Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin
Using arterial spin labelling and BOLD fMRI in healthy volunteers, intravenous psilocybin produced widespread decreases in cerebral blood flow and BOLD signal that were maximal in hub regions (thalamus, ACC, PCC and mPFC), with reduced mPFC activity predicting the intensity of subjective effects. The drug also decreased functional coupling between mPFC and PCC, suggesting psychedelic phenomenology arises from diminished activity and connectivity of key network hubs, permitting a state of unconstrained cognition.
Authors
- Robin Carhart-Harris
- David Nutt
- David Erritzoe
Published
Abstract
Psychedelic drugs have a long history of use in healing ceremonies, but despite renewed interest in their therapeutic potential, we continue to know very little about how they work in the brain. Here we used psilocybin, a classic psychedelic found in magic mushrooms, and a task-free functional MRI (fMRI) protocol designed to capture the transition from normal waking consciousness to the psychedelic state. Arterial spin labeling perfusion and blood-oxygen level-dependent (BOLD) fMRI were used to map cerebral blood flow and changes in venous oxygenation before and after intravenous infusions of placebo and psilocybin. Fifteen healthy volunteers were scanned with arterial spin labeling and a separate 15 with BOLD. As predicted, profound changes in consciousness were observed after psilocybin, but surprisingly, only decreases in cerebral blood flow and BOLD signal were seen, and these were maximal in hub regions, such as the thalamus and anterior and posterior cingulate cortex (ACC and PCC). Decreased activity in the ACC/medial prefrontal cortex (mPFC) was a consistent finding and the magnitude of this decrease predicted the intensity of the subjective effects. Based on these results, a seed-based pharmaco-physiological interaction/functional connectivity analysis was performed using a medial prefrontal seed. Psilocybin caused a significant decrease in the positive coupling between the mPFC and PCC. These results strongly imply that the subjective effects of psychedelic drugs are caused by decreased activity and connectivity in the brain's key connector hubs, enabling a state of unconstrained cognition.
Research Summary of 'Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin'
βBlossom's Take
Introduction
Psychedelic drugs such as psilocybin have a long history of ritual and therapeutic use, yet their neural mechanisms remain poorly understood. Earlier work has characterised the phenomenology of psilocybin and implicated serotonergic (particularly 5-HT2A) receptors, but direct, high-resolution imaging of the transition from normal waking consciousness into the psychedelic state has been lacking. Carhart-Harris and colleagues set out to characterise the neural correlates of the acute psychedelic state using task-free functional MRI. They combined arterial spin labelling (ASL) perfusion and blood-oxygen-level-dependent (BOLD) fMRI to map cerebral blood flow (CBF) and BOLD changes before and after intravenous infusions of placebo and psilocybin, aiming to capture short‑latency, phasic effects produced by a 2 mg i.v. dose that begins acting within seconds and peaks within minutes. The study focused on resting-state activity and connectivity, with particular attention to high-level association regions and connector hubs such as the medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), posterior cingulate cortex (PCC) and thalamus.
Methods
Two separate samples of healthy, hallucinogen-experienced volunteers were studied. For ASL perfusion imaging, 15 subjects (five female; mean age 34.1, SD 8.2) underwent two 18-minute task-free scans with a fixation cross; saline placebo was infused in the first scan and psilocybin (2 mg in 10 mL saline) in the second. Subjective intensity was rated on a 0–10 visual analogue scale at multiple time points (including 5 and 12 minutes post-infusion). For BOLD fMRI, a separate group of 15 subjects (two female; mean age 32.0, SD 8.9) underwent eyes-closed, task-free 12-minute BOLD scans on two visits about 14 days apart, with placebo and psilocybin infusions given in balanced order. Infusions in both protocols were administered manually over 60 s, beginning 6 minutes after scan start. Imaging: ASL perfusion used a single-shot pulsed PICORE-QUIPSSII sequence with 16 axial slices; 240 tag-control pairs were acquired. BOLD data were acquired with gradient-echo EPI (TR/TE 3000/35 ms, 53 slices, 3 × 3 × 3 mm voxels, 240 volumes). First-level models incorporated the tag-control difference (ASL) and a pharmacodynamically informed square function (BOLD) to estimate within-scan modulation by psilocybin; higher-level mixed-effects analyses contrasted post-infusion versus pre-infusion and psilocybin versus placebo. Statistical maps were cluster-thresholded (z > 2.3) and whole-brain corrected at P < 0.05. Functional connectivity/PPI: A ventromedial prefrontal (vmPFC) region of interest was defined from the CBF/BOLD decreases and used for psycho‑physiological interaction (PPI) analyses testing for changes in linear coupling associated with psilocybin infusion. Gray matter, white matter and CSF time series were entered as nuisance regressors. Physiological confounds were addressed by recording respiration, cardiac pulse and end‑tidal CO2; RETROICOR and GLM-based regressors were used to remove cardiac/respiratory harmonics and CO2-related variance. Cerebrovascular reactivity (CVR) was assessed with a breath‑hold task (paced breathing and 10-s breath-holds) to test whether psilocybin altered vascular responsiveness; BOLD responses to breath-hold were normalised to CO2 changes and compared voxel-wise between conditions. Ethical screening and exclusion criteria were applied (age ≥21, no personal/family psychiatric disorder, no substance dependence, no cardiovascular disease, no recent hallucinogen use within 6 weeks, etc.).
Results
Subjective effects: Psilocybin produced rapid, robust subjective effects. In the ASL group mean intensity ratings were 6.7 (±1.9) at 5 minutes post-infusion and 5.2 (±2.3) at 12 minutes; in the pooled data all ten subjective items scored significantly higher after psilocybin than after placebo (P < 0.01 as reported). ASL perfusion results: Group-level ASL analyses (n = 15) revealed significant decreases in CBF after psilocybin in multiple subcortical and cortical regions. Subcortical decreases included bilateral thalamus, putamen and hypothalamus. Cortical decreases were prominent in high‑level association and hub regions: PCC, retrosplenial cortex, precuneus, bilateral angular and supramarginal gyri, rostral and dorsal ACC, paracingulate gyrus, mPFC, frontoinsular cortex, lateral orbitofrontal cortex, frontal operculum, precentral gyrus and superior/middle/inferior frontal gyri. Temporal analyses of ROIs (thalamus, ACC, PCC) showed steep CBF reductions after infusion that were sustained for the duration of the scans. A correlation analysis indicated that larger CBF decreases in ROIs were associated with greater subjective intensity; the ACC CBF change correlated negatively with intensity (Pearson r = -0.55, P = 0.017, one-tailed). The extracted text reports trend‑level associations for thalamus and PCC but is ambiguous about exact statistics. BOLD fMRI results: The BOLD sample (n = 15) showed regional decreases in BOLD signal after psilocybin that broadly mirrored the ASL CBF decreases, including the mPFC, ventral PCC, putamen and subthalamic nuclei. Additional BOLD decreases were observed in higher‑order visual areas that were not seen in ASL. Importantly, no regional increases in CBF or BOLD signal were reported in either modality. Functional connectivity/PPI: Using a vmPFC seed, the PPI analysis identified a significant decrease in positive coupling between the mPFC/vmPFC and the PCC after psilocybin. The authors describe this as a reduced positive coupling rather than an emergence of genuine negative connectivity. Physiological correction: Removing physiological variance (heart rate, respiration rate and depth, end‑tidal CO2) from the BOLD data did not materially alter the significant maps. Breath-hold CVR testing found no difference in the BOLD response to hypercapnia between psilocybin and placebo, arguing against a direct vascular action of the drug on CVR.
Discussion
Carhart-Harris and colleagues interpret their findings as evidence that acute psilocybin decreases neural activity and functional coupling in key cortical and subcortical connector hubs, most notably the mPFC/ACC, PCC and thalamus, and that these decreases are related to the intensity of subjective psychedelic experience. They note that these results were unexpected because psychedelics are often assumed to increase neural activity; however, the authors point to supporting animal data showing broadband decreases in resting local field potential power after psilocybin and propose that decreased activity observed with fMRI is plausible. The authors contrast their fMRI results with prior PET work reporting global increases in glucose metabolism after oral psilocybin, suggesting a timescale difference: the PET tracer integrates activity over much longer periods and might therefore reflect rebound or later effects not captured by the phasic fMRI measures. Mechanistically, the team proposes that stimulation of 5-HT2A receptors, known to be central to psychedelic action, could lead indirectly to net inhibition of pyramidal cell activity via excitation of GABAergic interneurons, consistent with the observed deactivations in cortical regions rich in 5-HT2A receptors. They acknowledge that receptor-level mechanisms cannot be definitively established from these data. Functionally, the authors highlight that the most strongly affected regions are high‑baseline activity hubs within the default-mode network (DMN) and have unusually high cortico‑cortical connectivity. They argue that deactivation and decoupling of these hubs may reduce top‑down constraint on cognition, enabling an "unconstrained" or less‑constrained style of cognition seen subjectively during the psychedelic state. The observed decrease in vmPFC–PCC coupling is interpreted as a perturbation of reciprocal hierarchical interactions between prefrontal and parietal association areas, which could reflect reduced top‑down influence or a relative increase in bottom‑up influence. Clinical relevance and caveats: The discussion connects the findings to hypotheses about depression, noting that mPFC hyperactivity and increased mPFC connectivity have been implicated in depressive rumination; thus, acute mPFC deactivation by psilocybin may provide a putative biological mechanism for observed improvements in wellbeing and depressive symptoms in prior clinical reports, though the authors emphasise that further work is required to test this therapeutic hypothesis. They also mention decreased hypothalamic CBF as potentially relevant to anecdotal reports of relief in cluster headache. Limitations and uncertainties acknowledged by the authors include the need for more direct measures of neural activity to validate the fMRI inferences, incomplete resolution of receptor‑specific mechanisms, and the temporal differences between imaging modalities. They also report attempts to exclude non‑neural confounds: physiological regression and breath‑hold CVR testing argued against simple vascular explanations for the observed fMRI effects. In conclusion, the investigators propose that their multimodal fMRI approach provides a detailed account of the brain correlates of the psychedelic state, characterised principally by decreased activity and connectivity in connector hubs, which they suggest permits the altered, unconstrained cognition characteristic of high‑dose psilocybin experiences.
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RESULTS
ASL Perfusion fMRI. Fifteen healthy, hallucinogen-experienced subjects (five females), mean age 34.1 (SD 8.2) were scanned with ASL. Subjects underwent an anatomical scan followed by two task-free functional scans, each lasting 18 min. Subjects were instructed to relax and a fixation cross was displayed. Solutions were infused manually over 60 s, beginning 6 min after the start of each functional scan. Subjects received placebo (10-mL saline) in the first scan and psilocybin (2 mg in 10-mL saline) in the second. The intensity of the subjective effects was rated via button press on a 0-10 visual analog scale (10 = extremely intense effects) at the start of each functional scan, just before infusion, 5-min postinfusion, and 12-min postinfusion. The average rating 5-min postinfusion was 6.7 (±1.9), and 5.2 (±2.3) 12-min postinfusion. Earlier work showed that the effects of 2 mg i.v. psilocybin are comparable with ∼15 mg of orally administered psilocybin, which is considered a moderate dose. Nineteen additional items were rated immediately after each ASL scan. Fig.displays the top 10 rated items from the two studies. Ratings for all of the items used in the ASL and BOLD studies can be found in Table. The interaction between cerebral blood flow (CBF) and the infusion event was modeled, contrasting CBF before and after infusion. The subjective effects began toward the end of the infusion period and reached a sustained peak after ∼4 min. The first level results were entered into a higher level analysis, contrasting CBF after psilocybin with CBF after placebo for all 15 subjects. Fig.displays these results. The group level results (Fig.) revealed significant CBF decreases in subcortical (bilateral thalamus, putamen, and hypothalamus) and cortical regions [the posterior cingulate cortex (PCC), retrosplenial cortex, precuneus, bilateral angular gyrus, supramarginal gyrus, rostral and dorsal anterior cingulate cortex (ACC), paracingulate gyrus, medial prefrontal cortex (mPFC), frontoinsular cortex, lateral orbitofrontal cortex, frontal operculum, precentral gyrus, and superior, middle and inferior frontal gyrus] (Fig.). The decreases were localized to high-level association regions (e.g., the PCC and mPFC) and important connector hubs, such as the thalamus, PCC and ACC/mPFC. To assess the temporal dynamics of the CBF changes postinfusion, thalamic, ACC, and PCC masks were made; voxels within these were restricted to those that were significantly decreased after psilocybin. For each region of interest (ROI), the percent CBF change postinfusion was plotted against time (Fig.). All ROIs showed steep decreases in CBF after psilocybin that were sustained for the duration of the scan. To test for a relationship between regional CBF changes and subjective effects, we plotted each subjects' ROI CBF change postpsilocybin against their ratings of drug effects intensity (Fig.). For each ROI, it was evident that the greater the decreases in CBF, the more intense the subjective effects. BOLD fMRI. A separate sample of 15 subjects was scanned with BOLD fMRI. The BOLD scans took place ∼6 mo after the ASL. The sample included two females and had a mean age of 32 (SD 8.9). Subjects underwent an anatomical scan followed by an eyesclosed task-free BOLD scan, which lasted 12 min. This process occurred on two visits, ∼14 d apart. Placebo was given on one occasion and psilocybin on the other in a balanced order. Infusions began 6 min after the start of the scan, following the same procedure as the ASL study. The data were high-pass filtered with a cutoff of 300 s and the pharmacodynamics of intravenous psilocybin was used to model changes in the BOLD signal coinciding with the infusion event. The first level results were entered into a higher level analysis, contrasting BOLD signal changes before and after psilocybin, and before and after psilocybin versus before and after placebo (Fig., Upper). The regional decreases in BOLD signal were similar to the regional decreases in CBF observed with ASL, with consistent decreases in the mPFC, ventral PCC, putamen, and subthalamic nuclei (Fig., Lower). There were, however, additional BOLD signal decreases (e.g., in higher order visual areas) that were not observed with ASL (Fig., Upper, and Fig.). Pharmaco-Physiological Interaction. These results implicate the ACC/mPFC in the mechanism of action of psilocybin. The ACC/ mPFC showed decreased CBF (Fig.) and BOLD signal (Fig.) after psilocybin and the magnitude of CBF decreases correlated positively with the intensity of the drug's subjective effects (Fig.). Based on these results, a ventromedial prefrontal (vmPFC) ROI (Fig., red) was chosen for a psycho-physiological interaction (PPI) analysis. PPIs test for changes in linear coupling under a psychological factor. In our case, this factor was the administration of psilocybin. This finding means that, strictly speaking, we are looking at a pharmaco-physiological interaction. Although commonly referred to as analyses of functional connectivity, PPIs can also be regarded as tests for changes in effective connectivity under a simple linear model of the influence of one region upon another. Fig.. Subjective ratings (n = 30). Displayed are mean values + SEs. Ratings were given shortly after the scans. Subjects were instructed that "no more than usually" refers to normal waking consciousness. All 10 items were scored significantly higher after psilocybin than placebo (P < 0.01). For each subject, the vmPFC time series was entered into a model that included independent gray matter, white matter, and cerebrospinal fluid time series as regressors of no-interest. Fig.displays regions where activity was positively (yellow/orange) and negatively (blue) coupled to activity in the vmPFC throughout the placebo scan. However, the salient images are those shown as follows in Fig.: the middle row displays regions where activity became significantly less (blue) and more (red) coupled to activity in the vmPFC after psilocybin infusion and the bottom row displays these effects relative to those after placebo. Physiological Correction and Breath-Hold. BOLD and ASL fMRI measure changes in a vascular signal that is coupled to changes in neural activity. It is therefore important to address factors that may modulate brain vasculature without affecting neural activity. For example, increases in blood carbon dioxide that occur with changes in respiration can drive increases in CBF. Thus, to address the Fig.. Group CBF changes over time (Left) and CBF vs. subjective effects (Right). Plots on the left show blood flow changes over time for the thalamus, ACC, and PCC. These plots were made by calculating the postinfusion change in CBF as a percentage of the preinfusion CBF. This process was done for each ROI for each individual subject and then the group mean was plotted. Note, these plots are shown for display purposes; error bars are not included because the inclusion of error is implicit in the statistical parametric maps shown in Fig.. Plots on the right show the relationship between ROI CBF changes after psilocybin-infusion for each subject and their ratings of the intensity of the subjective effects given 5-and 12-min postinfusion (plotted are the average of these two ratings). There was a significant negative correlation between ACC CBF change postpsilocybin and intense subjective effects (Pearson's correlation, r = -0.55, P = 0.017, one-tailed) and CBF vs. intensity met a trend level significance for the thalamus and PCC (P < 0.01). possibility that the effects observed in this study were driven by nonneural physiological changes, physiological variance (i.e., heart rate, respiration rate, and respiration depth) was regressed from the functional data before repeating the BOLD analyses described above. This correction step did not significantly alter the statistical parametric maps (Fig.), suggesting that changes in physiological parameters were not responsible for the positive outcomes. Furthermore, to test the possibility that psilocybin had acted directly on the cerebral vasculature, we included a blocked breathhold paradigm at the end of each BOLD scan. Hypercapnia is known to significantly increase the BOLD signal via CO 2 -induced vasodilation (see ref.and Fig.); thus, it was reasoned that a direct effect of psilocybin on brain vasculature would cause an altered BOLD response to breath-hold. However, no difference was found in the BOLD response to breath-hold under psilocybin and placebo, implying that the drug had not acted directly on the vascular system.
CONCLUSION
The fMRI studies reported here revealed significant and consistent outcomes. Psilocybin significantly decreased brain blood flow and venous oxygenation in a manner that correlated with its subjective effects, and significantly decreased the positive coupling of two key structural hubs (the mPFC and the PCC). Our use of fMRI to measure resting-state brain activity after a psychedelic is unique, and because the results are unexpected, they require some explanation. The effect of psilocybin on resting-state brain activity has been measured before with PET and glucose metabolism. This study found a global increase in glucose metabolism after oral psilocybin, which is inconsistent with our fMRI results. One possible explanation for this discrepancy relates to the fact that the radiotracer used to measure glucose metabolism ( 18 F-fluorodeoxyglucose) has a long half-life (110 min). Thus, the effects of psilocybin, as measured by PET, are over much greater timescales than indexed by our fMRI measures. It is therefore possible that phasic or shortterm effects of psilocybin show some rebound that is detected by longer-term changes in glucose metabolism. More direct measures of neural activity will help inform this hypothesis, but in support of the inference that psilocybin does decrease neural activity, direct recordings of cortical local field potentials (LFPs) in rats found broadband decreases in resting state LFP power after psilocybin infusion-including γ-power (9)-changes in which are known to correlate with changes in the BOLD signal. It has been commonly assumed that psychedelics work by increasing neural activity; however, our results put this into question. Psilocin is a mixed serotonin receptor agonist, but there is a general consensus that the characteristic subjective and behavioral effects of psychedelics are initiated via stimulation of serotonin (5-Hydroxytryptamine, 5-HT) 2A receptors. It is possible that the deactivations observed in the present studies were caused by stimulation of 5-HT receptors other than 5-HT2A; however, this seems unlikely given that the affinity of psychedelics for the 5-HT2A receptor correlates with their potency (12) and 5-HT2A antagonists block the subjective effects of psychedelics. There is a large body of preclinical evidence that stimulation of 5-HT2A receptors increases GABAergic transmission and pyramidal cell inhibition (14-21), which may explain the deactivations observed here (Figs.and). fMRI studies with serotonergic compounds that stimulate other 5-HT receptors, such as the 5-HT2C () or (mainly) the 5-HT1A receptor, have not found comparable results to those shown here, and 5-HT2A receptors are present in high concentrations in the cortical regions that were significantly deactivated and decoupled after psilocybin (Table). Stimulation of the 5-HT2A receptor increases excitation in the host cell by reducing outward potassium currents. Thus, if the 5-HT2A receptor did mediate the observed deactivations, then it may have been via 5-HT2A-induced excitation of fast-spiking interneurons terminating on pyramidal cells (e.g., ref.or 5-HT2A-induced excitation of pyramidal cells projecting onto interneurons. Regardless of how these effects were initiated at the receptor level, it is necessary for us to offer a functional explanation for them. It is noteworthy that the regions which showed the most consistent deactivations after psilocybin (e.g., the PCC and mPFC) are also those that show disproportionately high activity under normal conditions. For example, metabolism in the PCC is ∼20% higher than most other brain regions (), yet psilocybin decreased its blood flow by up to 20% in some subjects. There is Fig.. Brain deactivations after psilocybin. (Upper) Regions where there was a significant decrease in the BOLD signal after psilocybin versus after placebo (z: 1.8-3). Mixed-effects analysis, z > 1.8, P < 0.05 whole brain cluster corrected, n = 15. (Lower) Regions where there was a consistent decrease in CBF and BOLD after psilocybin. For display purposes, significant BOLD decreases were calculated within a mask based on the ASL result (Fig.) at an uncorrected voxel level threshold of P = 0.05. Note, we observed no increases in CBF or BOLD signal in any region. (Top) Regions where activity was positively coupled to that of the vmPFC are shown in orange and regions where activity was "negatively" coupled to activity in the vmPFC are shown in blue (it should be noted however, that the appearance of negative connectivity is forced by regression of the global signal). (Middle) Significant increases (orange) and decreases (blue) in functional connectivity after psilocybin infusion. (Bottom) Increases and decreases in functional connectivity after psilocybin that were significantly greater than any connectivity changes after placebo. All analyses were mixed effects, z > 2.3, P < 0.05 whole-brain cluster corrected, n = 15. Note: The significant psycho-physiological interactions in the posterior PCC and left lateral parietal region suggest that the positive coupling (under placebo) has decreased significantly. This finding should not necessarily be interpreted as a negative coupling, simply a significant decrease in a positive coupling. some mystery about the function of the PCC; its large size, buffered location, and rich vasculature means that it is well protected from damage. The high metabolic activity of the PCC and the default-mode network (DMN) with which is it associatedhas led some to speculate about its functional importance, positing a role in consciousness () and high-level constructs, such as the selfor "ego". Indeed, the DMN is known to be activated during self-referencingand other high-level functions linked to the self-construct. Moreover, DMN regions are also known to host the highest number of cortico-cortical connections in the brain, making them important "connector hubs". These hubs may be critical for efficient information transfer in the brain by allowing communication between different regions via the fewest number of connections. However, such an integrative function would confer a significant responsibility on these regions, which may explain why their deactivation has such a profound effect on consciousness, as shown here. These results may have implications beyond explaining how psilocybin works in the brain by implying that the DMN is crucial for the maintenance of cognitive integration and constraint under normal conditions. This finding is consistent with Aldous Huxley's "reducing valve" metaphorand Karl Friston's "free-energy principle", which propose that the mind/brain works to constrain its experience of the world. The pharmaco-physiological interaction results were particularly intriguing, revealing significant decreases in the positive coupling between the PCC and mPFC after psilocybin. This result can be understood in terms of a regression of PCC activity on mPFC activity, in which the regression slope decreases. This finding can either be interpreted as a decrease in the (backward or top-down) connectivity from prefrontal to parietal regions or, equivalently, an increase in the reciprocal (forward or bottom-up) direction from parietal to prefrontal regions. This asymmetrical change in coupling, induced by psilocybin, is consistent with a reduction in the sensitivity of superficial pyramidal cells in the parietal region targeted by prefrontal afferents, which may or may not be associated with a compensatory increase in the influence of parietal regions on prefrontal activity. Whatever the underlying synaptic mechanisms, these results provide clear evidence for a perturbation in reciprocal coupling between these two association areas and speak to a rebalancing of hierarchical activity in distributed high-level modes. Finally, consistent with their history of use as adjuncts to psychotherapy, the idea has recently re-emerged that psychedelics may be useful in the treatment of certain psychiatric disorders. It seems relevant therefore that activity inand connectivity withthe mPFC is known to be elevated in depression and normalized after effective treatment. The mPFC was consistently deactivated by psilocybin (Fig.) and the magnitude of the deactivations correlated with the drug's subjective effects (Fig.). Depression has been characterized as an "overstable" state, in which cognition is rigidly pessimistic. Trait pessimism has been linked to deficient 5-HT2A receptor stimulation, particularly in the mPFC, and mPFC hyperactivity has been linked to pathological brooding. Recent work has shown that psilocybin can increase subjective well-being (4) and trait opennessseveral months after an acute experience, and depression scores in terminal cancer patients were significantly decreased 6 mo after treatment with psilocybin (2). Our results suggest a biological mechanism for this: decreased mPFC activity via 5-HT2A receptor stimulation. Further work is required to test this hypothesis and the putative utility of psilocybin in depression. We also observed decreased CBF in the hypothalamus after psilocybin (Fig.), which may explain anecdotal reports that psychedelics reduce symptoms of cluster headaches. Increased hypothalamic CBF was observed during acute headache in cluster headache sufferersand inhibition of the hypothalamus via direct electrical stimulation can provide therapeutic relief for this condition. To conclude, here we used an advanced and comprehensive fMRI protocol to image the brain effects of psilocybin. These studies offer the most detailed account to date on how the psychedelic state is produced in the brain. The results suggest decreased activity and connectivity in the brain's connector hubs, permitting an unconstrained style of cognition.
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Study Details
- Study Typeindividual
- Populationhumans
- Characteristicsbrain measuresopen label
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