Fast track — ArticlesVisual hallucinations in the diagnosis of idiopathic Parkinson's disease: a retrospective autopsy study
Introduction
Visual hallucinations (VH) and disturbances of visual perception occur in several neurodegenerative diseases, including Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In patients with PD the prevalence of VH has been reported to be between 6% and 60%.1, 2 VH in patients with Lewy body pathology are thought to be secondary to pathology in the basolateral nucleus of the amygdala and parahippocampus, and related to α synuclein pathology in the frontal cortex.3, 4, 5 The time from disease onset to first VH has been related to density of Lewy bodies in the parahippocampal and inferior temporal cortices.5 In patients with neurodegenerative dementias, the presence of VH is helpful in differentiating DLB from frontotemporal dementias and progressive supranuclear palsy, but not from Alzheimer's disease.6 Although the prevalence of VH has not been systematically studied in other pathologically diagnosed bradykinetic-rigid syndromes, there are some clinical reports of VH in multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration.7, 8, 9, 10 In these disorders, Lewy bodies do not typically occur in the frontal or temporal cortices, which suggests that when VH are present they are due to different mechanisms than in Lewy body parkinsonism (LBP). This distinction might be clinically helpful when diagnosing patients with bradykinetic-rigid syndromes, particularly for differentiating between PD and non-LBP. We aimed to investigate the relation between pathological diagnosis of a bradykinetic-rigid syndrome and VH and the relation between VH and other clinical factors, such as drugs.
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Patients
We studied cases with bradykinetic-rigid syndrome or parkinsonism archived at the Queen Square Brain Bank for Neurological Diseases. Donors were from the UK and died between 1988 and 2003. Cases had been diagnosed before death as well as pathologically confirmed; all met widely accepted pathological criteria for diagnosis.11, 12, 13, 14, 15, 16 Of 788 cases identified, 473 had PD, 44 had DLB (where cognitive dysfunction was recorded within the first year of disease onset), 127 had progressive
Results
44 cases were excluded from the study because of insufficient clinical data: 28 with PD, seven with progressive supranuclear palsy, five with multiple system atrophy, two with Alzheimer's disease, and two with vascular parkinsonism. Of the 744 cases included (table 1), 272 (37%) had VH. In four patients with progressive supranuclear palsy and three patients with multiple system atrophy VH were related only to dopaminergic drugs and ceased on withdrawal of the offending drug. These patients were
Discussion
VH are a useful clinical diagnostic feature in patients with PD. VH are a common symptom in patients with LBP and rarely occur in patients with other bradykinetic-rigid syndromes. The presence of VH predicted LBP with 93% accuracy. VH occurred in 50% of patients with PD, and in almost all of these VH occurred in the second half of the disease course. VH were only weakly correlated with use of selegiline and ergot dopamine agonists; they were not correlated with use of levodopa, amantadine, or
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