ISS could be seen as a cumulative and additional lesion to a cerebrovascular system already

impaired by chronic hypoxia. Moreover a recent study [17] pointed out that children with SCD have an impaired cerebral blood flow autoregulation compared with age-matched healthy subjects, independently from their hemolysis rate. It suggests Epigenetics inhibitor that children with SCD could have an impaired compensatory reaction to chronic hypoxia (that we consider a possible cause of cognitive impairment) without an increased intracranial blood flow velocities. So also a normal TAMM could be the expression of a pathological situation. Furthermore we have to consider the particular anatomy of the vessels in these patients [18], with an increase of tortuous course not necessarily related to stroke development. This situation could cause an increase in TAMM velocities without a consequent cognitive impairment. The higher brain plasticity of children compared to adult could explain why ISS detect by MRI do not correlate significantly with cognitive impairment. As altered TAMM are predictors of a high risk to develop ischemic stroke, it could express an initial damage that could induce a cognitive impairment after years. Only after a long-term follow-up of children with SCD and altered intracranial blood flow velocities a cognitive impairment

could become clinically relevant. This study has several intrinsic limits: the small sample size of the study population and the limits of TCD in children (large temporal acoustic windows with consequent LGK 974 errors in the measurements of intracranial blood flow velocities). It is necessary to continue the study with a greater number of SCD children and to follow them up in order to assess the positive predictive value to develop cognitive impairment with a non invasive method (TCD) that already demonstrated a high potentiality in children with SCD. “
“The two basic types

of sleep are non-rapid eye movement (NREM) and rapid eye movement (REM) Smoothened sleep. In humans NREM sleep is further subdivided into four stages, each associated with distinct states of altered consciousness [1] and [2]. When compared with baseline levels during wakefulness, cerebral blood flow (CBF) and cerebral metabolism (CM) decrease with the onset of sleep and during sleep stages land I–II and reach minimum values in all brain regions during slow-wave sleep (SWS; sleep stages III and IV) [3], [4], [5], [6], [7], [8], [9] and [10]. These changes are not uniformly distributed. Against this global fall in CBF are important regional variations with some brain regions (frontal cortex, basal ganglia, thalamus, pons, cerebellum) affected to a greater degree while others (temporal cortex) are relatively affected to a minor degree [7] and [11].