MBBS viva · Neurology
Peripheral neuropathy — the approach to numb and burning feet viva
A final-prof viva on the clinical approach to the patient with numb, tingling or burning feet. Examiner expects: pattern classification (which determines the differential), the focused bedside examination, nerve-conduction interpretation (axonal vs demyelinating), a structured differential using the DANG THERAPIST frame, and a rational, cause-directed management ladder that rejects opioids and protects the feet.
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Interpretation
The examiner presents a clinical scenario — a patient with progressive numbness and burning in the feet — and asks: "How do you classify this, what is your differential, and how do you investigate and manage it?"
- Classify by pattern first, because pattern predicts the cause. Distal symmetric (length-dependent) polyneuropathy — glove-and-stocking, longest nerves first — is by far the commonest and points to metabolic, toxic or hereditary causes (diabetes, alcohol, B12, drugs, CMT). Asymmetric or multifocal neuropathy points to vasculitis or mononeuritis multiplex, or to CIDP. Acute (days to weeks, ascending, motor) neuropathy points to GBS. Pure sensory points to paraneoplastic or B12; prominent autonomic to diabetic or amyloid.[3]
- The bedside examination confirms the distribution and fibre type: test vibration (128-Hz tuning fork at the hallux) and proprioception and a 10-g monofilament for large-fibre / protective-sensation loss; pinprick and temperature for small-fibre loss; ankle then knee reflexes; distal motor power and wasting; a positive Romberg for sensory ataxia; inspect the feet for ulcers, callus, deformity and Charcot changes; check an orthostatic BP for autonomic involvement.[1]
- Nerve conduction studies (NCS) interpret the pathology. Axonal neuropathy (diabetes, alcohol, B12, toxic) shows reduced amplitudes with near-normal conduction velocity. Demyelinating neuropathy (CIDP, GBS, CMT1) shows slowed conduction velocity, prolonged distal latency, conduction block and temporal dispersion with preserved amplitudes. A patient with burning feet but normal NCS may have small-fibre neuropathy — confirm with skin biopsy (intra-epidermal nerve fibre density).[3]
Key points
The examiner will probe each of these; be ready to defend them at viva depth:
- The differential — use DANG THERAPIST. Diabetes (commonest), Alcohol, Nutritional (B12/thiamine), Genetic (CMT); then Toxic (drugs/metals), Hereditary, Endocrine (hypothyroid), Renal (uraemic), Amyloid/paraprotein, Pyridoxine (B6 excess), Infection (HIV, leprosy), Systemic/vasculitis, Trauma/compression.[3]
- Length dependence explained. The longest axons (to the feet, up to a metre) have the greatest metabolic demand and least reserve, so metabolic and ischaemic insults strike the toes first and ascend — hence glove-and-stocking.[1]
- Diabetic mechanism is multifactorial. Chronic hyperglycaemia drives the polyol (sorbitol) pathway, mitochondrial oxidative stress, advanced glycation and microvascular ischaemia of endoneurial capillaries — producing length-dependent axonal degeneration.[2]
- Axonal vs demyelinating recovery. Axonal neuropathies recover slowly (nerve regrows at about 1 mm/day, roughly 1 inch/month) if the cause is removed and the cell body survives; demyelinating neuropathies can remyelinate and often respond to immunotherapy (CIDP, GBS).[4]
- Neuropathic pain — first-line by class, not opioids. A gabapentinoid (pregabalin/gabapentin), an SNRI (duloxetine, preferred for DPN) or a tricyclic (amitriptyline); start one, titrate, combine on partial response. Topical lidocaine or capsaicin for focal pain. Opioids are avoided — ineffective and addictive for chronic neuropathic pain.[2]
- Foot care prevents amputation. Loss of protective sensation on a 10-g monofilament predicts ulceration; daily inspection, well-fitting footwear, regular podiatry, never walk barefoot, and urgent treatment of any ulcer (offload with a total-contact cast, debride, treat infection).[1]
- The acute or asymmetric neuropathy is an emergency, not ordinary DPN. Rapid ascending weakness with areflexia (GBS), chronic proximal-and-distal demyelinating weakness (CIDP), or painful stepwise asymmetric mononeuritis multiplex (vasculitis) all demand urgent neurology, targeted investigations (CSF, NCS, biopsy) and specific therapy — not reassurance.[3][4]
References
- Selvarajah D, et al. Diabetic peripheral neuropathy. Lancet Diabetes Endocrinol 2019.[1]
- Sloan G, et al. Pathogenesis, diagnosis and clinical management of diabetic sensorimotor peripheral neuropathy. Nat Rev Endocrinol 2021.[2]
- Watson JC, Dyck PJB. Peripheral Neuropathy: A Practical Approach to Diagnosis and Symptom Management. Mayo Clin Proc 2015.[3]
- Lehmann HC, et al. Chronic inflammatory demyelinating polyneuropathy: update on diagnosis, immunopathology and treatment. J Neurol Neurosurg Psychiatry 2019.[4]
References4ShowHide
- [1]Selvarajah D, Kar D, Khunti K, et al. Diabetic peripheral neuropathy: advances in diagnosis and strategies for screening and early intervention. Lancet Diabetes and Endocrinology, 2019.PMID 31624024
- [2]Sloan G, Selvarajah D, Tesfaye S. Pathogenesis, diagnosis and clinical management of diabetic sensorimotor peripheral neuropathy. Nature Reviews Endocrinology, 2021.PMID 34050323
- [3]Watson JC, Dyck PJB. Peripheral Neuropathy: A Practical Approach to Diagnosis and Symptom Management. Mayo Clinic Proceedings, 2015.PMID 26141332
- [4]Lehmann HC, Burke D, Kuwabara S Chronic inflammatory demyelinating polyneuropathy: update on diagnosis, immunopathology and treatment. Journal of Neurology, Neurosurgery and Psychiatry, 2019.PMID 30992333