Localise common focal nerve lesions from motor, sensory and provoking patterns, distinguish them from root and plexus disease, and select urgent decompression, conservative care, neurophysiology or surgery appropriately.
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.
Carpal tunnel, cubital tunnel, spiral-groove and fibular-neck compression injure nerves at anatomically vulnerable passages, often worsened by posture or repetitive load.
Fracture, dislocation, surgery, injection and prolonged unconscious positioning can stretch, divide or compress an individual peripheral nerve.
Ganglion, tumour, anomalous muscle, scar or vascular lesion can create focal compression requiring imaging and sometimes surgical removal.
Diabetes, vasculitis, hereditary pressure-palsy susceptibility and generalised neuropathy lower the threshold for focal nerve injury or produce multifocal lesions.
Compression or stretch distorts myelin and impairs local endoneurial blood flow at the affected anatomical site.
Segmental demyelination slows or blocks impulses, producing weakness and paraesthesia that may recover after pressure is relieved.
Severe or prolonged injury disrupts axons, causing distal Wallerian degeneration, denervation, wasting and slow recovery dependent on regrowth distance.
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.
Dermatomal pain, myotomal weakness and reflex change across muscles supplied by different nerves favour a cervical or lumbar root lesion.
Patchy weakness and sensory loss spanning several terminal nerves, often with severe proximal pain, supports brachial or lumbosacral plexus disease.
Symmetrical length-dependent sensory loss and distal weakness indicate diffuse nerve disease, although focal entrapments may coexist.
Brisk reflexes, spasticity, sensory level or cortical signs redirect localisation to spinal cord or brain rather than one peripheral nerve.
Unrecovered denervation causes hand intrinsic wasting, wrist or foot drop and fixed shortening that impairs gait, grip and self-care.
Loss of protective sensation permits burns, pressure damage and unnoticed wounds, especially when diabetes or vascular disease impairs healing.
Ongoing compression and axonal injury can cause burning, allodynia and sleep disruption even after motor function improves.
Late decompression cannot restore irreversibly lost axons, while surgery itself carries scar, infection and recurrent-compression risk.
The palmar cutaneous median branch leaves before the carpal tunnel, so numb thenar eminence suggests a more proximal lesion despite classic finger symptoms.
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.
Posterior interosseous palsy causes finger drop without cutaneous sensory loss, while preserved wrist extension often pulls toward the radial side.
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.
After acute axonal injury, denervation takes time to emerge, so a premature study cannot guarantee continuity or benign prognosis.
Diagnosing entrapment from Tinel sign alone.
Calling all radial finger tingling carpal tunnel syndrome.
Missing a proximal median lesion when thenar-eminence sensation is abnormal.
Assuming wrist drop always means a radial lesion without testing other nerves.
Calling every foot drop common-peroneal palsy without testing inversion and hip abduction.
Waiting for electrophysiology before treating laceration or compartment syndrome.
Repeating injections while motor denervation progresses.
Your practice draft is saved in this browser.
A patient develops foot drop after prolonged leg crossing. Dorsiflexion and eversion are weak, sensation is reduced over the dorsum of the foot, but ankle inversion and hip abduction are normal. Where is the lesion most likely?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
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.
Check combination products and avoid presenting analgesia as definitive care when weakness, denervation or a structural lesion requires intervention.
Sedation, falls, anticholinergic effects, dependence and respiratory risk differ by agent; focal numbness alone is not an indication and benefit must be reviewed.