Peripheral nerve injuries and high-yield peripheral nerves

• A peripheral nerve injury can produce sensory loss, weakness, or pain in the territory of one named nerve, and the extent of recovery depends on which structural layers of the nerve are damaged.
• The three main degrees of injury are neurapraxia, in which the myelin is injured but the axon remains intact and recovery is usually complete; axonotmesis, in which the axon is damaged but its sheath survives; and neurotmesis, in which the whole nerve trunk is disrupted. ^[3]
• The motor deficits of the classic upper and lower limb nerve lesions can be localised from the pattern of weakness and sensory loss, with the fingers, wrist, shoulder, and foot being the areas most often affected.
• Entrapment neuropathies are the commonest focal nerve lesions in civilian practice; carpal tunnel syndrome and cubital tunnel syndrome are the two most common.
• Initial management of an uncomplicated entrapment is conservative; traumatic nerve injuries need urgent assessment, and any nerve that is not recovering within about 6 months needs surgical review.

By the end of this page you should be able to:

1. Classify a peripheral nerve injury using the Seddon (and Sunderland) scheme and predict its prognosis.
2. Localise a lesion to a specific upper or lower limb nerve from the motor and sensory deficit.
3. Choose the first-line investigation for a suspected entrapment and state when imaging, electrodiagnostic testing, or surgery are needed.
4. Outline the acute and delayed management of traumatic peripheral nerve injury, including timing of repair and rehabilitation.
5. Describe the recognition and first-line management of trigeminal neuralgia, and tell apart a focal mononeuropathy from stroke, radiculopathy, cauda equina syndrome, and polyneuropathy.

A peripheral nerve injury is damage to a named peripheral nerve, a plexus, or a nerve root that produces sensory, motor, or autonomic dysfunction in the territory of that structure.^[1] The term covers trauma, compression, entrapment, ischaemia, and iatrogenic injury. A mononeuropathy is involvement of a single nerve; mononeuritis multiplex is involvement of several non-contiguous nerves; a polyneuropathy is a generalised, usually length-dependent process.

Classification matters because it links what is seen clinically to the underlying pathology and to the expected recovery. Sir Herbert Seddon introduced his three-class scheme in 1942 while treating wounded soldiers, and Sir Sydney Sunderland later expanded it to five grades; Mackinnon and Dellon added a mixed sixth grade.^[1]

The nerve is built in layers, and each layer determines a step in the classification. The endoneurium surrounds each axon, the perineurium binds fascicles and forms the blood-nerve barrier, the epineurium is the tough outer coat, and the mesoneurium allows the nerve to glide in its bed.^[1] An injury that spares the endoneurial tube is the one that can recover by simple remyelination; once the basal lamina tube is lost, the regenerating axon may not find its target.

Traumatic peripheral nerve injuries are uncommon in trauma practice but carry heavy disability because they strike young, working-age adults. A European level I trauma centre identified nerve lesions in 5,026 of 110,667 trauma patients (4.54%).^[2] The median age of affected patients was 39.9 years, sick leave ranged from 11 to 1,109 days, and 30% of those with work-related nerve injuries received a work disability pension of at least 20%.^[2]

Upper limb injuries predominate in civilian practice. Traumatic radial, median, and ulnar nerve injuries and stretch injuries of the brachial plexus are the most frequent, while the sciatic nerve is the most commonly injured lower limb nerve.^[2] In children the pattern is different: lacerations account for 68.1% of nerve injuries, falls for 14.6%, road traffic collisions for 5.6%, and iatrogenic injury for 1.4%; in these cases the digital nerves are involved in almost half.^[2]

Iatrogenic injury is an important and often under-recognised cause. In one large case series 17.4% of peripheral nerve lesions were iatrogenic, and 94% of these followed a surgical procedure.^[2] Major procedures such as osteosynthesis, hernia repair, and knee, hip, or shoulder arthroplasty accounted for 45% of iatrogenic lesions; minor procedures such as lymph node biopsy and varicose vein surgery for 27%; and non-surgical measures such as injections, puncture, positioning, and dressings for 4%.^[2] Median (21.3%), accessory (18%), radial (15.6%), and peroneal (11.5%) nerves were the structures most often affected in that series.^[2]

Gunshot and blast injuries are a separate category, in which the damage from a high-velocity projectile, wound contamination, and debridement often delay nerve reconstruction until a clean soft-tissue bed is achieved.^[2]

For entrapment neuropathies the true population prevalence is poorly documented. Carpal tunnel syndrome is the commonest entrapment, with a prevalence of 3% in the general population (15% in the workforce), and cubital tunnel syndrome has been reported at 1.8% to 5.9% in one US metropolitan area.^[3]

Risk factors for entrapment include repetitive or prolonged pressure on a nerve, sustained abnormal limb posture, anatomic narrowing, tissue oedema, diabetes mellitus, rheumatoid arthritis, hypothyroidism, pregnancy, and inherited susceptibility to pressure palsy.^[1][4]

Every clinical picture follows from two processes: the immediate mechanical damage and the subsequent response of the nerve.

In compression and entrapment, the sequence is usually (i) mild ischaemia of the nerve from compression of the vasa nervorum, (ii) focal demyelination at the site of compression with conduction block, (iii) if compression persists, axonal degeneration, and (iv) fibrosis around and within the nerve.^[3] Prolonged compression of this kind is the mechanism behind carpal tunnel and cubital tunnel syndromes and most other entrapments. How long compression must be present before it produces permanent conduction loss or fibrosis is not well defined in the literature.^[3]

After transection, the distal nerve undergoes Wallerian degeneration with loss of axons and myelin. Sprouts emerge from the proximal stump and grow distally through the basal lamina tubes at about 1 to 3 mm per day. If motor axons reach their muscle within 12 to 18 months, good function can return; after that the motor end plate degenerates and reinnervation is no longer possible.^[2] This is why timing dominates the management of motor nerve injuries.

The symptoms of a focal nerve lesion are produced in the nerve's own territory, never in a root or dermatomal pattern. A lesion is suspected when weakness, pain, or paraesthesia is confined to the muscles and skin supplied by one nerve, with sparing of adjacent nerves and of the territory of spinal roots.^[1][4]

The examination should record all motor, sensory, and reflex functions, and should be repeated after any intervention.^[2] Knowledge of myotomes and dermatomes is essential because the differential diagnosis of a hand or foot deficit includes cervical or lumbar radiculopathy. The approach in short is:

• History. Onset (acute, subacute, or chronic), mechanism (trauma, compression, occupation, sleep posture, recent surgery, fracture), tempo, and aggravating and relieving factors.
• Sensory. Light touch, pinprick, temperature, and two-point discrimination in each dermatome and in each named nerve's sensory territory.
• Motor. Grade power (Medical Research Council 0 to 5) in the muscles supplied by each nerve, and look for wasting and fasciculation.
• Reflexes. Deep tendon reflex changes help separate a peripheral lesion from a spinal cord or root lesion.
• Special tests. Tinel, Phalen, Froment, and tests of opponens and adductor pollicis function; resisted pronation for pronator syndrome; tapping over the fibular neck for peroneal palsy.
• Regional examination. The cervical spine, shoulder, and hip girdle must be examined to exclude a proximal cause.

The brachial plexus is the commonest site of a stretch lesion in the upper limb. A stinger is a transient traction or compression injury in contact sport that gives paraesthesia and weakness radiating from the neck, most often in the C5 and C6 distribution; return to play is acceptable only after complete resolution and exclusion of cervical spine injury.^[3] Persistent or recurrent stingers need imaging for cervical stenosis or bony abnormality.^[3]

Entrapment syndromes deserve separate attention because they are the lesions most often seen outside specialist practice. A working knowledge of the relevant single-nerve territories is the key, because the sensory loss is limited to that territory even when pain spreads more diffusely.^[4]

Fine clinical points worth noting:

• Tinel and Phalen tests for carpal tunnel syndrome have wide and overlapping sensitivity and specificity (Tinel 38% to 100% sensitive and 54% to 98% specific; Phalen 42% to 85% sensitive and 55% to 100% specific), so they cannot be used alone.^[3]
• Foot drop from common peroneal palsy is distinguished from L5 radiculopathy by preserved ankle inversion in peroneal palsy.^[4]
• Brachial neuritis (Parsonage-Turner syndrome), an acute painful inflammatory neuropathy of the shoulder girdle, mimics many upper limb entrapments and should be considered in acute-onset painful weakness.^[4]

The first question is whether the presentation is a single nerve (mononeuropathy), several nerves (mononeuritis multiplex), a root or plexus lesion, or a central lesion. The second is whether one of the conditions in the table explains the whole picture better.

A few selected points on the conditions in the table that are common mimics:

• Trigeminal neuralgia is a paroxysmal, unilateral facial pain syndrome. The European Academy of Neurology guideline (2019) recommends classification as primary (classical or idiopathic, depending on the degree of neurovascular contact) or secondary (caused by pathology other than neurovascular contact), and MRI with three high-resolution sequences as part of the work-up, because no clinical characteristic excludes a secondary cause.^[5] In acute exacerbations, intravenous fosphenytoin or lidocaine can be used; for long-term treatment carbamazepine or oxcarbazepine are drugs of first choice; and microvascular decompression is recommended as first-line surgery in classical trigeminal neuralgia.^[5] Gabapentin, lamotrigine, pregabalin, baclofen, phenytoin, or botulinum toxin type A may be used alone or as add-on therapy.^{[5] [7]}
• Suspected neurological conditions (NICE, NG127, last updated 2023). Compression neuropathies of the radial, ulnar, or common peroneal nerve in adults with clear features and no radiculopathy should be splinted through orthotic services, with review at 6 weeks and neurological referral if there is no improvement; advise the patient to avoid further pressure on the nerve.^[6] Rapidly progressive symmetrical limb weakness or numbness over hours to days needs immediate neurological assessment.^{[6] [4]}

A careful history and examination localise most lesions. Instrumental tests confirm the diagnosis, grade severity, establish a baseline, and are essential when surgery is being considered.

• Nerve conduction studies and EMG. These are the principal ancillary tests. They localise the lesion, quantify axonal loss, distinguish neurapraxia from axonotmesis, and exclude mimics such as radiculopathy. The German S3 guideline recommends neurography in the first weeks if there is diagnostic uncertainty (informative after about 1 week) and needle EMG at 2 weeks to tell neurapraxia from axonotmesis.^[2] In entrapment, electrodiagnostic testing is an adjunct to history and examination and is indicated before surgical intervention.^[3]
• Imaging. Ultrasound is preferred for superficial nerves; MRI for deep or bone-adjacent structures and for surgical planning. For median nerve assessment at the carpal tunnel, a cross-sectional area of 9 mm2 or more at the inlet is 87.3% sensitive and 83.3% specific for carpal tunnel syndrome.^[3] Imaging is immediate in severe weakness or multiple nerve involvement; otherwise it can follow 6 to 8 weeks of conservative treatment.^[3] Ultrasound in particular can identify anatomic causes of entrapment and guide a focused operative approach.^[3]
• Blood tests. No blood test diagnoses an isolated focal nerve lesion. When a polyneuropathy is possible, screen for diabetes (blood glucose), thyroid function, vitamin B12 with metabolites, coeliac disease where appropriate, renal function, ESR, alcohol use, and dysproteinaemia; the American Academy of Neurology practice parameter notes that blood glucose, serum B12 with metabolites, and serum protein immunofixation electrophoresis are the screening tests with the highest yield of abnormality.^[6][8] Neurophysiological and other tests are useful as an adjunct, not as a substitute for clinical assessment.^[1][4]
• When to refer for specialist nerve assessment or studies. Electrodiagnostic testing is appropriate when it will change management; ultrasound or MRI is used to identify anatomic causes of entrapment; and, for refractory entrapments, to plan surgery.^[3][4]

The management pathway depends on the mechanism. The two common settings are an acute traumatic or iatrogenic injury and an entrapment neuropathy without significant trauma. A flowchart of the overall approach follows.

The time aspect is the dominant determinant of outcome.^[2] Notes on timing:

• Immediate exploration is required when a nerve is seen damaged during surgery or when an open injury crosses the nerve's course.^[2] If primary repair is not possible (for example with gunshot wounds, inadequate equipment, or multiple injuries), secondary repair should be carried out within 3 to 6 weeks, once the wound is clean, well perfused, and the diagnosis confirmed.^[2]
• Open injuries require immediate treatment; closed injuries with proven discontinuity should be reconstructed within 1 to 2 weeks; closed injuries without discontinuity that need neurolysis or adjuvant procedures within 2 to 6 weeks.^[2]
• Mixed nerves and pure sensory nerves differ in how urgently repair is needed; the exact cut-off for each nerve type varies between surgical standards, so check local pathways.
• Motor replacement by tendon transfer is a salvage option if reinnervation is not feasible or has failed.^[2] Distal nerve transfers are used when reconstruction is not feasible or unlikely to succeed, and they convert a proximal lesion into a distal one, shortening the reinnervation distance.^[2]
• If there has been no recovery, the treatment concept should be established within about 6 months of the trauma, but as early as possible; surgical exploration should be considered.^[2] Earlier repair improves the chance of good-to-excellent motor recovery.^[2]

Operative points from the guideline:

• Tension-free coaptation is required in every primary or secondary nerve suture.^[2]
• Primary and secondary sutures need microsurgical magnification, adequate lighting, appropriate instruments and suture, and intraoperative neurophysiological testing (grade A recommendation).^[2]
• For defects, autologous nerve grafting (often sural nerve) is the standard option; artificial conduits are reasonable for pure sensory nerves or small gaps.^[2]
• Following nerve reconstruction, occupational therapy and physiotherapy should start as soon as possible, including sensory re-education (mirror therapy, graded motor imagery, sensitivity training) and motor retraining (mirror therapy, electrical muscle stimulation, motor function training).^[2]

Initial treatment should be conservative: patient education, relative rest, activity modification, splinting, and physiotherapy.^[3] Specific measures include nocturnal wrist splinting for carpal tunnel syndrome, activity modification and a 45-degree night splint for cubital tunnel syndrome, and avoidance of provoking postures for peroneal palsy at the fibular neck. Steroid injection gives short-term relief in carpal tunnel syndrome for up to 1 month, and more recent studies show improvement up to 10 weeks with delay of surgery for up to 1 year.^[3] Surgical decompression is reserved for failed conservative care, significant weakness, atrophy, or evidence of moderate to severe damage on electrodiagnostic testing. Carpal tunnel release by open and endoscopic techniques are equally effective, but endoscopic recovery is shorter by about 8 days.^[3]

For neuropathic pain in peripheral nerve injury, NICE (CG173, last updated 2020) recommends offering a choice of amitriptyline, duloxetine, gabapentin, or pregabalin as initial treatment (except trigeminal neuralgia), switching to one of the remaining three if the first is ineffective or not tolerated, and reserving tramadol for acute rescue therapy.^[7] Capsaicin cream may be considered for localised neuropathic pain in patients who wish to avoid or cannot tolerate oral treatment. Cannabis sativa extract, morphine, oxcarbazepine, topiramate, venlafaxine, valproate, and long-term tramadol should not be started in non-specialist settings for neuropathic pain unless advised by a specialist.^[7] Doses are titrated to effect and tolerability per the BNF and product information, with slower titration in older adults and in renal impairment.

• Pregnancy. Entrapment is common in late pregnancy, especially carpal tunnel, and usually remits post partum. Treatment is conservative: splints, activity modification, and analgesia appropriate to pregnancy. For suspected polyneuropathy or progressive deficit in pregnancy, specialist neurological assessment is needed; the American Academy of Neurology practice parameter is a useful guide to the laboratory evaluation of polyneuropathy.^[8]
• Children. Nerve injuries in children arise mostly from laceration. Digital nerves are involved in nearly half. Iatrogenic nerve injury accounts for 1.4% of childhood nerve injuries.^[2] Growth and long recovery times alter expectations; early protected mobilisation and specialist follow-up are important.
• Older adults. Recovery from entrapment and traumatic injury is slower and axonal loss is more likely to be permanent. Neurotoxic and systemic contributors (diabetes, hypothyroidism, nutritional deficiency) are more common and should be screened for.^[6][8]

• Incomplete recovery and disability. Nerve lesions heal incompletely in many patients and cause lifelong functional impairment and high health-care costs.^[2]
• Chronic neuropathic pain, from neuroma formation or central sensitisation; treat as above.
• Recalcitrant neuroma, which may need surgical treatment by resection and targeted muscle reinnervation.^[2]
• Joint deformity and contracture from unopposed muscle action if range of movement is not maintained.^[6]
• Secondary depression and anxiety, from prolonged uncertain recovery; psychological support should be offered.^[2]
• Iatrogenic worsening from delayed recognition of compartment syndrome or missed nerve injury after fracture fixation.

Prognosis is set by the grade of injury, the type of nerve, the distance to the target, the patient's age, and the timing of repair. Neurapraxia recovers fully, usually in days to weeks. Axonotmesis recovers at 1 to 3 mm per day; motor nerves have 12 to 18 months before the motor end plate degenerates. Neurotmesis needs surgery. Mixed and motor nerve defects, and defects closed under tension, fare worst. Prompt, guideline-concordant treatment and interdisciplinary follow-up are the main modifiable factors.^[2]

• Primary prevention of trauma: road safety, safe use of machinery and sport equipment, and avoidance of habitual pressure on superficial nerves (not leaning on elbows, not crossing legs for prolonged periods).
• In hospital: pre- and post-intervention neurological documentation after every manipulation, injection, cast application, or operation, with a low threshold for senior review of a new deficit.^[2]
• Early recognition of compartment syndrome and urgent decompression prevent ischaemic nerve loss.
• Screening for polyneuropathy in diabetes, alcohol misuse, and nutritional deficiency, since an underlying polyneuropathy lowers the threshold for superimposed entrapment.^[6][8]

Pregnancy, children, and older adults are covered in the management section; immunocompromised patients with infection of a nerve injury should be treated according to the organism before surgery.^[2]

• Clinical examination and a sound knowledge of nerve territories are the diagnostic mainstay; imaging and electrodiagnostics are often unavailable and should never delay urgent surgical referral when a nerve has been transected or there is vascular compromise.
• A simple nerve conduction or EMG study, where available, is far more informative than CT or MRI for confirming and grading a peripheral nerve lesion.
• Splints, padding, activity modification, and physiotherapy are low-cost interventions with proven benefit and should be started early.
• Refer early to centres with microsurgical capability; delayed referral wastes the 12-to-18-month window for motor recovery.

Peripheral nerve topics that a student naturally reads next include acute limb ischaemia, stroke, cauda equina syndrome, and trigeminal neuralgia, together with diabetic and other polyneuropathies, radiculopathy, and fracture management.