Akademik Veri Yönetim Sistemi
MULTIPLE SCLEROSIS, cilt.13, sa.6, ss.737-741, 2007 (SCI-Expanded)
A close relationship between multiple sclerosis (MS) lesions and the cerebral vasculature has long been recognised. Some studies have suggested that vascular endothelial cell activation might be an early event in the evolution of MS, and demyelisation may have an ischemic basis in this condition. Hypoxia caused by breath holding (BH) results in autoregulatory vasodilatation, and an increase in CBF to the cortex. The increased CBF can be evaluated by transcranial Doppler (TCD), and can provide information about the vascular integrity. In this study, we aimed to examine the vascular integrity and assess the vasomotor reactivity of MS patients in response to BH in different activation phases of the disease by means of TCD. We studied 12 patients with clinically diagnosed relapsing remitting (RR) MS, according to the Poser criteria. The initial TCD examination was performed in the first two days of an acute exacerbation of disease and prior to any treatment. The second test was performed just after iv methylprednisolone (IVMP) treatment, and the third examination occurred one month later, when the patient was in the remission phase. A group of 11 healthy subjects was also examined by TCD as control. Blood flow velocities were recorded during 30 seconds of normal breathing and 15 seconds BH. Vasomotor reactivity was calculated as a ratio of difference of cerebral flow velocities during BH. There were no significant vasomotor reactivity differences between the controls (55.7%) and the patients during attacks (46.5%), as well as after treatment (48.3%) and during attack free periods (50.9%). There were also no significant changes amongst the patients groups throughout the study. In this study, in different disease activity stages, we observed non-significant cerebrovascular vasomotor reactivity difference between the RRMS patients and the healthy controls, although it was slightly lower in the MS patients. This observation suggests that cerebrovascular reactivity is normal in different disease activity levels.