British Journal of Radiology 75 (2002),990-933 © 2002 The British Institute of Radiology
Bilateral vocal cord paralysis caused by cervical spinal osteophytes
K Aydin, MD1,
T Ulug, MD2 and
T Simsek, MD1
Departments of 1 Radiology and 2 ENT, Istanbul University Medical School Capa Hospital, Capa, Istanbul, Turkey
Correspondence: Dr Kubilay Aydin, B.Mehmetpasa sokak Yavuz Apt. No:10/10, Camlikyolu, Etiler / Istanbul, Turkey
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Abstract
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Thyroid and cervical surgery, tracheal intubation, trauma and neurodegenerative and neuromuscular diseases may cause bilateral vocal cord paralysis. There are only a few reported cases of bilateral cord paralysis associated with cervical hyperostosis in the English literature. We report the MR and CT findings of a case of bilateral vocal cord paralysis caused by cervical spinal osteophytes compressing the recurrent laryngeal nerves.
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Introduction
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Iatrogenic injury of the recurrent laryngeal nerve is the most common cause of vocal cord paralysis. Trauma, malignancy, infection and neurodegenerative and neuromuscular diseases have all been reported to cause vocal cord paralysis [1–5]. Because of the longer course and mediastinal extension of the left recurrent laryngeal nerve, the majority of vocal cord palsies are left sided (56%) [1]. 9% of vocal cord paralyses are bilateral.
We report a case of bilateral vocal cord paralysis and respiratory obstruction caused by compression of the recurrent laryngeal nerves by cervical spinal osteophytes.
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Case report
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An 81-year-old male presented with sudden onset inspiratory stridor. Detailed clinical history revealed hoarseness to have started 2 days earlier and a history of neck stiffness for 2 years. There was no history of a recent interventional medical procedure, trauma, smoking or a known chronic disease. Head and neck examination was normal. Neurological examination revealed intact cranial nerves, normal deep tendon reflexes and muscular strength.
Laryngoscopy revealed immobility of the paramedian located vocal cords and a submucosal mass on the posterior wall of the pharynx. There was no mucosal lesion. Emergency tracheotomy was performed to relieve the severe respiratory obstruction. Blood and urine analysis revealed mild anaemia with a haemoglobulin level of 11.2 g dl-1. MR examination of the neck and upper mediastinum were performed to investigate the aetiology of the bilateral vocal cord paralysis and the nature of the submucosal lesion on a 1.0 T superconducting magnet (Magnetom impact; Siemens Medical Systems, Germany). MRI revealed the bilateral paramedian position of the vocal cords, which were narrowing the airway (Figure 1
). T1 and T2 weighted images showed hypointense osteophytes originating from the anterior cortex of cervical vertebral bodies. The osteophytes were compressing the post-cricoid area of the larynx. There was no mass lesion in the pathways of either the vagus or recurrent laryngeal nerves. The cervical spinal cord, upper mediastinum and skull base were normal. CT examination of the neck demonstrated osteophytes originating from the anterior surfaces of the cervical vertebral bodies and bridging to form a bony bar in the anterior prevertebral space from C3 to C7 (Figure 2 and Figure 3). Images at the level of the vocal cords revealed the paramedian localization of the vocal cords and the normal appearances of cricoid cartilage and cricoarytenoid articulations. Laryngeal electromyography demonstrated a peripheral neuropathic process. Laryngoscopic and MR findings did not show any change at 3-month and 6-month follow-up. Unilateral arythenoidectomy and cordopexy were performed to enlarge the airway.
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Figure 1. Axial T1 weighted image (repetition time 570ms, echo time 15ms, excitation 3) at the level of vocal cords reveals the paramedian location of vocal cords and severe obstruction of airway. Note the osteophyte (arrow) compressing on the post-cricoid area.
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Figure 2. (a) Sagittal reconstructed CT image of cervical spine demonstrates the osteophytes originating from the anterior of vertebral bodies. Bridging osteophytes form a bony bar in the anterior prevertebral space (arrow heads). (b) Sagittal T2 weighted image (repetition time 4000ms, echo time 112ms, excitation 3) shows the cervical spinal osteophytes compressing on the posterior wall of the larynx. Intervertebral discs show degenerative changes.
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Figure 3. (a) Axial CT image shows the close relation of cervical osteophyte (open arrows) with inferior cornu of thyroid cartilage (arrows). It demonstrates the severe narrowing of the pathway of recurrent laryngeal nerves, just behind the inferior cornu of thyroid cartilage (curved arrow). (b) Axial T1 weighted image demonstrates cervical osteophyte compressing the post-cricoid larynx. Note the severe narrowing of the spaces behind inferior cornu of thyroid cartilage (curved arrow).
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Discussion
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A detailed clinical history and head and neck examination usually reveal the cause of bilateral vocal cord paralysis in the majority of cases. The aetiology of unilateral and bilateral vocal cord paralysis are the same, but the percentages of causes are different [2, 6]. The most common cause of bilateral vocal cord paralysis is recurrent laryngeal nerve injury occurring during a surgical procedure. Vocal cord paralysis may develop after neck and mediastinal surgery. Blunt trauma to the neck and tracheal intubation are other common causes of vocal cord paralysis. Although unilateral vocal paralysis is caused by acute trauma during intubation, bilateral cases are usually owing to prolonged intubation [2]. In our case, there was no history of any surgical procedure or trauma.
A variety of central nervous system diseases, such as transient ischaemic attacks, hydrocephalus, myoclonus, Shy–Drager syndrome, multiple-system atrophy and amyotrophic lateral sclerosis, have been reported to produce vocal cord immobility [2]. There was no clinical history, neurological or electromyographical findings to suggest any of these diagnoses in our patient.
Cervical spinal osteophytes, either as a component of Forestier's disease or as a result of cervical spine disease, have been reported to be associated with dysphagia and dysphonia [7, 8]. Hassard [9] reported two cases of bilateral vocal cord paralysis caused by osteophytes compressing the post-cricoid area of the larynx, similar to our case. Laryngoscopic examination of both of these cases revealed post-cricoid ulceration and Hassard speculated that recurrent laryngeal neuritis due to superimposed infection of the post-cricoid ulcer might have caused the bilateral vocal cord paralysis. There was no mucosal ulceration or any finding of infection in our case.
Papakostas et al [10] reported a case of Forestier's disease in which cervical osteophytes were causing airway obstruction and acute stridor. Demuynck et al [11] reported a similar case of acute and severe upper airway obstruction caused by a cervical osteophyte. However, there was no impairment of vocal cord mobility in these cases.
Injury of recurrent laryngeal nerves by cervical osteophytes is the most probable mechanism for the development of vocal cord paralysis in our case. The right recurrent laryngeal nerve arises from the vagus nerve at the level of the subclavian artery and loops around it. The left recurrent laryngeal nerve leaves the vagus nerve on the left arch of aorta and winds below the arch. Both recurrent laryngeal nerves ascend in the trachea–oesophageal groove and enter the larynx just behind the articulation of the posterior cornu of thyroid cartilage with the cricoid cartilage. The section of the recurrent laryngeal nerve ascending in the trachea–oesophageal groove is safe from osteophyte compression. The most probable location for compression of the recurrent laryngeal nerve is behind the inferior cornu of the thyroid cartilage near the cricothyroid articulation, as in our case. Osteophytes were considerably narrowing the space behind the inferior cornu of the thyroid cartilage and the recurrent laryngeal nerves may have been impinged between the inferior cornu of thyroid cartilage and the osteophytes.
In our case, the sudden onset of stridor caused by a chronic aetiology seems contradictory. However, unilateral vocal cord palsy may precede bilateral paralysis and the patient may not notice hoarseness caused by the unilateral lesion. The development of bilateral paralysis following a possible unilateral lesion may explain the acute onset of stridor.
In conclusion, although rare, cervical osteophytes may cause bilateral vocal cord paralysis and respiratory obstruction, and should be considered in the differential diagnosis of vocal cord paralysis.
Received for publication January 4, 2002.
Revision received July 5, 2002.
Accepted for publication July 12, 2002.
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References
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Abstract
Introduction
