 Quote by Revenged
Why would Parkinson's Disease cause hallucination?
It is caused by a lack of dopamine in the brain to the striatum...
Whereas I thought hallucinations are thought to occur due to a release of glutamate or an effect on serotonin (5-HT)
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It's an interesting question – not an association I would have immediately made either. Unfortunately, 20-40% of Parkinson's patients develop cognitive disturbances, sometimes including hallucinations. Visual hallucinations apparently occur in about 25% of individuals with Parkinson's (Aarsland et al., 1999, Fénelon et al., 2000). Source of citations:
http://brain.oxfordjournals.org/cgi/...full/125/2/391
As you mentioned there is a degeneration in the dopamine production regions, and patients are treated with drugs like Levodopa to boost dopamine levels and compensate for the loss. Visual and auditory hallucinations occur sometimes as a side effect of this treatment, although I do not know the specific mechanisms behind it.
Other than that, the pathology of the disease itself may be to blame. One of the nasty things that can happen in the course of Parkinson's is a build-up of Lewy bodies in the neurons.
http://en.wikipedia.org/wiki/Lewy_body I was just reading a study published in 2002 examining the brains of deceased individuals who had suffered from Parkinsons (no dementia), Dementia with Lewy Bodies (DLB), or Parkinson's Disease with Dementia (PDD). Of particular interest was the concentration and distribution of Lewy bodies (LB) in the brain and the relationship to (reported) hallucinations that the patient had suffered from while alive.
http://brain.oxfordjournals.org/cgi/...full/125/2/391
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..there was a striking association between the distribution of temporal lobe LB and well-formed visual hallucinations. Cases with well-formed visual hallucinations had high densities of LB in the amygdala and parahippocampus, with early hallucinations relating to higher densities in parahippocampal and inferior temporal cortices. These temporal regions have previously been associated with visual hallucinations in other disorders.
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So, I read that and said, "fair enough, but what's the specific relationship to the vision system?" And I thought this would be of interest to you because you had asked about specific neurotransmitters.
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.. patients with Charles Bonnet syndrome, who report similar visual hallucinations to patients with LB, activate the anterior temporal projection of the ventral visual pathway when hallucinating about landscapes, figures, and vehicles with appropriate emotional context (ffytche et al., 1998 ; ffytche and Howard, 1999 ; Santhouse et al., 2000 ). These hallucinations are thought to occur because of a lack of occipital stimulation due to ocular pathology (ffytche et al., 1998 ; ffytche and Howard, 1999 ; Santhouse et al., 2000 ). Downstream ventral association cortices increase their activity as a result of cortical disinhibition with this abnormal activity in visual processing regions activating complex visual hallucinations. It would appear more than coincidental that the same brain regions concentrating LB in our patients with visual hallucinations were those activated by visual hallucinations in patients with the Charles Bonnet syndrome (Santhouse et al., 2000 ), particularly as decreased occipital glucose metabolism also occurs in patients with LB (Imamura et al., 1999 , 2001; Lobotesis et al., 2001 ). The reduction in occipital metabolism occurs without underlying pathological inclusions, with a recent study suggesting that white matter abnormalities contribute to this metabolic deficit (Higuchi et al., 2000 ). In addition, DLB patients have preserved glucose metabolism in ventral temporal lobe regions, particularly those cases with visual hallucinations (Imamura et al., 1999 ; Higuchi et al., 2000 ; Lobotesis et al., 2001 ). These data suggest that activity in ventral visual pathways in association with underactivity of the primary visual cortices contributes to the well-formed visual hallucinations reported in cases with LB.
While it is generally believed that intracytoplasmic inclusions are a sign of neurodegeneration, several studies quantifying cortical neuronal loss in patients with DLB have shown a remarkable neuronal preservation (Gómez-Isla et al., 1999 ; Broe et al., 2001 ), suggesting that cortical LB may not signify neurodegeneration. If these cortical inclusions do not disrupt neuronal metabolism sufficiently to cause degeneration, they may disrupt cell mechanisms sufficiently to cause an increase in metabolic demand for neuronal survival. This may contribute to the association between the concentration of temporal lobe LB and well-formed visual hallucinations found in the present study. In fact, the overall pattern of temporal lobe LB formation appears to be more relevant to the onset of visual hallucinations than to the onset of dementia in cases with cortical LB disease.
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However, I was thinking of a more recent fMRI study when I originally posted the comment about Parkinson's and visual hallucinations:
http://neuro.psychiatryonline.org/cg...tract/18/3/402
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ABSTRACT
Using functional magnetic resonance imaging (fMRI), the authors examined visual cortex function in Parkinson's disease patients who did and did not experience visual hallucinations. Patients with visual hallucinations demonstrated increased activation in the visual association cortex and deficits in the primary visual cortex, suggesting that visual hallucinations are associated with an abnormality of visual-cortex function.
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Anyway, I don't know very much about the role of specific neurotransmitters during hallucinations so maybe I can pick your brain on this - pun intended.

I would like to learn more if you have any studies/links you could direct me to.