Table 2.

Causes of polyneuropathy according to mode of presentation

Mode of presentation	Distinctive clinical features	Examples of causes
Acute	Rapid progression from onset to nadir, typically <4 weeks	GBS, vasculitis, porphyria, toxins, infections (e.g. Lyme disease, diphtheria), critical illness neuropathy
Subacute	Progression from onset to nadir = 4–8 weeks	Vasculitis, SIDP, vitamin B12 deficiency
Multifocal	Patchy, asymmetrical, non-length-dependent	Vasculitis, HNPP, MMN, diabetes mellitus, leprosy, sarcoidosis, malignant infiltration, occasionally CIDP
Demyelinating, predominantly motor	Weakness disproportionate to wasting, nerve hypertrophy, postural upper limb tremor	AIDP, SIDP, CIDP, CMT1, CMTX, paraproteinaemic, amiodarone
Large-fibre sensory neuropathy/neuronopathy	Sensory ataxia, pseudo-athetosis, loss of vibration and joint position sensation	Sjögren's syndrome, paraneoplastic, idiopathic, occasionally CIDP, paraproteinaemic, vitamin B12 deficiency
Small-fibre	Neuropathic pain, autonomic involvement	Diabetes mellitus, idiopathic, amyloidosis, HIV, HSN, Fabry disease
Hypertrophic	Palpable (and sometimes visible) nerves, e.g. ulnar, superficial radial, common peroneal, greater auricular	Leprosy, CIDP, CMT1, Refsum's disease, amyloidosis, neurofibromatosis
‘Default’	Chronic, axonal, length-dependent	Diabetes mellitus, idiopathic, CMT2, HIV, alcohol, thiamine deficiency, chronic kidney disease, many drugs and toxins

GBS, Guillain–Barré syndrome; SIDP, subacute inflammatory demyelinating polyradiculoneuropathy; HNPP, hereditary neuropathy with liability to pressure palsies; MMN, multifocal motor neuropathy; CIDP, chronic inflammatory demyelinating polyradiculoneuropathy; AIDP, acute inflammatory demyelinating polyradiculoneuropathy; CMT1, autosomal dominant demyelinating Charcot–Marie–Tooth disease; CMTX, X-linked Charcot–Marie–Tooth disease; HSN, hereditary sensory neuropathies; CMT2, autosomal dominant axonal Charcot–Marie–Tooth disease.