Kl. Newell et Bk. Kleinschmidtdemasters, CENTRAL PONTINE MYELINOLYSIS AT AUTOPSY - A 12 YEAR RETROSPECTIVE ANALYSIS, Journal of the neurological sciences, 142(1-2), 1996, pp. 134-139
Central pontine myelinolysis (CPM) was first described in 1959 and onl
y later was associated with a rapid, sustained rise in serum sodium fr
om a hyponatremic baseline. This discovery in 1981 led to modification
s in recommendations for clinical treatment of hyponatremia. Our inter
est has been in tracking the incidence of CPM found at autopsy by year
to see whether changes in medical treatment in hyponatremia have resu
lted in a decrease in CPM over time. Clinically asymptomatic CPM found
at autopsy has always been at least as frequent as cases diagnosed pr
emortem and serves as a reasonable indicator for the incidence of the
disease, In over 3,000 autopsies, on most of which the brain was exami
ned macroscopically and microscopically by the same neuropathologist,
we have discovered 15 cases of asymptomatic, small pontine CPM. Of the
se 15, 6 were active lesions and 9 were remote; in the active group, 5
of the 6 cases were associated with a rapid, sustained rise in serum
sodium during the appropriate time period. The incidence of asymptomat
ic CPM has remained steady over the 13-year time period. In contrast,
we have encountered no cases of CPM diagnosed premortem that have come
to autopsy in the same time period. These cases emphasize that CPM st
ill occurs, but most often as an asymptomatic disorder with small, mid
line pontine lesions. When small active CPM is found, it still is asso
ciated with a rapid sustained rise in serum sodium.