Common patterns of clinical motor dysfunction

✍ Scribed by Nathaniel H. Mayer; Alberto Esquenazi; Martin K. Childers

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 339 KB
• Volume: 20
• Category: Article
• ISSN: 0148-639X
• DOI: 10.1002/(sici)1097-4598(1997)6+<21::aid-mus4>3.0.co;2-l

✦ Synopsis

Lesions of the central nervous system often produce an upper motoneuron (UMN) syndrome. Characteristics of the upper motoneuron syndrome include the presence of spasticity, weakness, and a variety of motor control abnormalities that impair the regulation of voluntary movement. The adult spastic disorders are outlined by Gormley, 4 and the pathophysiology of spasticity is discussed by Mayer elsewhere in this syllabus. In patients with an upper motoneuron syndrome (particularly those who develop the syndrome after traumatic brain injury, anoxic encephalopathy, and stroke), focal but variable patterns of muscle dysfunction are commonly observed which lead to deformity across upper and lower extremity joints. Identifying specific muscles that contribute to deformity across a joint is a useful evaluation strategy because denervation techniques, such as the use of neurolytic or chemodenervation agents or surgical approaches, can take therapeutic advantage of such information. In the text below, we discuss frequently observed patterns of deformity associated with problematic spasticity, paresis, contracture, and impaired voluntary motor control. Muscle involvement is summarized in Table . It should be remembered that not all muscles will be involved in a deformity in a particular patient. Further, some spastic muscles are weaker than their non-spastic agonists. Spasticity in this situation may not lead to deformity or functional impairment, and so may not be an appropriate target for chemodenervation. Treatment decisions are often best regarded as hypotheses to be tested and evaluated by clinical trial and the follow-up assessment.