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Wise - what do you make of this?

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  • Wise - what do you make of this?

    Thanks Leo for posting the FensForum site.

    Wise, one article worries me a bit under 'spinal cord repair.'


    In this extract V Dietz says "A preserved amplitude of the motor action potentials following repetitive peripheral nerve stimulation indicates a spinal site of impairment. In patients who participated in a locomotor training programme lasting up to 13 weeks no positive effect on the slope of exhaustion was seen. It is concluded that a degradation of spinal neuronal activity takes place following a SCI. If in the future regeneration of spinal tract fibres becomes feasible in patients with complete SCI, such an approach can only become functionally successful if neuronal activity below the level of lesion is maintained. This might be achieved by a continuous training approach starting early after injury."

    Dietz seems to be suggesting that in chronic patients the lower neurons are irreversibly degenerated unless continuous training is started early after injury.


    Help Wise, what do you make of this?

  • #2
    Bump - Wise?

    My thoughts were that this is inconclusive- to walk without fatigue you have said the central pattern generator (CPG) at T12, L1 needs to be doing the walking more than the brain and people get fatigued when they need to use their brain too much because of incomplete communication with the CPG.


    • #3
      Chris2, it is hard to tell from the abstract of the talk exactly what Volker Dietz is referring to. He uses some unusual words to describe the neurophysiological activity. I presume that his use of the word "exhaustion" refers to the more standard term "fatigue". His statement "A preserved amplitude of the motor action potentials following repetitve peripheral nerve stimulation inducates a spinal site of impairment" probably refers to a response called the M-response which is the direct muscle response to stimulation of the peripheral nerve. Since the M-response remains constant. They probably saw fatigue of the reflexive response of the spinal cord (probably the H-reflex) to repetitive stimulation. Because a 13-week course of locomotor training did not change the tendency of the H-reflex to fatigue, it suggests that weight-supported ambulaton training was not able to change the rapid fatigue of the muscle. I don't think that this finding alone would justify the conclusion. It just suggests that their locomotor training program is not affecting the spinal fatigue. I would have to see other test results to understand the situaiton.



      • #4
        Thanks Wise - I was kinda hoping you'd say that. It only proves their therapy didn't reduce fatigue. If the brain could be reconnected again to the lower neurons the fatigue may diminish with excercise as with most excercise programmes.


        • #5
          chris2, that is indeed an interesting alternative interpretation of the findings, that some of the so-called "learned non-use" may be related to a form of atrophy of denervated neural circuitry in the spinal cord and that "forced-use" alone may not be sufficient, and that reinnervation may be necessary to reverse the changes in the neural circuit. Such a hypothesis can only be tested if and when there is regeneration.

          A second potential interpretation may be related to the intensity and duration of exercise. The abstract does not provide details of the exercise program that was used, whether they used electrical stimulation in the exercise, and the levels of the patients.

          A third interpretation is that there may have been some damage to the lower spinal cord. There is a very interesting paper in the 1980's by Dimitrijevic and his colleagues studied the reflex activity of the lower spinal cord and found that as many as 15% of patients with upper spinal cord injuries may have had lower spinal cord damage that was masked by the upper damage. I must say that I have now seen a number of patients who have inexplicable flaccidity in their legs even though their level of injury should not be associated with flaccidity. This has been puzzling me for quite a while.

          I think that the conclusion of this paper, unless it is backed up by other evidence not presented in the abstract, is premature. Nonetheless, it does suggest that there are limits to what weight-supported ambulation training can do for the lower spinal cord. This is of course not unanticipated. Weight-supported ambulation is not a cure for spinal cord injury. It is just one method. The U.S. study of weight-supported ambulation indicating that it does not improve locomotor function significantly more than "standard rehabilitation" suggests that there are other approaches that may be as effective. There are very likely to be nuances to the training effect that we will find out as research continues. I am very glad that people like Dietz and others are continuing to examine this issue. It is very important, in my opinion.