Stress-promoting system is known to be involved in course and outcome of acute stage of
ischemic stroke. An important predictor of an unfavorable course of
stroke is so-called "
low T3-syndrome".
Therapy with drugs increasing T3 level on the background of reduced reaction of oxidative stress is one of a perspective direction of neuroprotection. The study aimed at investigating
thyroliberin influence on a
clinical course and an outcome of ischemic atherothrombotic
stroke as well as on
thyroid hormones level in 46 patients (27 women and 19 men) aged 55-75 years admitted to the hospital at the first 24 hours of the disease. Twenty-one patients were switched to
thyroliberin in dosage 500 mcg twice a day during 5 days. A control group included 25 patients. Neurological status of the patients was evaluated on days 1, 3, 7 and 21 using the Orgogozo scale and functional recovery was assessed on day 21 with the Bartel scale. Radioimmunoassay of TTH level, cT3 and free
thyroxine (cT4) in blood plasma was conducted on days 1, 2, 3 and 7 using test-kit IRMA TTG CT (Belorus). Atherosclerotic changes of MAG were measured with USDG on day 1. All the patients underwent MRI of the brain on days 1, 7 and 21 using tomograph Ellips (Russia) 0.15 Tesla. The dynamics of regress of neurological disturbances in patients receiving
thyroliberin appeared as the higher total score on the Orgogozo scale on days 3, 7 and 21 especially in a severe course of the diseases compared to the control group (p<0,007 on day 7). The T3 level in these patients was significantly higher (p<0,05) on days 2, 3 and 7 and the
thyroxine level was increased significantly on the 3rd day of
stroke (p<0,005) as compared to the control group. In patients with moderate severity of the disease, the TTH level was significantly higher on the 2nd day of
stroke (p=0,0004). However, in patients with a severe course TTH and T4 concentrations did not differ in both groups. The results of the study suggest that the use of
thyroliberin in an acute stage of
ischemic stroke prevents development of "
low T3 syndrome" that promotes more rapid and essential regress of neurological disturbances.