01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Focal neuropathy can result from external pressure, entrapment in a fibro-osseous tunnel, stretch, trauma, diabetes, pregnancy, oedema, ganglion, tumour or inflammatory disease. The bedside examination determines where along the nerve the lesion lies. A distal lesion weakens only branches below it and removes sensation only where cutaneous fibres still travel. Root disease crosses nerve boundaries, often adds neck or back pain and may alter a corresponding reflex. Plexopathy affects several named nerves in a patchy regional pattern.
Median lesions range from carpal tunnel to pronator syndrome and anterior interosseous palsy. Ulnar lesions commonly occur behind the medial epicondyle or in cubital tunnel and less often at the wrist. Radial injury occurs in the axilla, spiral groove or posterior interosseous branch. The common peroneal nerve is vulnerable where it winds around the fibular neck after weight loss, leg crossing, squatting, casts, surgery or prolonged immobility. Diabetes and inherited pressure-palsy syndromes increase susceptibility at multiple sites.
Management depends on severity, cause and axonal continuity. Transient neurapraxia can recover after pressure relief; axonal injury requires months of regeneration and may leave fixed weakness; laceration or ongoing compression needs earlier surgery. Electrodiagnostic testing is often best after sufficient time for denervation, but an obvious traumatic transection should not wait for it. Splints and therapy preserve joints during recovery. Corticosteroid injection is evidence-based for selected carpal tunnel syndrome but should not be extrapolated casually to every nerve.
Key points
- Localise before naming: identify every weak movement, reflex change and sensory territory, then compare muscles supplied by the same root through different peripheral nerves.
- Carpal tunnel syndrome causes nocturnal paraesthesia in thumb, index, middle and radial ring fingers with later thenar weakness; sensation over the thenar eminence is often spared because the palmar cutaneous branch travels outside the tunnel.
- Anterior interosseous neuropathy is motor only, weakening flexor pollicis longus and index flexor digitorum profundus so the patient cannot make a round thumb-index OK sign.
- Ulnar neuropathy at the elbow causes small-finger and ulnar-ring sensory symptoms with weak finger abduction, adduction and pinch; sustained elbow flexion or leaning commonly aggravates it.
- A lesion in Guyon's canal can spare dorsal ulnar hand sensation because the dorsal cutaneous branch arises proximal to the wrist, helping distinguish wrist from elbow localisation.
- Radial neuropathy at the spiral groove causes wrist and finger drop with triceps preserved, while posterior interosseous neuropathy weakens finger and thumb extension without cutaneous sensory loss.
- Common-peroneal neuropathy at the fibular neck weakens dorsiflexion and eversion with dorsal-foot sensory change; ankle inversion is relatively preserved, unlike many L5 radiculopathies.
- Provocative tests such as Phalen, Tinel and elbow flexion modestly shift probability but cannot diagnose entrapment in isolation or substitute for a neurological examination.
- Nerve-conduction studies localise demyelination or axonal loss and grade severity, while ultrasound or MRI identifies swelling, ganglion, tumour, anomalous muscle or compressive anatomy.
- Remove pressure and improve mechanics early, use a night wrist splint for carpal tunnel or an ankle-foot orthosis for foot drop, and refer severe, progressive or denervating lesions for timely surgical review.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Entrapment and external pressure
Carpal tunnel, cubital tunnel, spiral-groove and fibular-neck compression injure nerves at anatomically vulnerable passages, often worsened by posture or repetitive load.
Trauma and iatrogenic injury
Fracture, dislocation, surgery, injection and prolonged unconscious positioning can stretch, divide or compress an individual peripheral nerve.
Mass and anatomical lesion
Ganglion, tumour, anomalous muscle, scar or vascular lesion can create focal compression requiring imaging and sometimes surgical removal.
Systemic nerve vulnerability
Diabetes, vasculitis, hereditary pressure-palsy susceptibility and generalised neuropathy lower the threshold for focal nerve injury or produce multifocal lesions.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Focal mechanical stress
Compression or stretch distorts myelin and impairs local endoneurial blood flow at the affected anatomical site.
- 2Conduction block
Segmental demyelination slows or blocks impulses, producing weakness and paraesthesia that may recover after pressure is relieved.
- 3Axonal degeneration
Severe or prolonged injury disrupts axons, causing distal Wallerian degeneration, denervation, wasting and slow recovery dependent on regrowth distance.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Nocturnal tingling, shaking the hand for relief, sensory loss in radial three-and-a-half digits and weak thumb abduction or opposition localises to the wrist.
Weak thumb interphalangeal and index distal-interphalangeal flexion creates a flattened pinch, with no cutaneous numbness because the branch is purely motor.
Symptoms worsen with elbow flexion, dorsal and palmar ulnar sensation may be affected and first dorsal interosseous weakness produces impaired finger abduction and Froment sign.
Wrist, finger and thumb extension fail after prolonged upper-arm compression while elbow extension remains intact and dorsal first-web-space sensation may be reduced.
Finger and thumb drop occurs without sensory loss; wrist extension may persist but deviates radially because extensor carpi radialis longus is spared.
Foot drop with weak eversion, preserved inversion and numbness over anterolateral leg or dorsum of foot points to the fibular neck rather than L5 root.
Deficit after fracture, dislocation, deep laceration, tourniquet or expanding painful swelling requires immediate orthopaedic, plastic or vascular assessment.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Motor and sensory localisation examinationFirst step - Why
- Distinguish named nerve, branch, root and plexus lesions before testing.
- Interpretation and limitations
- Test individual movements against resistance, relevant reflexes and autonomous sensory zones; compare inversion and hip abduction for foot drop and thenar-eminence sensation for median lesions.
- 02
Nerve-conduction studies - Why
- Localise conduction slowing or block and quantify axonal sensory and motor loss.
- Interpretation and limitations
- Focal slowing across wrist, elbow or fibular head supports entrapment; normal sensory potentials can occur in a root lesion because the dorsal-root ganglion is distal to pathology.
- 03
Needle electromyography - Why
- Identify active denervation, chronic reinnervation and root or plexus involvement.
- Interpretation and limitations
- Timing matters because fibrillation develops after axonal degeneration; paraspinal abnormalities support radiculopathy but sensitivity is imperfect.
- 04
Peripheral nerve ultrasound - Why
- Show focal enlargement, subluxation, ganglion or external compression dynamically.
- Interpretation and limitations
- Cross-sectional area thresholds depend on nerve and laboratory; imaging complements rather than overrides concordant symptoms and electrophysiology.
- 05
MRI nerve, joint or spine - Why
- Investigate mass, trauma, anomalous anatomy, plexus disease or a root differential.
- Interpretation and limitations
- Select the scan from localisation; common degenerative spinal findings should not be blamed unless level, side and weak muscles agree.
- 06
Radiographs after trauma or deformity - Why
- Detect fracture, dislocation, callus or bony narrowing affecting a nerve.
- Interpretation and limitations
- Urgent post-traumatic images and examination guide surgical action, whereas normal radiographs do not exclude soft-tissue entrapment.
- 07
Targeted metabolic screen - Why
- Find systemic susceptibility when neuropathies are bilateral, recurrent or multifocal.
- Interpretation and limitations
- HbA1c, thyroid, B12, renal profile, paraprotein or inflammatory studies follow context; routine large panels add noise in a clear single compression.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Radiculopathy
Dermatomal pain, myotomal weakness and reflex change across muscles supplied by different nerves favour a cervical or lumbar root lesion.
Plexopathy
Patchy weakness and sensory loss spanning several terminal nerves, often with severe proximal pain, supports brachial or lumbosacral plexus disease.
Polyneuropathy
Symmetrical length-dependent sensory loss and distal weakness indicate diffuse nerve disease, although focal entrapments may coexist.
Central motor lesion
Brisk reflexes, spasticity, sensory level or cortical signs redirect localisation to spinal cord or brain rather than one peripheral nerve.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01LocaliseBuild a movement-and-sensation mapFirst stepA patient presents with focal hand weakness, wrist drop or foot drop.+
- 1Establish onset, pressure, posture, injury, weight loss, surgery, pregnancy, diabetes and neck or back pain, noting progression and any sphincter or systemic symptoms.
- 2Test each affected movement, reflex and autonomous sensory zone, then test same-root muscles supplied by other nerves to distinguish mononeuropathy from radiculopathy.
- 3EscalationEscalate acute traumatic, vascular, compartment, cauda-equina or rapidly progressive patterns immediately before arranging routine electrophysiology.
02Conservative entrapmentRemove pressure and preserve movementA mild or moderate compressive neuropathy has no major axonal weakness or urgent structural cause.+
- 1Modify the specific pressure: neutral wrist at night for carpal tunnel, avoid prolonged elbow flexion or leaning for ulnar neuropathy, and protect the fibular neck.
- 2Use hand therapy, ergonomic change or ankle-foot orthosis to maintain safe function and range while treating diabetes, oedema or nutritional vulnerability when present.
- 3Review at a defined interval with objective power and sensation, obtaining nerve conduction or imaging if weakness progresses, diagnosis is uncertain or recovery stalls.
03Carpal tunnel interventionEscalate median entrapment proportionatelyEscalationMedian symptoms persist despite splinting or examination suggests significant motor involvement.+
- 1Confirm the clinical diagnosis, account for pregnancy, diabetes, thyroid disease, arthritis and proximal median or cervical mimics, and grade thenar power.
- 2Offer locally commissioned corticosteroid injection for temporary benefit in selected patients or refer for decompression when symptoms are severe, recurrent or denervation is present.
- 3Do not delay surgical opinion for fixed sensory loss, thenar wasting or major neurophysiological axonal loss, explaining that recovery may be incomplete after prolonged damage.
04Motor recoveryProtect function during axonal regenerationRadial, ulnar or common-peroneal palsy has caused clinically important motor loss.+
- 1Remove compression and provide wrist, hand or ankle support that prevents contracture and falls while allowing safe movement of unaffected muscles.
- 2Repeat examination and appropriately timed electromyography for continuity and reinnervation, imaging the nerve when a mass or constriction remains possible.
- 3Refer to peripheral nerve or orthopaedic surgery when laceration, persistent conduction block, absent recovery or a time-sensitive tendon or nerve transfer is considered.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Local corticosteroid for carpal tunnel
A trained clinician uses the locally approved corticosteroid and dose, commonly with local anaesthetic, after confirming anatomy, consent and contraindications.Avoid intraneural injection; discuss transient pain, skin change, tendon or nerve injury, glucose elevation and variable duration, and do not use repeated injection to postpone necessary decompression.
Paracetamol
Use the current BNF adult oral regimen for short-term associated musculoskeletal pain, reducing the maximum for low body weight or liver risk.Check combination products and avoid presenting analgesia as definitive care when weakness, denervation or a structural lesion requires intervention.
Neuropathic pain medicine
Select amitriptyline, duloxetine, gabapentin or pregabalin through the NICE neuropathic-pain pathway with low initiation, titration and organ-dose adjustment.Sedation, falls, anticholinergic effects, dependence and respiratory risk differ by agent; focal numbness alone is not an indication and benefit must be reviewed.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Persistent weakness and contracture
Unrecovered denervation causes hand intrinsic wasting, wrist or foot drop and fixed shortening that impairs gait, grip and self-care.
Sensory injury and ulceration
Loss of protective sensation permits burns, pressure damage and unnoticed wounds, especially when diabetes or vascular disease impairs healing.
Chronic neuropathic pain
Ongoing compression and axonal injury can cause burning, allodynia and sleep disruption even after motor function improves.
Incomplete surgical recovery
Late decompression cannot restore irreversibly lost axons, while surgery itself carries scar, infection and recurrent-compression risk.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Grade the same key muscles serially, such as abductor pollicis brevis, first dorsal interosseous, finger extensors, tibialis anterior and ankle evertors.
- Map autonomous sensory zones rather than asking only whether numbness is better, watching for ulcers, burns and loss of protective sensation.
- Check splint and orthosis fit, skin pressure and functional benefit, especially after oedema, weight change or recovering power alters mechanics.
- Repeat nerve conduction or electromyography only when severity, reinnervation or surgical timing will change management rather than on a fixed calendar.
- Review diabetes, thyroid, pregnancy-related oedema, weight loss and workplace or sleep pressure that may perpetuate entrapment.
- Escalate any progressive weakness, new root or cord signs, intractable pain or lack of expected recovery to the relevant nerve, spine or surgical service.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Thenar skin is spared
The palmar cutaneous median branch leaves before the carpal tunnel, so numb thenar eminence suggests a more proximal lesion despite classic finger symptoms.
Dorsal ulnar sensation localises
Sparing of the dorsal ulnar hand supports a lesion in Guyon's canal because that sensory branch has already left the nerve above the wrist.
PIN has no numbness
Posterior interosseous palsy causes finger drop without cutaneous sensory loss, while preserved wrist extension often pulls toward the radial side.
Inversion tests L5 elsewhere
Tibialis posterior is L5 but supplied by the tibial nerve; weak inversion with foot drop therefore favours L5 root or plexus over common-peroneal entrapment.
A normal early EMG is limited
After acute axonal injury, denervation takes time to emerge, so a premature study cannot guarantee continuity or benign prognosis.
11Common pitfallsFrequent interpretation and management errors.
- 01
Diagnosing entrapment from Tinel sign alone.
- 02
Calling all radial finger tingling carpal tunnel syndrome.
- 03
Missing a proximal median lesion when thenar-eminence sensation is abnormal.
- 04
Assuming wrist drop always means a radial lesion without testing other nerves.
- 05
Calling every foot drop common-peroneal palsy without testing inversion and hip abduction.
- 06
Waiting for electrophysiology before treating laceration or compartment syndrome.
- 07
Repeating injections while motor denervation progresses.