Brain glycogen metabolism: A possible link between sleep disturbances, headache and depression.

The functions of sleep and its links with neuropsychiatric diseases have long been questioned. Among the numerous hypotheses on sleep function, early studies proposed that sleep helps to replenish glycogen stores consumed during waking. Later studies found increased brain glycogen after sleep deprivation, leading to "glycogenetic" hypothesis, which states that there is a parallel increase in synthesis and utilization of glycogen during wakefulness, whereas decrease in the excitatory transmission creates an imbalance causing accumulation of glycogen during sleep. Glycogen is a vital energy reservoir to match the synaptic demand particularly for re-uptake of potassium and glutamate during intense glutamatergic transmission. Therefore, sleep deprivation-induced transcriptional changes may trigger migraine by reducing glycogen availability, which slows clearance of extracellular potassium and glutamate, hence, creates susceptibility to cortical spreading depolarization, the electrophysiological correlate of migraine aura. Interestingly, chronic stress accompanied by increased glucocorticoid levels and locus coeruleus activity and leading to mood disorders in which sleep disturbances are prevalent, also affects brain glycogen turnover via glucocorticoids, noradrenaline, serotonin and adenosine. These observations altogether suggest that inadequate astrocytic glycogen turnover may be one of the mechanisms linking migraine, mood disorders and sleep.

Memory and prefrontal functions in earthquake survivors: differences between current and past post-traumatic stress disorder patients.

OBJECTIVE: Many studies reported deficits in cognitive functions in post-traumatic stress disorder (PTSD). Most were, however, conducted on man-made trauma survivors. The high comorbidity of alcohol use and depression with PTSD in these studies further complicated the interpretation of their results. We compared prefrontal lobe functions and memory in three earthquake survivor groups: current PTSD, past PTSD and no PTSD. We hypothesized that prefrontal performances of the current and past PTSD groups would be worse than that of control group. METHOD: Survivors of the 1999 earthquakes in Turkey were evaluated for current and lifetime PTSD. Memory and prefrontal functions were assessed by a neuropsychological test battery. RESULTS: Current PTSD patients performed worse on attention, verbal memory, verbal fluency, and psychomotor speed. Past PTSD group was similar to the controls on most cognitive measures, except for their vulnerability to proactive interference and low performance in verbal fluency for animal names. CONCLUSION: Our findings indicate that the prefrontal organization and monitorization of verbally processed information are defective in earthquake-related PTSD patients, more so in the current PTSD group.