Pathogenesis Of Visual Hallucinations Research Articles

Vision loss and hallucinations: perspectives from neurology and ophthalmology.

The aim of this article is to summarize the evidence for visual impairment as a risk factor for visual hallucinations in neurologic disease and recent advances in our understanding of the central visual pathways that mediate this association. Recent studies have described the prevalence Charles Bonnet syndrome and questioned its lack of association with cognitive impairment, used advanced neuroimaging to show that disinhibition of the occipital lobe is involved in the pathogenesis of visual hallucinations in Parkinson's disease, and demonstrated that visual impairment because of eye disease is a consistent risk factor for visual hallucinations across a number of different neurodegenerative disease populations. Through connections between the primary visual cortex and other brain structures, visual function is closely tied to visual hallucinations. Given that the vast majority of vision loss is caused by ophthalmic disease, much of which is preventable or treatable, the detection and treatment of vision loss in at-risk populations may reduce the burden and consequences of visual hallucinations in older adults.

Management of visual hallucinations in dementia and Parkinson's disease.

We undertook a systematic review of the visual hallucinations in dementia, searching studies published between January 1980 and July 2017 using PubMed with the search terms visual hallucinations AND review AND (dementia OR parkinson*). We found 645 articles and screened them for relevance, finally including 89 papers (11 meta-analyses, 34 randomized controlled trials, six other trials and a number of relevant review articles). Only six of the trials reported visual hallucination outcomes separately from other neuropsychiatric symptoms. Atypical antipsychotics were frequently studied, but with the exception of clozapine in Parkinson's disease dementia, results were equivocal. There was some evidence that acetylcholinesterase inhibitors may help visual hallucinations. Overall, effect sizes for most treatments were small and there were few studies with long term follow up. Treatments need to be carefully weighed up with the risks and reviewed often, and many patients improved without treatment. There is a lack of data regarding visual hallucinations due to the grouping of psychotic symptoms together in commonly used rating scales. The lack of a specific rating scales, or analyzable items within other scales, for visual hallucinations, limited efficacy of current and small evidence base with short follow up are important areas for future studies to address.

Ventral striatal dopaminergic defect is associated with hallucinations in Parkinson's disease.

Visual hallucinations (VHs) are a common complication of Parkinson's disease (PD). The pathogenesis of VHs in PD is still largely unclear. The aim of this study was to investigate the dopaminergic mechanisms of VHs and specifically whether the degree of striatal dopamine transporter (DAT) function or extrastriatal serotonin transporter (SERT) function can predict the appearance of VHs in patients with PD. Twenty-two PD patients scanned with [123 I]FP-CIT single photon emission computed tomography at an early stage of their disease who later developed VHs were identified and compared with 48 non-hallucinating PD patients. The groups were matched for age, medication, disease duration and motor symptom severity. Clinical follow-up after the scan was a median (range) of 6.9 (3.8-9.6) years. Imaging analyses were performed with both regions-of-interest-based and voxel-based (Statistical Parametric Mapping) methods for the striatal and extrastriatal regions. The median interval between the scan and the emergence of VHs was 4.8 years. Patients who developed VHs had 18.4% lower DAT binding in the right ventral striatum (P = 0.009), 16.7% lower binding in the left ventral striatum (P = 0.02) and 18.8% lower binding in the right putamen (P = 0.03) compared to patients who did not develop VHs. Low striatal DAT function may predispose PD patients to VHs, and the regional distribution of the findings suggests a particular role of the ventral striatum. This is in line with non-PD research that has implicated ventral striatal dysfunction in psychosis.

Caudate dopaminergic denervation and visual hallucinations: evidence from a ¹²³I-FP-CIT SPECT study.

The pathogenesis of visual hallucinations (VHs) in Parkinson's disease (PD) has been considered multifactorial. In the pathophysiology of VHs a combination of impaired visual processing and attention has been reported. Imaging studies evidenced a role of the primary visual system and visual association areas as well as a dysfunctional activation of frontal areas in the occurrence of VHs. Due to the functional connections between basal ganglia and frontal areas, a role of basal ganglia and of the fronto-striatal circuits in the pathogenesis of VHs may be postulated. Aim of this study is to unveil whether a presynaptic dopamine deficiency at baseline may predict the development of VHs. A group of 18 non demented PD patients with VHs was matched with 18 non demented PD patients without VHs as regards age of onset of disease, disease duration and severity and levodopa equivalent dose. We retrospectively analyzed the (123)I-FP CIT SPECT performed on the two groups at the onset of their disease. The striatal uptake values in the two groups were examined, in order to evaluate nigrostriatal differences between the groups with different behavioral phenotype. The group of patients with VHs had a significant reduction (p < 0.05) in right caudate uptake values at baseline when compared with patients without VHs. No significant differences were found between the groups regarding left caudate and putaminal uptake values. The frontal impairment reported in PD patients with VHs may be due to a right caudate dysfunction, as it is connected to the frontal brain areas via neuronal loops.

Attentional and perceptual impairments in Parkinson's disease with visual hallucinations

Visual hallucinations (VH) are common in Parkinson's Disease (PD). Both deficits of perception and attention seem to play a role in the pathogenesis of VH in PD. However, the possible coexistence of impairments in attention and visual perception in PD with VH is not known. This study investigated both attention and visual perception in non-demented PD patients with VH, compared to PD patients without VH and healthy controls. Fourteen participants were included in each group. All patients were assessed with sustained visual attention and object and space perception tests. Only PD patients with VH showed impairments on object and space perception. In addition, PD patients with and without VH showed impairments on sustained visual attention, being more severely affected in PD patients with VH. Only in PD patients with VH sustained visual attention was associated with a decreased object and space perception. The results of our study thus suggest that in PD patients with VH an impairment of object and space perception, possibly in association with a decreased sustained visual attention, might play a role in the pathogenesis of VH.

Charles Bonnet Syndrome: successful treatment of visual hallucinations due to vision loss with selective serotonin reuptake inhibitors

Visual hallucinations are a common and often distressing consequence of vision loss, particularly in age-related macular degeneration. Charles Bonnet Syndrome (CBS) is defined by the triad of complex visual hallucinations, ocular pathology causing visual deterioration and preserved cognitive status. So far, although this condition is frequent, no established treatment for CBS has been stated. We report here the case of a 78-year-old woman, who came in our hospital because of a 4-week long mild depressive symptomatology. For 1 year she experienced daily sudden, unexpected, vivid and elaborate hallucinations. Insight was completely present, so the patient stated that the hallucinations were unreal and that the faces, geometrical figures and animals she saw every day were possibly due to her vision loss. The Mini Mental State Examination, digit span and verbal fluency were administered and no cognitive impairment was reported. The visual acuity was hand motion. After 4 days of treatment with venlafaxine the hallucinations completely disappeared. This is the first case to show that selective serotonin (and noradrenalin) reuptake inhibitors may be an effective and well-tolerated treatment for visual hallucinations associated with vision loss, and it adds to evidence implicating serotonergic pathways in the pathogenesis of visual hallucinations.