Intrathecal Administration of Baclofen for Treatment of Spasticity: Neurobiological Principles and First Clinical Results
The term “spasticity,” as defined by LANCE (7) as “a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks,” includes a clinical phenomenon which is produced by spinal and supraspinal lesions in the central nervous system: The transection of the brain stem at midbrain level, a condition that SHERRINGTON (16) called “decerebrate rigidity,” and the condition after spinal cord trauma are combined with clinical and electrophysiological findings identical to the above-mentioned definition. Nevertheless, it certainly cannot be excluded that different mechanisms of neuronal interactions are involved in the formation of spasticity. Although the imbalance between the different descending systems, including the reticulospinal and vestibulospinal tracts, could play a major role in the spasticity triggered by supraspinal lesions, the “sprouting” theory is gaining more and more importance in the light of growing knowledge of the plasticity of the adult central nervous system. McCOUCH et al. (9) and LIU and CHAMBERS (8) found in monkeys and cats a sprouting of segmental afferent terminals below a spinal cord transection area. It appeared that sprouts and terminals of dorsal root fiber axons in part take over vacated synaptic sites originally occupied by terminations of descending, now degenerated, fibers.
KeywordsCatheter Depression Respiration Neurol Baclofen
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