Acute paralysis in Guillain-Barre syndrome

                                                                                                                                                                                                                                           
Acute paralysis in Guillain-Barre syndrome                                                        is related to Na negligence.


Na (sodium): Na is the chemical symbol for sodium. From natrium, a synonym for sodium.

Sodium is the major positive ion (cation) in fluid outside of cells. The chemical notation for sodium is Na+.  When combined with chloride (Cl), the resulting substance is table salt (NaCl).

Excess sodium (such as from fast food hamburger and fries) is excreted in the urine. Too much or too little sodium can cause cells to malfunction, and extremes can be fatal.

Normal blood sodium level is 135 - 145 milliEquivalents/liter (mEq/L), or in international units, 135 - 145 millimoles/liter (mmol/L).

Morbid and iatrogenic events involving IV salt and water may occur unpredictably in this patient group, resulting in SIADH. It results from a deficit of sodium, or surplus of water due to iatrogenic fluid overload. Na overload is almost always iatrogenic, ie. water overload and not enough potassium. It occurs in patients with Guillian Barre syndrome, meningitis, encephalitis, pneumonia, septicemia, severe malaria, bronchiolitis, RSV infection, or as a direct result of clinical insult. SIADH can sometimes be the first symptom of Guillain Barre syndrome. Na+ channel blocking factor in the cerebrospinal fluid may predispose.

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 used for the treatment of pain. 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 multiple sclerosis (MS).

Hyponatremia is a common fluid-electrolyte disturbance, particularly in patients with neurologic disorders, in part because of the major role the central nervous system (CNS) plays in the regulation of sodium and water homeostasis. Hyponatremia is the most common accompanying electrolyte imbalance in fluid overload states. Rapid correction of hyponatremia can cause osmotic brain demyelination.

Several neurologic disorders including Guillain-Barre 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-Barre 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-Barre 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.

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

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 as to suggest that Guillain Barre Syndrome is also an iatrogenic disorder. Serum sodium: Hyponatermia is common due to osmolar compensation for hyperglycemia. f or normal Na+ indicates severe water loss.

As with sodium, the presence of hyperglycemia leads to a shift of water and potassium from the intracellular to the extracellular space. Patients with low-normal or low serum potassium concentration on admission have severe total-body potassium deficiency and require very careful cardiac monitoring and more vigorous potassium replacement, because treatment lowers potassium further and can provoke cardiac dysrhythmia.

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