Visual hallucinations in dementia with Lewy bodies : transcranial

Visual hallucinations are a feature of many psychiatric disorders, including schizophrenia and bipolar disorder as well as proto-typical conditions such as Charles Bonnet syndrome. However, their prevalence is particularly high in Lewy body diseases including Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy bodies; and in the latter up to 80% of individuals are affected. 1 Untreated, visual hallucinations in dementia with Lewy bodies can markedly impair quality of life 2 and significantly increase caregiver distress. 3 However, although a number of causative models for complex visual hallucinations have been proposed (see, for example, Collerton et al, 4 Diederich et al, 5 ffytche et al 6 and Manford & Andermann 7) no specific model has yet been proved definitive. Deafferentation models of visual hallucinations, favoured in conditions such as Charles Bonnet syndrome, suggest that defective sensory input from the eye to the visual cortex can lead to the 'release' of visual cortical areas and subsequent visual hallucinations. 6,7 A similar deafferentation process leading to hyperexcitability of the visual cortex could also occur in dementia with Lewy bodies; certainly across the Lewy body disease spectrum there is evidence for pregeniculate dysfunction, including disturbances in retinal dopaminergic circuitry, altered inter-retinal neural transmission and neuropathological abnormalities in photoreceptors and outer plexiform layers (for review, see Archibald et al 8). Others have speculated that dysfunction in association areas or impaired attentional binding is crucial to visual hallucination formation in Lewy body disease. 4,9 In dementia with Lewy bodies, Lewy bodies in the inferior temporal cortex at autopsy have been linked with visual hallucinations during life, 10 there is extensive parietal hypoperfusion 11 and significant glucose hypometabolism in visual association areas; 12 these abnormalities combined with posterior white matter disruption 12,13 may lead to perturbations in visual processing with disturbances in afferent inputs and recurrent feedback loops. In support of this, a functional magnetic resonance imaging (fMRI) study examining visual object processing 9 found that people with Parkinson's disease with visual hallucinations had reduced blood oxygen level-dependent activation in lateral occipital and extrastriate temporal areas compared with individuals with Parkinson's disease who did not hallucinate prior to image recognition. The authors argued that this favoured the role of impaired bottom-up processing from early visual areas to association areas in the pathogenesis of visual hallucinations. One way to provide further insights into the aetiology of visual hallucinations in dementia with Lewy bodies is to …