Do frontal dysfunctions play a role in visual hallucinations in Alzheimer's disease as in Parkinson's disease? A comparative study.

Abstract

Recent studies have demonstrated that nondemented patients with Parkinson's disease with visual hallucinations had lower scores on frontal-executive tasks than parkinsonian patients without hallucinations, most likely due to defective cholinergic circuitry. The aim of the present study is to investigate whether development of visual hallucinations in patients with Alzheimer's disease may also be related to more severe frontal dysfunctions. In the present study, 36 patients were included who were affected by probable Alzheimer's disease (18 with visual hallucinations and 18 without) and 38 patients affected by idiopathic Parkinson's disease (19 with visual hallucinations and 19 without). Patients completed a neuropsychological test battery and a short questionnaire to collect information about hallucination types and features. Multivariate analysis showed that patients with Alzheimer's disease scored significantly lower than patients with Parkinson's disease and that patients with hallucinations scored significantly lower than patients without hallucinations. Within both the Alzheimer's disease group and the Parkinson's disease group, patients with visual hallucinations scored significantly lower than patients without visual hallucinations, particularly on tests evaluating frontalexecutive functions. These results demonstrate that patients with visual hallucinations show a significant impairment on tests tapping frontal-executive functions in Alzheimer's disease, as previously demonstrated (and verified here) in Parkinson's disease. On this basis it seems likely that analogous cognitive mechanisms underlie development of visual hallucinations in both degenerative diseases. Moreover, we may speculate that a defective circuitry of the prefrontal cortex is crucial for the genesis of hallucinations.

Acute LSD effects on response inhibition neural networks

“…A previous study could show that Parkinson patients with visual hallucination have substantially greater impairments of inhibitory ability than those without visual hallucination (Barnes & Boubert, 2008). Another study supported this result by showing that within patients with Parkinson's and Alzheimer's disease, those with visual hallucinations scored significantly lower than patients without visual hallucinations, particularly on tests evaluating prefrontal-executive functions such as inhibition (Grossi et al 2011). Theoretical reflections propose that 5-HT 2A R activation may cause a cognitive disability to integrate new perception that subsequently triggers the formation of aberrant feelings and visual perception (Vollenweider & Geyer, 2001; Geyer & Vollenweider, 2008).…”

The treatment of behavioural and psychological symptoms in dementia: pragmatic recommendations

“…11,12 The same pathophysiology may be responsible for the hallucinations and disinhibition in some cases of atypical AD. 17 However, the majority of psychotic symptoms observed in AD patients are secondary or reactive to the cognitive deficit. 3,9,18 As a result of the memory loss induced by dementia, a patient may actually believe that a family member has stolen their belongings because they cannot remember where they were, or that a close relative has been replaced by a lookalike because they can no longer feel their emotional correlates.…”

“…They result from atrophy and neuronal loss in the frontal and temporal lobe networks involved in behavioural control, aggregates of abnormal tau or TDP‐43 proteins in these same regions, and serotonin and dopaminergic dysregulation involved in mood, impulsivity, and reward processing 11,12 . The same pathophysiology may be responsible for the hallucinations and disinhibition in some cases of atypical AD 17 …”