Abstract

Occlusive processes of the internal carotid artery (ICA) lead to chronic hypoperfusion on the affected side. Severe ICA-stenosis and ICA-occlusion are associated with impaired cognition; but the underlying mechanisms are not fully understood ( Balucani and Silvestrini, 2011 ), and neurophysiological alterations of cortical function in chronic hypoperfusion are poorly investigated so far. To study the effect of hypoperfusion on cortical plasticity and cortical excitability in patients with severe ICA-stenosis on both affected and unaffected side. 10 Patients (61 ± 14 years, range 30–74 years, 3 females) with severe unilateral ICA-stenosis ( n = 3) or ICA-occlusion ( n = 7) were included. Severe hypoperfusion on the affected side was diagnosed by transcranial doppler sonography. Using transcranial magnetic stimulation, cortical excitability was assessed bilaterally by resting motor threshold (rMT), GABAB-activity in the cerebral cortex by the cortical silent period (CSP) at 120% and 130% rMT bilaterally, long term potentiation (LTP)-like cortical plasticity using a paired associative stimulation (PAS) protocol bilaterally, comparing motor evoked potentials (MEP) before, and 0, 15 and 30 min after PAS. For all experiments, the investigator was blinded to the side of the stenosis. rMT was significantly lower on the side of the stenosis, as compared to the contralateral side ( p = 0.02). CSP at 120% rMT showed a trendwise decrease on the side of the stenosis, as compared to the contralateral side ( p = 0.06) ( Fig. 1 ). With regard to cortical plasticity, a repeated measures ANOVA revealed a significant interaction of STENOSIS X TIME ( F = 4.05, p = 0.02), and main effect of STENOSIS ( F = 9.51, p = 0.018). Post-hoc t -tests revealed significant differences in favour of the side contralateral to the stenosis at time point T1 (p). As reported previously ( List et al., 2012 ), LTP-like cortical plasticity was decreased in chronic hypoperfusion. Moreover, we demonstrated enhanced cortical excitability on the side of the stenosis, possibly due to reduced cortical inhibitory GABA-activity. Further evaluations (structural MRI, motor learning tests, neuropsychological tests in both patients and age-matched healthy controls; all ongoing) will help elucidate the complex relationship between hypoperfusion, cortical excitability and cortical plasticity, and cognition.

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