Mohammed T. Abou-Saleh

508 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRY48. Rabins P, Pauker S, Thomas J. Can schizophrenia occur after age 44?Comp Psychiat 1984; 25: 290–3.49. Jorgensen P, Munk-Jorgensen P. Paranoid psychoses in the elderly.Acta Psychiat Scand 1985; 72: 358–63.50. Castle DJ, Murray RM. The epidemiology of late onsetschizophrenia. Schizophren Bull 1993; 19: 691–700.51. Almeida OP, Howard RJ, Levey R, David AS. Cognitive and clinicaldiversity in psychotic states arising in late life (late paraphrenia).Psychol Med 1995; 25: 699–714.52. Castle DJ. Gender and age at onset in schizophrenia. In Howard R,Robins P, Castle D, eds, Late-onset Schizophrenia. Petersfield:Wrightson Biomedical, 1999; 147–64.53. Bleuler M. Late schizophrenic clinical pictures (in German). ForschrNeurol Psychiat 1943; 15: 259–90.54. Rokhlina ML. A comparative clinico-genetic study of attack-likeschizophrenia with late and early manifestations with regard to age(in Russian). Zhurnal Nevropatalogii i Psiikhiatrii Imeni SS Korsakova1975; 75: 417–24.55. Volavka J. Late-onset schizophrenia: a review. Comp Psychiat 1985;26: 148–56.56. Castle DJ, Murray RM. Schizophrenia: aetiology and genetics. InCopeland JRM, Abou-Saleh MT, Blazer DG, eds, Principles andPractice of Geriatric Psychiatry 1st edn. Chichester: Wiley, 1994;653–9.Brain Imaging in Schizophrenia-like andParanoid Disorders in Late LifeRobert HowardInstitute of Psychiatry and Maudsley Hospital, London, UKTwo general conclusions can be drawn from the results of brainimaginginvestigations of patients with an onset in late life of aschizophrenia-like psychosis. First, the established neuroimagingabnormalities reported in early adult life-onset schizophrenia arealso seen in later life-onset patients. Second, imaging has notimplicated focal or generalized neurodegenerative abnormalitiesthat can be implicated in psychosis aetiology, as has been the casefor late-onset affective disorders.STRUCTURAL IMAGINGComputed tomography (CT) studies of onset after 45 years 1 and60 years 2 patients have shown lateral and third ventricle volumeenlargement that does not approach the ventriculomegaly seen inAlzheimer’s disease. Structural magnetic resonance imaging(MRI) has confirmed these findings, as well as indicating possiblereductions in left temporal lobe and superior temporal gyrusvolumes 3–5 . MRI studies of patients with so-called ‘‘late-lifepsychosis’’ have included patients with organic as well asschizophrenia-like psychoses and, not surprisingly, have reportedan excess of focal structural abnormalities within deep grey andwhite matter structures 6 . Similar studies of patients with morerigorously defined late-onset schizophrenia, with exclusion ofindividuals who are cognitively impaired or have clinical evidenceof focal cerebrovascular disease, have found no significantincrease in such focal brain lesions compared to age-matchedcomparison subjects 7,8 .FUNCTIONAL IMAGINGResting bloodflow abnormalities have been reported with singlephotonemission computed tomography (SPECT) in ‘‘late-lifepsychosis’’, which may include patients with organic psychoses 9 .To date no bloodflow studies using cognitive activation paradigmshave been reported in late-onset patients. A singleneuroreceptor positron emission tomography study has reportedincreased binding values for dopamine D2 receptors 3 , althoughage-matched control subjects were not examined for comparison.In a small group of drug-naive onset 60+ patients, we wereunable to demonstrate any absolute increase in striatal D2receptor number compared with elderly controls using SPECT 10 .Hence, the issue as to whether or not neuroreceptor levels areabnormal in late-onset cases mirrors the dispute in the early-onsetschizophrenia literature.Although brain imaging studies to date have supported theconcept that early- and late-onset cases of schizophrenia sharecommon structural and neuroreceptor brain abnormalities, moresophisticated future studies may show differences. These may helpto settle which of two current hypotheses concerning theaetiopathology of late-onset schizophrenia and very late-onsetschizophrenia-like psychosis are most likely to be correct. Ifschizophrenia arising at any point in life is essentially a unitarycondition, then we cannot expect neuroimaging studies of evenremarkable sophistication to reveal differences between early- andlate-onset cases 11 . If (and the author favours this secondhypothesis) the later-onset cases represent a subtle organicphenocopy of schizophrenia, then application of novel imagingmethodologies, such as diffusion tensor imaging, which allow highresolution definition of white matter structures in vivo should beinformative in the next few years.REFERENCES1. Rabins PV, Pearlson G, Jayaram G et al. Increased ventricle-to-brainratio in late-onset schizophrenia. Am J Psychiat 1987; 144: 1216–18.2. Naguib M, Levy R. Late paraphrenia: neuropsychological impairmentand structural brain abnormalities on computed tomography. Int JGeriat Psychiat 1987; 2: 83–90.3. Pearlson GD, Tune LE, Wong DF et al. Quantitative D2 receptor PETand structural MRI change in late-onset schizophrenia. Schizophr Bull1993; 19: 783–95.4. Howard RJ, Almeida OP, Levy R et al. Quantitative magneticresonance imaging volumetry distinguishes delusional disorder fromlate-onset schizophrenia. Br J Psychiat 1994; 165: 474–80.5. Howard RJ, Mellers J, Petty R et al. Magnetic resonance imagingvolumetric measurements of the superior temporal gyrus,