Neuroleptic-Induced Dysphagia

Lisa Guttman Sokoloff, BSc (C.D.), MS1 and Rosemarie Pavlakovic, BSc, Phm2

Services of1Speech Pathology, Rehabilitation Institute of Toronto (formerly The Queen Elizabeth Hospital), Toronto, Ontario, Canada and2Pharmacy, Sunnybrook Health Science Centre, University of Toronto, North York, Ontario, Canada

Abstract. Neuroleptic medications may result in extra-pyramidal symptoms that can affect swallowing. Bothoral and pharyngeal phases of swallowing may be af-fected. Unlike the more common causes of dysphagia,especially in the elderly, drug-induced dysphagia may bereversible. This report describes a case of neuroleptic-induced dysphagia in an elderly male with Alzheimer’sdisease. When the loxapine was discontinued, the dys-phagia improved significantly.

Key words: Neuroleptic — Extrapyramidal — Loxa-pine — Parkinsonism — Dysphagia — Deglutition —Deglutition disorders.

Dysphagia in the elderly is usually due to neurologicaldisease or structural changes in the oro-pharynx [1].Medications such as neuroleptics are an uncommoncause of dysphagia but important to recognize becausethe effect may be reversible (Table 1) [2,3]. This reportdocuments a case of neuroleptic-induced dysphagia in anelderly gentleman.

Neuroleptics, sometimes referred to as antipsy-chotics or major tranquilizers, are used for the treatmentof psychoses such as schizophrenia. In the elderly de-mented population, neuroleptics are commonly used forcontrol of aggressive or disruptive behavior [4]. Thisclass of medication is divided into subgroups based onpotency and adverse effect profiles. All agents are con-sidered to be equally effective in comparable doses, sothe choice of neuroleptic is often based on adverse ef-fects. The most common include cardiovascular (e.g.,orthostatic hypotension), anticholinergic (e.g., dry

mouth, blurred vision), sedation, and extrapyramidalsigns (i.e., parkinsonism, akathisia, or dystonia). Lowpotency neuroleptics, such as chlorpromazine or thiorid-azine, are associated with a low incidence of extrapy-ramidal side effects, but frequently cause sedation, or-thostatic hypotension, and dry mouth whereas high po-tency agents, such as haloperidol, are more likely tocause extrapyramidal side effects, and less likely to causeanticholinergic effects. Moderate potency agents such asloxapine are thought to have an intermediate potential forall effects [5–7].

The mechanism of action of neuroleptics in-volves blocking of dopamine receptors in the basal gan-glia. Neuroleptic-induced parkinsonism occurs in 12%–45% of patients and is more common in the elderly [8].Drug-induced parkinsonism, like idiopathic Parkinson’sdisease, may present as tremor at rest, rigidity of limbsand trunk, bradykinesia, masked face, and a lack of au-tomatic body movements. Drug-induced parkinsonismcan occur within days to weeks of instituting drugtherapy and resolves when the medication is discontin-ued but may take several months [8].

Drug-induced parkinsonism may have seriousimplications for swallowing [2]. Up to 50% of patientswith Parkinson’s disease may have some degree of dys-phagia [9,10] with abnormalities in both the oral andpharyngeal phases. Robbins et al, [11] have suggestedthat rigidity and bradykinesia may be responsible forimpairment in the oral phase of swallowing and aspira-tion. The severity of dysphagia does not necessarily cor-relate with the overall severity of the Parkinson’s disease[12].

Oral phase impairments in Parkinson’s diseaseinclude defective tongue movements [13], repetitivetongue pumping [11], tongue tremor with reduced initia-tion of lingual movement, and slowed oral transit time[14]. Pharyngeal phase abnormalities include delayedinitiation of the swallow, irregular epiglottic movement,

This study was completed at Sunnybrook Health Science Centre, Uni-versity of Toronto, North York, Ontario, CanadaCorrespondence to:Lisa Guttman Sokoloff, Speech Pathology, Reha-bilitation Institute of Toronto, 550 University Avenue, Toronto, On-tario, Canada, M5G 2A2

Dysphagia 12:177–179 (1997)

© Springer-Verlag New York Inc. 1997

vallecular and pyriform fossae stasis [15], silent aspira-tion [11,16], misdirected swallowing, abnormal pharyn-geal motility [17], delayed swallow reflexes, slowed pha-ryngeal transit time, inadequate laryngeal closure, andcricopharyngeal dysfunction [14].

Case Report

A 79-year-old man with Alzheimer’s disease was admitted for long-term care in January, 1994. Other relevant medical history includedhypertension. A computed tomography (CT) scan on December 11,1984 was normal except for mild atrophy. A follow-up CT on Novem-ber 13, 1986 was unchanged. Magnetic resonance imaging (MRI) scanon February 8, 1991 revealed moderate cerebral atrophy. A singlephoton emission computed tomography (SPECT) scan on March 15,1991 indicated decreased perfusion to the posterior parietal lobes bi-laterally, suggestive of Alzheimer’s disease. A repeat SPECT scan inJune 1993 was unchanged.

Prior to admission, aggressive behavior necessitated haloperi-dol and thioridazine. His wife gave him either one 0.5 mg tablet ofhaloperidol or two 10 mg tablets of thioridazine as needed, requiring onaverage, two to three doses per week.

On admission, haloperidol and thioridazine were not effectivefor controlling his aggressive episodes. As an alternative, the admittingphysician ordered loxapine 5 mg three times daily as needed, orally orintramuscularly. The patient required an increasing number of ‘‘asneeded’’ doses of loxapine to control aggressive behavior and there-fore, on March 3, 1994, loxapine 5 mg daily was prescribed on aregular basis. Over the course of a week the dose was increased gradu-ally to 5 mg two times daily. Approximately 1 week later, the patient’sprimary nurse observed ‘‘choking on medication’’ and requested liquiddosage forms. The patient’s wife confirmed that this choking had notbeen present at home. Nursing notes reported that his chest soundedcongested. In light of the recent choking episodes, a speech-languagepathologist was consulted.

Initial Swallowing Evaluation

An initial evaluation indicated difficulty with both thin and thick liq-uids. While drinking, the patient consistently presented with a wetsounding vocal quality, and aspiration was suspected. Chewing wasmildly impaired, however, his dentures were loose which may havecontributed to this impairment. Minced food textures were suggested tocompensate for his chewing difficulties. Liquids were removed becauseof the wet vocal quality, congestion, and suspected aspiration, andmedications were changed back to tablet form.

On March 16, a modified barium swallow following the vid-eofluoroscopy procedure described by Logemann [18] was performed.Only lateral views were taken, with the patient seated upright. Thefollowing textures were presented: thin liquid, semi-thick liquid, thickliquid, puree, minced, minced in a sandwich, and chopped. All textureswere mixed with barium powder to allow for contrast.

The videofluoroscopic evaluation indicated moderate to severeoral-pharyngeal dysphagia characterized by reduced chewing ability,tongue pumping, defective tongue movements, and reduced base oftongue movement (most likely due to tongue rigidity), all resulting inreduced oral control. Pharyngeal phase difficulties included a delay ininitiating a swallow, pooling of residue in the valleculae (due to re-duced base of tongue movement) and pyriform sinuses (due to reducedlaryngeal movement) after the swallow for all food and liquid textures,penetration of this pooled residue, and significant silent aspiration of

thin fluids. Minced and chopped textures could not be assessed as thepatient stated that they were ‘‘too difficult’’ and he removed them fromhis mouth.

Following this evaluation, management recommendations in-cluded continuation of a fluid-free diet, change to pureed food, admin-istration of medications in tablet form crushed with mixed with apple-sauce, and supervision while eating. Over the next 10 days the patientrefused to eat or drink and required intravenous hydration. On March28, loxapine was discontinued and chlorpromazine was given in a doseof 10 mg every 8 hours; this medication was selected because it wasless likely to result in extrapyramidal side effects [7]. A second clinicalevaluation 1 week later indicated an improvement in swallowing withno significant signs of oral or pharyngeal dysphagia.

A second videofluoroscopic evaluation on April 14, 1994 indi-cated improvement in both the oral and pharyngeal phases. Changes inthe oral phase included adequate base of tongue movement (reducedrigidity), no tongue pumping or incoordination, and an ability to takeall textures and not remove any from his mouth. Pharyngeal phasechanges included significantly reduced pooling for all textures, no velarpumping, or aspiration. Chewing abilty remained mildly impaired ashis denture repairs had not yet been completed. Recommendations atthis time included upgrading his meal plans to minced textures withspecific chopped items and thin and thick fluids.

Currently, the patient’s aggressive behavior is well controlledon 40 mg/day of chloropromazine in three divided doses (i.e., 20 mg inthe morning and 10 mg in the afternoon and at bedtime). The patient’swife and primary nurse indicate that he is tolerating all foods andliquids. Medications are all taken in tablet form. There have been noreports of coughing or choking at meals and no pneumonia, chestcongestion, or infections.

Table 1. Drug-induced dysphagia

Mechanism Drug/drug classification

Xerostomia (dry mouth) AnticholinergicsAntihypertensivesCardiovascular agentsDiureticsOpiatesAntipsychoticsAntiemeticsAntidepressantsMuscle relaxantsAntihistamines

Reduced lower esophageal Theophyllinesphincter pressure (promoting Nitratesgastroesophageal reflux) Calcium antagonists

AnticholinergicsDiazepamMorphine

Esophageal injury AntibioticsAscorbic acidASA and NSAIDSFerrous sulfatePrednisonePotassium chlorideQuinidineTheophylline

Extrapyramidal effects (compromising Antipsychoticsmuscle function in the oropharynx Metoclopramideand esophagus) Prochlorperazine

178 L.G. Sokoloff and R. Pavlakovic: Neuroleptic-Induced Dysphagia

Discussion

Our patient developed dysphagia while receiving a neu-roleptic with significant potential to cause extrapyrami-dal side effects. By changing this to a neuroleptic lesslikely to cause extrapyramidal effects, his dysphagia alsoresolved. There are few reports of neuroleptic-inducedoropharyngeal dysphagia in the literature. In 1993, Sliwaand Lis [19] reported a patient who presented with dif-ficulty swallowing while receiving haloperidol to controlaggressive behavior secondary to a traumatic brain in-jury. Videofluoroscopy confirmed moderate oropharyn-geal dysphagia which progressed to moderate-severe ona second study 2 weeks later. He developed aspirationpneumonia. The haloperidol was discontinued with noimmediate improvements in swallowing; however, 8weeks later, his dysphagia resolved.

Hughes et al. [20] described a patient who devel-oped severe dysphagia after addition of haloperidolwhile also receving the neuroleptic flupenthixol for psy-chiatric complications of systemic lupus erythematosus(SLE). Swallowing improved 2 weeks after discontinu-ation of haloperidol.

Leopold [21] recently described a case of drug-induced dysphagia in a patient who was receiving theneuroleptic trifluoperazine for depression. The patientpresented with parkinsonism and dysphagia, and bothresolved rapidly after discontinuation of the neuroleptic.

Neuroleptics are commonly used in elderly de-mented patients who are at significant risk for develop-ing parkinsonism. Atypical neuroleptics, such as cloza-pine and risperidone, are less likely to cause extrapy-ramidal syndromes, and therefore may be preferable inthis population. However, these agents may produceother serious adverse effects which require regular moni-toring [22,23].

Although neuroleptic-induced dysphagia is notfrequently reported, it is important to be aware that itdoes occur and may potentially be reversed. Therefore,when dysphagic symptoms occur, the adverse effects ofneuroleptic and other medications should not be over-looked as a potential cause.

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