# Peripheral Neuropathy Approach > Peripheral neuropathy approach for NEET-PG Medicine covering axonal versus demyelinating patterns, mononeuritis multiplex, nerve conduction clues and causes. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/peripheral-neuropathy-approach - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-08 - Last updated: 2026-10-08 - Reference basis: Bradley's Neurology in Clinical Practice; Harrison's Principles of Internal Medicine; Davidson's Principles and Practice of Medicine - How to cite: "Peripheral Neuropathy Approach", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/peripheral-neuropathy-approach ## Direct answer A peripheral neuropathy approach starts by sorting the pattern as length-dependent, asymmetric or multifocal, then uses nerve conduction studies to separate axonal from demyelinating disease. Axonal neuropathy shows reduced compound muscle and sensory action potentials with near-normal velocity, while demyelinating neuropathy shows marked slowing, prolonged distal latency, conduction block or temporal dispersion. Common causes include diabetes, alcohol, vitamin B12 deficiency and drugs, and a multifocal pattern raises vasculitis or leprosy. ## What you must remember - **Length-dependent pattern:** symmetrical stocking-and-glove sensory loss from the toes, typical of diabetes, alcohol, uraemia and B12 deficiency. - **Axonal pattern:** reduced amplitudes with near-normal velocity, pointing to metabolic, toxic or nutritional causes. - **Demyelinating pattern:** conduction velocity reduced by about 30 per cent or more below normal, with prolonged distal latency and temporal dispersion, as in CIDP and CMT1A. - **Conduction block:** an amplitude fall of about 30 per cent or more between proximal and distal stimulation, suggesting acquired demyelination. - **Mononeuritis multiplex:** asymmetric involvement of separate nerves, suggesting vasculitis, diabetes, leprosy, sarcoidosis, amyloidosis or lymphoma. - **Anti-MAG neuropathy:** IgM monoclonal antibody against myelin-associated glycoprotein, causing distal sensory ataxia and tremor with demyelinating studies. - **Leprosy neuropathy:** thickened ulnar, common peroneal and great auricular nerves, with hypopigmented anaesthetic skin patches. ## A stepwise route from a glove-and-stocking complaint A 58-year-old man with diabetes reports two years of numb feet. 1. **Confirm length dependence:** Check ankle reflexes, which are usually lost first, and test vibration and joint position sense. 2. **Interpret the sensory loss:** Loss of pain and temperature alone points to small-fibre disease, as in diabetes. Loss of vibration with a positive Romberg test points to large-fibre disease, as in B12 deficiency or CIDP. 3. **Decide the nerve pattern:** Nerve conduction studies separate axonal from demyelinating patterns, and an absent sural response supports distal axonal loss. 4. **Send the laboratory tests:** Fasting glucose and HbA1c, B12 with methylmalonic acid, TSH, renal and liver function, serum protein electrophoresis with immunofixation, and HIV serology are sent. A history of isoniazid or high-dose pyridoxine is checked. 5. **Widen the search if the pattern changes:** If the pattern is asymmetric, multifocal or progressive, vasculitis, sarcoidosis and amyloidosis move up the list, and nerve or muscle biopsy is considered. 6. **Treat acute ascending weakness at once:** Acute ascending weakness with areflexia is handled differently, because Guillain-Barre syndrome needs prompt intravenous immunoglobulin or plasma exchange without waiting for the full work-up. ## Where the axonal and demyelinating labels get mixed up The labels below are mixed up most often, and each has a clear discriminator. - **Trap:** reading a reduced amplitude as demyelination. — **Correct:** amplitude loss is the axonal signal, while slowing or conduction block is the demyelinating signal. - **Trap:** mixing up CMT1A and CMT2. — **Correct:** CMT1A has uniformly slow conduction, thickened nerves and a positive family history, whereas CMT2 is axonal with normal velocity. - **Trap:** attributing an asymmetric, painful neuropathy to diabetes. — **Correct:** diabetes is the commonest cause, but that pattern points to vasculitis or a focal process rather than distal diabetic polyneuropathy (diabetic amyotrophy is a recognised exception). - **Trap:** treating multifocal motor neuropathy with steroids. — **Correct:** it is motor-only with conduction block and no sensory involvement, and it is treated with immunoglobulin rather than steroids. ## Frequently asked questions ### Which nerve conduction finding separates axonal from demyelinating neuropathy? Axonal neuropathy shows reduced compound muscle and sensory action potential amplitudes with only modest slowing of conduction velocity. Demyelinating neuropathy shows marked slowing, prolonged distal motor latency, temporal dispersion or conduction block, with relatively preserved amplitudes in early disease. ### Which tests should follow a diagnosis of mononeuritis multiplex? Mononeuritis multiplex calls for a search for systemic vasculitis, diabetes, leprosy, sarcoidosis, amyloidosis and lymphoma. Initial tests usually include blood sugar, HbA1c, ESR or CRP, ANCA, cryoglobulins, serum protein electrophoresis and HIV serology, with nerve biopsy directed by the clinical pattern. ### When should Guillain-Barre syndrome be suspected in a patient with neuropathy? Guillain-Barre syndrome is suspected when weakness ascends symmetrically over days to weeks with areflexia, often after an infection such as Campylobacter jejuni. CSF typically shows albuminocytologic dissociation, and treatment with intravenous immunoglobulin or plasma exchange should not be delayed. ### How is CIDP distinguished from Guillain-Barre syndrome? Chronic inflammatory demyelinating polyneuropathy is distinguished from Guillain-Barre syndrome by its course, which progresses over more than eight weeks or relapses repeatedly. Both are demyelinating and respond to immunotherapy, but CIDP needs longer treatment and monitoring for relapse.