Postgrad Med J (1994) 70, 581 - 583 i) The Fellowship of Postgraduate Medicine, 1994

Severe dysphagia associated with major tranquillizertreatment

T.A.T. Hughes, G. Shone' G. Lindsay2 and C.M. Wiles

Department ofNeurology and 'Department ofEar Nose and Throat Surgery, University Hospital of Wales,Heath Park, CardiffCF4 4XW, and 2General Practitioner, 350 Cyncoed Road, Cardif, UK

Summary: A 56 year old patient with psychiatric complications of systemic lupus erythematosusdeveloped severe dysphagia complicated by weight loss and aspiration. Following investigation it wasconcluded that the addition of haloperidol to her treatment was the major precipitating cause andwithdrawal of the drug was followed by an objective improvement in swallowing. Patients taking majortransquillizers may be at increased risk ofsevere dysphagia; regular observation ofswallowing is suggestedas a useful addition to the clinical examination of these patients.

Introduction

Dysphagia is a recognized complication ofidiopathic Parkinson's disease but it is not widelyappreciated that significant dysphagia may alsooccur in drug-induced parkinsonism and in othersyndromes associated with major tranquillizers.

Case report

In 1976 a 41 year old woman presented with discoidlupus confirmed on skin biopsy and was treatedsuccessfully with topical steroids. In 1984 shepresented with agitated depression with somepsychotic features and required admission to hos-pital. She improved with flupenthixol 20 mg every 2weeks. In December 1990 she presented withweight loss, malaise and myalgia. Investigationsincluded haemoglobin (Hb) 7.1 g/l, platelets132 x 109/l, white blood cell count 2.4 x 109/l, ESR78 mm in one hour, anti-nuclear factor (ANF) of1/320, antibody to double-stranded DNA (anti-DNA) of 1/320 and subnormal levels of comple-ment C3 and C4. A diagnosis of systemic lupuserythematosus (SLE) was made and she respondedwell to prednisolone and azathioprine. InDecember 1991 she became hyperactive withimpaired memory and judgement, and requiredhospital admission for worsening agitation andparanoia. There was no evidence ofactive SLE andher symptoms were eventually controlled withmedication; drugs prescribed on discharge inMarch 1992 were flupenthixol 20 mg every 2 weeks,procyclidine 5 mg three times a day, haloperidol

Correspondence: T.A.T. Hughes, M.R.C.P.Accepted: 10 January 1994

1.5 mg and diazepam 10 mg four times a day,prednisolone 15 mg daily and azathioprine 25 mgthree times a day.

In June 1992, whilst still on the medication listedabove, she presented with an 8 week history ofworsening, intermittent, painless dysphagia forsolids and liquids with accompanying weight lossof 10 kg. She had no other specific complaints.There was no other past medical history of note.She was a retired schoolteacher, married with twochildren and had no family history of neurologicalor psychiatric disease.On admission she weighed 33 kg, was clearly

malnourished but walked unaided. She hadmarked postural hypotension and inspiratorycrackles were audible at the left lung base;abdominal examination was normal. She wasagitated and restless. Cranial nerve examinationrevealed a lack of facial expression, but palatal andpharyngeal sensation and reflexes were normal andtongue movements were normal. She had a quiethoarse voice with a persistent productive coughand on attempting to drink water she coughedviolently during and after the first mouthful andwas unable to proceed. She had cogwheel rigidityand some bradykinesia in the limbs but no otherneurological signs.

Investigations revealed a normochromic normo-cytic anaemia with Hb 10.7 g/l, ESR 70 mm/hour,C-reactive protein (CRP) 116 mg/I (normal range1-4), normal complement levels, normal chestX-ray, negative ANF and a negative anti-DNA. Acomputerized tomographic scan of the brain andcerebrospinal fluid examination were normal.Indirect laryngoscopy showed chronic inflam-mation of the larynx, pooling of secretions andsaliva in the pyriform fossae but normal move-

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582 CLINICAL REPORTS

ments ofthe vocal cords. Videofluoroscopy showedcomplete failure of laryngeal elevation and closure,and failure of cricopharyngeal opening. Pooling

occurred in the pyriform fossae and above thecricopharyngeus, and there was aspiration of con-trast into the larynx and trachea (Figure 1).

Figure I Videofluoroscopy image showing gross pooling in the pyriform fossae (straight arrow), failure ofopening ofthe cricopharyngeus and tracheal aspiration (curved arrow).

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Figure 2 Repeat videofluoroscopy showing the bolus passing freely from pharynx to oesophagus without pooling ortracheal aspiration.

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CLINICAL REPORTS 583

In the absence of a structural lesion or ofevidence of active SLE causing her dysphagia, herneuroleptic medication was suspected, particularlyin view of her definite but mild extrapyramidalsigns. Her case was discussed with her psychiatristand over the next 8 days the haloperidol wasstopped and the procyclidine and diazepam eachreduced to 5 mg twice a day; the dosages of otherdrugs were not changed. Since she had clinical andradiographic evidence of aspiration, oral feedingwas stopped and a nasogastric tube used. Twoweeks later she was able to swallow clear fluids. Thespeech therapist and dietician then gradually intro-duced suitable textures of food and after 6 weeksthe patient was taking a normal diet withoutdifficulty. On discharge repeat videofluoroscopyshowed normal elevation of the larynx and normalopening of the cricopharyngeus without pooling oraspiration (Figure 2); ESR and CRP were normaland her weight had increased to 41.4 kgs. Despitethe withdrawal of haloperidol there was animprovement in her psychiatric symptoms duringthis period.

Discussion

In this case a patient with SLE already on long-term flupenthixol treatment developed severe dys-phagia following the addition of haloperidol, pro-cyclidine and diazepam to her treatment. Follow-ing withdrawal of the haloperidol and a reductionin the dosage of diazepam and procyclidine theswallowing problem gradually resolved suggestingthat it was the addition of haloperidol to theexisting treatment that was mainly responsible forthe dysphagia.The mild signs of parkinsonism, the absence of

any lower cranial nerve signs and the videofluoro-scopy findings ofcomplete failure ofvoluntary andreflex swallowing suggests that the drugs producedan akinesia or bradykinesia of the swallowingprocess; the term 'bradykinetic dysphagia' has beenused by other authors to describe this type ofproblem.' There was no good evidence of a dys-tonia of the larynx or pharynx or of tardivedyskinesia, both of which cause swallowing prob-lems and have been associated with drugs of themajor tranquillizer group.2'3 The evidence for SLE

being active during the illness was poor; the initiallyabnormal ESR was probably the result of lunginfection secondary to aspiration as it returned tonormal with management of the dysphagia alone.The small reduction in the dose ofprocyclidine mayhave contributed to the improvement seen butrecovery occurred despite continuation of the drugat a dose of 10 mg/day.An assessment of swallowing is not routinely

included in the clinical examination ofpatients whoare on large doses of major tranquillizers despitereports suggesting an association between thesedrugs and unexplained fatal choking episodes inpsychiatric in-patients.4 Some authors have sug-gested that the gag reflex should be regularlyobserved in patients on neuroleptic drugs thoughtto be at risk of developing a swallowing problem.'If closely observed the gag reflex may give usefulinformation about the sensory and motor innerva-tion of the palate and the posterior pharyngealwall, but it does not provide information aboutswallowing; as in this case a patient may havesevere dysphagia and exhibit all the components ofa normal gag reflex. For this reason observation ofthe patient actually swallowing is an essential partof the bedside examination; obvious caution andslowing of drinking, coughing during swallowing,an alteration in voice quality post swallow ordifficulty in initiating a swallow when the bolus isheld in the mouth are easily detected warning signsof impaired swallowing. Conversely, if recurrentchest infections, cough or unexplained weight lossraise the possibility of aspiration in this group ofpatients, a detailed clinical evaluation supported byvideofluoroscopy should be carried out.The case demonstrates the dramatic effect

neuroleptic medication may have on swallowing.Dysphagia may be associated with a significantmorbidity and mortality in patients on neurolepticdrugs, and a high level of clinical awareness andregular observation of the patient swallowing mayhelp to improve detection of this problem.

Acknowledgement

We are grateful to Dr Dafydd Huws and Dr RichardMoore for permission to report details of a patient undertheir care, and to Dr Brian Lawrie for thevideofluoroscopy images.

References

1. Bazemore, P.H., Tonkonogy, J. & Ananth, R. Dysphagia inpsychiatric patients: clinical and videofluoroscopic study.Dysphagia 1991, 6: 2-5.

2. Newton-John, H. Acute upper airway obstruction due tosupraglottic dystonia induced by a neuroleptic. Br MedJ 1988,297: 964-965.

3. Massengill, R. & Nashold, B. A swallowing disorder denotedin tardive dyskinesia patients. Acta Oto-laryngol 1969, 68:457-458.

4. Craig, T.J. Medication use and deaths attributed to asphyxiaamong psychiatric patients. Am J Psychiat 1980, 137:1366-1373.

5. Craig, T.J. & Richardson, M.A. Swallowing, tardive dys-kinesia, and anticholinergics. Am J Psychiat 1982, 138: 1083.

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