The Pathology of Human Striated Muscle Following Denervation

Aird, Robert B.; Naffziger, Howard C.

doi:10.3171/jns.1953.10.3.0216

Cited by 33 publications

(9 citation statements)

References 8 publications

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“…113: , 2004 In the clinical setting, the reversal of skeletal muscle denervation atrophy and the recovery of contractile function upon reinnervation tend to be unsatisfactory when the denervation period is extended either because of a long distance from the nerve lesion or a delayed nerve repair. [1][2][3][4][5] Experimental data are consistent with these clinical observations, but the mechanisms responsible for the failure of longterm denervated muscle to become reinnervated and to resume function are unclear. 6 -8 Previous data from our laboratory support the working hypothesis that there are two general classes of mechanisms that affect skeletal muscle contractility after denervation and reinnervation: (1) mechanisms that affect primarily muscle mass and (2) mechanisms that affect muscle force capacity independent of muscle mass.…”

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confidence: 68%

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Force Deficits in Skeletal Muscle after Delayed Reinnervation

Aydın

Mackinnon

et al. 2004

Plastic and Reconstructive Surgery

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Using a rat hindlimb model, the authors tested the hypothesis that, in muscles reinnervated after long-term denervation, atrophy-dependent and atrophy-independent mechanisms operate independently to produce force deficits. In adult rats, gastrocnemius muscles were subjected to denervation via tibial nerve transection. Reconstruction of the nerve lesion was delayed for periods ranging from 2 weeks to 1 year. After a minimum recovery period of 6 months after nerve repair, muscle mass and maximum isometric tetanic force were measured and specific force was calculated for each muscle (n = 40 muscles from 23 animals). After recovery, observed deficits in muscle mass and maximum tetanic force were directly proportional to the denervation interval. On the other hand, the deficit in specific force was not proportional to the denervation interval; all groups in which the nerve reconstruction was delayed for a month or longer demonstrated a deficit of 30 percent to 50 percent. These data support our hypothesis that, after prolonged denervation followed by reinnervation, the magnitude of the deficit in whole muscle force does not parallel the deficit in specific force. These data support the idea that mechanisms governing muscle atrophy are independent of those resulting in specific force deficits.

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confidence: 68%

“…Intramuscular fibrosis has been suggested to impair mechanical function by also altering transmission of contraction to the tendons. 1 Denervation, depending on its duration, may render permanent ultrastructural changes to muscle fibers that cause a failure in maximal force capacity of the contracting fiber even if it is fully reinnervated.…”

Section: Resultsmentioning

confidence: 99%

Force Deficits in Skeletal Muscle after Delayed Reinnervation

Aydın

Mackinnon

et al. 2004

Plastic and Reconstructive Surgery

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“…The time necessary for muscle reinnervation and the number of regenerating axons that successfully reinnervate the muscle play a major role in motor recovery after nerve injury 3-8 . With extended denervation times, Schwann cells (SCs) in the distal nerve become less supportive of regenerating axons 9-11 , the denervated muscle begins to atrophy resulting in profound muscle changes including apoptosis and fibrosis 3,4,6-8,12-17 , and fewer motor neurons from the proximal nerve regenerate 4,7,11,16,18,19 . Replacement of muscle fibers by adipose tissue has also been seen with chronic denervation 16,20 .…”

Section: Introductionmentioning

confidence: 99%

Supercharge Nerve Transfer to Enhance Motor Recovery: A Laboratory Study

Farber¹,

Glaus²,

Moore³

et al. 2013

The Journal of Hand Surgery

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Purpose To investigate the ability of a supercharge end-to-side (SETS) nerve transfer to augment the effect of regenerating native axons in an incomplete rodent sciatic nerve injury model. Methods Fifty-four Lewis rats were randomized to 3 groups. The first group was an incomplete recovery model (IRM) of the tibial nerve complemented with a SETS transfer from the peroneal nerve (SETS-IRM). The IRM consisted of tibial nerve transection and immediate repair using a 10mm fresh tibial isograft to provide some, but incomplete, nerve recovery. The 2 control groups were IRM alone and SETS alone. Nerve histomorphometry, electron microscopy, retrograde labeling, and muscle force testing were performed. Results Histomorphometry of the distal tibial nerve showed significantly increased myelinated axonal counts in the SETS-IRM group compared to the IRM and SETS groups at 5 and 8 weeks. Retrograde labeling at 8 weeks confirmed increased motoneuron counts in the SETS-IRM group. Functional recovery at 8 weeks showed a significant increase in muscle specific force in the SETS-IRM group compared to the IRM group. Conclusions A SETS transfer enhanced recovery from an incomplete nerve injury as determined by histomorphometry, motoneuron labeling within the spinal cord, and muscle force measurements. Clinical Relevance A SETS distal nerve transfer may be useful in nerve injuries with incomplete regeneration such as proximal Sunderland II or III degree injuries, where long regeneration distance yields prolonged time to muscle reinnervation and suboptimal functional recovery.

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“…The effect of the experimental injection of alcohol into the subarachnoid space of cats was studied by Aird and Naffziger (1935). They found widespread degenera tion involving posterior rootlets, posterior funiculi, posterolateral tracts, anterior rootlets and antero-lateral columns.…”

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confidence: 99%

The neuropathological effects resulting from the intrathecal injection of chemical substances

Wolman

1966

Spinal Cord

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The Pathology of Human Striated Muscle Following Denervation

Cited by 33 publications

References 8 publications

Force Deficits in Skeletal Muscle after Delayed Reinnervation

Force Deficits in Skeletal Muscle after Delayed Reinnervation

Supercharge Nerve Transfer to Enhance Motor Recovery: A Laboratory Study

The neuropathological effects resulting from the intrathecal injection of chemical substances

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