A peripheral nerve injury (PNI) involves damage to the Peripheral Nervous System (PNS)—the network of nerves outside the brain and spinal cord. The PNS acts as a communication relay between the Central Nervous System (CNS) and the rest of the body. Unlike the CNS, peripheral nerves are more vulnerable to external physical forces and systemic conditions. Their fundamental role is to transmit both motor signals for movement and sensory information like touch, temperature, and pain.
Anatomy and Causes of Peripheral Nerve Damage
A peripheral nerve is a complex structure composed of bundled nerve fibers, or axons. Many axons are wrapped in a fatty myelin sheath, which acts like insulation and allows for rapid signal transmission. Individual fibers are supported by the endoneurium and grouped into larger bundles called fascicles, each encased by the perineurium. Finally, the entire nerve is bound by the outer epineurium, which protects the structure and contains its blood supply. Damage to any of these components interrupts the flow of electrical and chemical signals.
Peripheral nerve damage arises from three primary mechanisms. Acute physical trauma, such as a deep cut or severe stretch injury, can partially or completely sever the nerve fibers and their sheaths. Chronic compression, seen in entrapment syndromes like carpal tunnel syndrome, causes localized damage due to persistent pressure and lack of blood flow. Systemic diseases, most notably diabetes mellitus, cause a type of damage called neuropathy by chemically altering and weakening the nerve fibers over time.
Categorizing Nerve Injury Severity
Nerve injuries are categorized based on the degree of structural damage to the axon and supporting connective tissue sheaths. The mildest form is neurapraxia, involving a temporary block of nerve conduction, often due to focal compression. Only the myelin sheath is affected, while the axon remains intact. Since the nerve fiber is undamaged, this injury usually resolves completely within days to weeks once pressure is relieved.
Axonotmesis is a more severe injury involving the complete disruption of the axon, while the surrounding connective tissue layers remain intact. Preserved sheaths guide the regenerating axon, offering a good prognosis for recovery, though the process is slow. The most severe injury is neurotmesis, where both the axon and all connective tissue sheaths are completely severed. The lack of an intact guidance tunnel makes spontaneous, functional recovery highly unlikely, often necessitating surgical intervention. The prognosis is directly linked to which of the nerve’s internal structures have been compromised.
Manifestation and Biological Repair
Manifestations depend on the type of nerve fibers affected, leading to three categories of functional loss. Damage to motor nerves results in muscle weakness, cramps, or paralysis in the affected area. Injury to sensory nerves causes symptoms like numbness, tingling, burning sensations, or chronic pain. Autonomic nerve damage impacts involuntary functions such as sweating, blood pressure regulation, and digestion.
Following an injury that severs the axon, Wallerian degeneration begins within 24 to 48 hours. In this process, the nerve segment distal to the injury site breaks down and is cleared away by immune cells. The nerve attempts repair through axonal sprouting, where the proximal segment of the axon regrows toward its target.
Successful regeneration occurs slowly, at about one millimeter per day, and relies on the integrity of the endoneurial tubes remaining from the original nerve. These preserved sheaths act as a scaffold to guide the regenerating axon sprouts to their correct endings. However, regeneration is often imperfect; axons may become misdirected or fail to reach their target, resulting in incomplete recovery of function. The peripheral nervous system exhibits a remarkable capacity for repair compared to the CNS.