Acute Inflammatory Demyelinating Polyradiculoneuropathy Guillainbarre Syndrome

Until approximately a decade ago, GBS was considered to be a single clinical entity, a rapidly evolving sensorimotor polyradiculoneuropathy resulting from widespread demyelination in the PNS and due to inflammation. Consequently, GBS was viewed as synonymous with AIDP. However, it is now obvious that demyelination is only one of the causes for the combination of clinical features labeled GBS; different pathological processes can lead to the same clinical presentation (,TabJ,e,49z1). [13' , [14] In 1986, Feasby and co-workers reported that some patients who were considered to have GBS had axon loss rather than SD as their underlying pathophysiology; these cases have been labeled the acute axonal form of GBS. y More recently, it has been appreciated that this subdivision must be further separated into two groups: the first with both motor and sensory fibers affected, labeled the acute motor-sensory axonal neuropathy pattern, y and the second with only motor fibers affected, particularly at the root level, labeled the acute motor axonal neuropathy pattern or acute motor neuropathy. y , y The following discussion reflects the prototype of GBS and these variations.

_TABLE 49-1 -- ACQUIRED DEMYELINATING DISORDERS OF THE PERIPHERAL NERVOUS SYSTEM

Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

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