Mohammed T. Abou-Saleh

530 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRYSchizophreniaThe schizophrenic illness itself may be a risk factor 59,61 . Longbefore the advent of antipsychotic drugs, a variety of motordisorders were described in psychiatric patients, particularly thosewith catatonic schizophrenia 72–74 and other types of schizophrenia75–77 . These movements would seem to be principallydisturbances of voluntary motor activity and may be classifiedas stereotypes and mannerisms, preservative movements, tics,grimaces and general clumsiness, awkwardness and lack ofcoordination. However, Kraepelin 78 , and then later Farran-Ridge 75 , observed spasmodic movements, mainly involving theorofacial muscles, which they considered choreiform in nature.Nevertheless, Marsden et al. 79 concluded that true chorea andathetosis were scarce in chronic psychiatric patients before drugtreatment, and that much of the motor disorder seen wasattributable to organic neurological disorder, such as encephalitisand syphilis. Further, the terminology used is confused, reflectingvarious conceptual notions of the aetiology of the motorphenomena observed 80,81 . Kleist 73 and Farran-Ridge 75 commentedthat the similarity between the manifestations of dementiapraecox and epidemic encephalitis was such that difficulties indifferential diagnosis could arise. However, there is no doubt thatsome of the movements described would be scored on currentrating scales for tardive dyskinesia if seen now in patientsreceiving antipsychotic drugs.There would seem to be three possible interpretations of theseobservations 59 . First, the type of motor disturbance historicallydescribed is not specifically associated with schizophrenia, butrather the product of organic brain disease. The two conditionsalso occur together when the brain disease is also responsible forsymptomatic schizophrenia, as, for example, when schizophreniaappears in patients with encephalitis, Wilson’s disease orHuntington’s disease, among other conditions 82 . Second, theassociation of motor disturbance and schizophrenia may be morespecific, in that an underlying neuropathological process iscapable of producing both psychological and motor impairments.Third, as Kraepelin and Bleuler tended to suggest, the movementsmay be secondary to the schizophrenic disturbance of will,thought and emotion. However, the distinctions between the threeexplanations cannot be too sharply drawn, and more than onemay be relevant.In a relevant contemporary study, Owens et al. 83 comparedchronic schizophrenia inpatients with and without a history ofantipsychotic drug treatment, and found a similar prevalence ofabnormal involuntary movements in the two groups. This findingconfirmed the occurrence of spontaneous movement disorder inschizophrenia. However, the contribution of drug therapy wasacknowledged, in that when the age difference between the twopatient samples was taken into account in further analysis of thedata, there was a significant linear relationship between theprevalence of abnormal involuntary movements and exposure toantipsychotic drugs 84 . Grouping movements into clinically recognizablesyndromes revealed a particular susceptibility to orofacialdyskinesia in the drug-treated patients. Nevertheless, the schizophrenicillness, at least in some forms, may be seen as apsychomotor disorder with an inherent, increased risk ofdyskinesia. Antipsychotic drug treatment may interact with thedisease process and age-related cerebral deterioration to hasten orprovoke the appearance of such movement disorder 59,85 .DementiaAccepting that organicity is a risk factor for tardive dyskinesia, itmight be expected that the neurodegenerative changes ofAlzheimer’s disease would be associated with a relatively highrisk of spontaneous dyskinesia and also a greater risk of tardivedyskinesia when antipsychotic drugs are administered. Molsaet al. 86 assessed abnormal involuntary movements in 177 patientswith Alzheimer’s disease, with a mean age of 75 years. In the 143patients who had never received antipsychotic drugs, theprevalence of dyskinesia was 17%, while for the 34 patientstreated with antipsychotic drugs the figure was 53%. As part of alarger study, Ramsay and Milard 53 looked at 40 patients on longstaypsychogeriatric wards. Of the 13 (32.5%) patients withdyskinesia, 12 had a history of treatment with antipsychoticdrugs. These findings suggest a vulnerability to tardive dyskinesiain dementia patients receiving antipsychotic drugs.O’Keane and Dinan 54 assessed 78 patients with an age range of65–91 years, all of whom fulfilled DSM-III criteria for seniledementia of the Alzheimer type. The scales used included theMini-Mental State (MMS) 87 and Abnormal Involuntary MovementsScale (AIMS) 88 . They reported that 62 patients (69%) hadevidence of orofacial dyskinesia, a figure the authors noted to beover 10 times that reported in healthy elderly adults, and alsoconsiderably higher than the prevalence found in populations ofpatients with chronic schizophrenia. Orofacial dyskinesia was byfar the most common abnormal movement rated. The mean dosesof antipsychotic drug for those with and without abnormalmovements were modest, and although the former group wasreceiving a higher mean dosage, the differences between the twogroups was not statistically significant.Molsa et al. 86 found that the severity of orofacial dyskinesia intheir sample of patients with Alzheimer’s disease increased withthe degree of cognitive deficit. Bakchine et al. 89 studied a group of91 patients with dementia of the Alzheimer type and examined therelationships between primitive reflexes, extrapyramidal symptomsand severity of cognitive impairment. They failed to find anysignificant relationship between ‘‘buccolinguofacial dyskinesias’’and a low score on intellectual functioning, but their methodologywas criticized by O’Keane and Dinan 54 , who pointed out that theyonly rated abnormal movement as either present or absent, ratherthan qualifying the movements using a standardized scale. In theirown study O’Keane and Dinan found that there were nosignificant differences in terms of age or length of illness betweenthose patients with and without abnormal movements, and bothgroups showed evidence of severe intellectual impairment.However, those patients with abnormal movements had asignificantly greater degree of cognitive impairment, as judgedon mean MMS scores. On the basis of this finding, O’Keane andDinan suggested that orofacial dyskinesia might prove to be auseful indicator of the severity of intellectual decline in patientswith Alzheimer’s disease.Acute Extrapyramidal Side Effects:Parkinsonism and AkathisiaSusceptibility to acute drug-induced extrapyramidal side effects asa predictor of tardive dyskinesia was first suggested by Crane in1972 90 . He considered that tardive dyskinesia was more likely toemerge in patients who had developed parkinsonism as an acuteside effect of antipsychotic drug treatment than in those who hadnot.Based on clinical observation, Chouinard et al. 91 suggested thatpatients with tremor or akathisia, which they described as‘‘hyperkinetic’’ symptoms of parkinsonism, were more likely tomanifest tardive dyskinesia than patients with ‘‘hypokinetic’’symptoms, such as bradykinesia and rigidity. De Veaugh-Geisset al. 92 elaborated on this idea, suggesting that in some casesakathisia represented a stage in a progression from parkinsonismto the development of orofacial and trunk and limb dyskinesia.Consistent with this notion, Barnes and Braude 93 reported two