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Electrophysiological Assessment of Spinal Circuits in Spasticity by Direct Dorsal Root Stimulation

 

作者: Victor Fasano,   Giancarlo Barolat‐Romana,   Sergio Zeme,   Angelo Sguazzi,  

 

期刊: Neurosurgery  (OVID Available online 1979)
卷期: Volume 4, issue 2  

页码: 146-151

 

ISSN:0148-396X

 

年代: 1979

 

出版商: OVID

 

关键词: Cerebral palsy;Dorsal root electrostimulation;Spasticity;Spinal circuits

 

数据来源: OVID

 

摘要:

&NA;Experimental researchers have shown that, because of normal inhibitory processes, repetitive orthodromic stimulation of the dorsal spinal roots induces a depression of the reflex discharge in the spinal motoneurons that is a function of the stimulation rate. Because a lack of inhibitory processes is considered to be the basic mechanism of spasticity, intraoperative stimulation of dorsal spinal roots from L‐1 to S‐1 bilaterally was performed in 80 patients affected by cerebral palsy. In these patients spasticity (exaggerated stretch reflexes, marked increase of proprioceptive reflexes, and clonus) was the main symptom. We stimulated the dorsal roots adjacent to the spinal cord and recorded motor responses by electromyogram (EMG) in the corresponding muscle groups. The most important findings were that: (a) variable inhibition (diminished, increased, or normal) was encountered in the spinal circuits of the spastic patient; and (b) the individual roots and rootlets can have different effects upon segmentary output. The absence of normal inhibitory processes was the most common finding; surgical sectioning of the corresponding roots resulted in immediate reduction in muscle tone in the related muscles. Selecting the dorsal roots for section results in a remarkable reduction of negative side effects that may follow total or random rhizotomy (marked hypotonia, ataxia, sensory defects) and of the percentage of late recurrences. This procedure results in additional positive effects at segmentary and suprasegmentary levels. These results confirm the idea that the basic mechanism of spasticity is a central defect in the traffic regulation of peripheral afferents as they are transmitted to the spinal cord. This defect causes segmentary and suprasegmentary adaptive reactions that extend the negative outcome of the local increase of muscle tone.

 

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