Two major noncortical inputs to the striatum originate from the substantia
nigra and the thalamic centre median-parafascicular complex. Although it is
established that in Parkinson's disease there is degeneration of the nigra
l dopaminergic neurons, there has been little analysis of the glutamatergic
centre median-parafascicular complex. We therefore evaluated these and nei
ghboring thalamic nuclei (for specificity of any changes) in 9 Parkinson's
disease patients and 8 age-matched controls. Degeneration in the substantia
nigra and centre median-parafascicular complex was estimated by using quan
titative neuronal counts. On average, 70% of the pigmented nigral neurons d
egenerated and there was 30% to 40% neuronal loss in the centre median-para
fascicular complex in Parkinson's disease. Thalamic degeneration was marked
in neuronal subpopulations (50% loss of parvalbumin-positive neurons in th
e parafascicular, and 70% loss of non-parvalbumin-positive neurons in the c
entre median nuclei). In contrast, adjacent thalamic nuclei did not degener
ate, which supports a selective neurodegeneration of the centre median-para
fascicular complex. Our results show that the thalamic centre median-parafa
scicular complex is an additional nondopaminergic site of neurodegeneration
in Parkinson's disease. Because this thalamic region provides important se
nsorimotor feedback to the striatum, degeneration of this region is likely
to exacerbate the clinical signs and symptoms of Parkinson's disease.