© Priory Lodge Education Limited, 1996.
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1. Side effects of anticholinergic drugs

Anticholinergic drugs have side effects of their own which has been suggested as a valid reason for not using anticholinergic drugs by several authors. Several studies on the use of anticholinergic drugs in neuroleptic-induced EPS suggest that the incidence of anticholinergic side effects is actually low (Grove & Crammer, 1972; Goldstein et al, 1964; Winslow et al, 1986). However, there are other reports which suggest that in some patients at least, these side effects are reasons to avoid these agents (DiMascio & Demirgian, 1970). Several central and peripheral anticholinergic side effects are recognised which can be distressing and can affect compliance (Kazamatsuri et al, 1972; Johnson, 1972; Gerlach et al, 1974). The mnemonic for the effects of parasympathetic blockade is a useful reminder of anticholinergic side effects "-- hot as a hare, blind as a bat, dry as a bone, red as a beet and mad as a hen". All anticholinergic drugs can produce dry mouth, blurred vision, hot, dry skin and hyperpyrexia. In addition, all centrally acting anticholinergic drugs cause changes in behaviour and cognition.

Psychiatric effects are of particular concern and range from mild impairment of recent memory to acute confusional states (Quinn, 1984; Molloy & Brooymans, 1989). The risk of these side effects increases with age, dose, and the presence of pre-existing mental impairment. Changes in awareness and cerebration are also known. In elderly patients impairment in learning and memory storage of new material has been observed (Potaminos & Kellett, 1982). Anticholinergic drugs can cause inattention, slowness of thought processes, aggression and paranoid behaviour or ideas, visual and less commonly tactile hallucinations or changes in mood and restlessness (Parkes, 1981).

Approximately 19-30% of patients with parkinsonism given anticholinergics may develop anxiety, excitement, restlessness, depression, confusion, delusions or hallucinations (Editorial, 1974). Such effects may be precipitated by concomitant administration of other drugs with anticholinergic properties such as antihistamines, phenothiazines, tricyclics or other antiparkinsonian drugs or by intercurrent infection. Anticholinergic drugs by their central action may cause vagal stimulation which may result in decreased heart rate. It may also cause peripheral vagal depression which normally results in slight increase in heart rate (Parkes, 1981).

Treatment with anticholinergic drugs results in decreased production of sweat, bronchial, lacrimal, nasal, gastric and intestinal secretion. It also results in decreased gut motility and inhibition of micturition and urinary retention. Anticholinergic drugs have also been reported to cause eczema (Cant, 1969), retrosternal pains due to increased oesophageal reflux (Piper & Heap, 1972) and cardiac infarction (Scherf, 1973).

With anticholinergic medication dry mouth (xerostomia, hyposialorrhoea) results because of decreased salivation. This may be a useful side effect in some patients as it may decrease sialorrhoea induced by neuroleptics, however, it may be a bitter complaint and extreme dryness of mouth can result in parotiditis and almost total loss of teeth (Winer & Bahn, 1967). Saliva protects the epithelium of the mouth from drying and acts as a mechanical cleansing solution. It facilitates speech and antagonises the abrasive action of food by adding lubrication. Saliva is thought to produce a medium in which the apatite crystals of tooth enamel can acquire ions such as calcium and phosphates that make teeth more resistant to decay (Mason & Chrisholm, 1975). The main secretomotor action of saliva is by parasympathetic outflow and all drugs with anticholinergic action cause substantial decrease in salivation.

Anticholinergic drugs used alone may give rise to abnormal movements usually buccolingual-masticatory, particularly in elderly females (Fahn & David, 1972) and occasionally, though less commonly, cause involuntary movements of the limbs (Birket-Smith, 1974).

Severe toxicity following ingestion of anticholinergic drug has been documented (Stephens, 1967). Confusional states and delirium are reported when toxicity develops, however, elderly patients with cerebrovascular diseases are particularly likely to develop confusional states even on therapeutic doses. Clinical signs of anticholinergic overdose or toxicity include a flushed excited patient with dry skin, fever, confusion, pupillary dilatation, tachycardia, arrhythmias and rapid breathing. Toxic doses of anticholinergic drugs result in widely dilated pupils, flushed dry skin, fever, increased intraocular pressure, tachycardia, palpitations, arrhythmias, urinary retention and constipation. Rapid respiration may also result from peripheral cholinergic blockade. Difficulty in focussing is due to mydriatic and cycloplegic effects. Atropine causes long lasting ocular effects which may last for days but most anticholinergic drugs cause less prolonged ocular effects than atropine. Photopsia may occur and very rarely loss of vision may result by precipitation of angle closure glaucoma (Friedman and Newman, 1972). Cognitive impairment following acute intoxication is generally reversible although it has been reported to persist in some (Crawshaw & Mullen, 1984).