Lesions as therapy: rigidity and Parkinson's disease.
Since James Parkinson (1817) first characterized the shaking palsy as a unique condition, significant confusion has remained concerning the causes and treatments of Parkinson's disease (PD). Through the 19th century, a wide variety of approaches were attempted in an effort to reduce its cardinal signs--rigidity, tremor, and bradykinesia--but to little effect. Today, approaching 200 years after Parkinson's seminal work, this disorder is commonly treated by surgical means, inducing a lesion in one specific portion of a small nucleus in the central nervous system (Desaloms et al., 1998, Lang et al., 1999). The notion of providing a lesion to the nervous system as a therapy for PD, however, began in earnest at the beginning of the 20th century. The first attempt to alleviate the symptoms of PD through surgical means involved a section of the dorsal roots of the spinal cord supplying the affected limb (also known as dorsal rhizotomy). Although ultimately resulting in disastrous effects, these early surgical attempts proceeded from a firm body of clinical and experimental research on both the central and peripheral nervous systems. After briefly reviewing the use and failure of dorsal rhizotomy as a treatment for parkinsonian rigidity, this paper will examine the manner in which clinicians and scientists justified the procedure.
Clower
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University of Pittsburgh, W1640 BST, Pittsburgh, PA 15261, USA. clowerw@pitt.edu
D003655:Decerebrate State / Q000266:history; D049672:History, 19th Century; D049673:History, 20th Century; D006801:Humans; D009127:Muscle Rigidity / Q000266:history* / Q000601:surgery; D010300:Parkinson Disease / Q000266:history* / Q000601:surgery; D019051:Rhizotomy / Q000266:history