Acute paralysis in Guillain-Barré syndrome (GBS) is related to a Na negligence.

Acute paralysis in Guillain-Barré syndrome (GBS) is related to a Na negligence. It is associated with morbid and iatrogenic events involving IV salt and water, and channel blocking factor in the cerebrospinal fluid. Na, from natrium, is the chemical symbol/synonym for sodium.

Several neurologic disorders including Guillain-Barré syndrome (GBS) are associated with hyponatremia. Hyponatremia and its overly fast correction have major implications to the course of the underlying neurologic disease. Sudden onset of CNS dysfunction suggests acute onset of hyponatremia. Hyponatremia is reported to occur in up to one-third of patients with Guillain-Barré syndrome (GBS). Hyponatremia can be associated with low, normal, or high tonicity. An association of SIADH with GBS has been documented in a number reports.

The neurophysiological abnormalities seen in Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and multiple sclerosis, traditionally regarded as the result of demyelination, may also be explained by sodium channel dysfunction commonly regarded as electrolyte disorders. Disruption of the blood-brain barrier (BBB) following a rapid increase in serum sodium concentration is considered to play a critical role in the pathogenesis of osmotic demyelination.

Demyelination of the white matter is associated with breakdown of the blood brain barrier and the development of vasogenic edema. Vasogenic edema is the most common type of edema results from local disruption of the blood brain barrier. Once the barrier is breached, hydrostatic and osmotic forces work together to extravasate intravascular fluid. Once extravasated, fluid is retained outside the vasculature, mostly in the white matter of the brain, and within the bundles of myelinated axons of long tracts and commissural fibers.

Active demyelination can be detected with the use of gadolinium-enhanced MRI and usually indicates that there has been a breach in the blood-brain barrier. Alteration in the permeability of the blood-brain barrier may predispose.

Osmotic Demyelination Syndrome occurs with rapid correction of Hyponatremia. It is characterized by acute paralysis, dysarthria, dysphagia and other neurological symptoms.

Anti-GM1 antibody is one of the causative factors of conduction abnormality in GBS patients. Breakdown of the blood-nerve barrier, inflammation of the nerve roots and conduction block are leading symptoms. Antibodies are known to reversibly block the voltage-gated Na+-channels of nerve cells. The demyelination as a secondary event may actually be displaying a pronounced "blood-brain barrier breach".

A novel Na+ channel blocker may exhibit analgesic effects in some. The assumed mechanism of action to effect analgesia is the acute blocking of sodium channels. The role of analgesic and/or antiepileptic drugs with “sodium channel–blocking” properties are the very same drugs known to exacerbate autonomic dysfunction encountered in Guillain-Barré syndrome (GBS) and multiple sclerosis (MS). Autonomic dysfunction is a frequent and severe complication of Guillain-Barre syndrome, giving rise to the hypothesis that some GBS cases may therefore have a subclinical peripheral neuropathy of osmotic aetiology and that Guillain Barre Syndrome is also an iatrogenic disease.