Neuropraxia is a type of peripheral nerve injury, and is known as the mildest form of nerve injury. It is classified as a transient conduction block of motor or sensory function without nerve degeneration, although loss of motor function is the most common finding. In cases of neuropraxia, autonomic function is preserved. Patients are usually able to fully recover within a period of weeks to months.
Nerve damage is classically described in terms of anatomical injury. Nerves are comprised of the endoneurium that surrounds axons. These include both individual axons that are covered in myelin and groups of axons than are unmyelinated. These collections are surrounded by a layer called perineurieum, and the epineurium forms the outermost layer. Vascular networks are contained within the epineurium to supply the capillaries to the endoneurium. Neuropraxia by definition does not involve damage to the axon.
Neuropraxia was originally described in 1943 by Seddon  as the mildest form of nerve injury that is comprised of transient demyelination, compared to axonotmesis, which involves disruption of the axon itself with an intact epineurium and neurotmesis, which is complete nerve disruption extending through the endometrium. Neuropraxia is characterized by transient functional loss, with a recovery in 6–8 weeks. Sunderland later reclassified peripheral nerve injury from Seddon’s original classification to five degrees of injury, with neuropraxia identified as first-degree injury .
The exact pathophysiology of neuropraxia is unknown. It is thought to be a local reaction to periods of ischemia that result in ion-induced conduction blockade. There is demyelination of the axon initially, which eventually recovers. Loss of function occurs until remyelination occurs, sometimes rapidly over days, or at times up to 12 weeks .
Neuropraxia occurs as a traumatic peripheral nerve injury, which can include penetrating, crush, traction, blast, and burn injuries. These traumatic events cause a period of ischemia to the nerve, rather than a direct injury to the nerve. After a traumatic event, the vasculature of the epineurium becomes relatively more permeable than that of the endoneurium, which contributes to local ischemia both by the direct decrease in flow and also by the contribution to edema, which leads to compression and secondary injury .
The clinical manifestations of neuropraxia are many. It is the underlying etiology of such cultural references as “honeymooner’s palsy” (a radial nerve neuropraxia) and “crossed leg palsy” (a peroneal nerve neuropraxia). For the surgeon, however, it is most commonly encountered after the use of pneumatic tourniquets in extremity surgery, or the use of lithotomy position for pelvic surgeries. The true incidence of postoperative neuropraxia is unknown as there are no reporting requirements, and there is no long-term morbidity associated with the condition. The other clinical scenario commonly encountered by physicians is posttraumatic cervical cord neuropraxia, when an athlete presents with quadriplegia after an impact that resolves, usually, within 24 h.
The diagnosis of neuropraxia is usually clinical, and can classically be identified postoperatively when a patient experiences functional loss in a nerve distribution related to an area of compression related to patient positioning under anesthesia. Commonly, the presentation can also occur with athletes who have spinal stenosis and present with quadriplegia after impact injuries. The mechanism of injury combined with the neurological deficit is sufficient to make the diagnosis.
The diagnosis can also be made or confirmed with conduction studies or electromyography (EMG). These studies will reveal a conduction block proximal to the lesion, and sustained action potentials distal to the lesion. Remyelination leads to resolution of these electromyographic findings in most cases, although remyelination is usually not as robust as myelination before the injurious event and slowing of conduction may persist even with full functional recovery.
There is disagreement as to when to conduct EMG studies if the clinician feels they are necessary to make the diagnosis. While the classic findings of sustained action potentials distal to the lesion may not be fully present until 3 weeks after the mechanism of injury, the immediate EMG post-injury will demonstrate lack of conduction. The exact localization of the nerve injury may not be possible at this time, but abnormal findings are enough to confirm diagnosis in the appropriate clinical scenario, and exact localization is unlikely to change management of this injury, which is focused on the functional disability of the patient.
Neuropraxia is most commonly encountered with nerve compression after positioning during surgery. Neuropraxia has been described after tourniquet use after orthopedic extremity surgery, although there is limited data about the rates of this complication. Neuropraxia is also a known complication when the patient is in the lithotomy position during surgery. Retrospective studies have suggested that rates of lower-extremity neuropraxia are as high as 1% after surgery in the lithotomy position. Risks for neuropraxia include age over 70, surgery duration of 180 min or greater, and inappropriate positioning . Prevention of neuropraxia in surgery requires optimal positioning and minimizing operation time. Animal studies have demonstrated that occasional reperfusion during periods of ischemia do not change rates of neuropraxia . This inference implies that periodic relaxations of the tourniquet or from the lithotomy position may not be an appropriate response to prevent neuropraxia.
Therapy for neuropraxia involves monitoring to ensure resolution of the symptoms in an appropriate time line. Patients can also pursue physical and occupational therapy depending on the deficit. There is limited evidence that other interventions, such as steroid administration, have any impact on outcome, and these lesions will resolve on their own without any intervention. More research is needed in this area to optimize time to recovery.
Cervical Cord Neuropraxia
Cervical cord neuropraxia is a different clinical syndrome from what has been described postoperatively. It is described as occurring in athletes who have subclinical cervical stenosis of the spinal cord. When these athletes are involved in a high-impact collision, such as in tackling in football, these patients can experience over 24 h of transient quadriplegia . The typical mechanism of this injury is hyperextension of the neck, which creates a period of transient ischemia and causes the athlete to lose motor function in all four extremities. Frequently, the athlete may regain function by the time they arrive at the hospital.
Cervical cord neuropraxia has been estimated to have an incidence as high as 0.06% . There have been several high-profile incidences of cervical cord neuropraxia. These athletes are at high risk for a second incident, although given the small numbers of cases that are reported, it is difficult to derive broadly applicable conclusions about the natural history of this injury.
Therapy for cervical cord neuropraxia is similarly limited to therapy for postoperative neuropraxia. Given the concern for greater damage to the spinal cord and associated morbidity and mortality, many individuals receive steroids on arrival to the hospital. However, steroid administration for spinal cord injury has currently come under scrutiny, and may not change outcome even in more serious forms of spinal cord injury. The greatest question in these cases is if there is a more significant underlying injury. Once these injuries have been ruled out and the patient has returned to normal functioning, return to play is not contraindicated. If players have continuing deficits, more significant underlying injury should be sought.
Overall, the risk of neuropraxia in traumatic and postoperative settings appears to be low. This condition, while transient, does have significant morbidity for the duration of functional losses. The pathophysiology of this condition is poorly understood, and its incidence low enough that there are a few studies examining the best approach to treating these patients. Diagnosis is usually made with the appropriate mechanism of injury and clinical setting, although given the functional loss, EMG is frequently used to confirm the diagnosis and educate patients about prognosis. Prognosis in these cases is excellent, but more research is necessary to explore ways to shorten the duration of morbidity given the high burden of functional motor loss.