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TREATMENT OF GBS, Neuropathy, CIDP
What is Neuropathy management? or CIDP ?
Journal of Neurology Neurosurgery and Psychiatry 2003;74:ii9
MANAGEMENT OF INFLAMMATORY NEUROPATHIES
Robert D M Hadden1 and Richard A C Hughes2
Inflammatory neuropathies are uncommon but important to diagnose because they are treatable. This review summarises the clinical approach to diagnosis and treatment of Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and related neuropathies which are thought to be causedby direct autoimmune attack on peripheral nerves. Features that suggest that a neuropathy is likely to be inflammatory includeloss of reflexes without muscle wasting, elevated cerebrospinalfluid (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 neuropathyhas 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.
GUILLAIN-BARRé SYNDROME (GBS)
GBS is a clinically defined syndrome with several underlying pathologies. It affects 1–4 per 100 000 per year, men slightly more often than women. Diagnostic criteria1 include progressive weakness of two or more limbs reaching a maximum within four weeks, reduced or absent tendon reflexes in the weak limbs, and exclusion of alternative causes (box 1).2 Somecases may be so mild that medical attention is never sought. Most cases are caused by acute inflammatory demyelinating polyradiculoneuropathy (AIDP), but some are caused by acute motor axonal neuropathy (AMAN) or acute motor and sensory axonal neuropathy (AMSAN).3Primary axonal GBS is thought to be caused by an autoimmun eattack on axonal antigens, and is common in Asia, but is responsible for less than 5% of GBS cases in Europe and North America. Reflexesare sometimes preserved in AMAN. Rarer variants of GBS are thepharyngo-cervico-brachial pattern, acute oropharyngeal palsy(not to be confused with diphtheria), involvement of the lowerbut not upper limbs, and a pure motor and a pure sensory form. Acute pandysautonomia and acute sensory neuronopathy may also be related.
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