Approach to Peripheral Neuropathy
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Direct answer
Peripheral neuropathy is solved by pattern, not by test menus: define the temporal course, the fibre and modality involved, the distribution (symmetrical length-dependent versus asymmetric multifocal versus focal) and the family history, then let nerve conduction separate demyelinating from axonal pathology. In India the dominant causes are diabetes, leprosy, vitamin B12 deficiency, alcohol and drugs, with Guillain-Barré syndrome and CIDP as the immune acute and chronic forms. The pattern determines both the shortlist and the first investigation.
What you must remember
- Nerve conduction dichotomy: demyelinating disease shows slowed conduction, prolonged distal and F-wave latencies and conduction block (Guillain-Barré, CIDP, CMT1, multifocal motor neuropathy); axonal disease shows reduced amplitudes with preserved conduction (metabolic, toxic, most hereditary distal neuropathies).
- Uniform demyelination with slowed conduction everywhere suggests inherited CMT1; non-uniform slowing with blocks suggests acquired CIDP — the single most useful discrimination in the electrophysiology report.
- Indian length-dependent causes: diabetic (screen with monofilament; small-fibre burning with normal conduction is common), vitamin B12 deficiency (posterior column signs, macrocytosis, methylmalonic acid and homocysteine), alcohol, hypothyroidism, uraemia and drugs — isoniazid always with pyridoxine, vincristine, metronidazole.
- Leprosy remains the great Indian neuropathy: thickened tender nerves (ulnar at the elbow, great auricular, common peroneal), mononeuritis multiplex or symmetric neuropathy with anaesthetic skin patches, and a pure neuritic form with normal skin; treat with WHO multidrug therapy plus corticosteroids for reactions and nerve function impairment.
- Immune neuropathies: CIDP produces proximal and distal weakness beyond eight weeks with hypertrophic nerves and cytoalbuminologic dissociation, responding to steroids, immunoglobulin or plasma exchange; multifocal motor neuropathy produces asymmetric motor blocks with anti-GM1 antibodies, responding to immunoglobulin and worsening with steroids.
- Mononeuritis multiplex (asymmetric, painful, stepwise) implies vasculitis until excluded: screen vasculitic markers, cryoglobulins and hepatitis B and C, and consider nerve biopsy.
- Hereditary pointers: family history, high arches, hammer toes, inverted-champagne calves and uniform slowing in CMT1A (PMP22 duplication); recurrent pressure palsies suggest PMP22 deletion; small-fibre with autonomic neuropathy and family history suggests transthyretin amyloidosis.
Common confusion
CIDP versus Guillain-Barré is a time question — eight weeks of progression is the customary dividing line, and steroid responsiveness belongs only to the chronic form. CMT versus CIDP traps candidates into immunosuppressing a hereditary neuropathy; family history, foot deformity and uniform slowing point to CMT. Small-fibre neuropathy with normal conduction studies is not functional: diabetes and glucose intolerance are the usual culprits. Finally, a stocking-glove sensory level with brisk reflexes localises to cord or ganglion — though B12 deficiency straddles both territories and deserves the methylmalonic acid test.
Exam-focused takeaway
Answer in the examiner's order: pattern first, conduction second, cause third. The examinable pairs are uniform versus non-uniform demyelination, mononeuritis multiplex with vasculitis, anti-GM1 with multifocal motor neuropathy, and the thickened ulnar nerve with leprosy. In any Indian sensory neuropathy, the safest additions to the workup are vitamin B12 metabolites and a meticulous skin and nerve examination.
Frequently asked questions
How are demyelinating and axonal neuropathies distinguished on nerve conduction?
Demyelination slows velocity and prolongs latencies with conduction block; axonal loss reduces amplitudes with preserved velocity.
Which treatable neuropathies are common in India?
Diabetic, vitamin B12 deficiency, leprosy, alcohol-related, hypothyroid and drug-induced — several preventable or reversible when caught early.
What is mononeuritis multiplex?
Stepwise painful involvement of individual nerves, classically vasculitic, requiring urgent serological workup and often nerve biopsy.
How does leprosy present neurologically?
Thickened tender nerves with anaesthetic hypopigmented patches, mononeuritis multiplex or a pure neuritic symmetric neuropathy — entirely treatable.
What distinguishes CIDP from CMT?
CIDP is acquired, progressive beyond eight weeks, non-uniformly demyelinating and steroid-responsive; CMT is hereditary, uniform and unresponsive to immunotherapy.