Negative myoglobin staining in hemiplegic muscle of acute stroke patients predicts functional recovery

There is little information on skeletal muscle changes in patients with acute stroke, despite the repeated observation that levels of serum creatine kinase (CK) and myoglobin (Mb) increase in the initial phase of strokes. It is also not clearly known whether the CK and Mb are derived from skeletal muscle or myocardium.

Biceps muscle biopsies of the hemiplegic side were obtained from 157 ischemic stroke patients on the second day of stroke onset and were examined for immunoreactivity to Mb, and measurements of Mb, total CK, troponin T, epinephrine, and norepinephrine were made on the same day. The degree of disability of patients was assessed at 7 days and at 12 mos after stroke using the Barthel index and the Scandinavian Stroke Scale. The control group consisted of 159 healthy volunteers matched in age and sex.

Lack of Mb immunoreactivity was observed in 109 patients. The prevalence of negatively stained muscle fibers ranged from 0.0% to 22.0%, with a mean of 5.9% +/- 6.0%. The mean values of serum Mb, CK, troponin T, and norepinephrine were higher in patients than those in the control group (P < 0.0001 for all indices; percentage differences were 658% for Mb, 529% for CK, and 258% for norepinephrine). A positive correlation was observed between the prevalence of negative Mb immunostaining in fibers and the Mb (r2 = 0.968, P < 0.0001), CK (r 2= 0.910, P < 0.0001), and norepinephrine levels (r2 = 0.835, P < 0.0001). During the 12-mo study period, Barthel index and Scandinavian Stroke Scale values improved. The percentage change of the Barthel index and Scandinavian Stroke Scale correlated positively with the prevalence of negative Mb immunostaining in fibers.

It was speculated that ischemia, resulting from vasoconstriction induced by an increase in norepinephrine, may be responsible for the occurrence of fibers with negative immunoreactivity for Mb. Patients with higher negative immunostaining for Mb fibers had poor functional recovery of hemiplegia 12 mos after stroke onset. This implies that these muscular alterations may hamper functional recovery.