Citation

Hedera P, Friedman JH. Neurology 2014; 82(17): 1488-1489.

Affiliation

From the Department of Neurology (P.H.), Vanderbilt University, Nashville, TN; Movement Disorders Program (J.H.F.), Butler Hospital, Providence; and the Department of Neurology (J.H.F.), Alpert Medical School of Brown University, Providence, RI.

Copyright

(Copyright © 2014, Lippincott Williams and Wilkins)

DOI

10.1212/WNL.0000000000000370

PMID

24682972

Abstract

Idiopathic Parkinson disease (PD) is an α-synucleinopathy, one of several proteinopathies characterized by intracellular and extracellular accumulation of abnormal filament proteins.(1) Relentless progression of neuropathologic changes, consisting of α-synuclein-positive Lewy bodies and Lewy neurites, and widespread neuronal loss closely correlate with clinical worsening of motor and nonmotor PD symptoms. Typically, unilateral onset of tremor, rigidity, or bradykinesia, the cardinal motor features, is followed by contralateral spread of disease signs. The presence of midline problems, such as gait disorder and balance impairment, generally represents a more advanced phase of the disease, used as the central criteria in Hoehn & Yahr staging.

Language: en