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,
Serum amyloid A1 Serum amyloid A1 Serum amyloid A1 (SAA1) is a protein that in humans is encoded by the "SAA1" gene. SAA1 is a major acute-phase protein mainly produced by hepatocytes in response to infection, tissue injury and malignancy. When released into blood circulation, SAA1 is present as an apolipoprotein associated with high-density lipoprotein (HDL). SAA1 is a major precursor of amyloid A (AA), the deposit of which leads to inflammatory amyloidosis. The gene coding for human SAA1 is one of the 4 SAA genes mapped to a region in the short arm on Chromosome 15. Two of these genes, SAA1 and