The Effect of Mindfulness Meditation on Impulsivity and its Neurobiological Correlates in Healthy Adults.

Interest has grown in using mindfulness meditation to treat conditions featuring excessive impulsivity. However, while prior studies find that mindfulness practice can improve attention, it remains unclear whether it improves other cognitive faculties whose deficiency can contribute to impulsivity. Here, an eight-week mindfulness intervention did not reduce impulsivity on the go/no-go task or Barratt Impulsiveness Scale (BIS-11), nor produce changes in neural correlates of impulsivity (i.e. frontostriatal gray matter, functional connectivity, and dopamine levels) compared to active or wait-list control groups. Separately, long-term meditators (LTMs) did not perform differently than meditation-naïve participants (MNPs) on the go/no-go task. However, LTMs self-reported lower attentional impulsivity, but higher motor and non-planning impulsivity on the BIS-11 than MNPs. LTMs had less striatal gray matter, greater cortico-striatal-thalamic functional connectivity, and lower spontaneous eye-blink rate (a physiological dopamine indicator) than MNPs. LTM total lifetime practice hours (TLPH) did not significantly relate to impulsivity or neurobiological metrics. Findings suggest that neither short- nor long-term mindfulness practice may be effective for redressing impulsive behavior derived from inhibitory motor control or planning capacity deficits in healthy adults. Given the absence of TLPH relationships to impulsivity or neurobiological metrics, differences between LTMs and MNPs may be attributable to pre-existing differences.

Acute effects of meditation training on the waking and sleeping brain: Is it all about homeostasis?

Our recent finding of a meditation-related increase in low-frequency NREM sleep EEG oscillatory activities peaking in the theta-alpha range (4-12 Hz) was not predicted. From a consolidated body of research on sleep homeostasis, we would expect a change peaking in slow wave activity (1-4 Hz) following an intense meditation session. Here we compared these changes in sleep with the post-meditation changes in waking rest scalp power to further characterize their functional significance. High-density EEG recordings were acquired from 27 long-term meditators (LTM) on three separate days at baseline and following two 8-hr sessions of either mindfulness or compassion-and-loving-kindness meditation. Thirty-one meditation-naïve participants (MNP) were recorded at the same time points. As a common effect of meditation practice, we found increases in low and fast waking EEG oscillations for LTM only, peaking at eight and 15 Hz respectively, over prefrontal, and left centro-parietal electrodes. Paralleling our previous findings in sleep, there was no significant difference between meditation styles in LTM as well as no difference between matched sessions in MNP. Meditation-related changes in wakefulness and NREM sleep were correlated across space and frequency. A significant correlation was found in the EEG low frequencies (<12 Hz). Since the peak of coupling was observed in the theta-alpha oscillatory range, sleep homeostatic response to meditation practice is not sufficient to explain our findings. Another likely phenomenon into play is a reverberation of meditation-related processes during subsequent sleep. Future studies should ascertain the interplay between these processes in promoting the beneficial effects of meditation practice.

Neurobiological correlates of impulsivity in healthy adults: Lower prefrontal gray matter volume and spontaneous eye-blink rate but greater resting-state functional connectivity in basal ganglia-thalamo-cortical circuitry.

Studies consistently implicate aberrance of the brain's reward-processing and decision-making networks in disorders featuring high levels of impulsivity, such as attention-deficit hyperactivity disorder, substance use disorder, and psychopathy. However, less is known about the neurobiological determinants of individual differences in impulsivity in the general population. In this study of 105 healthy adults, we examined relationships between impulsivity and three neurobiological metrics - gray matter volume, resting-state functional connectivity, and spontaneous eye-blink rate, a physiological indicator of central dopaminergic activity. Impulsivity was measured both by performance on a task of behavioral inhibition (go/no-go task) and by self-ratings of attentional, motor, and non-planning impulsivity using the Barratt Impulsiveness Scale (BIS-11). Overall, we found that less gray matter in medial orbitofrontal cortex and paracingulate gyrus, greater resting-state functional connectivity between nodes of the basal ganglia-thalamo-cortical network, and lower spontaneous eye-blink rate were associated with greater impulsivity. Specifically, less prefrontal gray matter was associated with higher BIS-11 motor and non-planning impulsivity scores, but was not related to task performance; greater correlated resting-state functional connectivity between the basal ganglia and thalamus, motor cortices, and prefrontal cortex was associated with worse no-go trial accuracy on the task and with higher BIS-11 motor impulsivity scores; lower spontaneous eye-blink rate was associated with worse no-go trial accuracy and with higher BIS-11 motor impulsivity scores. These data provide evidence that individual differences in impulsivity in the general population are related to variability in multiple neurobiological metrics in the brain's reward-processing and decision-making networks.

Short Meditation Trainings Enhance Non-REM Sleep Low-Frequency Oscillations.

STUDY OBJECTIVES: We have recently shown higher parietal-occipital EEG gamma activity during sleep in long-term meditators compared to meditation-naive individuals. This gamma increase was specific for NREM sleep, was present throughout the entire night and correlated with meditation expertise, thus suggesting underlying long-lasting neuroplastic changes induced through prolonged training. The aim of this study was to explore the neuroplastic changes acutely induced by 2 intensive days of different meditation practices in the same group of practitioners. We also repeated baseline recordings in a meditation-naive cohort to account for time effects on sleep EEG activity. DESIGN: High-density EEG recordings of human brain activity were acquired over the course of whole sleep nights following intervention. SETTING: Sound-attenuated sleep research room. PATIENTS OR PARTICIPANTS: Twenty-four long-term meditators and twenty-four meditation-naïve controls. INTERVENTIONS: Two 8-h sessions of either a mindfulness-based meditation or a form of meditation designed to cultivate compassion and loving kindness, hereafter referred to as compassion meditation. MEASUREMENTS AND RESULTS: We found an increase in EEG low-frequency oscillatory activities (1-12 Hz, centered around 7-8 Hz) over prefrontal and left parietal electrodes across whole night NREM cycles. This power increase peaked early in the night and extended during the third cycle to high-frequencies up to the gamma range (25-40 Hz). There was no difference in sleep EEG activity between meditation styles in long-term meditators nor in the meditation naïve group across different time points. Furthermore, the prefrontal-parietal changes were dependent on meditation life experience. CONCLUSIONS: This low-frequency prefrontal-parietal activation likely reflects acute, meditation-related plastic changes occurring during wakefulness, and may underlie a top-down regulation from frontal and anterior parietal areas to the posterior parietal and occipital regions showing chronic, long-lasting plastic changes in long-term meditators.

Reversal of cortical information flow during visual imagery as compared to visual perception.

The role of bottom-up and top-down connections during visual perception and the formation of mental images was examined by analyzing high-density EEG recordings of brain activity using two state-of-the-art methods for assessing the directionality of cortical signal flow: state-space Granger causality and dynamic causal modeling. We quantified the directionality of signal flow in an occipito-parieto-frontal cortical network during perception of movie clips versus mental replay of the movies and free visual imagery. Both Granger causality and dynamic causal modeling analyses revealed an increased top-down signal flow in parieto-occipital cortices during mental imagery as compared to visual perception. These results are the first direct demonstration of a reversal of the predominant direction of cortical signal flow during mental imagery as compared to perception.

Experienced mindfulness meditators exhibit higher parietal-occipital EEG gamma activity during NREM sleep.

Over the past several years meditation practice has gained increasing attention as a non-pharmacological intervention to provide health related benefits, from promoting general wellness to alleviating the symptoms of a variety of medical conditions. However, the effects of meditation training on brain activity still need to be fully characterized. Sleep provides a unique approach to explore the meditation-related plastic changes in brain function. In this study we performed sleep high-density electroencephalographic (hdEEG) recordings in long-term meditators (LTM) of Buddhist meditation practices (approximately 8700 mean hours of life practice) and meditation naive individuals. We found that LTM had increased parietal-occipital EEG gamma power during NREM sleep. This increase was specific for the gamma range (25-40 Hz), was not related to the level of spontaneous arousal during NREM and was positively correlated with the length of lifetime daily meditation practice. Altogether, these findings indicate that meditation practice produces measurable changes in spontaneous brain activity, and suggest that EEG gamma activity during sleep represents a sensitive measure of the long-lasting, plastic effects of meditative training on brain function.

Hypothalamic osmoregulation is maintained across the wake-sleep cycle in the rat.

In different species, rapid eye movement sleep (REMS) is characterized by a thermoregulatory impairment. It has been postulated that this impairment depends on a general insufficiency in the hypothalamic integration of autonomic function. This study aims to test this hypothesis by assessing the hypothalamic regulation of body fluid osmolality during the different wake-sleep states in the rat. Arginine-vasopressin (AVP) plasma levels were determined following intracerebroventricular (ICV) infusions of artificial cerebrospinal fluid (aCSF), either isotonic or made hypertonic by the addition of NaCl at three different concentrations (125, 250 and 500 mM). Animals were implanted with a cannula within a lateral cerebral ventricle for ICV infusions and with electrodes for the recording of the electroencephalogram. ICV infusions were made in different animals during Wake, REMS or non-REM sleep (NREMS). The results show that ICV infusion of hypertonic aCSF during REMS induced an increase in AVP plasma levels that was not different from that observed during either Wake or NREMS. These results suggest that the thermoregulatory impairment that characterizes REMS does not depend on a general impairment in the hypothalamic control of body homeostasis.

Cold exposure and sleep in the rat: REM sleep homeostasis and body size.

STUDY OBJECTIVES: Exposure to low ambient temperature (Ta) depresses REM sleep (REMS) occurrence. In this study, both short and long-term homeostatic aspects of REMS regulation were analyzed during cold exposure and during subsequent recovery at Ta 24 degrees C. DESIGN: EEG activity, hypothalamic temperature, and motor activity were studied during a 24-h exposure to Tas ranging from 10 degrees C to -10 degrees C and for 4 days during recovery. SETTING: Laboratory of Physiological Regulation during the Wake-Sleep Cycle, Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna. SUBJECTS: 24 male albino rats. INTERVENTIONS: Animals were implanted with electrodes for EEG recording and a thermistor to measure hypothalamic temperature. MEASUREMENTS AND RESULTS: REMS occurrence decreased proportionally with cold exposure, but a fast compensatory REMS rebound occurred during the first day of recovery when the previous loss went beyond a "fast rebound" threshold corresponding to 22% of the daily REMS need. A slow REMS rebound apparently allowed the animals to fully restore the previous REMS loss during the following 3 days of recovery. CONCLUSION: Comparing the present data on rats with data from earlier studies on cats and humans, it appears that small mammals have less tolerance for REMS loss than large ones. In small mammals, this low tolerance may be responsible on a short-term basis for the shorter wake-sleep cycle, and on long-term basis, for the higher percentage of REMS that is quickly recovered following REMS deprivation.

Lithium affects REM sleep occurrence, autonomic activity and brain second messengers in the rat.

The effects of a single intraperitoneal administration of lithium, a drug used to prevent the recurrence of mania in bipolar disorders, were determined in the rat by studying changes in: (i) the wake-sleep cycle; (ii) autonomic parameters (hypothalamic and tail temperature, heart rate); (iii) the capacity to accumulate cAMP and IP(3) in the preoptic-anterior hypothalamic region (PO-AH) and in the cerebral cortex (CC) under an hypoxic stimulation at normal laboratory and at low ambient temperature (T(a)). In the immediate hours following the injection, lithium induced: (i) a significant reduction in REM sleep; (ii) a non-significant reduction in the delta power density of the EEG in NREM sleep; (iii) a significant decrease in the concentration of cAMP in PO-AH at normal laboratory T(a); (iv) a significant increase of IP(3) concentration in CC following exposure to low T(a). The earliest and most sensitive effects of lithium appear to be those concerning sleep. These changes are concomitant with biochemical effects that, in spite of a systemic administration of the substance, may be differentiated according to the second messenger involved, the brain region and the ambient condition.