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Management of Neurogenic Dysphagia

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Management of Neurogenic Dysphagia 694 Postgrad Med J 2001;77:694–699 Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from Management of neurogenic dysphagia A M O Bakheit Dysphagia is common in patients with neuro- of the cerebral cortex, basal ganglia, brain logical disorders. It may result from lesions in stem, cerebellum, and lower cranial nerves may the central or peripheral nervous system as well result in dysphagia. Degeneration of the as from diseases of muscle and disorders of the myenteric ganglion cells in the oesophagus, neuromuscular junction. Drugs that are com- muscle diseases and disorders of neuromusc- monly used in the management of neurological ular transmission, for example myasthenia conditions may also precipitate or aggravate gravis and Eaton-Lambers syndrome, are other swallowing diYculties in some patients. Neuro- less common causes. genic dysphagia often results in serious compli- cations, including pulmonary aspiration, dehy- CEREBRAL CORTEX dration, and malnutrition. These The commonest condition associated with complications are usually preventable if the dysphagia resulting from cortical lesions is stroke. Acute stroke is complicated by dys- dysphagia is recognised early and managed 1 appropriately. phagia in about 25%–42% of all cases. Dysphagia in these patients is usually associ- Physiological mechanisms of neurogenic ated with hemiplegia due to lesions of the brain stem or the involvement of one or both dysphagia The act of swallowing may be viewed as three hemispheres. However, on rare occasions, dys- discrete but inter-related physiological stages: phagia may be the sole manifestation of a cer- the oral, pharyngeal, and oesophageal phases. ebrovascular event. Dysphagia in the absence of other neurological symptoms and signs has The oral phase is initiated voluntarily and been reported in patients with lacunar infarcts serves to prepare the food bolus and deliver it in the periventricular white matter2 and after to the pharynx. An adequately prepared and discrete vascular brain stem lesions.3 suYciently large and cohesive food bolus Dysphagia in stroke is usually transient. triggers the swallow reflex by stimulating the Recovery of the swallowing ability occurs in sensory receptive field in the soft palate, almost 90% of cases within two weeks. dorsum of the tongue, epiglottis, and posterior However, the symptoms persist in about 8% of pharyngeal wall. Simultaneously the larynx patients for six months or more.4 The occur- closes and the velum retracts upwards to rence of dysphagia in acute stroke does not prevent the entry of food and fluid into the appear to depend on the size or the site of the nasal cavity. Coordination of respiration and lesion. Interestingly, when it persists for a swallowing is necessary to prevent the penetra- month or more after the stroke onset it is usu- http://pmj.bmj.com/ tion of food into the airways. This is achieved ally associated with right parietal lobe involve- by transient cessation of breathing, a process ment. known as deglutition apnoea. The pharyngeal phase is followed by a prolonged expiration to BASAL GANGLIA avert mist aspiration, that is inhalation of air Dysphagia is usually a late feature in Parkin- held in the pharynx (which is usually saturated son’s disease but is sometimes reported by with fluid and food particles). The swallow patients in the early stages and may even be the reflex triggers the oesophageal peristaltic presenting symptom in some cases. More than on September 24, 2021 by guest. Protected copyright. movements and causes relaxation of the 80% of patients with Parkinson’s disease have circopharyngeal sphincter. This, combined dysphagia but, as a rule, this is mild and has with the eVects of gravity, facilitates the trans- little or no eVect on the patient’s nutritional mission of food down into the stomach. status. However, in about 10% of dysphagic Several factors contribute to the swallowing parkinsonian patients the symptoms are severe diYculties encountered in patients with neuro- and this generally correlates with the severity genic dysphagia. These include weakness of the and duration of the disease. Tremor and speech oral musculature and tongue movements, disturbances have been found to be the main failure to form a cohesive food bolus, reduced predictors of dysphagia in these patients.5 sensitivity of the pharyngeal receptors, and The swallowing diYculties most frequently buccolingual apraxia. Although the abnormali- associated with Parkinson’s disease relate to the ties of swallowing associated with neurological oral phase (diYculties with lip closure and disease predominantly aVect the oropharyn- tongue movements) and the pharyngeal stage geal phase, occasionally neurogenic dysphagia (complaints of food sticking in the throat). On Stroke Unit, Mount may result from disorders of innervation of the videofluoroscopy these abnormalities are seen Gould Hospital, oesophagus. Plymouth PL4 7QD, as abnormal bolus formation, multiple tongue UK elevations, delayed swallow reflex, and prolon- Causes of neurogenic dysphagia gation of the pharyngeal transit time with Correspondence to: Normal swallowing depends on the anatomical repetitive swallows to clear the throat. Drool- Professor Bakheit and functional integrity of numerous neural ing, which is commonly seen in patients with Submitted 23 February 2001 structures and extensive pathways in the parkinsonism, is not due to excessive salivation Accepted 2 July 2001 central and peripheral nervous system. Lesions but is an indication of bradykinesia of the www.postgradmedj.com Neurogenic dysphagia 695 Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from oropharyngeal musculature. Other parkinso- by anticholinergic drugs. The benzodiazepines nian syndromes, for example Shy-Drager can adversely aVect swallowing in at least two syndrome, multisystem atrophy, etc result in ways. Dysphagia in patients taking these drugs similar, but usually more severe symptoms. is usually associated with depressed level of Dysphagia is also common in spasmodic consciousness but has also been reported in torticollis. In one study it was observed on vid- alert subjects.7 The latter eVect could be eofluoroscopy in more than 50% of a randomly explained by a direct inhibition of brain stem selected patients’ sample.6 Interestingly, only neurones that regulate swallowing. This is in two thirds of the study patients were sympto- keeping with observations from animal experi- matic and the occurrence of dysphagia did not ments.8 correlate with the patient’s age or disease dura- The most widely used drug that causes dys- tion. phagia due to inhibition of neural transmission at the neuromuscular junction is botulinum CEREBELLUM AND BRAIN STEM toxin type A. It is the drug of first choice for the Cerebellar disease and brain stem lesions treatment of spasmodic torticollis and may resulting in bulbar and pseudobulbar palsy cause dysphagia in 10%–28% of these patients. mainly aVect the oral phase of swallowing. Poor This adverse eVect is usually mild and coordination of the activity of the orofacial transient, lasting 10–14 days. Clinical observa- musculature may lead to inadequate lip seal, tions suggest that the incidence of dysphagia is diYculties with the timing of the voluntary ini- increased when a large dose of the drug is tiation of the swallow reflex, preparation of a injected (for example 750 units or more of cohesive food bolus, and delivery of the bolus botulinum toxin type A), especially if the dose to the pharynx. is divided between multiple sites in the muscle. PERIPHERAL NERVES AND MUSCLES Clinical manifestations of dysphagia and Isolated peripheral nerve lesions and degenera- pulmonary aspiration tion of autonomic ganglion cells in the lower Patients with mild or moderately severe neuro- two thirds of the oesophagus (which results in genic dysphagia may not be aware of their achalasia) are rare causes of dysphagia. Achala- swallowing diYculties. However, on direct sia is characterised by stasis of food and dilata- questioning most of these patients would admit tion of the oesophagus due to reduced peristal- that they have been avoiding certain foods sis and incomplete relaxation of the lower which they found diYcult to chew or swallow. oesophageal sphincter. In addition to dys- Weight loss may be the first presentation in phagia, patients typically present with halitosis. some cases. Drooling occurs in dysphagic The diagnosis is confirmed with endoscopy patients when they are sitting up and aspiration and studies of oesophageal motility. is common in the recumbent position, espe- Abnormalities of neuromuscular transmis- cially during sleep. Occasionally interrupted sion, for example in myasthenia gravis, fre- sleep may be the only indication of swallowing quently cause diYculties with swallowing. In diYculties. Pain on swallowing (odynophagia) addition to dysphagia, patients with disorders is not a symptom of neurogenic dysphagia and http://pmj.bmj.com/ of the neuromuscular junction often have dys- suggests the diagnosis of oesophagitis, usually phonia and dysarthria. Obvious weakness of secondary to candida infections. Nasal regurgi- oral and facial muscles may or may not be tation of fluids occurs when palatal weakness is present. The diagnosis of the underlying disor- present. der can usually be confirmed with single fibre electromyography. Assessment Assessment of swallowing function starts with a DRUGS AND DYSPHAGIA careful examination of the oral cavity. The
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