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,
Hypotonic hyponatremia a side effect of certain medicines, lung problems such as pneumonia or abscess, brain disease, or certain cancers (most often small cell lung carcinoma). The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used. SIADH can also be treated with specific antagonists of the ADH receptors, such as conivaptan or tolvaptan. Another cause is psychogenic polydipsia. A third group of people with hyponatremia are often said to be "hypervolemic". They are identified by the presence of peripheral edema. In fact, the term