The Subthalamic Nucleus in Parkinsonʼs Disease and Progressive Supranuclear Palsy

• Published in: Journal of neuropathology and experimental neurology 1997-02, Vol.56 (2), p.132-142
• Main Authors: HARDMAN, CRAIG D, HALLIDAY, GLENDA M, MCRITCHIE, DEBORAH A, MORRIS, JOHN G.L
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Biological and medical sciences; Calbindin 2; Calbindins; Calcium binding proteins; Care and treatment; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Humans; Immunohistochemistry; Medical sciences; Middle Aged; Neurology; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parvalbumins - metabolism; Progressive supranuclear palsy; Protein binding; S100 Calcium Binding Protein G - metabolism; Supranuclear Palsy, Progressive - metabolism; Supranuclear Palsy, Progressive - pathology; tau Proteins - metabolism; Thalamic Nuclei - metabolism; Thalamic Nuclei - pathology
• ISSN: 0022-3069; 1554-6578
• DOI: 10.1097/00005072-199702000-00003

The subthalamus has become a promising target for the neurosurgical treatment of parkinsonian symptoms. We have used unbiased counting techniques to quantify the neuronal populations of the subthalamic nucleus in patients with idiopathic Parkinsonʼs disease and progressive supranuclear palsy. In addition, the type of calcium binding proteins contained within these subthalamic neurons was established using immunohistochemistry. Most of the 550,000 subthalamic neurons contain either parvalbumin or calretinin calcium binding proteins, and patients with idiopathic Parkinsonʼs disease sustained no damage to this nucleus. This is consistent with current theories of basal ganglia circuitry, which postulate that overstimulation of this excitatory nucleus contributes to the inhibition of the motor thalamus via the activation of inhibitory relays. In contrast, we found that there was substantial cell loss in the subthalamus in progressive supranuclear palsy (45 to 85% neuronal reduction) and that both cell types were equally affected. Extracellular neurofibrillary tangles as well as tau-positive glia were observed in the subthalamus of these cases. As the patients, with Parkinsonʼs disease and progressive supranuclear palsy all had overlapping parkinsonian symptoms, the loss of subthalamic stimulation within the basal ganglia of progressive supranuclear palsy cases is puzzling, unless their parkinsonian symptoms were generated by an alternate mechanism.