Neurology Case Challenge: Drooling and Dysphagia in a Man Who Can’t Speak

Elena Cecilia Rosca, MD, PhD; Cristina Dijmarescu, MD; Mihaela Simu, MD


April 04, 2022

The acute onset of dysphagia and anarthria should be differentiated from a lateral medullary syndrome (Wallenberg syndrome) due to vertebral artery occlusion or to posterior inferior cerebellar artery occlusion. The ipsilateral signs of a lateral medullary lesion include the following:

  • Dysarthria and dysphagia

  • Loss of taste from the posterior third of the tongue (due to lesions of cranial nerves IX, X, XI, and XII)

  • Ataxia (caused by damage to the inferior cerebellar peduncle and cerebellum)

  • Reduced corneal reflex temperature loss and facial pain (due to cranial nerve V damage)

  • Nystagmus

  • Hypoacousia (due to a cranial nerve VIII lesion)

  • Horner syndrome (caused by a lesion of the descending sympathetic fibers)

Contralateral findings include loss of pain and temperature sensation, indicating a lesion of the anterior spinothalamic tract. Other clinical signs of Wallenberg syndrome include tachycardia and dyspnea caused by cranial nerve X dysfunction.

Other causes of acute bulbar muscle dysfunction must also be considered. Botulism is an acute neurologic disease that causes severe paralysis due to a neurotoxin produced by Clostridium botulinum. In adults, botulism can be caused by the introduction of toxin-producing spores into wounds from injury involving contaminated soil; intravenous use of contaminated drugs; or ingestion of preformed neurotoxins in high-risk foods, including home-canned or home-processed fruits and vegetables, fish and fish products, condiments such as relish, and chili peppers. Most patients present with three to five of the following signs:

  • Dysphagia

  • Diplopia

  • Fixed mydriasis

  • Nausea

  • Vomiting

  • Dry mouth unrelieved by drinking fluids

Cranial nerve symptoms consist of dysarthria; dysphagia; suppressed gag reflex; extraocular muscle weakness; diplopia; and fixed, dilated pupils. Patients also present with descending paralysis of the motor and autonomic nerves. The patient in this case had only one of the major botulism symptoms, no oculomotor nerve involvement, and no lower motor neuron signs.

Another entity in the differential diagnosis is myasthenia gravis, an autoimmune disorder that involves the neuromuscular junction. The initial symptom is usually extraocular muscle weakness, tending to spread to the facial and bulbar muscles. Bulbar muscle involvement is common and is accompanied by weakness of head extension and flexion. As the disease progresses, truncal and limb muscles can be also affected. However, the weakness is fatigable, increased by sustained activity and alleviated by rest. The disease typically progresses over weeks or months, with exacerbations and remissions. Myasthenia gravis is diagnosed using clinical, laboratory (anti-acetylcholine receptor antibodies or autoantibodies to muscle-specific kinase), and electrophysiologic investigations.

In the present case, the bulbar muscle weakness was isolated, with no extraocular, neck, or trunk muscle involvement. Furthermore, the onset was acute and without fluctuations in the deficit.


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