Pain and dyskinesia in Parkinson's disease
Carlos Juri (1, 2), María C. Rodríguez-Oroz (1), Juan A. Burguera (3), Jorge Guridi (1), Jose A. Obeso (1)
(1) Neurosciences Division, Department of Neurology and Neurosurgery, Clínica Universitaria and Medical School, CIMA and CIBERNED, University of Navarra, Pamplona, Spain
(2) Deptartment of Neurology, Medical School, Pontificia Universidad Católica de Chile, Santiago, Chile
(3) Service of Neurology, Hospital Universitario La Fe, Valencia, Spain
Lerner and Bagic1 have to be congratulated for their hypothesis on PD pathogenesis. They suggest that the sequence of the brain changes in PD follows specific and repeatable patterns in all cases, as well as that a prion-like process underlies neurodegeneration. These ideas could explain several features of PD, such as the high prevalence of olfactory, autonomic, or sleep abnormalities. However, any pathogenic hypothesis should also explain:
- The variable rate of progression.
- The heterogeneous presentation.
- The persistent asymmetry of motor symptoms and signs.
- The progressive worsening and somatotopic spreading of the same symptom, meaning that neurons displaying similar gene expression profile, intracellular enzymatic machinery, and signaling pathways are differentially affected by the process.
- The case of young-onset cases: whereas they must have severe disease to present so early, disability progresses slowly.
CITATION Mov Disord. 2010 Jan 15;25(1):130-2