3 research outputs found

    Diurnal rhythms in seizures detected by intracranial electrocorticographic monitoring: an observational study

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    Few studies have evaluated human seizure occurrence over the 24-hour day, and only one group has employed intracranial electrocorticography monitoring to record seizures. Circadian patterns in seizures may have important implications in diagnosis and therapy and provide opportunities in research. We have analyzed spontaneous seizures in 33 consecutive patients with long-term intracranial EEG and video monitoring. Several aspects of seizures were noted, including time of day, origin, type, and behavioral state (sleeping/awake). We recorded 450 seizures that showed an uneven distribution over the day, depending on lobe of origin: temporal lobe seizures occurred preferentially between 1100 and 1700 hours, frontal seizures between 2300 and 0500 hours, and parietal seizures between 1700 and 2300 hours. In the awake state, larger proportions of clinical seizures were seen from 0500 to 1100 hours and from 1700 to 2300 hours. During sleep, larger proportions occurred from 1100 to 1700 hours and from 2300 to 0500 hours. Our results suggest that seizures from different brain regions have a strong tendency to occur in different diurnal patterns

    Chronotypes and subjective sleep parameters in epilepsy patients:A large questionnaire study

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    Accumulating evidence suggests epilepsy and seizures may influence circadian rhythms and that circadian rhythms may influence epilepsy. It is also conceivable that seizure timing influences the timing of daily activities, sleeping, and wakefulness (i.e., chronotype). Only one group has studied the distribution of chronotypes of epileptics, showing significant differences between the diurnal activity patterns in two groups of patients with different epilepsy syndromes. The authors performed a questionnaire-based study of 200 epilepsy patients to compare the distribution of chronotypes and subjective sleep parameters of sleep duration and time of mid-sleep on free days to the distribution in the general population (n = 4042). Within this large group of epilepsy patients, we also compared the chronotypes of subsamples with well-defined epilepsy syndromes, i.e., temporal lobe epilepsy [TLE; n = 46], frontal lobe epilepsy [FLE; n = 30], and juvenile myoclonic epilepsy [JME; n = 38]. In addition, 27 patients who had had surgery for TLE were compared with those with TLE who had not had surgery. Both the Morningness-Eveningness Questionnaire and Munich Chronotype Questionnaire were used to determine chronotypes and subjective sleep parameters. Significant differences in morningness/eveningness distribution, timing of mid-sleep (corrected for sleep duration), and total sleep time on free days were found between epileptics and healthy controls. Those with epilepsy were more morning oriented, had earlier mid-sleep on free days, and longer sleep duration on free days (p <.001). However, distributions of chronotypes and sleep parameters between the groups of people with TLE, FLE, and JME did not differ. Persons who had surgery for TLE had similar morningness-eveningness parameters and similar sleep durations compared to those without surgery, but mid-sleep on free days was earlier in operated patients (p = .039). In conclusion, this is the first large study focusing on chronotypes in people with epilepsy. We show that the distribution of chronotypes and subjective sleep parameters of epileptics, in general, is different from that of healthy controls. Nevertheless, no differences are observed between patients with specified epilepsy syndromes, although they exhibit seizures with different diurnal patterns. Our results suggest that epilepsy, itself, rather than seizure timing, has a significant influence on chronotype behavior and subjective sleep parameters. (Author correspondence: [email protected]

    Wnt2 Regulates Progenitor Proliferation in the Developing Ventral Midbrain*

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    Wnts are secreted, lipidated proteins that regulate multiple aspects of brain development, including dopaminergic neuron development. In this study, we perform the first purification and signaling analysis of Wnt2 and define the function of Wnt2 in ventral midbrain precursor cultures, as well as in Wnt2-null mice in vivo. We found that purified Wnt2 induces the phosphorylation of both Lrp5/6 and Dvl-2/3, and activates β-catenin in SN4741 dopaminergic cells. Moreover, purified Wnt2 increases progenitor proliferation, and the number of dopaminergic neurons in ventral midbrain precursor cultures. In agreement with these findings, analysis of the ventral midbrain of developing Wnt2-null mice revealed a decrease in progenitor proliferation and neurogenesis that lead to a decrease in the number of postmitotic precursors and dopaminergic neurons. Collectively, our observations identify Wnt2 as a novel regulator of dopaminergic progenitors and dopaminergic neuron development
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