Yoga is an ancient Indian science and way of life that has been described in the traditional texts as a systematic method of achieving the highest possible functional harmony between body and mind. Yogic practices are claimed to enhance the quality of sleep. Electrophysiological correlates associated with the higher states of consciousness have been reported in long-term practitioners of transcendental meditation during deep sleep states. The present study was carried out to assess sleep architecture in Sudarshan Kriya Yoga (SKY) and Vipassana meditators. This was to ascertain the differences, if any, in sleep architecture following yogic practices. Whole night polysomnographic recordings were carried out in 78 healthy male subjects belonging to control and yoga groups. The groups studied were aged between 20 and 30-years-old (younger) and 31 to 55-years-old (middleaged). The sleep architecture was comparable among the younger control and yoga groups. While slow wave sleep (non-REM (rapid eye movement) S 3 and S 4 ) had reduced to 3.7 percent in the middleaged control group, participants of the middle-aged yoga groups (both SKY and Vipassana) showed no such decline in slow wave sleep states, which was experienced by 11.76 and 12.76 percent, respectively, of the SKY and Vipassana groups. However, Vipassana practitioners showed a significant enhancement (P < 0.001) in their REM sleep state from that of the age-matched control subjects and also from their SKY counterparts. Yoga practices help to retain slow wave sleep and enhance the REM sleep state in the middle age; they appear to retain a younger biological age as far as sleep is concerned. Overall, the study demonstrates the possible beneficial role of yoga in sleepwakefulness behavior.
Intense meditation practices influence brain functions in different ways and at different levels. Earlier studies have shown that meditation practices help to organize sleep-wake behavior. In the present study, we evaluated the sleep architecture of vipassana meditators across different age groups. Whole-night polysomnography was carried out in healthy male subjects between 30 and 60 years of age from control (n = 46) and meditation (n = 45) groups. They were further divided into younger-(30-39 years), middle-(40-49 years), and older-aged (50-60 years) groups. Sleep variables were evaluated from subjects who had a sleep efficiency index more than 85%. The sleep architecture of vipassana meditators was different from that of control groups. Vipassana meditators showed enhanced slow wave sleep and rapid eye movement sleep states with an enhanced number of sleep cycles across all age groups. When compared to meditators, the control groups exhibited pronounced age-associated decrease in slow wave sleep states. Our study suggests that vipassana meditation helps to establish a proper sleep structure in old age, probably through its capacity to induce neuronal plasticity events leading to stronger network synchronization and cortical synaptic strengthening.
This study demonstrates the clinical efficacy of Manasamitra Vataka and Shirodhara (Ayurvedic treatments) over clonazepam in preserving slow wave sleep and promoting sleep quality in patients of generalized anxiety disorder (GAD) with co-morbid generalized social phobia. Whole night polysomnography was carried out to assess the sleep architecture and spindledelta dynamics. The study highlights the sleep promoting and preserving nature of Manasamitra Vataka and Shirodhara in GAD patients with co-morbid generalized social phobia. Ayurvedic treatments were helpful in improving the subjective quality of sleep and preserve sleep organization. Further studies are needed to confirm the potential of Ayurvedic interventions as a treatment of choice in the management of anxiety disorders.
This contribution aims to integrate findings of our recently reported three brain imaging studies on young narcolepsy-cataplexy patients [1][2][3]. All brain images were acquired using 3.0 Tesla MRI. In our prior study of a voxel-based morphometry [1], narcoleptic patients showed gray matter (GM) deficits in the hypothalamus and fronto-limbic areas. Hypothalamic GM deficits correlated with severity of narcolepsy. In our diffusion tensor imaging study that assessed global white matter (WM) integrity [2], narcoleptic patients had decreased WM integrity especially in fronto-limbic areas, which were associated with sleepiness and attention deficit. Prefrontal metabolite concentration was measured in a proton magnetic resonance spectroscopy [3]. Narcoleptic patients had higher GABA levels in the medial prefrontal areas. This is potentially related to the compensation of nocturnal sleep disturbance. Hypothalamus seems to be a key structure in narcoleptic symptoms. However, both GM and WM abnormalities of fronto-limbic areas were also related to narcolepsy and its symptoms. Compensatory alteration of GABA was also found in the areas. Taken together, our reports suggest that fronto-limbic area, as well as hypothalamus, may be implicated in narcolepsy. References[1] Gray matter deficits in young adults with narcolepsy. Acta Neurol Scand 2009;119:61-7. [2] Decreased fractional anisotropy values in brains of young narcoleptic patients. 2009; presented in APSS. [3] Increased GABA levels in medial prefrontal cortex of young adults with narcolepsy.Two types of monoamine oxidase (MAO), type A (MAO-A) and type B (MAO-B), have been identified. Generally, MAO-A is highly expressed in noradrenergic/adrenergic neurons such as the locus coeruleus, whereas MAO-B is highly expressed in serotonergic and histaminergic neurons and distinct populations of glia such as tanicytes. On the other hand, it has been reported that non-catecholaminergic neurons also express MAOs in an adult rat brain. Extracellular serotonin (5-HT), norepinephrine / epinephrine (NE/E), and dopamine (DA) appear to be removed by a reuptake mechanism; subsequently, they are metabolized by intracellular MAO activity. In the hypothalamus, 5-HT and DBHpositive varicosities densely distribute around hypothalamic nucleus, likely MAO activity affecting the neuronal functions. In the present study, we investigated the distribution of MAOs and the anatomical relation to the neuropeptide-expressing neurons in the rat hypothalamus. We performed enzyme histochemistry for MAO-A or MAO-B, and use specific antibodies for MAO-A and MAO-B. In the result, we found moderate MAO-A enzyme activities in the distinct neuronal populations, and strong MAO-B activity in some glial cells including tanicytes. MAO-A-immunoreactivities (IR) were found in the varicosities of noradrenergic/adrenergic neurons and in the cell bodies of some neuropeptides-expressing neurons in the lateral hypothalamus. Especially, orexin neurons robustly express MAO-A, but not MAO-B. Objective:We have elucidated the p...
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