Visual dysfunction in Parkinson disease without dementia
Rizzo M, Anderson SW, Qian S, Rodniztky RL and Dawson JD;
Commented by , 22 Mar 2006
Background
Cognitive dysfunction already in non-demented patients has been increasingly better recognized. Among these visual dysfunction may be one of the earliest and most prominent ones. This has, however, not been studied in large patient populations.
Objectives
The objective of this study was to determine the profile of visual dysfunction and its relationship to motor, cognitive dysfunction and to overall disability in patients with mild to moderate PD without dementia.
Methods
This was a prospective study with a patient and normal control group. Seventy-six independently living patients with mild to moderate PD and 161 neurologically normal older adults were studies using a comprehensive neuropsychological test battery to assess visual acuity, contrast sensitivity (CS), visual speed of processing and attention, spatial and motion perception, visuo-constructional abilities, visual and verbal memory, executive functions, depression, and motor function.
Results
Patients with PD scored significantly worse on all tests of vision and cognition compared to normal elderly persons. Reduced CS contributed to deficits on tests of spatial and motion perception and attention in patients. Impairments in visual attention and spatial perception predicted worse cognitive function.
Worse performances on tests of visual speed of processing and attention, spatial and motion perception, visual construction, and executive functions correlated with measures of postural instability and gait difficulty as measured with UPDRS. Impairments in motor function, visual memory, mood, and executive functions predicted worse disability as measured by Schwab-England ADL scale.
Professor Emre's comments
In contrast to the earlier perceptions that PD is a purely motor disorder cognitive deficits, also in those patients who are seemingly normal, have been increasingly better identified. It was shown in an incident cohort of newly diagnosed patients with PD, that 35% of them had cognitive deficits at the time of diagnosis (ref. 1), the recent report on the 15 years follow-up of the longitudinal Sydney study demonstrated that 15 years after the diagnosis 85% of the patients had cognitive impairment (ref. 2).
Visual impairment was suggested to be one of the earlier and more prominent of the cognitive deficits already in 80s (ref. 3), but was not properly studied in large patient populations, What makes this study important is that an extensive neuropsychological test battery was employed in a large population of non-demented patients with mild to moderate disease as compared to a large number of controls.
This study clearly demonstrates that PD patients without apparent complaints have deficits in peripheral (contrast sensitivity) as well as in central visual processing. More simple functions such as impaired contrast sensitivity may be due to dopaminergic cell loss in the retina, but what is the impairment in central processing due to?
There is a prominent loss of cholinergic innervation in cortex of patients with PD, a recent functional imaging study re-confirmed what has been reported before (ref. 4). On the other hand it was suggested that visual hallucinations in PD may be due to impaired cholinergic innervation in visual association cortices (ref. 5), visual hallucinations were found to be more frequent in those patients with more severely impaired visual perception (ref. 6), recently a regional cerebral blood flow study demonstrated that in PD patients with non-psychotic visual hallucinations there was hyperperfusion in areas of temporal cortex associated with visual object recognition (ref. 7).
All these findings may nicely tie together that impairment in cholinergic modulation of visual processing in visual association cortices may be responsible for the widespread dysfunction in visual functions in PD. What remains to be demonstrated is a correlation between the severity of visual impairment and severity of cholinergic impairment.
References
1. Foltynie T, Brayne CEG, Robbins TW and Barker RA. The cognitive ability of an incident cohort of Parkinson’s patients in the UK. The CamPaIGN study. Brain 2004; 127 (pt 3); 1-11 (Free full text article)
2. Hely MA, Morris JG, Reid WG and Trafficante R. Sydney Multicenter Study of Parkinson’s disease: non-L-dopa-responsive problems dominate at 15 years . Movement Disorders 2005; 20 (2); 190-199
3. Girotti F, Soliveri P, Carella F, Piccolo I, et al. Dementia and cognitive impairment in Parkinson's disease . Journal of Neurology Neurosurgery and Psychiatry 1988; 51 (12); 1498-1502
4. Hilker R, Thomas AV, Klein JC, et al. Dementia in Parkinson’s disease: functional imaging of cholinergic and dopaminergic pathways . Neurology 2005; 65 (11); 1716-1722
5. Perry EK and Perry RH. Acetylcholine and hallucinations: disease-related compared to drug-induced alterations in human consciousness . Brain and Cognition 1995; 28 (3); 240-258
6. Mosimann UP, Mather G, Wesnes KA, O'Brien JT, et al. Visual perception in Parkinson disease dementia and dementia with Lewy bodies . Neurology 2004; 63 (11); 2091-2096
7. Oishi N, Udaka F, Kameyama M, et al. Regional cerebral blood flow in Parkinson disease with nonpsychotic visual hallucinations . Neurology 2005; 65 (11); 1708-1715