Mohammed T. Abou-Saleh

AETIOLOGY, GENETICS AND RISK FACTORS 505Table 91.2Selected series of late-onset schizophrenia patients reporting gender ratioReference No. No. of cases Ascertainment method Diagnosis Age (years) Ratio female:male25 57 Hospital admissions Late paraphrenia a 460 5.3:143 47 Hospital admissions Systematized delusion+hallucinations; not demented 465 22.5:144 644 Hospital admissions Late-onset schizophrenia; not organic 440 1.8:145 6064 First admissions ICD-8 schizophrenia 440 1.6:146 320 Hospital admissions Late paraphrenia a 465 6:147 25 Consecutive referrals Late paraphrenia a 460 3.2:148 35 Hospital admissions Persistent delusional state; absence of mood or cognitive Onset 440 10.7:1disorder49 106 First admissions ICD-8 schizophrenia, paranoid state, reactive psychosis, 460 2.2:1other psychoses6 37 Case register Late paraphrenia a (13 cases considered ‘‘organic’’ at460 7:1–3:1 bfollow-up)50 477 Case register ICD-9 schizophrenia and related disorders, paraphrenia, 460 4.4:151 47 Referrals from a numberof psychiatric settingsa Akin to Roth’s 1 criteria.b Dependent on whether ‘‘organic’’ cases included.From ref. 52, with permission.atypical psychosesLate paraphrenia a 465 9:1PREMORBID CHARACTERISTICSIt has been consistently reported that a higher proportion ofpatients with late-onset paranoid psychoses have abnormalpremorbid personality traits, most commonly described as‘‘suspicious’’, ‘‘hostile’’ and ‘‘reclusive’’. Some workers haveconsidered that the occurrence of paranoid psychosis in individualswith such personality traits is an ‘‘understandabletransition’’, while Retterstol 13 has suggested that psychoticbreakdown is a reaction to stress in a ‘‘hypersensitive’’ personality.Post 14 proposed that the paranoid/schizoid personality traitsreflect a long-standing latent schizophrenic disorder that manifestsitself only when additional factors come into effect. Suchfactors might include social deprivation, sensory deprivation(deafness and possibly visual loss, as discussed below), frankcerebral pathology, or even ordinary ageing processes in the brain.Moreover, such personality traits could be expected to result insocial isolation and reclusiveness, which in turn would exacerbatethe paranoid imaginings characteristic of the illness.In contrast to their early-onset counterparts, late-onset schizophreniapatients are generally neither educationally noroccupationally compromised. This again suggests that they mayhave a form of disease that is relatively distinct from the severeearly-onset ‘‘dementia praecox’’ type.SOCIAL ISOLATIONAgeing often results in increasing social isolation. It appears,however, that patients with late-onset schizophrenia have agreater likelihood of being socially isolated than age-matchednormals or affective disorder patients. Low rates of marriage, fewoffspring and paranoid premorbid personality traits could all beexpected to contribute to such isolation. Paranoid ideation in thedisease itself is often directed at neighbours, resulting in furtherreclusiveness. Thus, social isolation in late-life psychosis mightwell be a consequence rather than a cause of the illness.SENSORY DEFICITSA number of general population studies have found an associationbetween paranoid ideation and sensory impairment in theelderly. This perhaps understandable association has also beeninvestigated as potentially causal in late-onset paranoid illnesses.For example, Post 14 reported that 25% of 72 elderly paranoidpsychotic patients had hearing loss, compared with 11% of anaffective disorder group; the mode of audiometric assessment wasnot stated. Cooper et al. 15 found that 25 (46%) of a group of 65elderly paranoid patients were ‘‘socially deaf’’, compared with 12(21%) of 67 patients with affective illness. Audiometry andotological examination of an enlarged sample (27 paranoid and 18affective deaf subjects) revealed that the paranoid group weremore likely to have long-standing conductive hearing loss, asopposed to later-onset sensorineural loss in the affective group.Visual impairment, mostly due to cataracts, was found in 30(56%) of 54 of the paranoid group, and 21 (37%) of 57 of theaffective group.From such data, Kay et al. 16 and Cooper 17 concluded that in theelderly, long-standing conductive deafness is an independent riskfactor for paranoid, as opposed to affective, psychosis. Thisprobably does not apply in earlier-onset schizophrenia patients,neither are persons with profound (prelingual) deafness predisposedto schizophrenia. The association with visual impairment isless robust, possibly because determination of functional visualimpairment is difficult.More recently, however, Prager and Jeste 18 failed to confirm anexcess of constitutional (‘‘uncorrected’’) visual and hearingimpairment in late-onset schizophrenia patients; they did, however,find that such patients were more likely than controls to havesensory deficits that were not adequately ‘‘corrected’’, e.g. byspectacles or hearing aids. Thus, these data are complex andinterpretation of causality problematic. Furthermore, there is noconsistent association between particular modalities of sensoryloss and any specific psychotic symptom. For example, it is notthe case that hearing impairment is necessarily associated withauditory hallucinosis. Likewise, the association between visualimpairment and visual hallucinations, so dramatically representedin the Charles–Bonnet syndrome 19 , does not appear to be found inlate-life schizophrenia.The social and psychological consequences of sensory impairments(social withdrawal and ostracization; misinterpretation ofsocial cues) may result in suspiciousness and hostility, leading toparanoid ideation. Abnormal percepts associated with reducedsensory input might result in hallucinations, as in the Charles–Bonnet syndrome, although secondary delusional elaboration is