Year : 2013 | Volume
: 3 | Issue : 3 | Page : 318--319
Lateral medullary syndrome presenting with acute central stridor secondary to bilateral vocal cord palsy
Ajay Mishra, Nikhil Dave, Manan Mehta
Department of Medicine, Pramukhswami Medical College, Karamsad, Anand, Gujarat, India
Department of Medicine, Pramukhswami Medical College, Karamsad, Anand, Gujarat
Lateral medullary syndrome is a conglomeration of symptoms suggestive of tract involvement at the level of lateral medulla, with classic clinical findings. We report an 82-year-old male with lateral medullary syndrome who developed acute stridor secondary to bilateral vocal cord palsy.
|How to cite this article:|
Mishra A, Dave N, Mehta M. Lateral medullary syndrome presenting with acute central stridor secondary to bilateral vocal cord palsy.Int J Nutr Pharmacol Neurol Dis 2013;3:318-319
|How to cite this URL:|
Mishra A, Dave N, Mehta M. Lateral medullary syndrome presenting with acute central stridor secondary to bilateral vocal cord palsy. Int J Nutr Pharmacol Neurol Dis [serial online] 2013 [cited 2021 Oct 19 ];3:318-319
Available from: https://www.ijnpnd.com/text.asp?2013/3/3/318/114835
Wallenberg's syndrome is well-defined clinically; the lateral medullary infarction is the most frequent cause, among others. The triad of Horner's syndrome, ipsilateral ataxia, and ipsilateral hyperalgesia clinically identify patients with the lateral medullary syndrome. Although the combinations of various signs and symptoms are helpful for the clinical diagnosis of lateral medullary syndrome, the presence of the different signs and symptoms may vary from patient to patient.  Among these symptoms and signs, dysphagia, dysphonia, hiccoughs and failure of automatic breathing are described in association with lateral medullary syndrome; development of central stridor due to the bilateral vocal cord palsy is rare.
We are reporting an unusual presentation of a patient with features of lateral medullary syndrome that developed acute stridor due to bilateral vocal cord palsy leading to acute life-threatening upper respiratory obstruction.
An 82-year-old male presented with imbalance while walking with difficulty in swallowing and change in voice for 2 days before presentation. Neurological examination revealed clinical features, suggestive of left lateral medullary syndrome; dysphagia, dysarthria, hoarseness, anisocoria, left ptosis, sensory loss on the left side of the face and right half of the body and left limb ataxia. Deep tendon reflexes were symmetrically exaggerated and planter responses bilateral extensor. Cerebellar signs as ataxia, dysdiadochokinesia, past pointing and intention tremor were present on the left side. His past medical history included hypertension, diabetes mellitus type 2 and permanent cardiac pacemaker implant for complete heart block.
A presumptive diagnosis of the brain stem stroke of ischemic origin, secondary to cardiac embolism or vertebrobasilar thrombosis was considered. Magnetic resonance imaging was not possible as he had a pacemaker in situ. A computed tomography (CT) head brain with CT angiography was planned. However, shortly after arrival, patient developed stridor with severe respiratory distress. Laryngoscopy demonstrated both vocal cords to be fixed in the midline in severe spasm with mild slit-like airway opening with respiration making endotracheal intubation impossible despite neuromuscular paralysis. An emergency tracheostomy was performed and patient was shifted to the intensive care unit for mechanical ventilator support. Arterial blood gas analysis revealed respiratory acidosis and hypoxia (pH 7.29, pCO 2 59.6 mm Hg, pO 2 63.6 mm Hg on 60% oxygen). Hematological and biochemical parameters including, random blood sugar, serum electrolytes, lipid profile and renal, liver and thyroid function tests were within the normal range. Hepatitis B surface antigen, hepatitis C virus and human immunodeficiency virus serology was negative. Electrocardiography showed pacemaker rhythm. 2D echocardiography and chest X-ray did not reveal any abnormality. After hemodynamic stabilization, CT brain imaging revealed no hemorrhage. CT angiography revealed mild diffuse narrowing of the basilar artery in the mid part, without major stenosis in other cranio-cervical arteries, thus confirming thrombotic ischemic stroke as cause of stroke. Patient required mechanical ventilation for about 24 h after, which he was able to maintain saturation on room air with T-piece ventilation. Bulbar functions improved after 2 weeks. He was decannulated and underwent neurological rehabilitation. He had significant recovery in his ataxic hemiparesis and could walk without the aid at discharge at 3 weeks.
The relationship between stroke and functional impairment is complex. Approximately, 80% of patients with acute stroke presents with focal weakness or paralysis.  Lateral medullary infarctions comprise approximately 2% of ischemic stroke.  It usually presents with dysphonia and dysphagia, but clinical presentations can vary depending on specific nuclei and fibers involved. Rostral lesions were usually associated with more severe dysphagia, hoarseness and the presence of ipsilateral facial paresis for the involvement of the nucleus ambiguus and the looping corticobulbar fibers destined to the facial nucleus respectively. Caudal lesions were correlated with more marked vertigo, nystagmus and gait ataxia by the involvement of the vestibular nuclei, vestibulocerebellar pathway and restiform body or the spinocerebellar pathway. Nausea, vomiting and Horner sign were common regardless of the lesion location without rostrocaudal difference.  Vocal cord palsy is usually ipsilateral in lateral medullary syndrome and contralateral in lesions cranial to the nucleus ambiguous.  Unilateral medullary lesion is commonly associated with an unilateral vocal cord palsy that usually does not cause upper airway obstruction. 
A review of the literature revealed few case reports of upper airway obstruction due to bilateral vocal cord palsy secondary to ischemic cortical and lateral medullary infarction. ,, In one of the case reports, unilateral vocal cord palsy, stridor and ventilator failure was associated with lateral medullary syndrome secondary to hemorrhage in left dorsolateral quadrant of the medulla. 
The simultaneous involvement of the nucleus ambiguus and peri-ambigual reticular formation in unilateral medullary lesion may cause simultaneous ipsilateral and contralateral vocal cord palsy.  A previous study using the squirrel monkeys suggests that the corticobulblar laryngeal control pathway synapses in the ipsilateral dorsal reticular nucleus and is divided into two components: One component runs directly to the ipsilateral nucleus ambiguus and the other crosses to the contralateral nucleus ambiguus after having synapses in the ipsilateral peri-ambigual reticular formation. 
Clinician should be aware of this rare, but potentially fatal complication in patients presenting with features of the brain stem stroke. Centrally-mediated vocal cord palsy may result in acute respiratory obstruction and requires emergency tracheostomy.
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