Case reports

The Intensive Care Society 2009

Lateral medullary syndrome causing vocal cord palsy and stridor

J Nicholson, U Paralkar, G Lawton, P Sigston
We report a 63-year-old patient with lateral medullary syndrome secondary to a medullary haemorrhage, causing unilateral vocal cord palsy which precipitated respiratory failure sufficient to warrant intubation and ventilation. The patient recovered completely following neurological rehabilitation and was discharged home a month later. Centrally-mediated vocal cord palsy is a rare cause of stridor, but should be suspected in cases where no other local cause can be found.
Keywords: lateral medullary syndrome; vocal cord palsy; stridor, medullary haemorrhage; respiratory failure; ventilation

Case report
A 63-year-old man was admitted under the general physicians with a seven-day history of dizziness and fever, four days of dry cough, tinnitus, nausea and vomiting, and two days of feeling unsteady on his feet, associated with a headache. He had no other signicant past medical history. On examination the patient had a pulse of 92 beats per minute, a temperature of o 38.8 C and was found to be hypertensive with a blood pressure of 184/111 mm Hg with normal heart sounds. He was tachypnoeic, with a respiratory rate of 20 breaths per minute; auscultation of the chest revealed crepitations at the left base. Neurologically, examination of both cranial and peripheral nervous systems was unremarkable, as were his routine blood results. Chest Xray showed a left basal pneumonia and he received intravenous uids and antibiotics. On the third day after his admission, he developed a hoarse voice, increasing hypertension, diplopia and dysarthria with type II respiratory failure and stridor. Arterial blood gas analysis revealed a respiratory acidosis (pH 7.33, pCO2 8.8 kPa, on 60% oxygen). Flexible pharyngopO2 10.9 kPa laryngoscopy was performed on the ward by the ENT team and revealed a left vocal cord palsy. A head CT scan demonstrated a high-density lesion measuring 25 7 mm consistent with haemorrhage in the territory of the left Xth cranial nerve nucleus in the lateral brainstem (Figure 1). Shortly after arrival on the ICU, the patients respiratory function deteriorated rapidly, necessitating intubation and mechanical ventilation. He was sedated with alfentanil and propofol, and ventilated with pressure-controlled synchronised intermittent mandatory ventilation (SIMV) with 60% oxygen. His arterial blood gas tensions were promptly corrected. On the rst day of his ICU stay, his tracheal tube was changed for a tracheostomy. A labetolol infusion (0-20 mg) was used to maintain his mean arterial pressure in the range of 90 to 100 mm Hg. After withholding sedation, repeat neurological examination revealed left gaze nystagmus. By day three, he was weaned to spontaneous breathing with a tracheostomy mask.
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Figure 1 Head CT scan showing a 25 x 7 mm high-density haemorrhage in the left Xth cranial nerve nucleus in the lateral brainstem.

Repeat exible pharyngo-laryngoscopy demonstrated left vocal cord palsy, swollen arytenoids and pooling of saliva. A further neurological examination found marked left-sided ataxia but no demonstrable numbness, weakness or diplopia. His reexes and sensation were normal. Throughout his admission, there were no positive microbiology results from sputum or blood. Magnetic resonance imaging (MRI) of his brain with magnetic resonance angiography (MRA) of the posterior circulation conrmed a small haemorrhage in the left dorsolateral quadrant of the medulla. There was associated mass effect with surrounding T2/FLAIR hyper-dense signal oedema.
Volume 10, Number 3, July 2009 JICS

Case reports

Anatomical location Spinothalamic tract Spinal trigeminal nucleus Nucleus ambiguus

Presenting symptoms Contralateral loss of pain and temperature sensation Ipsilateral facial loss of pain and temperature Supplies vagus and glossopharyngeal nerves; dysphagia/dysphonia/ diminished gag reflex Vertigo/diplopia/nystagmus/ vomiting Ipsilateral Horners syndrome Palatal clonus Ataxia

Inferior vestibular nucleus Sympathetic fibres Central trigeminal tract Inferior cerebellar peduncle

Table 1 Clinical picture of lateral medullary syndrome.

Another hyper-dense lesion was also noted at the right pontomedullary junction, but this was considered insignicant. The MRA showed a normal vascular pattern. He was decannulated once bulbar function returned and underwent further neurological rehabilitation until he was nally discharged home a month later.

the efferent supply to the vocal cords is via the recurrent laryngeal nerve, a branch of the vagus. While dysphonia is an almost universal nding in lateral medullary syndrome when ischaemic in origin, our literature search revealed only one recent case report giving an account of concurrent lateral medullary syndrome (secondary to thrombosis of the vertebral 1 artery) and stridor. It is possible that haemorrhagic events, with associated mass effect can involve contralateral nuclei which would cause some adduction of the contralateral cord making airway narrowing more signicant. Indeed, the initial magnetic resonance imaging reports suggest a lesion on the right side; it was suggested at the time that this could signify change in crossing white matter tracts of the medulla. Other than ventilatory failure, the other main indication for intubation was airway protection given his diminished gag reex. Indeed, the pneumonia present on admission may have been due to aspiration in the early stages of the illness. Treatment of lateral medullary syndrome is usually supportive, which may involve speech and swallowing therapy. Adequate pain relief should be ensured in these patients if the spino-thalamic tract is involved.

Acknowledgement
The authors are grateful to the patient for his consent to publish this case report.

Discussion
The posterior inferior cerebellar artery is the largest branch of the vertebral artery, supplying the cerebellum and choroid plexus of the fourth ventricle. It divides into medial and lateral branches with the medial branches lying between the two hemispheres of the cerebellum while the lateral branch supplies the under-surface of the cerebellum. Lateral medullary syndrome also called Wallenberg's syndrome or posterior inferior cerebellar artery syndrome, was rst described in 1808 by Gaspard Vieusseux. First descriptions by Wallenberg were in 1895, when he described in detail the classical picture caused by infarction of the lateral medulla oblongata following occlusion of the posterior inferior cerebellar artery. It usually presents with dysphonia and dysphagia, but clinical presentations can vary depending on which specic nucleii and bres are involved (see Table 1). However, although dysphonia and dysphagia are common symptoms of lateral medullary syndrome, hiccoughs can also be the main presenting complaint. This case demonstrates a centrally-mediated cause of stridor. In our patient, symptoms and signs were predominantly secondary to nucleus ambiguus and vestibular involvement as

References
1. Vaidyanathan S, Capper R, Chadha D. Stridor: an unusual presentation of lateral medullary syndrome. J Laryngol Otol 2007; 121:e9. 2. Kim JS, Lee JH, Choi CG. Patterns of lateral medullary infarction: vascular lesion magnetic resonance imaging correlation of 34 cases. Stroke 1998;29:645-52. 3. Shaw GL. Airway obstruction due to bilateral vocal cord paralysis as a complication of stroke. South Med J 1987;80: 1432-33

James Nicholson Specialist Registrar in Anaesthesia and

Intensive Care

Ulka Paralkar Specialist Registrar in Anaesthesia and

Intensive Care doculka@hotmail.com

Greg Lawton Consultant Anaesthetist and Intensivist Paul Sigston Consultant Anaesthetist and Intensivist
Department of Anaesthesia and Intensive Care, Kent and Sussex Hospital, Maidstone and Tunbridge Wells NHS Trust

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