Motor correlates of occipital glucose hypometabolism in Parkinson’s disease without dementia

Objective: To determine whether occipital reduction in regional cerebral glucose metabolism in PD reflects retinal versus nigrostriatal dopaminergic degeneration. We hypothesized that occipital glucose metabolic reduction should be symmetric if parkinsonian retinopathy is responsible for the reduction. Methods: PD patients without dementia (n = 29; age 63 ± 10 years) and normal controls (n = 27; age 60 ± 12 years) underwent [18F]fluorodeoxyglucose PET imaging. Regional cerebral glucose metabolic rates were assessed quantitatively. Results: When compared with normal controls, PD patients showed most severe glucose metabolic reduction in the primary visual cortex (mean −15%, p < 0.001). Occipital glucose metabolic reduction was greater in the hemisphere contralateral to the side of the body affected initially or more severely in PD. There was an inverse correlation between side-to-side asymmetries in finger-tapping performance and occipital glucose metabolic reduction (r = −0.45, p < 0.05; n = 28). The correlation was strongest in patients with a relatively early stage of PD with more unilateral motor impairment (Hoehn and Yahr stage I, r = −0.74, p < 0.01; n = 10). Conclusion: The results indicate a pathophysiologic association between nigrostriatal dysfunction and occipital glucose metabolic reduction in PD.

[1]  M. Hoehn,et al.  Parkinsonism , 1967, Neurology.

[2]  S. Folstein,et al.  "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. , 1975, Journal of psychiatric research.

[3]  R A Koeppe,et al.  Alternative Approach to Single-Scan Estimation of Cerebral Glucose Metabolic Rate Using Glucose Analogs, with Particular Application to Ischemia , 1984, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[4]  D Comar,et al.  Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease. , 1984, Journal of neurology, neurosurgery, and psychiatry.

[5]  D E Kuhl,et al.  Patterns of local cerebral glucose utilization determined in Parkinson's disease by the [18F]fluorodeoxyglucose method , 1984, Annals of neurology.

[6]  C. Bulens,et al.  Effect of levodopa treatment on contrast sensitivity in Parkinson's disease , 1987, Annals of neurology.

[7]  Stephen M. Stahl,et al.  Cerebral metabolism of Parkinsonian primates 21 days after MPTP , 1988, Experimental Neurology.

[8]  M. Torrens Co-Planar Stereotaxic Atlas of the Human Brain—3-Dimensional Proportional System: An Approach to Cerebral Imaging, J. Talairach, P. Tournoux. Georg Thieme Verlag, New York (1988), 122 pp., 130 figs. DM 268 , 1990 .

[9]  T. Di Paolo,et al.  Decreased dopamine in the retinas of patients with Parkinson's disease. , 1990, Investigative ophthalmology & visual science.

[10]  T. Joh,et al.  Neuropathology of immunohistochemically identified brainstem neurons in Parkinson's disease , 1990, Annals of neurology.

[11]  K. Jellinger,et al.  Pathology of Parkinson's disease. Changes other than the nigrostriatal pathway. , 1991, Molecular and chemical neuropathology.

[12]  M Schulzer,et al.  Cerebral glucose metabolism in Parkinson's disease with and without dementia. , 1992, Archives of neurology.

[13]  J. Fuh,et al.  Cognition and 99Tcm-HMPAO SPECT in Parkinson's disease. , 1992, Nuclear medicine communications.

[14]  Peter Ford Dominey,et al.  A cortico-subcortical model for generation of spatially accurate sequential saccades. , 1992, Cerebral cortex.

[15]  M. Tagliati,et al.  The visual system in Parkinson's disease. , 1993, Advances in neurology.

[16]  R. Koeppe,et al.  Anatomic standardization: linear scaling and nonlinear warping of functional brain images. , 1994, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[17]  William J. Jagust,et al.  Cortical glucose metabolism in Parkinson's disease without dementia , 1994, Neurobiology of Aging.

[18]  O. Hikosaka,et al.  Visual hemineglect induced by unilateral striatal dopamine deficiency in monkeys. , 1995, Neuroreport.

[19]  Alan C. Evans,et al.  Extraretinal modulation of cerebral blood flow in the human visual cortex: implications for saccadic suppression. , 1995, Journal of neurophysiology.

[20]  O. Hikosaka,et al.  Eye movements in monkeys with local dopamine depletion in the caudate nucleus. I. Deficits in spontaneous saccades , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[21]  R. Koeppe,et al.  A diagnostic approach in Alzheimer's disease using three-dimensional stereotactic surface projections of fluorine-18-FDG PET. , 1995, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[22]  R. Albin,et al.  Fluoro-deoxyglucose positron emission tomography in diffuse Lewy body disease , 1996, Neurology.

[23]  G. Orban,et al.  The influence of stimulus location on the brain activation pattern in detection and orientation discrimination. A PET study of visual attention. , 1996, Brain : a journal of neurology.

[24]  A Weindl,et al.  Deactivation of human visual cortex during involuntary ocular oscillations. A PET activation study. , 1996, Brain : a journal of neurology.

[25]  T. Trottenberg,et al.  Directional bias of initial visual exploration. A symptom of neglect in Parkinson's disease. , 1996, Brain : a journal of neurology.

[26]  R. Albin,et al.  Cerebral metabolic differences in Parkinson's and Alzheimer's diseases matched for dementia severity. , 1997, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[27]  Richard S. J. Frackowiak,et al.  Functional localization of the system for visuospatial attention using positron emission tomography. , 1997, Brain : a journal of neurology.

[28]  K. Heilman,et al.  Neglect and Related Disorders , 1984, Seminars in neurology.