Peripheral nerve injuries (PNIs) by trauma are the most common neuronal injury in civilian and military populations and significantly burden health care systems. Mammals (including humans) with PNIs experience: (1) immediate loss of sensory and motor functions mediated by the denervated target tissues; (2) rapid (3-7d) Wallerian Degeneration (WD) of severed distal axonal segments; and, (3) slow (~1mm/day) regeneration by naturally occurring axonal outgrowths from surviving, severed proximal stumps that produce poor (if any) functional recovery because of slow axonal regeneration for long distances and lack of axonal guidance. Denervated muscle fibers and sensory organs often atrophy before any re-innervation can occur.
The most common traumatic PNI is a peripheral segmental nerve gap or ablation defect. i.e., a segmental-loss peripheral nerve injury (PNI), as opposed to a simple cut PNI that can be primarily repaired by using microsutures through the epineurium/perineurium to appose the severed proximal/distal nerve ends (neurorrhaphy), a major advance in treatment of PNIs made many decades ago. Segmental-loss PNIs in more proximal portions of limbs and/or PNIs that involve ablations of > 5mm often especially have very poor, if any, restoration of function or coordinated voluntary behaviors. This morbidity is a major public health problem because current options for treating such PNIs often fail or lead to only partial recovery that leaves patients permanently disabled. Recently, however significant advances have been made in peripheral nerve repair that leads to significant functional recovery of voluntary behaviors is experimental animals. This issue focuses on those advances and their translation to clinical practice.
The articles in this Research Topic focus on recent advances in cellular/molecular mechanisms that demonstrably restore voluntary behavioral functions after traumatic injuries to peripheral nerves in mammals. Each article should concentrate on the cellular/molecular mechanisms, but also demonstrate that these mechanisms lead to voluntary behavioral recovery—as opposed to increased numbers of regenerating axons or electrical activity per se. The emphasis and goal of each article should be translation to clinical recovery.
Peripheral nerve injuries (PNIs) by trauma are the most common neuronal injury in civilian and military populations and significantly burden health care systems. Mammals (including humans) with PNIs experience: (1) immediate loss of sensory and motor functions mediated by the denervated target tissues; (2) rapid (3-7d) Wallerian Degeneration (WD) of severed distal axonal segments; and, (3) slow (~1mm/day) regeneration by naturally occurring axonal outgrowths from surviving, severed proximal stumps that produce poor (if any) functional recovery because of slow axonal regeneration for long distances and lack of axonal guidance. Denervated muscle fibers and sensory organs often atrophy before any re-innervation can occur.
The most common traumatic PNI is a peripheral segmental nerve gap or ablation defect. i.e., a segmental-loss peripheral nerve injury (PNI), as opposed to a simple cut PNI that can be primarily repaired by using microsutures through the epineurium/perineurium to appose the severed proximal/distal nerve ends (neurorrhaphy), a major advance in treatment of PNIs made many decades ago. Segmental-loss PNIs in more proximal portions of limbs and/or PNIs that involve ablations of > 5mm often especially have very poor, if any, restoration of function or coordinated voluntary behaviors. This morbidity is a major public health problem because current options for treating such PNIs often fail or lead to only partial recovery that leaves patients permanently disabled. Recently, however significant advances have been made in peripheral nerve repair that leads to significant functional recovery of voluntary behaviors is experimental animals. This issue focuses on those advances and their translation to clinical practice.
The articles in this Research Topic focus on recent advances in cellular/molecular mechanisms that demonstrably restore voluntary behavioral functions after traumatic injuries to peripheral nerves in mammals. Each article should concentrate on the cellular/molecular mechanisms, but also demonstrate that these mechanisms lead to voluntary behavioral recovery—as opposed to increased numbers of regenerating axons or electrical activity per se. The emphasis and goal of each article should be translation to clinical recovery.
