Central pontine myelinolysis sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function. The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem. The most common cause is overly rapid correction of low blood sodium levels (hyponatremia). Apart from rapid correction of hyponatraemia,
Cerebral edema (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly known as hyperosmolar non-ketotic acidosis (HONK). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, which can cause progressive cerebral edema, resulting in a spectrum of signs and symptoms from headache and ataxia to seizures