sixth) cranial nerves. Spinal motor nerves and, less commonly, upper motor neurons are sometimes affected, giving a picture resembling amyotrophic lateral sclerosis (ALS; 105400). The onset of the disease is usually in the second decade, but earlier and later onset have been reported. Hearing loss tends to precede the onset of neurologic signs, mostly progressive muscle weakness causing respiratory compromise. However, patients with very early onset may present with bulbar palsy and may not develop hearing loss until later. The symptoms, severity, and disease duration are variable (summary by Green et al., 2010). Genetic Heterogeneity of Brown-Vialetto-Van Laere Syndrome See also BVVLS2 (614707), caused by mutation in the SLC52A2 gene (607882) on chromosome 8q.
Neuronopathy, distal hereditary motor, type 7A
MedGen UID:
322474
Concept ID:
C1834703
Disease or Syndrome
Autosomal dominant distal hereditary motor neuronopathy-7 (HMND7) is a neurologic disorder characterized by onset in the second decade of progressive distal muscle wasting and weakness affecting the upper and lower limbs and resulting in walking difficulties and hand grip. There is significant muscle atrophy of the hands and lower limbs. The disorder is associated with vocal cord paresis due to involvement of the tenth cranial nerve (summary by Barwick et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant distal HMN, see HMND1 (182960).
Neuronopathy, distal hereditary motor, type 7B
MedGen UID:
375157
Concept ID:
C1843315
Disease or Syndrome
The spectrum of DCTN1-related neurodegeneration includes Perry syndrome, distal hereditary motor neuronopathy type 7B (dHMN7B), frontotemporal dementia (FTD), motor neuron disease / amyotrophic lateral sclerosis (ALS), and progressive supranuclear palsy. Some individuals present with overlapping phenotypes (e.g., FTD-ALS, Perry syndrome-dHMN7B). Perry syndrome (the most common of the phenotypes associated with DCTN1) is characterized by parkinsonism, neuropsychiatric symptoms, hypoventilation, and weight loss. The mean age of onset in those with Perry syndrome is 49 years (range: 35-70 years), and the mean disease duration is five years (range: 2-14 years). In most affected persons, the reported cause/circumstance of death relates to sudden death/hypoventilation or suicide.
Paragangliomas 3
MedGen UID:
340200
Concept ID:
C1854336
Disease or Syndrome
Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues distributed along the paravertebral axis from the base of the skull to the pelvis) and pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas cause catecholamine excess; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base and neck (referred to as head and neck PGL [HNPGL]) and sometimes in the upper mediastinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically lead to catecholamine excess. Symptoms of PGL/PCC result from either mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for developing metastatic disease is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas.
Ptosis-vocal cord paralysis syndrome
MedGen UID:
349807
Concept ID:
C1860403
Disease or Syndrome
A rare hereditary disorder with the combination of congenital bilateral recurrent laryngeal nerve paralysis and congenital bilateral ptosis. There have been no further descriptions in the literature since 1983.
Paragangliomas 2
MedGen UID:
357076
Concept ID:
C1866552
Disease or Syndrome
Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues distributed along the paravertebral axis from the base of the skull to the pelvis) and pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas cause catecholamine excess; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base and neck (referred to as head and neck PGL [HNPGL]) and sometimes in the upper mediastinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically lead to catecholamine excess. Symptoms of PGL/PCC result from either mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for developing metastatic disease is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas.
Paragangliomas 1
MedGen UID:
488134
Concept ID:
C3494181
Neoplastic Process
Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues distributed along the paravertebral axis from the base of the skull to the pelvis) and pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas cause catecholamine excess; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base and neck (referred to as head and neck PGL [HNPGL]) and sometimes in the upper mediastinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically lead to catecholamine excess. Symptoms of PGL/PCC result from either mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for developing metastatic disease is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas.
Charcot-Marie-Tooth disease type 2R
MedGen UID:
815985
Concept ID:
C3809655
Disease or Syndrome
A rare subtype of axonal hereditary motor and sensory neuropathy characterised by early-onset axial hypotonia, generalised muscle weakness, absent deep tendon reflexes and decreased muscle mass. Electromyography reveals decreased motor nerve conduction velocities with markedly reduced sensory and motor amplitudes. There is evidence the disease is caused by homozygous or compound heterozygous mutation in the TRIM2 gene on chromosome 4q.
Lethal congenital contracture syndrome 8
MedGen UID:
896058
Concept ID:
C4225385
Disease or Syndrome
Lethal congenital contracture syndrome-8 (LCCS8), an axoglial form of arthrogryposis multiplex congenita, is characterized by congenital distal joint contractures, reduced fetal movements, and severe motor paralysis leading to death early in the neonatal period (Laquerriere et al., 2014). For a general phenotypic description and a discussion of genetic heterogeneity of lethal congenital contracture syndrome, see LCCS1 (253310).
Intellectual disability, autosomal dominant 54
MedGen UID:
1614787
Concept ID:
C4540484
Mental or Behavioral Dysfunction
Feingold syndrome type 1
MedGen UID:
1637716
Concept ID:
C4551774
Disease or Syndrome
Feingold syndrome 1 (referred to as FS1 in this GeneReview) is characterized by digital anomalies (shortening of the 2nd and 5th middle phalanx of the hand, clinodactyly of the 5th finger, syndactyly of toes 2-3 and/or 4-5, thumb hypoplasia), microcephaly, facial dysmorphism (short palpebral fissures and micrognathia), gastrointestinal atresias (primarily esophageal and/or duodenal), and mild-to-moderate learning disability.
DEGCAGS syndrome
MedGen UID:
1794177
Concept ID:
C5561967
Disease or Syndrome
DEGCAGS syndrome is an autosomal recessive syndromic neurodevelopmental disorder characterized by global developmental delay, coarse and dysmorphic facial features, and poor growth and feeding apparent from infancy. Affected individuals have variable systemic manifestations often with significant structural defects of the cardiovascular, genitourinary, gastrointestinal, and/or skeletal systems. Additional features may include sensorineural hearing loss, hypotonia, anemia or pancytopenia, and immunodeficiency with recurrent infections. Death in childhood may occur (summary by Bertoli-Avella et al., 2021).
Congenital myopathy 15
MedGen UID:
1824046
Concept ID:
C5774273
Disease or Syndrome
Congenital myopathy-15 (CMYP15) is a skeletal muscle disorder characterized by symptom onset soon after birth. Affected infants are hypotonic and have severe respiratory insufficiency and feeding problems, sometimes requiring mechanical ventilation or tube feeding. The disorder is unique in that there is gradual improvement of the severe muscle weakness with time, although forced vital capacity remains decreased. Additional features include facial weakness, scoliosis, joint contractures, and persistent ptosis or external ophthalmoplegia (van de Locht et al., 2021). For a discussion of genetic heterogeneity of congenital myopathy, see CMYP1A (117000).

Professional guidelines

PubMed

Sin JH, Shafeeq H, Levy ZD
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Burch HB, Cooper DS
JAMA 2015 Dec 15;314(23):2544-54. doi: 10.1001/jama.2015.16535. PMID: 26670972

Recent clinical studies

Etiology

Ortega Beltrá N, Martínez Ruíz de Apodaca P, Matarredona Quiles S, Nieto Curiel P, Dalmau Galofre J
Acta Otorrinolaringol Esp (Engl Ed) 2022 Nov-Dec;73(6):376-383. Epub 2022 Oct 10 doi: 10.1016/j.otoeng.2021.11.002. PMID: 36228989
Sanchez-Jacob R, Cielma TK, Mudd PA
Pediatr Radiol 2022 Aug;52(9):1619-1626. Epub 2021 Nov 29 doi: 10.1007/s00247-021-05235-0. PMID: 34841448
Viana Baptista SIR, Lott DG, Almeida SCC, Cid MO, Vera-Cruz PS, Zagalo C
J Voice 2021 Sep;35(5):809.e1-809.e6. Epub 2020 Jan 28 doi: 10.1016/j.jvoice.2019.12.024. PMID: 32005624
Engeseth MS, Olsen NR, Maeland S, Halvorsen T, Goode A, Røksund OD
Paediatr Respir Rev 2018 Jun;27:74-85. Epub 2017 Nov 15 doi: 10.1016/j.prrv.2017.11.001. PMID: 29336933
Butskiy O, Mistry B, Chadha NK
JAMA Otolaryngol Head Neck Surg 2015 Jul;141(7):654-60. doi: 10.1001/jamaoto.2015.0680. PMID: 25973887

Diagnosis

Sanchez-Jacob R, Cielma TK, Mudd PA
Pediatr Radiol 2022 Aug;52(9):1619-1626. Epub 2021 Nov 29 doi: 10.1007/s00247-021-05235-0. PMID: 34841448
Volk GF, Guntinas-Lichius O
Adv Otorhinolaryngol 2020;85:18-24. Epub 2020 Nov 9 doi: 10.1159/000456680. PMID: 33166978
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Therapy

Sanchez-Jacob R, Cielma TK, Mudd PA
Pediatr Radiol 2022 Aug;52(9):1619-1626. Epub 2021 Nov 29 doi: 10.1007/s00247-021-05235-0. PMID: 34841448
Yang Y, Li B, Yi J, Hua R, Chen H, Tan L, Li H, He Y, Guo X, Sun Y, Yu B, Li Z
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Duan Q, Zhang F, Wang G, Wang H, Li H, Zhao J, Zhang J, Ni X
Eur J Pediatr 2021 Apr;180(4):1059-1066. Epub 2020 Oct 13 doi: 10.1007/s00431-020-03830-1. PMID: 33048238
Engeseth MS, Olsen NR, Maeland S, Halvorsen T, Goode A, Røksund OD
Paediatr Respir Rev 2018 Jun;27:74-85. Epub 2017 Nov 15 doi: 10.1016/j.prrv.2017.11.001. PMID: 29336933
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Dtsch Arztebl Int 2015 May 8;112(19):329-37. doi: 10.3238/arztebl.2015.0329. PMID: 26043420Free PMC Article

Prognosis

Patel J, Boon M, Spiegel J, Huntley C
Ear Nose Throat J 2021 Sep;100(5_suppl):608S-613S. Epub 2020 Jan 5 doi: 10.1177/0145561319894414. PMID: 31903781
The Lancet
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Clinical prediction guides

Ridgway C, Bouhabel S, Martignetti L, Kishimoto Y, Li-Jessen NYK
JAMA Otolaryngol Head Neck Surg 2021 Aug 1;147(8):745-752. doi: 10.1001/jamaoto.2021.1050. PMID: 34110365
Viana Baptista SIR, Lott DG, Almeida SCC, Cid MO, Vera-Cruz PS, Zagalo C
J Voice 2021 Sep;35(5):809.e1-809.e6. Epub 2020 Jan 28 doi: 10.1016/j.jvoice.2019.12.024. PMID: 32005624
Engeseth MS, Olsen NR, Maeland S, Halvorsen T, Goode A, Røksund OD
Paediatr Respir Rev 2018 Jun;27:74-85. Epub 2017 Nov 15 doi: 10.1016/j.prrv.2017.11.001. PMID: 29336933
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Recent systematic reviews

Haddad R, Ismail S, Khalaf MG, Matar N
Laryngoscope 2022 Aug;132(8):1630-1640. Epub 2021 Dec 11 doi: 10.1002/lary.29965. PMID: 34894158
Lin RJ, Klein-Fedyshin M, Rosen CA
Laryngoscope 2019 Apr;129(4):943-951. Epub 2018 Nov 19 doi: 10.1002/lary.27530. PMID: 30450691
Engeseth MS, Olsen NR, Maeland S, Halvorsen T, Goode A, Røksund OD
Paediatr Respir Rev 2018 Jun;27:74-85. Epub 2017 Nov 15 doi: 10.1016/j.prrv.2017.11.001. PMID: 29336933
Walton C, Conway E, Blackshaw H, Carding P
J Voice 2017 Jul;31(4):509.e7-509.e22. Epub 2016 Dec 19 doi: 10.1016/j.jvoice.2016.11.002. PMID: 28007326
Butskiy O, Mistry B, Chadha NK
JAMA Otolaryngol Head Neck Surg 2015 Jul;141(7):654-60. doi: 10.1001/jamaoto.2015.0680. PMID: 25973887

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