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

A M O Bakheit

Dysphagia is common in patients with neuro- of the , basal ganglia, brain logical disorders. It may result from lesions in stem, cerebellum, and lower cranial nerves may the central or peripheral 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 . 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. 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 , 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 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 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 . 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 on September 24, 2021 by guest. Protected copyright. Many drugs may precipitate or aggravate swal- presence of dysphagia and its severity can then lowing diYculties. This eVect is usually dose be confirmed at the bedside by observing the dependent and is often reversible with discon- patient during “trial swallows”. Swallowing tinuation of the drug. Sometimes reduction of behaviour can be observed while the subject is the drug dose is suYcient. The mechanisms taking food and fluids of diVerent consistencies implicated in drug induced dysphagia are under “normal” everyday conditions. Cough- diverse. These include depression of the level ing, splattering, and choking while eating are of consciousness (sedatives and hypnotics), obvious signs. Change in the pattern of breath- interference with the oropharyngeal phase of ing or change in voice quality may also occur. swallowing, a direct eVect on brain stem Some patients attempt to compensate for their neurones or blocking of acetylcholine release at swallowing diYculties by taking small, frequent the neuromuscular junction. Some drugs drinks during the meal in order to “wash mediate their eVect on swallowing by more down” the food bolus. Inspection of the oral than one mechanism. cavity usually reveals pooling of secretions or Neuroleptic drugs delay the initiation of the food residue in the mouth. swallow reflex, sometimes in the absence of In recent years a simple bedside measure- obvious extrapyramidal features. On the other ment of the swallowing speed has been hand, dopaminergic agents may cause orofacial suggested as a diagnostic test for neurogenic which aVects the preparation of the dysphagia.9 The test, which has been shown to food bolus and its delivery to the pharynx. be specific and sensitive, consists of measuring Dysphagia due to poor preparation of the food the speed with which the patient drinks 150 ml bolus may also result from xerostomia caused of cold tap water while sitting up. A swallowing

www.postgradmedj.com 696 Bakheit Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from speed of less than 10 ml/s suggests the presence have a normal bolus transit time and seldom of dysphagia. This test has obvious advantages complain of diYculties with eating or drinking. over other methods of assessment such as vid- eofluoroscopy and nasendoscopy, especially Complications of dysphagia when regular and frequent monitoring of the A serious complication of dysphagia is pulmo- patient’s condition is necessary. nary aspiration. Severe swallowing diYculties, Videofluoroscopy is considered the gold even for relatively short periods, may also lead standard for the evaluation of dysphagia. It to dehydration, reduced calorie intake, and permits the observation of the oral preparatory malnutrition. phase, the reflex initiation of swallowing, and Pulmonary aspiration is defined as penetra- the pharyngeal transit of the food bolus. How- tion of food or fluid into the airways below the ever, it is not suitable for repeated assessments true vocal cords. It may result in severe because of the undesirability of frequent expo- morbidity and sometimes mortality. About a sure to radiation and the cost of the procedure. third of patients with dysphagia aspirate food An alternative method is fibreoptic nasendos- or fluid into their airways and in 40% of them copy. This procedure consists of introducing an aspiration is silent, that is does not trigger endoscope through the nose into the nasophar- coughing or cause symptoms or signs of ynx and placing the tip just above the soft pal- distress. Paradoxically, aspirating patients fre- ate. The patient is then given food and drink quently do not complain of swallowing diYcul- coloured with a dye and before and after swal- ties and there are no reliable clinical signs of lowing pharyngeal pooling is observed. Nasal this complication. Interestingly, a weak cough endoscopy is a reliable method for assessing which is generally associated with the ability to dysphagia and the risk of pulmonary aspiration protect the airways, is more likely to be present but special expertise is necessary to carry out in aspirating rather than non aspirating dys- the procedure and to interpret its results. phagic patients.11 Similarly, a diminished or Another useful method of bedside diagnosis absent gag reflex does not diVerentiate aspirat- of dysphagia and pulmonary aspiration is pulse ing from non-aspirating patients. The detec- oximetry. The use of this method is based on tion of silent aspiration, therefore depends the premise that aspiration of food or fluid in largely on a high index of clinical suspicion and the airways causes reflex bronchoconstriction may be confirmed by non-invasive bedside that leads to ventilation-perfusion mismatch. investigations such as pulse oximetry.10 The resulting oxygen desaturation of arterial blood can be readily measured with pulse oxi- Management metry. In a recent study pulse oximetry The aim of management is to prevent pulmo- predicted aspiration or the lack of it in 81.5% nary aspiration, to maintain adequate food and of dysphagic stroke patients.10 This method is fluid intake, and to correct nutritional deficien- non-invasive, quick, and repeatable but its cies when present. Oral feeding has important results must be interpreted with caution in social and psychological significance to pa- smokers (high carboxyhaemoglobin concentra- tients and their families and should be contin-

tions may give false negative results) and in ued whenever possible. In some patients oral http://pmj.bmj.com/ those with chronic lung disease. intake is often not adequate even in the absence Oesophageal manometry enables measure- of significant swallowing diYculties. This may ments of the intraoesophageal pressure be due to excessive fatigue or cognitive impair- gradient and is useful in the evaluation of dys- ment. In these patients oral food intake may be function of the circopharyngeus muscle and supplemented with gastrostomy tube feeding. abnormalities of oesophageal motility. It is preferable that such supplements are given at night. Withholding morning gastrostomy

DiVerential diagnosis feeds usually stimulates the patient’s appetite. on September 24, 2021 by guest. Protected copyright. A careful medical history and physical exam- An interdisciplinary team approach is essential ination (supplemented by special investigations for the optimal management of patients with in some cases) are necessary to establish the neurogenic dysphagia. The core team should cause of the swallowing diYculty and to consist of a speech and language therapist, a exclude coincidental dysphagia due to obstruc- dietitian, a nurse, and a physician. tive lesions. In contrast to dysphagia due to Dysphagia in some patients may result from oesophageal strictures or tumours, patients poor preparation of the food bolus because of with neurogenic dysphagia find fluids more ill fitting dentures or due to disease of the oral diYcult to swallow than solids. This is probably cavity, such as mouth ulcers or candida because a solid (and more cohesive) food bolus infections. These causes should be routinely is more likely to result in adequate pharyngeal looked for and treated. Care should be taken to stimulation and trigger a swallow reflex. avoid feeding when the patient is tired or Dysphagia resulting from discrete brain stem distracted (for example while watching televi- lesions or confluent periventricular infarction sion). Talking while eating also increases the may aVect predominantly the volitional initia- risk of aspiration and patients (and their carers) tion of swallowing and spare reflexive degluti- should be made aware of this. It is sometimes tion. In these circumstances the patient’s useful to plan the timing of meals so that they symptoms are often ascribed to globus hysteri- coincide with periods when the patient’s func- cus. However, in the latter condition a “lump in tional abilities are maximal, for example, the throat” is a characteristic complaint and the during the “on periods” in parkinsonian symptoms are usually associated with emo- patients with “on/oV” motor fluctuations. Fre- tional distress. Patients with globus hystericus quent suction of copious saliva may be

www.postgradmedj.com Neurogenic dysphagia 697 Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from necessary in some cases. In dysphagic patients descriptive terms such as syrup or yoghurt who have a tracheostomy, occlusion of the consistency. This has the disadvantage that flu- stoma with a speaking valve during swallowing ids with low viscosity may be served and result reduces the risk of pulmonary aspiration in pulmonary aspiration. On the other hand, presumably by normalising the pressure in the fluids that are too thick are usually unpalatable upper airways. The eVects of posture on and are often rejected by patients. The use of a swallowing are well recognised. For example, viscometer for the preparation of the pre- “chin tuck” decreases the pharyngeal transit scribed fluid thickness has been shown to time of the food bolus, whereas “chin up” has improve the dietary management in these the opposite eVect. Head tilt to one side to cases.14 maximise the eVect of gravity on the unaVected side of pharynx is also a useful strategy on some TUBE FEEDING occasions. The direct delivery of nutrients into the stom- It has been shown that patients with weak ach (or rarely into the jejunum) via a feeding tongue movements and those with poor tube is frequently used as the sole method of pharyngeal clearance of the food bolus benefit nutritional support of severely dysphagic pa- from the use of gravity and posture to facilitate tients who are at risk of pulmonary aspiration if safe swallowing. Lying down on one side (at 45 fed orally. Tube feeding should be considered if degrees from flat) may be associated with less the subject aspirates approximately 10% or risk of aspiration than feeding in the upright more of the food bolus (M Collins, personal position.12 13 communication) or shows evidence of slow transit of the food bolus, that is more than 10 15 REVIEW OF PATIENT’S MEDICATION seconds, on videofluoroscopy. However, in Sedative and other drugs that reduce the some cases, for example when easy fatiguability patient’s level of arousal should be discontin- makes swallowing unsafe, tube feeding can be ued whenever possible. In patients with Parkin- used to supplement the daily oral intake. The son’s disease drug induced dyskinesia may patients will then be able to take their favourite cause or aggravate dysphagia and the success- foods orally and the rest of the calorie require- ful management of this complication usually ments will be given through the tube. improves swallowing. Sometimes it is suYcient The use of a gastrostomy tube is preferred to to avoid feeding during periods of peak dose naso-oesophageal intubation, especially when dyskinesia. Drooling in parkinsonian patients is dysphagia is expected to be present for more primarily due to swallowing diYculties rather than a few days. Nasogastric tube feeding is than the excessive production of saliva. Anti- usually poorly tolerated and may make the cholinergic drugs should be avoided in these patient irritable or even agitated. Extubation by cases as they aggravate dysphagia by increasing patients is common and the volume of feeds the viscosity of oral secretions. Viscid secre- delivered in this way is usually not adequate. In tions interfere with bolus preparation and pre- one study patients who were fed using a dispose to the formation of a mucous plug. nasogastric tube received 55% of their feeds,

Prescribing of benzodiazepines to dysphagic whereas those fed with a gastrostomy tube had http://pmj.bmj.com/ patients is not desirable and it is sensible that 93% of their prescribed daily intake.16 When anticonvulsants are taken as a single dose at nasogastric tube feeding is prescribed the use bedtime if possible. of fine bore tubes, for example Ryle’s tube, is preferred to large bore ones. However, fine DIETARY MODIFICATION bore tubes are more likely to dislodge, kink, or Maintenance of hydration and nutrition can be block. They also deliver feeds at a relatively achieved safely in most patients with neuro- slow rate.

genic dysphagia with dietary modification. Some patients with neurological disease on September 24, 2021 by guest. Protected copyright. Simple, but eVective, measures include avoid- develop gastrointestinal ileus and in these ance of dry and sticky food and eating food patients enteral nutrition could be established with uniform consistency. The use of starch with the intrajejunal administration of low resi- based fluid thickeners, for example “Thick and due solutions. Duodenal intubation is often Easy” and Vitaquick, is also an important facilitated by an intravenous injection of 20 mg management strategy. Tube feeding is usually of metoclopramide a few minutes before the required in only a minority of patients. procedure. (Metoclpramide increases stomach Patients with neurogenic dysphagia experi- peristalsis and relaxes the pyloric sphincter.) ence more diYculties with fluids than with Prolonged nasogastric tube feeding is not solid food. This is probably due to the diYculty desirable. It often results in numerous compli- in controlling a thin bolus and/or a delay or cations including nasopharyngitis, oesoph- absence of triggering the swallow reflex. The agitis, oesophageal strictures, epistaxis, pneu- rationale for the use of fluid thickeners is that mothorax, and nasopharyngeal oedema with by increasing the viscosity of ingested fluids the associated otitis media. Furthermore, nasogas- resistance to flow of the bolus is increased. In tric tube feeding does not fully protect against addition, the duration of cricopharyngeal aspiration and the association between na- opening and the oropharyngeal transit time are sogastric tube feeding and this complication is increased. However, the optimal viscosity of well documented. Ciocon et al have found that fluids that ensures safe swallowing in patients 43% of dysphagic patients aspirated in the first with neurogenic dysphagia has not been estab- two weeks after nasogastric tube feeding was lished. In practice the required fluid thickness started.17 Elevation of the head of the bed dur- is judged subjectively and recorded using ing and for 1–2 hours after bolus nasogastric

www.postgradmedj.com 698 Bakheit Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from tube gastric and intrajejunal feeding reduces feeding may prevent diarrhoea, nausea, and the risk of aspiration in these patients. vomiting). Feeding via a gastrostomy tube should be considered when dysphagia is likely to be pro- SWALLOWING THERAPY gressive or to persist for long periods. For A range of remedial therapies and training in example, most clinicians would consider gas- the use of compensatory strategies may be trostomy tube feeding in stroke patients if there helpful in the treatment of neurogenic dys- are no signs of recovery of swallowing after the phagia. These include exercises to strengthen first week. However, there are no conclusive the orofacial musculature, manoeuvres to data to support this at present, but the results improve poor laryngeal elevation and laryngeal of a large ongoing multicentre study are eagerly closure during swallowing, and techniques to 18 awaited. In patients with motor neurone stimulate the swallow reflex. These methods disease the option of percutaneous endoscopic are usually used before starting direct swallow- gastrostomy (PEG) tube feeding should be ing practice. oVered early after the onset of dysphagia to Exercises to enhance the function of the oro- supplement the oral intake and help maintain facial muscles are used to improve lip seal, the muscle mass. Insertion of the feeding tube mastication, and tongue movements. A simple through a PEG, rather than a surgical gastros- technique known as “the supraglottic swallow” tomy, is a relatively simple, safe, and cost eVec- may improve the elevation and closure of the tive technique. PEG tube feeding is eVective larynx during swallowing. During this manoeu- and is usually acceptable to patients and their vre the subject holds his/her breath and carers. Transient, self limiting abdominal pain swallow and they release the air by coughing. and diarrhoea may occur in the early postop- Patients with delayed or absent swallow reflex erative period. Long term complications in- often benefit from thermal stimulation of the clude tube obstruction and wound infection. oropharyngeal receptors. The procedure has In some patients who are fed via a PEG tube been claimed to improve triggering of the swal- pulmonary aspiration may occur and routine lowing action and to reduce the bolus transit intrajejunal feeding has been suggested for time. It involves the repeated application of a these cases. However, technically it is easier to small laryngeal mirror dipped in ice to the insert a gastric rather than an intrajejunal feed- anterior faucial arch. Sensitisation may be ing tube. An additional advantage is that bolus repeated between swallows. Direct swallowing gastric tube feeding is more physiological, par- therapy can be started with small amounts of ticularly with respect to insulin secretion. Fur- food (of the right consistency) under the thermore, because the feeds can be given inter- supervision of a speech and language therapist mittently it allows greater patient freedom when the risk of pulmonary aspiration is (intrajejunal feeding should be given continu- deemed to be low. ously rather than intermittently). Direct intra- jejunal delivery of nutrients should probably be SURGICAL TREATMENT OF NEUROGENIC reserved for patients with gastro-oesophageal

DYSPHAGIA http://pmj.bmj.com/ reflux, hiatus hernia, or recurrent aspiration on Cricopharyngeal myotomy has been shown to gastrostomy feeding. be an eVective method of treatment of Entral feeding can be started a few hours dysphagia in a number of neurological disor- after the insertion of the PEG tube. The ders including stroke, muscular dystrophy, and volume of feed is usually restricted in the first a significant proportion of patients with motor 24 hours to one litre and is given at a rate of 50 neurone disease. However, the careful selection ml/hour. The volume of feed and the rate of its of patients for this procedure is essential and

administration are then gradually increased two conditions must be satisfied. First, failure on September 24, 2021 by guest. Protected copyright. over the following 3–4 days until the patient’s of relaxation of the pharyngeal sphincter must daily nutritional requirements are met. Some be demonstrated on videofluoroscopy. Sec- clinicians prescribe “starter feeding regimens” ondly, the oral phase of swallowing, that is lip in the first postoperative week. These are feeds seal, voluntary initiation of swallowing, and the diluted with sterile water. The concentration propulsive action of the tongue must also be and osmolality are gradually increased over preserved. Poor tongue movements (demon- several days to full strength feeds. Starter regi- strated on videofluoroscopy by the inability to mens with clear water or diluted enteral propel or retrieve the food bolus) is a contrain- solutions are thought to improve tolerance to dication to cricopharyngeal myotomy. Patients feeds and reduce diarrhoea, but this has not with absent pharyngeal peristalsis or delayed been confirmed. In fact, a randomised control- triggering of the swallow reflex by 10 seconds led study demonstrated the poor relationship or more are also unlikely to benefit from this between osmolality of the feeds and the occur- treatment. Surgery for cricopharyngeal dys- rence of diarrhoea in these patients.19 Further- function after stroke and more, patients who were randomised to the should be considered after the first three starter regimen group received 20% less nutri- months of the disease onset. ents in the first seven days than the control Relaxation of the cricopharyngeus can also subjects. Diarrhoea in patients on enteral feed- be achieved with “chemical cricopharyngeal ing is usually due to treatment with antibiotics myotomy” using botulinum toxin type A injec- for coincidental infections, bacterial contami- tions.20 The location of the cricopharyngeal nation of the feed and bolus feeding (the use of muscle is determined with direct oesophagos- enteral feeding pumps to control the rate of copy and electromyography (using a hooked

www.postgradmedj.com Neurogenic dysphagia 699 Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from wire electrode) and the toxin is injected trans- 6 Riski JE, Horner J, Nashold BS. Swallowing function in patients with spasmodic torticollis. 1990,40: cutaneously into the dorsomedial part and into 1443–5. the ventrolateral party of the muscle on both 7 Wyllie E, Wyllie R, Cruse RP, et al. The mechanism of nitrazepam-induced drooling and aspiration. N Engl J Med sides. A total dose of botulinum toxin type A of 1986,;14:35–8. 80–120 units is usually suYcient and the mean 8 Hockman CH, Bieger D. Inhibitory eVect of diazepam on beneficial eVect of treatment is five months. reflexly-induced deglutition. Proceedings of the Canadian Federation of Biological Sciences 1979;2:85. The procedure usually requires a light general 9 Nathadwarawala KM, Nicklin J, Wiles CM. A timed test of anaesthetic. swallowing capacity for neurological patients. J Neurol Neu- rosurg Psychiatry 1992;55:822–5. 10 Collins MJ, Bakheit AMO. Does pulse oximetry reliably Summary detect aspiration in dysphagic stroke patients? Stroke 1997; 28:1773–5. Dysphagia is a common impairment in patients 11 Horner J, Massey W.Silent aspiration following stroke. Neu- with neurological disease and may be caused rology 1988;38:317–19. 12 Ekberg O. Posture of the head and pharyngeal swallowing. by lesions at any level of the neuroaxis. Acta Radiol 1986;27:691–6. Frequently the swallowing diYculties are 13 Drake W, O’Donoghue S, Bartram C, et al. Eating in side lying facilitates rehabilitation in neurogenic dysphagia. aggravated by sedatives and other drugs. The Brain Inj 1997;11:137–42. management, as well as the clinical outcome of 14 Goulding R, Bakheit AMO. Evaluation of the benefits of dysphagia depend on the underlying pathology. monitoring fluid thickness in the dietary management of dysphagic stroke patients. Clin Rehabil 2000;14:119–24. In stroke, for example, most patients recover in 15 Park RHR, Allison MC, Lang J, et al. Randomised compari- the first month and only a small minority will son of percutaneous endoscopic gastrostomy and nasogas- tric tube feeding in patients with persisting neurological require long term nutrition and hydration dysphagia. BMJ 1993;304:1406–9. through a PEG feeding tube. 16 Wilson PS, Johnson AP, Bruce-Lockhart FJ. Videofluoros- copy in motor neurone disease prior to cricopharyngeal myotomy. Ann R Coll Surg Engl 1990;72:375–7. 1 Kidd D, Lawson J, Nesbitt R, et al. Aspiration in acute 17 Ciocon JO, Silverstone FA, Graver LM, et al. Tube feeding stroke: a clinical study with videofluoroscopy. QJMed in elderly patients. Indications, benefits and complications. 1993;86:825–9. Arch Intern Med 1988;148:429–33. 2 Celifarco A, Gerard G, Faegenburg D, et al. Dysphagia as 18 The FOOD trial (Feed Or Ordinary Diet)—a multicentre the sole manifestation of bilateral . Am J Gastroenterol trial to evaluate various feeding policies in patients admitted 1990;85:610–13. to hospital with a recent stroke. National Research Register 3 Buchholz DW. Clinically probable brain stem stroke 2001, issue 2. presenting as dysphagia and nonvisualised by MRI. 19 Keohane PP, Attrill H, Love M, et al. Relation between Dysphagia 1993;8:235–8. osmolality of diet and gastrointestinal side eVects in entral 4 Smithard DG, O’Neill PA, Martin DF, et al. The natural nutrition. BMJ 1984;288:678–80. history of dysphagia following stroke. Dysphagia 1997;12: 20 Schneider I, Thumfart WF, Potoschnig C, et al. Treatment 188–93. of dysfunction of the cricopharyngeal muscle with botuli- 5 Coates C, Bakheit AMO. Dysphagia in Parkinson’s disease. num A toxin: introduction of a new non-invasive method. Eur Neurol 1997;38:49–52. Ann Otol Rhinol Laryngol 1994;103:31–5. http://pmj.bmj.com/ on September 24, 2021 by guest. Protected copyright.

www.postgradmedj.com