Problems of Spasticity in the Treatment of Spinal Cord Injuries

  • Jerzy Kiwerski


Spinal cord injury is immediately followed by a state of deficiency, or lowered irritability, of the spinal cord isolated from the influence of higher centers. Since 1841 this condition is known as spinal shock a term proposed by Marshall Hall [64]. Most investigators believe that spinal shock is a manifestation of deranged interneuronal activity but the mechanisms of this phenomenon and its variations are not adequately clarified. Contemporary definitions of spinal shock are based on the work of Sherrington and his school [122]–[125], which suggests that transient hyporeflexia in the spinal cord below its transection is a result of acute disturbance of the dominant influence of supraspinal structures due to interruption of synaptic conduction. More recently, Eccles and his collaborators [31]–[36], whose studies were concerned with the mechanisms of synaptic stimulation and inhibition, have demonstrated that areflexia in spinal shock is mainly a result of reduction of the influence of spindle receptors due to relaxation of intrafusal fibers in consequence of acute deficiency of control of the spindles by gamma motoneurons [60]. According to Walsh [138], spinal shock depends on interruption of the output of stimuli from the brain to the spinal cord, independently of disorders of blood supply of the spinal cord. This is supported by the fact that a second tran-section below the level of the first, made after return of reflex activity, does not again abolish it. Rosen [112] is of the opinion that during spinal shock the function of anterior horn cells is impaired, leading to functional block, which subsides partly after spinal shock status. Yamada and Mitchell [144] consider that three factors are essential for the development of spinal shock:
  1. (1)

    loss of irritability of the descending pathways

  2. (2)

    inhibition of the sacrolumbar segments

  3. (3)

    retrograde degeneration of interneurons after transection of their axons.



Spinal Cord Spinal Cord Injury Spastic Paralysis Motor Unit Obturator Nerve 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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© Springer Science+Business Media New York 1977

Authors and Affiliations

  • Jerzy Kiwerski

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