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Chronic inflammatory demyelinating polyneuropathy, an acquired immunologically mediated disorder, is clinically similar to Guillain-Barr syndrome except that it has a relapsing or steadily progressive course over months or years and that autonomic dysfunction is generally less common It may present as an exclusively motor disorder or with a mixed sensorimotor disturbance In the relapsing form, partial recovery may occur after some relapses, but in other instances there is no recovery between exacerbations Although remission may occur spontaneously with time, the disorder frequently follows a progressive downhill course leading to severe functional disability Electrodiagnostic studies show marked slowing of motor and sensory conduction, and focal conduction block Signs of partial denervation may also be present owing to secondary axonal degeneration Nerve biopsy may show chronic perivascular inflammatory infiltrates in the endoneurium and epineurium, without accompanying evidence of vasculitis However, a normal nerve biopsy result or the presence of nonspecific abnormalities does not exclude the diagnosis Corticosteroids may arrest or reverse the downhill course Treatment is usually begun with prednisone, 60 mg daily, continued for 2 3 months or until a definite response has occurred If no response has occurred despite 3 months of treatment, a higher dose may be tried In responsive cases, the dose is gradually tapered, but most patients become corticosteroid-dependent, often requiring prednisone, 20 mg daily on alternate days, on a long-term basis IVIG can be used in place of or in addition to corticosteroids and is best used as the initial treatment in pure motor syndromes When both IVIG and corticosteroids are ineffective, plasma exchange may be worthwhile Immunosuppressant or immunomodulatory drugs (such as azathioprine) may be added when the response to other measures is unsatisfactory or to enable maintenance doses of corticosteroids to be lowered Symptomatic treatment is also important

Albers JW et al Porphyric neuropathy Muscle Nerve 2004 Oct;30(4):410 22 [PMID: 15372536]

When the diagnosis is made, the history and appropriate laboratory studies should exclude the possibility of porphyric, diphtheritic, or toxic (heavy metal, hexacarbon, organophosphate) neuropathies The temporal course excludes other peripheral neuropathies Poliomyelitis, botulism, and tick paralysis must also be considered as they cause weakness of acute onset The presence of pyramidal signs, a markedly asymmetric motor deficit, a sharp sensory level, or early sphincter involvement should suggest a focal cord lesion

Most patients eventually make a good recovery, but this may take many months, and about 20% of patients are left with persisting disability

Treatment with prednisone is ineffective and may prolong recovery time Plasmapheresis is of value; it is best per-

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Bolton CF Neuromuscular manifestations of critical illness Muscle Nerve 2005 Aug;32(2):140 63 [PMID: 15825186] Briemberg HR et al Inflammatory neuropathies Curr Neurol Neurosci Rep 2005 Feb;5(1):66 71 [PMID: 15676111] Hughes RA et al Corticosteroids for Guillain-Barr syndrome Cochrane Database Syst Rev 2006 Apr 19;(2): CD001446 [PMID: 16625544] Hughes RA et al European Federation of Neurological Societies/ Peripheral Nerve Society guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: report of a Joint Task Force of the European Federation of Neurological Societies and the Peripheral Nerve Society Eur J Neurol 2006 Apr;13(4):326 32 [PMID: 16643309] Hughes RA et al Guillain-Barr syndrome Lancet 2005 Nov 5;366(9497):1653 66 [PMID: 16271648] Krishnan AV et al Uremic neuropathy: clinical features and new pathophysiological insights Muscle Nerve 2007 Mar;35(3): 273 90 [PMID: 17195171] Stamboulis E et al Clinical and subclinical autonomic dysfunction in chronic inflammatory demyelinating polyradiculoneuropathy Muscle Nerve 2006 Jan;33(1):78 84 [PMID: 16184605]

nostic studies show evidence of partial denervation in weak muscles Peripheral nerve tumors are uncommon, except in Recklinghausen s disease, but also give rise to mononeuropathy This may be distinguishable from entrapment neuropathy only by noting the presence of a mass along the course of the nerve and by demonstrating the precise site of the lesion with appropriate electrophysiologic studies Treatment of symptomatic lesions is by surgical removal if possible

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The median nerve gives off its motor branch, the anterior interosseous nerve, below the elbow as it descends between the two heads of the pronator teres muscle A lesion of either nerve may occur in this region, sometimes after trauma or owing to compression from, for example, a fibrous band With anterior interosseous nerve involvement, there is no sensory loss, and weakness is confined to the pronator quadratus, flexor pollicis longus, and the flexor digitorum profundus to the second and third digits Weakness is more widespread and sensony changes occur in an appropriate distribution when the median nerve itself is affected The prognosis is variable If improvement does not occur spontaneously, decompressive surgery may be helpful

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