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nflammatory neuropathies are uncommon but important to diagnose because they are treatable. This review summarises the clinical approach to diagnosis and treatment of Guillain-Barr syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and related neuropathies which are thought to be caused by direct autoimmune attack on peripheral nerves. Features that suggest that a neuropathy is likely to be inflammatory include loss of reflexes without muscle wasting, elevated cerebrospinal fluid (CSF) protein, positive sensory symptoms such as pain or tingling, asymmetry, and proximal weakness. Nerve conduction studies show features of demyelination, especially motor nerve conduction block and temporal dispersion. Inflammatory neuropathy has been arbitrarily classified according to the time from symptom onset until maximal severity, where "acute" is less than four weeks and "chronic" is more than eight weeks, with a rare intermediate "subacute" group. Assessing the efficacy of potential treatments is difficult because the natural history is variable and may include spontaneous improvement. However, some progress has been made in conducting the randomised trials and systematic reviews as a basis for management decisions.
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Robert D. M. Hadden (2003) studied this question.
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