This is the reinnervation of denervated muscle fibers by small nerve sprouts that arise from nearby uninjured and intact axons. The second form of peripheral neurological recovery is terminal collateral sprouting.
This usually happens somewhere between 18 and 24 months. Chronically denervated muscle will eventually become fibrotic and electrically inactive. Muscle tissue must also remain viable and electrically active if a regenerating axon is going establish a connection with a functional neuromuscular junction. If the denervated muscle becomes fibrotic, these factors may no longer be released. These factors act as a catalyst to stimulate the axon to regenerate. This is necessary for the release of nerve growth factors from denervated muscle. Neurological recovery is also dependent on healthy viable muscle tissue. This process occurs at a rate of 3–4 mm/day so axonal regeneration is length-dependent. The proximal axon forms a bud that begins to regenerate distally through the endoneurial tube toward the denervated muscle. When axonal injury occurs, the axon distal to the site of injury undergoes Wallerian degeneration, whereas the proximal axonal component usually remains intact. For axonal regeneration to occur, there must be an intact anterior horn cell also known as the motor neuron cell body and an intact channel for regeneration, the endoneurial tube. True axonal regeneration occurs at the site where the nerve has been injured and where axonal degeneration begins. Peripheral neurological recovery occurs in two forms: true axonal regeneration and the reinnervation of denervated muscle fibers by terminal collateral sprouting. However, electrodiagnostic studies can never truly tell whether there is axon transection or not.ĮMG testing can be used to demonstrate neurological recovery. The limitation here is that one can not differentiate a conduction block where the nerve/axon remains intact from axonal degeneration or from nerve/axon transection. Nerve conduction studies across an injured segment of nerve will also be abnormal immediately. These early findings can help to localize the site of injury and to some extent the degree of injury. However, when there is significant axonal injury or even a severe neuropraxia (conduction block), a decreased rate of motor unit recruitment will instantaneously become abnormal and a skilled electromyographer can often determine this. This is a length-dependent process so that the longer the length of the injured axon, the longer Wallerian degeneration will take. It is true that the degree of muscle denervation that occurs after nerve injury can not be determined until Wallerian degeneration is complete and this can take as short as 1 week or as long as 4 weeks. One of the most common myths about EMG tests is that one must wait 2–3 weeks following a nerve injury before reliable information can be obtained.
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