ACUTE ELEVATION AND RECOVERY OF INTRACELLULAR [MG2-ISCHEMIA(] FOLLOWING HUMAN FOCAL CEREBRAL)

We used P-31 magnetic resonance spectroscopy (MRS) to investigate chan ges in brain intracellular [Mg2+] following human focal cerebral ische mia. Mean brain pMg (where pMg = -log[Mg2+]) was significantly lower i n the ischemic focus of all stroke patients (pMg = 3.34 +/- 0.28, n = 45, p < 0.01) when compared with normal controls (pMg = 3.50 +/- 0.08, n = 25). Ischemic brain pMg was also significantly reduced when the p H of the stroke region was acidotic (pH < 6.90, pMg = 3.07 +/- 0.44, n = 11, p < 0.01) and when the phosphocreatine index (PCrI = PCr/[PCr P(i) (inorganic phosphate)]) was reduced (PCrI < 0.47, pMg = 3.12 +/- 0.42, n = 13, p < 0.01). Mean brain pMg was significantly reduced at days 0 to 1 (acute) poststroke (pMg = 3.32 +/- 0.28, n = 26, p < 0.01) and at days 2 to 3 (subacute) poststroke (pMg = 3.38 +/- 0.28, n = 21 , p = 0.03). There was also a significant (p < 0.01) correlation betwe en decreased pMg and increased relative signal intensity of P(i) (norm alized by total phosphate signal, P(i)/TP) for all stroke groups studi ed. During the temporal evolution of stroke, pH returned to normal lev els by days 2 to 3, and pMg returned to normal by days 4 to 10 (subacu te). PCrI and P(i)/TP returned toward normal levels after 10 days (chr onic), at a time when ischemic brain pH had become significantly alkal otic (pH = 7.10 +/- 0.24, n = 15, p < 0.01). Elevation of ischemic bra in [Mg2+] is temporally linked to the acidotic phase of human stroke a s well as the breakdown of energy metabolism. These acute changes in [ Mg2+] may contribute to, or be a marker for, cellular injury.