In 1942, Seddon classified the severity of peripheral nerve injury (PNI) in three types; neurapraxia, axonotmesis, or neurotmesis. A few years later, in 1951, Sunderland classified them in five different degrees. Neurapraxia is the mildest type of PNI commonly induced by focal demyelination or ischemia. It corresponds to grade 1 in Sunderland classification. In neurapraxia, the conduction of nerve impulses is blocked in the injured area. Motor and sensory conduction are partially or entirely lost. All the structures of the nerve stump, including the endoneurium, perineurium, and epineurium, remain intact.
Neurapraxia occurs when the myelin sheath of the nerve is damaged. If the nerve is stimulated distal to the injured area, conduction is preserved. Neurapraxic injuries generally have a good prognosis. Spontaneous clinical and electrodiagnostic recovery of this type of injury is expected in three months when the nerve completes remyelination.
Frequently, the word neuropraxia is incorrectly used in the literature. In the original 1942 classification by Seddon, neurapraxia was used; therefore, its correct use should continue in the scientific world.
Etiologies of neurapraxia are multiple.
Transient neurological deficits can occur following interscalene brachial plexus block, axillary brachial plexus blocks, and femoral nerve blocks with an incidence of 2.84%, 1.48%, and 0.34%, respectively. Permanent neurological deficits will occur in only 0.04/1000 blocks. Following ultrasound-guided nerve blocks, the incidence of transient neuropathies is 1.8/1000. Causes are mechanical by direct puncture of the nerve, pressure around the nerve, vascular/ischemic compromise by vasoconstriction, and inflammatory by scar.
Incorrect or careless patient positioning during anesthesia is an avoidable complication. Ulnar nerve injury has an incidence of 1:215 to 1:385. The majority of ulnar nerve injuries occur in patients with pre-operative subclinical abnormalities of ulnar nerve conduction. During childbirth in the lithotomy position, the common peroneal nerve and the sciatic nerve can be injured due to nerve traction or compression. The radial nerve suffers injury due to compression between the humerus and the edge of the operating table. In the early postoperative period, patients complain of pain, paraesthesia, or weakness in the distribution of the nerve.
High-velocity trauma, lacerations, and penetrating injury usually produce axonotmesis or neurotmesis.
The exact incidence and prevalence of neurapraxia are not clearly defined as it is usually combined with other types of PNI. The incidence of traumatic nerve injuries is approximately 350,000/year. Traumatic nerve injuries occur more frequently in young adults, with an average age of 20 to 39. Male sex is associated with 74% of traumatic injuries. Neurapraxia injury may a similar incidence since most cases are secondary to traumatic injuries or high contact sports.
During the Iraq and Afghanistan war conflicts, 45% of the nerve injuries were due to neurapraxia of the ulnar, common peroneal, and tibial nerves. In non-conflict time, mononeuropathies of the upper extremity are involved in 75% of the cases, commonly involving the ulnar nerve, alone or in combination. Other reports consider the radial nerve as the most frequently involved, followed by the ulnar nerve, and then, the median nerve. Combined lesions most commonly involved the ulnar and median nerves. Penetrating injuries to the common peroneal nerve and sciatic nerve are the most frequent lesions in the lower extremity.
The most common cause of PNI is vehicular accidents (46.4%), which affected mostly young men. Other causes include penetrating trauma (23.9%), falls (10.9%), gunshot wounds (6.6%), pedestrians involved in car accidents (2.7%), sports-related (2.4%), and miscellaneous (7.2%).
Neural Anatomy: A nerve is composed of axons and connective tissue and the associated blood supply. Axons may be myelinated or unmyelinated. The endoneurium, perineurium, epineurium form the connective tissue to support the axons. The endoneurium surrounds each axon. Several axons are group together as a fascicle which is surrounded by the perineurium. The epineurium groups multiple fascicles. This last external connective tissue has an internal component (epifascicular) that encases the fascicles and an external component (epineural), which encases the entire nerve proper. External to the epineurium, there is a loose connective tissue called the mesoneurium or perineurium, which supports the nerve and contains the blood supply.
Vascular Anatomy: The blood supply to the nerve is external to the epineurium. Extrinsic blood vessels join to form an anastomosing plexus of epineurial macro vessels. This anastomosing vasa nervorum penetrates the perineurium. Microvessels with non-fenestrated endothelium penetrate the endometrium and provide blood to axons.
Neurapraxia is induced by focal demyelination or ischemia. All the structures of the nerve, including the endoneurium, perineurium, and epineurium, remain intact. The mechanism usually involves crush, traction, ischemia, and less common mechanisms such as thermal, electric shock, radiation, percussion, and vibration. Increased pressure in a confined compartment (compartment syndrome), traction of the surrounding tissue, synovial tissue hypertrophy, tenosynovitis, hematoma, aneurysm, pseudoaneurysm, tissue edema, or local anesthetic injection proximal to the nerve can also produce neurapraxia.
Compression of a nerve can be acute or chronic. Compression at small openings and superficial nerve locations can damage the nerve and its blood supply. Scar tissue formation and inflammation can produce nerve entrapment. During surgery, nerve injury occurs by focal compression or traction from the retractor. If a force is applied at a right angle to the nerve, compression occurs along the long axis of the nerve, resulting in a decrease of the diameter of the nerve. If the force is applied along the axis of the nerve, traction occurs, resulting in lengthening of the nerve.
As a consequence of focal demyelination or ischemia, the nerve will have a decrease in conduction velocity and an increase in the latency. Compound muscle action potential (CMAP) amplitude evoked with stimulation above the injury is absent or markedly reduced, as compared with stimulation below the injury. The CMAP amplitudes with stimulation below the injury usually remain normal or are only slightly reduced because it reflects the sum of all the motor unit potentials stimulated. Electromyography (EMG) does not show significant changes in neurapraxia, except for reduced MUP recruitment. Due to the myelin injury, motor nerves are affected more than sensory nerves, and weakness predominates.
Neurapraxia had been studied in a rat model in which compression of 60 g/mm2 to the sciatic nerve produced a complete paralysis, which became normal in 14 days. An entire motor conduction block occurred if stimulated above the injured site, but below the compression site, remained normal. Wallerian degeneration signs were limited.
Information regarding the mechanism of injury is essential as it will guide decisions about the management. The physical examination will point toward the specific nerve involved. The sensory and motor distribution of the nerve affected is tested.
Alteration in the nerve structure can produce motor impairment (weakness, hyporeflexia, and atrophy in chronic cases) and sensory impairment (pain, allodynia, hyperesthesia, hypoesthesia, paresthesia). A combination of these is usually present, but motor deficits are more prominent. If there is a complete nerve injury, there will be anesthesia of the sensory distribution, and the muscles will show flaccid paralysis. If the damage is incomplete, some degree of preserved sensation or motion will be present. The presence of a Tinel sign indicates conduction along with the injured site.
Laboratory workup will include complete blood count, blood glucose, liver function, renal function, erythrocyte sedimentation rate, vitamin B12 levels, and thyroid-stimulating hormone.
Needle EMG is the most sensitive study. The motor response amplitude decrement begins around days 2–3 and is complete by day 6. EMG is most useful 2 to 3 weeks after the injury as the involved muscles had undergone denervation. EMG is done every six weeks. Stimulation of the nerve below the lesion will result in a CMAP wave from the neurapraxic axons. If there is an absence of CMAP upon stimulation, a complete injury had occurred, which has a poor prognosis. When small-amplitude, short-duration (SASD) motor unit potentials are detected, the prognosis for recovery is excellent.
In a complete neurapraxia lesion, no motor unit action potentials (MUAPs) are elicited under voluntary control. EMG can differentiate if the cause of weakness is neuropathic or myopathic. In neurapraxic lesions, the muscle does not reveal any abnormal spontaneous activity (fibrillation and positive sharp waves). On follow-up, the presence of MUAPs indicates that reinnervation is taking place.
In neurapraxia, CMAP and sensory nerve action potential (SNAP) can be elicited distal to the injury. Proximal to the injury, stimulation shows a partial or complete conduction block with varying degrees of decreased CMAP and SNAP associated with reduced conduction velocity. Remyelination improves the changes partially or entirely. Electrodiagnostic studies done two weeks after the injury will show CMAP and SNAP with distal stimulation and will differentiate from a neurotmesis or axonotmesis injury.
Ultrasound can help to identify the continuity of the nerve and exclude neurotmesis injuries.
A computed tomographic scan of the affected area can be helpful to show unreduced fractures causing compression or misplaced hardware.
Magnetic resonance imaging (MRI) of the lumbar spine and pelvis should be done immediately in traumatic and post-operative cases presenting deficits to rule out a compressive source of neuropathy. Diffusion tensor tractography with three-dimensional maps of fiber tracts showing the nerve fiber bundles within the tissue can be obtained using diffusion-weighted imaging and diffusion tensor imaging.
For neurapraxic injuries, conservative treatment is recommended. This includes orthotic measures with splints and limb supports, physical rehabilitation, avoidance of the aggravating activity, and neuropathic pain medications (analgesics, antidepressants, anticonvulsants, corticosteroids, anesthetics). Serial examinations and electrodiagnostic studies are performed to assess for evidence of improvement.
If there is compression by a hematoma, urgent surgical decompression is performed. If it is due to a fracture, surgical decompression may be required. In compartment syndrome, fasciotomy is needed.
If there is no clinical and electrophysiological recovery after 3–6 months, surgical intervention can be required as scar tissue may be preventing improvement. The nerve can have a simple decompression or a decompression with transposition.
Rehabilitation should include psychological support and pain control. Pain control is challenging in PNI. Nerve injury produces a characteristic burning sensation and dysesthesias along with the nerve distribution. Tricyclic antidepressants, serotonin reuptake inhibitors, anticonvulsants (carbamazepine, phenytoin, lamotrigine, gabapentin, and pregabalin), and baclofen can be used. For short-term use, nonsteroidal anti-inflammatory drugs, tramadol, and opioids can be used.
Prevention should be emphasized, especially for iatrogenic damage. Repeat injury should be prevented. Persistent compression can result in a delayed recovery or full recovery.
Neurapraxia resembles many other nerve and muscle illnesses; therefore, the following differentials should be kept in mind when assessing such patients.
Neurapraxia has an excellent prognosis. It is a non-axonal injury, and most patients experience recovery within 2–3 months. Young age favors a better functional outcome, but permanent disability can occur in up to 30% of cases. Those with profound injuries can have long, sick-leave periods.
For ulnar nerve injury, patients should be informed that half of the cases recover within six weeks; however, the remaining half can still be impaired at two years. Brachial plexus injuries after improper positioning during general anesthesia had a full recovery in 82% of the cases.
Neurapraxia, apart from medical complications, had a considerable impact on the life of the individual. The following are a few complications of neurapraxia.
Evaluation and management of neurapraxia is a multidisciplinary approach. Following specialties while working in collaboration can improve outcomes in these patients.
Prevention is the initial step in dealing with neurapraxia. Rehabilitation of these injuries will significantly impact the wellbeing of patients and improve the management of this condition to improve outcomes. Patients must be educated and counseled to seek medical attention as soon as possible to evaluate for treatable causes. Patients can have several weeks of no return of sensory or motor functions, but they should be encouraged to maintain physical therapy and rehabilitation sessions. In approximately three months, the nerve should have recovered.
Neurapraxia frequently poses a diagnostic dilemma and should be differentiated from axonotmesis or neurotmesis. The causes of neurapraxia are many, but the prognosis is usually excellent.
While the neurosurgeon is almost always involved in the care of patients presenting with neurapraxia, it is essential to consult with an interprofessional team of specialists that include a physiatrist and the rehabilitation team. The physiatrist will evaluate the patient and do the appropriate electrodiagnostic studies to enhance and restore functional ability and quality of life to the patient with physical impairments. Physical therapists will help patients in rehabilitation. Prompt consultation with an interprofessional group of specialists is recommended to improve outcomes. Periodic clinical and electrodiagnosis exams are recommended to evaluate for the improvement of nerve function.
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