Phys · neurological
Peripheral Neuropathy
Also known as peripheral neuropathy · polyneuropathy · distal symmetric polyneuropathy · DSPN · diabetic neuropathy · mononeuritis multiplex · Guillain-Barre syndrome · GBS · chronic inflammatory demyelinating polyradiculoneuropathy · CIDP · Charcot-Marie-Tooth disease · CMT · vasculitic neuropathy · small fibre neuropathy · critical illness polyneuropathy
Consultant-physician-depth systematic approach to peripheral neuropathy. Covers the four classification axes — fibre type (motor, sensory, autonomic, mixed), distribution (distal symmetric, mononeuropathy, mononeuritis multiplex, polyradiculoneuropathy), time course (acute, subacute, chronic), and pathology (axonal versus demyelinating — the key NCS discriminator). The full differential by cause: diabetes (the most common, with DSPN and cranial and lumbosacral variants), alcohol and thiamine, B12 and folate, B1 beriberi, B6 toxicity, vitamin E, drug-induced (vincristine, cisplatin, isoniazid, amiodarone, metronidazole, phenytoin, statins), toxins (lead, arsenic, mercury, organophosphates), hereditary (CMT, HNPP), autoimmune (GBS, CIDP, vasculitis), paraproteinaemic (MGUS, myeloma, amyloid, POEMS), uraemic, and critical illness (CIP/CIM). Investigation pathway (NCS/EMG, bloods, CSF, genetics, biopsy) and management (treat the cause, neuropathic pain, foot care, falls and burns prevention). Structured for FRACP DWE and DCE preparation.
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Red flags
- Acute ascending flaccid paralysis with areflexia progressing over days — Guillain-Barre syndrome until proven otherwise; monitor forced vital capacity and admit for respiratory and autonomic monitoring
- Painful asymmetric stepwise multifocal neuropathy with motor and sensory loss — mononeuritis multiplex from vasculitis; urgent sural nerve biopsy and high-dose immunosuppression to prevent irreversible disability
- Rapidly progressive weakness over weeks with respiratory decline or bulbar involvement — consider GBS, CIDP, or vasculitic neuropathy; urgent NCS and CSF, and early IV immunoglobulin or plasma exchange
- Neuropathy with significant orthostatic drop, gastroparesis, or resting tachycardia — severe autonomic neuropathy with risk of syncope, injury, and sudden cardiac death
- A warm, swollen, relatively painless foot in a diabetic — Charcot neuroarthropathy; offload immediately and refer, to prevent fracture dislocation and the rocker-bottom deformity
- A painless foot ulcer in a diabetic — combined neuropathy, ischaemia, and deformity; urgent podiatric and vascular assessment to prevent deep infection and amputation
- Distal weakness with hand involvement, respiratory weakness, or weight loss in a longstanding neuropathy — consider amyloidosis, POEMS, or a paraneoplastic process; check serum free light chains and a paraprotein screen
Peripheral Neuropathy
[1]The answer first
Peripheral neuropathy is a disorder of the peripheral nerves that produces a stereotyped constellation of sensory disturbance (numbness, tingling, burning, pain), motor loss (weakness, wasting, reduced reflexes), and autonomic dysfunction (orthostatic hypotension, gastroparesis, bladder and bowel and sexual dysfunction). It is among the most common problems in general neurology and general medicine — up to 8 per cent of the general population and over 50 per cent of patients with long-standing diabetes have some degree of peripheral neuropathy. [1]
The key to the systematic approach is classification along four axes — fibre type, distribution, time course, and pathology. Of these, two dominate the diagnostic reasoning. Distribution — distal symmetric, mononeuropathy, mononeuritis multiplex, or polyradiculoneuropathy — is the single most powerful clinical clue to the cause. And pathology — axonal versus demyelinating, determined by nerve conduction studies — is the single most powerful paraclinical discriminator, because it partitions the differential into two non-overlapping lists [3].
The most common pattern is distal symmetric polyneuropathy (DSPN), and the most common cause of DSPN is diabetes mellitus, producing a length-dependent, slowly progressive, mixed sensorimotor neuropathy with loss of ankle reflexes and vibration sense [1]. The most common hereditary neuropathy is Charcot-Marie-Tooth disease (CMT) [7]. The two neuropathies that demand emergency recognition are Guillain-Barre syndrome (GBS) — an acute demyelinating polyradiculoneuropathy that can cause respiratory failure within days [5] — and vasculitic neuropathy, presenting as mononeuritis multiplex, which causes irreversible nerve infarction unless treated urgently with immunosuppression [9].
Management rests on three pillars: treat the underlying cause (glycaemic control, immunotherapy, vitamin replacement, toxin removal, dialysis), control neuropathic pain (gabapentinoids, serotonin-noradrenaline reuptake inhibitors, tricyclic antidepressants) [10], and prevent complications (foot care and ulceration, falls, burns, and Charcot neuroarthropathy).
DCE trap: The candidate who, faced with a neuropathy long case, immediately generates a list of twenty causes has already failed. The correct approach is to classify first — state the distribution pattern and the axonal-versus-demyelinating status from the nerve conduction studies — and only then generate a focused, structured differential. This single discipline separates a pass from a distinction. [1]
References10ShowHide
- [1]Tesfaye S, Boulton AJ, Dyck PJ, et al. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments Diabetes Care, 2010.PMID 20876709
- [2]Tesfaye S, Boulton AJ, Dickenson AH. Mechanisms and management of diabetic painful distal symmetrical polyneuropathy Diabetes Care, 2013.PMID 23970715
- [3]England JD, Gronseth GS, Franklin G, et al. Practice Parameter: evaluation of distal symmetric polyneuropathy: role of laboratory and genetic testing (an evidence-based review). Report of the American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Academy of Physical Medicine and Rehabilitation Neurology, 2009.PMID 19056666
- [4]England JD, Gronseth GS, Franklin G, et al. Practice Parameter: evaluation of distal symmetric polyneuropathy: role of autonomic testing, nerve biopsy, and skin biopsy (an evidence-based review) [RETIRED]. Report of the American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Academy of Physical Medicine and Rehabilitation Neurology, 2009.PMID 19056667
- [5]Willison HJ, Jacobs BC, van Doorn PA Guillain-Barré syndrome Lancet, 2016.PMID 26948435
- [6]Van den Bergh PYK, van Doorn PA, Hadden RDM, et al. European Academy of Neurology/Peripheral Nerve Society guideline on diagnosis and treatment of chronic inflammatory demyelinating polyradiculoneuropathy: Report of a joint Task Force-Second revision J Peripher Nerv Syst, 2021.PMID 34085743
- [7]Pareyson D, Marchesi C Diagnosis, natural history, and management of Charcot-Marie-Tooth disease Lancet Neurol, 2009.PMID 19539237
- [8]Latronico N, Bolton CF Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis Lancet Neurol, 2011.PMID 21939902
- [9]Collins MP, Dyck PJ, Gronseth GS, et al. Peripheral Nerve Society Guideline on the classification, diagnosis, investigation, and immunosuppressive therapy of non-systemic vasculitic neuropathy: executive summary J Peripher Nerv Syst, 2010.PMID 21040139
- [10]Attal N, Cruccu G, Baron R, et al. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision Eur J Neurol, 2010.PMID 20402746