This action might not be possible to undo. Are you sure you want to continue?
THE NEAR-DEATH EXPERIENCE: A CEREBELLAR METHOD TO PROTECT BODY AND SOUL—LESSONS FROM THE IBOGA HEALING ;CEREMONY IN GABON Süster Strubelt, , , Uwe Maas, ,
Dip Psych Dip Soc MPH MD DrMed
The root bark of the Iboga shrub (Tabernanthe iboga) is used in Gabon, Africa, to induce a near-death experience for spiritual and psychological purposes. The pharmacology of ibogaine, a psychoactive indole alkaloid extracted from the bark, has been investigated extensively because of its putative qualities to treat addiction. This review of these studies and neuroscientiﬁc approaches to the near-death experience compared with ﬁeld studies of traditional African rituals has generated new insights into the neurological correlates and the psychological effects and after-effects of the near-death experience. Ibogaine stimulates the cerebellar fastigial nucleus in the same manner as ischemia and leads to a medium-term protection of the brain against glutamate-induced neurotoxicity. At the same time, it induces changes in the autonomic nervous and the cardiovascular systems, which aid in the survival of ischemia: iboga intake and ischSüster Strubelt, Dip Psych, Dip Soc, MPH, is a development worker for the Austrian development service “HorizonT3000” in Harare, Zimbabwe. Uwe Maas, MD, DrMed, a clinical pediatrician, is a development worker in Harare.
emia both lead to slowing of electroencephalogram (EEG) activity (dominance of theta and delta waves), a stimulation of the limbic system, and a dominance of a phylogenetically older branch of the vagus nerve, originating in the dorsal motor nucleus, which lowers the metabolic rate of the body. In conclusion, the near-death experience seems to be the result of a dominance of phylogenetically and ontogenetically old neurological structures and brain waves, which are allowed to show their (para)psychological abilities in the absence of cortical dominance. If parts of the neocortex are still active and permit observation and memory performance, the experience can be integrated within the personality. The newly learned peaceful state of vagal and subcortical dominance can be actively self-induced. Implications of this model for alternative healing are discussed. (Altern Ther Health Med. 2008;14(1):30-34.) without similar recollection). The observed psychological differences between the groups in their study were more pronounced after 8 years of follow-up than after 2 years.10 However, the causes of these effects remain unclear. Neurological attempts to formulate an explanation hold the endorphins responsible for the exalted mood during the near-death experience. 11-13 The visions are presumed to be caused by a disengagement of external stimuli13,14 and a cerebral increase in activity,11 in particular, an overactivation of the temporal lobe11,13,15 and the hippocampus.11,14,16 Blanke et al report they could provoke an out-of-body experience from a woman diagnosed with epilepsy by electric stimulation of the right angular gyrus.17 On the other hand, Woerlee holds malfunction of several brain areas (prefrontal cortex, motor cortex, parietal cortex, angular gyrus, amygdala, and hippocampus) caused by ischemia and resuscitation responsible for near-death experiences during cardiac arrest.18 Reader explains the near-death experience as a parasympathetic response to excessive sympathetic stimulation caused by extreme stress in situations of danger.19 Jansen proposes that the near-death experience serves to protect the brain from the effects of ischemia by blocking N-methyl d-aspartate (NMDA)–type glutamate receptors.13 Studies about near-death experiences have several limitations because of their unexpected occurrence, the priority of life-saving measures,18 and the impossibility of communication with the person experiencing near-death. The Iboga vision is, on the other hand, provoked in a controlled situation with a speciﬁc musical and psy-
n the Republic of Gabon in central Africa, an initiation ritual is performed with the consumption of the root bark of the Iboga shrub and is supported by complex musical accompaniment. Gabonese healers expect the initiate to experience a “vision” of “death and rebirth.”1-4 Reports of Europeans being initiated and interviews with Gabonese people by ethnologists show all the typical elements of a near-death experience: a life review; out-of-body experience and floating over various landscapes; an encounter with deceased people; gliding through a tunnel into an ulterior world; an encounter with a divine entity; the arrival at a point of no return, which is not to be surpassed by the living; and the return to life.1-4 Also, Gabonese expectations of a successful initiation coincide with the research results of the effects of near-death experiences: acceptance of responsibility, reduction of dependencies, increase in spirituality, and reduced fear of death, as well as a new love for people and environment, are unanimously observed as effects of the encounter with death.5(pp52-57)-9 Lommel et al were able to prove these effects in a longitudinal study. In this study, patients who had a near-death experience related to cardiac arrest were compared with a control group (also with heart failure but
ALTERNATIVE THERAPIES, jan/feb 2008, VOL. 14, NO. 1
Lessons From the Iboga Healing Ceremony in Gabon
indicated by a gradual slowing of EEG activity.36 In cases of mild or beginning ischemia. Glutamate.41 Theta-rhythms with a frequency spectrum of 4-8 Hz are generated in different parts of the hippocampus42 and develop in humans within the ﬁrst years of their lives. In addition. Harding et al were able to demonstrate that despite the loss of almost all activity in Purkinje cells.45.5-4 Hz Lower activity of Purkinje cells Activation of fastigial nucleus Autonomous nervous system: Vagal dominance Change in cerebral functions Resistance Life against reviews? ischemia FIGURE Neurogenic Pathways of the Near-Death Experience here fits well with the results of a recent study carried out by Schutter et al. no obvious cellular damage was seen. ibogaine also increases this rhythm. additional augmentation of the theta-rhythm results from the polyrhythmic ritual mouth bow (in male initiations) and harp music (in female initiations). Welsh et al discovered that ibogaine in very high concentration caused patterns of cell degeneration in rats that mimic global ischemia. who could induce an out-of-body experience by transcranial stimulation of the cerebellum. a transition to delta waves can be Lessons From the Iboga Healing Ceremony in Gabon ALTERNATIVE THERAPIES.46 However.43(p56) Alpha activity shows a slower onset and becomes dominant in puberty.29 Reis et al could reduce the infarct volume after focal ischemia by up to 50% after electrical stimulation of the fastigial nucleus. the most important psychoactive alkaloid of the Iboga shrub. The Induction of a Cerebral Delta-Rhythm In the course of ischemia. can produce “excitotoxicity” in Purkinje cells.23-26 It could be presumed that this mechanism serves as a protection in case of ischemia. Though classiﬁed as an illegal drug in the United States and most European countries. a protective effect that could be observed for weeks. Our research questions were as follows: • Are Iboga visions and near-death experiences based on a common neurological mechanism? • Can ibogaine research help to detect structural changes in brain function during a near-death experience? • Are there neurological correlates for the personality changes after near-death experiences and after Iboga visions? RESULTS: PHARMACOLOGY AND PHYSIOLOGY OF THE NEAR-DEATH EXPERIENCE UNDER IBOGA A Cerebellar Emergency Program Through an unknown mechanism. Gabon. ibogaine induces a rhythm of 8-12 Hz in the inferior olive. the fastigial nucleus induces neuroprotective mechanisms in the brain. normally inhibiting the fastigial nucleus.33. which might occur in situations of real as well as anticipated ischemia.20 RESEARCH QUESTIONS The aim of this study was to gain new insights into neurological correlates of near-death experiences. integrating the results of a literature review of neuroscience with ethnological investigations and our own field studies in the region of Lambaréné. NO. thereby inducing protection against subsequent ischemic insults.38 Similarly.34 Presumably as a measure of protection. If inhibition through these cells fails. a theta-rhythm of 5-6 Hz in human beings37 is intensiﬁed. 1 31 . jan/feb 2008. ibogaine.40 During the Gabonese initiation ceremony.39 probably through its stimulating effect on the fastigial nucleus.25 Schutter and van Honk were able to induce this reaction by transcranial stimulation of the cerebellum.35. we tried to gather as much information as possible about the topic. during a fall or the rollover of a car. this phase lasts for several hours and enables the participant to confront childhood problems.43(pp70-78) While theta-rhythms serve the formation of episodic memories and the encoding of new information. Parallels can be drawn to near-death experiences. so we hypothesize that the phase of dominance of the theta-rhythms is responsible for the episodic life review in near-death experiences. between the years of 1999 and 2005.28 This ischemic preconditioning also seems to stimulate the fastigial nucleus. this relationship is reversed.30.44 Normally. which is played in an absolutely constant measure of 5-6 Hz.18. for example. has been extensively investigated pharmacologically in animal studies because of its putative properties to treat addiction. thereby inducing neuroprotection and allowing extraordinary ways of thinking.35. Using a model of mild ischemia in sheep fetuses. Through a comparison of international science and traditional knowledge in a qualitative study design. VOL. 14.21 Although the death of Purkinje cells in rats could be demonstrated only after large doses of ibogaine were administered. After a person consumes ibogaine.21.chological accompaniment.31 The model we suggest Ibogaine Ischemia Belief to die Gabonian ritual music Slowing of brain waves: Theta-rhythm 5-6 Hz Delta-rhythm 0. it is used by self-help groups and private clinics to cure addiction. is claimed to be the ﬁrst danger in cases of ischemia. the most important excitatory neurotransmitter.32 The Induction of a Hippocampal Theta-Rhythm Enhanced release of the stimulating neurotransmitter glutamate. in ischemia. and normal inhibitions are removed. alpha-rhythms serve to memorize semantic matters. This blockage is supposed to be more distinct in fearful people. It can be assumed that the recall of memories is facilitated by the same EEG frequencies that were present during memory formation. a process that is psychotherapeutically guided by the healers. which can be neurotoxic not only to Purkinje cells. slower rhythms in the brain are inhibited by faster ones.27 the protective properties are presumably effective with smaller doses. are especially vulnerable to neurodegeneration. They become dominant in the waking EEG at the age of 6-7 years.22 Certain groups of cells.26 It can be concluded that ibogaine induces this type of protective reaction against (prospective) oxygen deprivation in the brain. higher cerebral functions are reduced under oxygen deprivation. This rhythm leads to enhanced synaptic excitation in cerebellar Purkinje cells through a glutamatergic pathway (Figure).
51 which are more resistant to ischemia than are the neurocognitive networks of mammals. consists not only of images but also strong emotions that are experienced as being exceptional. We suppose that meditation initiates similar processes of conscious inﬂuence on the autonomic nervous system. These may be recalled later and felt as long-term shaping. the coordination of breathing and heart rate).to delta-rhythms is also facilitated by the Gabonese ceremonial music during the induction of a possession-trance. which is also accompanied by a sympathetic overreaction.5-4 Hz) also induced by ibogaine. reduced respiratory rate. This “new vagus” is connected with neuromuscular regions (eg.43(p56) Jacobs and Nadel claim that the hippocampus and the hippocampal theta-rhythm are not yet functioning in infants. With that vision.18. NO. 32 ALTERNATIVE THERAPIES.66 Humans need it presumably mainly at birth.55 which is observed under Iboga2 and during near-death experiences30 and seems to be reasonable in cases of ischemia to save energy. The vision symbolizes the elements of the tunnel.2.67 whereas higher reptiles and mammals have 2 vagal branches: the evolutionary older one. This exceptional vagal stimulation during near-death experience might explain that the situation is perceived as completely new and beyond comparison with other “real” experiences. seem to generally inhibit vagal reactions.” Only a remembered vision is considered successful. new spiritual contents of the unconscious mind as well as knowledge of interior processes are opened to the conscious mind. The similarity to ischemia during birth is reﬂected in the Gabonese description.30. Maintaining Neocortical Functions In contrast to the possession/trance.observed. the ability to memorize and the ability to verbally communicate are preserved during the Iboga “vision. the initiated or those experiencing near-death can recall the feelings of the experience later and continuously activate a new awareness of life. Benson et al showed that Buddhist monks were able to reduce their need for oxygen by up to 70%.53 This offers one explanation for the special performance of space and time during the near-death experience.20.52 Delta-rhythms also dominate the waking EEG in newborns. and reduced metabolism. and other autonomic parameters. the facial muscles) and therefore allows different emotions and forms of communication (eg. That cortical functions are not always maintained might be the reason why neardeath experiences are rare. If the new feeling of vagal dominance is connected with cerebral networks. as if belonging to another person (interpreted as “possession” by a ghost). like other spiritual experiences.66 Phylogenetically old reptiles have only an energy-saving mode (vagal excitement) and an activity mode (sympathetic excitement).69 Trauma victims who have experienced extreme situations of helplessness and often dissociations. head movement and mimicking.71 The Induction of Neurogenesis in the Hippocampus In Gabon. and therefore.54 are strange behavioral patterns.35 a frequency spectrum (0. During the Iboga initiation ceremony. with the addition of decreased body temperature and an extreme deceleration of body movement. however. 1 Lessons From the Iboga Healing Ceremony in Gabon . as observed by Bourguignon in several African cultures. no verbal exchange with the environment takes place.68 This “vagal competence” could also be effective psychologically. The traditional initiation may last several weeks. the fastigial nucleus inﬂuences the brain but also breathing. they are not able to memorize information about space and time. originating in the dorsal motor nucleus of the nervus vagus. divine light. seem to be responsible for the suppression of motor responses.56-61 Ischemia causes bradycardia.62. This demonstrates that they were unable to use the vagal system adequately for their own relaxation. jan/feb 2008. A transition from theta. and the “re”birth. and a second branch. the maintenance of the cortical functions is considered to be very important therapeutically.65. the night of the vision is only the beginning of the healing process. Sahar et al discovered that patients with posttraumatic stress disorder demonstrate a stronger sympathetic activation than a control group when presented with a mathematical problem.41 Characteristic features of this trance.” the ﬁght of the body for survival. sucking and tasting. Lommel et al found that 80% of patients did not remember anything after cardiac arrest. call-outs.47 Gabbard was able to observe a transition from theta to delta waves in the EEG of adults who were able to self-induce an out-of-body experience in a motionless rest position. The “old” energy-saving vagus is dominant in mammals only in situations of extreme danger. We interpret the loss of the cortical functions of speech and memory as indication of the dominance of subcortical networks during this possession/trance.6-9 In emergency situations. even though in most cases during the experience. even out-of-body experiences. dominate the waking EEG of reptiles.48 Whinnery observed the same effect in pilots who had near-death experiences during fast accelerations. originating in the nucleus ambiguus. and conditions are prepared to transfer them into long-term memory.65.64 According to Porges’ polyvagal theory.50 Wettach interprets these delta wave patterns in humans’ waking EEG as a shift of the brain to evolutionary older structures. the different emotions of higher mammals are made possible through a complicated cooperation of the 2 antagonists of the autonomic nervous system. especially those of the prefrontal lateral cortex.63 Ibogaine has the same effects.18 In Gabon. the inability to speak. and subsequent amnesia.70 Mash et al were able to demonstrate an improvement after ibogaine treatment using a self-rating depression scale. which in adults normally only occur during fatigue or sleep. 14. the healers demand constant verbal communication about the observed matters and their possible meanings and request target-oriented activities in the “hereafter. VOL.49. as indicated by clearly structured and linguistically formulated memories.10 The Acquisition of “Vagal Competence” The near-death experience. that one dies and is reborn. The Iboga vision might enable them to experience a massive vagal reaction in a situation of safety and therefore make it once again available for their own experience. Certain cerebral functions. the sympathetic and vagal systems. “point of no return.30 Delta-rhythms. because of the circumstances. heart rate. The mechanism for the maintenance of the cortical function is unclear.” The access to neocortical functions also seems to be intact during near-death experiences. In cases of depression.
Münster: Lit-Verlag.78 Hippocampal neurogenesis also seems to be part of the effect of electroconvulsive therapy79 and antidepressants. Konstanz: Universitätsverlag. 6. he is continuously accompanied by healers and other initiated people in the processing of the experiences.358(9298):2039-2045. eds.6:70-111. and willingness to share their knowledge with us. initiation is induced in cases in which an individual has a problem with the deceased.81 Keeping the person isolated and in permanent company of healers after the initiation ceremony in Gabon in the period of neurogenesis. 2005:221-227. Maas U. extensive support. 2006. Interestingly enough. Lancet. Meyers V. Our study permits the assumption that these structures are also leading in other types of spiritual performance. Neocortical structures seem to inhibit these processes under normal circumstances. Gabon).74-76 which also can be shown in cases of depression77 and alcohol dependency. Bonenfant R.”84 We propose that in future research. 10. Soeffner H. Todesnähe. which is expected not to be “hallucinogenic. Ethisches Handeln in den Grenzbereichen von Medizin und Psychologie. 2006:52-57. Ethnotherapies in the Cycle of Life. personality changes are not induced by resolving or reliving life problems but by a transcendental experience. ed. jan/feb 2008. consistent with the period of retreat in the traditional initiation ceremony.1 The psychological changes could be based on neurological changes as the brain responds after ischemia72 or epilepsy73 with increases in neurogenesis in the hippocampus. Die Iboga-Heilungszeremonie im Gabun: Gelenkte Nah-Todes-Erfahrung als Psychotherapie. In: Gottschalk-Batschkus CE. In the resulting exceptional state. The Iboga-healing ceremony in Gabon. München: Ethnomed. near-death experiences do not always cause personality changes. 11. Kevelaer: MatthiasGrünewald-Verlag. Wissenschaftliche Zugänge zu einem außergewöhnlichen Phänomen. In: Knoblauch H. an approach that ﬁts with studies about neurogenesis after life-threatening situations. The near-death experience is therefore the result of a dominance of phylogenetically and ontogenetically old neurological structures and brain waves. 1999:65-97. 1982:470-493. Groth-Marnat G. For this reason. 1999:32-67. Aftercare and the importance of the spiritual experience are also underestimated in ibogaine therapies against drug addiction performed by private clinics in several industrial countries.82 CONCLUSIONS Iboga-induced visions and the near-death experience seem to be attributed to a common neuronal mechanism. aftercare should be a therapeutic concern. 5. Although drug addicts often report elements of near-death experiences after the intake of ibogaine. Blackmore S.After the consumption of Iboga. van Lommel P. 9. To experience a life-threatening situation in a peaceful and beatiﬁed manner can heal basic life fears. traditional healers in Mitoné/Lambaréné (Gabon) for their conﬁdence.6-7:39-56. which lasts several weeks. Implications for Alternative Healing During an ibogaine-induced or “natural” near-death experience. 12. ed. Nahtoderfahrungen: Hinweise auf ein Leben nach dem Tod. Psychedelic Monographs and Essays.20 Glick et al even developed an Iboga alkaloid congener to treat addiction. Altered beliefs. In: Kick. 1998. Sillans R. aftercare is as important as the vision itself. 8. 2. He is in a state of regression and relives childhood experiences. Konstanz: Universitätsverlag. Pharmacodynamics and therapeutic applications of Iboga and Ibogaine. however. J Humanistic Psychol. 14. To our knowledge. They result from a protective cerebellar reaction against real or anticipated oxygen deprivation. van Wees R. This is a potential that is underused in Western psychotherapy. Fernandez JW. eds. Wissenschaftliche Zugänge zu einem außergewöhnlichen Phänomen. Lage: Jacobs-Verlag. Summers R. Maas U. 7. Considering the high number of neardeath experiences in Western societies (Knoblauch found a rate of near-death experience reports of 4% in a representative survey in Germany83). Strubelt S. In: Knoblauch H. impacts of aftercare on the long-term effects of near-death experiences have not yet been investigated. Strubelt S. Gollnhofer O. 4. Soeffner H.80 Gould was able to conﬁrm these effects in a study using rats: a relatively small population of immature new cells could exert a substantial functional inﬂuence over hippocampal function. Ein Vergleich afrikanischen Wissens mit internationalen Forschungsergebnissen. in both cases. 1 33 . To be sure. Schröter-Kunhardt M. Jansen KL. 13. In Gabon. A comparative study of near-death experience and non-near-death experience outcomes in 56 survivors of clinical death.72 may serve to consolidate personality changes. Nah-Todeserfahrungen aus psychiatrisch-neurologischer Sicht. the person to be initiated will be sheltered from the outer world for several days and is accompanied by healers. which are allowed to show their (para) psychological abilities in the absence of cortical dominance. We presume that cortical inﬂuences (the belief that death is impending) may also be a possible cause. which can be induced pharmacologically in the fastigial nucleus. attitudes and behaviors following near-death experiences. Green JC. For African healers. Acknowledgments We would like to thank Antoine Makondo and Jeannette Moussouma. Clark emphasizes the importance of a sensitive and respectful treatment of near-death experienced in the hospital setting.22(3):155-178. 3. Based on extensive clinical experience. eds. The initiatory rite of the Bwiti religion (Ndea Narizanga sect. Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands. Bwiti: An Ethnography of the Religious Imagination of Africa. NO. In: Lyttle T. 2006. Ewald G. Only when parts of the cortex are no longer inhibiting but still active (permitting observation and memory performance) can the experience be integrated within the personality. Gabonian healers always emphasize how important it is not to “forget” the initiation.72 This could be important because long-term stress or trauma results in a reduction of hippocampal volume. The physiology of spiritual experiences and concomitant spiritual phenomenona of physiological processes are worthy of further investigation. Organic alterations in the brain during a controlled near-death-experience. Those experiencing near-death usually lack this period of retreat and counseling and only casually (particularly if they are hospitalized) have the time to consolidate and integrate their experiences in a comprehensive atmosphere without the demands of daily life.38(3):110-125. the brain reduces its activity and re-activates infantile brain rhythms and networks that are exceptionally resistant to oxygen deprivation. REFERENCES 1. VOL. Schröter-Kunhardt M. Jahrbuch für Ethnomedizin und Bewusstseinsforschung. H. 2001. Nah-Todeserfahrung—Grundlage neuer Sinnﬁndung. The ketamine model of the NDE: a central role for the N-Methyl-D-Aspartate recep- Lessons From the Iboga Healing Ceremony in Gabon ALTERNATIVE THERAPIES. Many people who had near-death experiences also have solved a problem with the afterlife: the fear of death. J Near-Death Stud.5(pp44-52) these are neglected by the pharmacological research or are considered as being disturbing and without inﬂuence on the success of the therapeutic process. Todesnähe. physiology and spirituality should no longer be considered separately. Neurophysiologische Erklärungen der Nah-Todeserfahrung. 1998. These changes last for several weeks. Samorini G. 2002:59-70. Goutarel R. Princeton: Princeton University Press. the adult person relives a condition of massive vagal dominance that is not normally at his disposal. 2000. Elfferich I.
83. Takasawa K. J Neurochem. Glick SD. Bremner J. London. Golanov EV. Polyrhythms supporting a pharmacotherapy. 60. 2000. 2000. 42. Schmid RS. Hippocampal changes in patients with a ﬁrst episode of major depression. 2002. J Neurosci. Kinney GG. 53. Free and forced diving in birds.818(2):304-315. Reis DJ. 2000. 2006. et al. González J. 55. Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. Whinnery JE. 2002. Meisenzahl EM. Ann Neurol. Warburton S. Stress. Central neurogenic neuroprotection: protection of brain from focal ischemia by cerebellar stimulation.274(6 Pt 2):H2035-H2045. Near death experiences in cardiac arrest: visions of a dying brain or visions of a new science of consciousness. Sahar T. Underwood MD. Hulbert AJ. Reis DJ. 26. 1998. In: Gazzaniga MS. Brain Res. Neural systems underlying the suppression of unwanted memories. Lutherer LO.419(6904):269-270. J Near-death Stud.660:341-345. J Near-death Stud. Klinische Elektroenzephalographie des Kindes. 2001. 79. Molliver ME. Neocortical rhythmic slow activity during wakefulness and paradoxical sleep in rats. Cardiac arrest and near-death experience. Hopkins PJ. Depressed mood is related to high-frequency heart rate variability during stressors. second ed.370(2):378-382.94(1):95-104. 66. 1965.16(1):5-26. Else PL. Golanov EV. 45. 1999. Bengzon J.635(1-2):27-36. 57. 40. 1984:203. 51. 38. Alteration in electroencephalogram and monoamine concentrations in rat brain following ibogaine treatment. 1997. Vagal control of heart rate and cardiac shunts in reptiles: relation to metabolic state. Mash DC.22(3):299-307.1(1):35-40. in vitro. concerns for safety. Ochsner KN. Brain Res. Nestler EJ. Newport J. VOL.10(4):871-885. 1976. Frazier DT. 62. 68.75(3 Pt 1):899-903. The olivocerebellar projection mediates Ibogaine-induced degeneration of Purkinje cells: a model of indirect. 1987. 1995. Abe A. 2001. 1994. Increased neurogenesis in a model of electroconvulsive therapy. Placantonakis DG.18(3):160-168. Near-death and transcendental experiences: neurophysiological correlates of mystical traditions. Am J Psychiatry. Brain Res. Strubelt S. Golanov EV. Sakura S. Brain Res. NO. 25. 33(4):1227-1231. Chida K. Acta Physiol Scand. Kovera CA. 1987. Personality trait of behavioral inhibition is associated with oscillatory systems reciprocal relationships. Zhao X. Schmidt D. second ed. 28. Lutherer BC. Consciousness. cognition and emotion: frontal theta EEG activity to single-pulse cerebellar TMS. A novel vasodepressor response elicited from the rat cerebellar fastigial nucleus: the fastigial depressor response.78:242-254. Groover ME. 1996. Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia. Iadecola C. Gabbard G. Transcendence.52:555-566. Brain Res. Martner J. 1988. van Honk J. 49. Thomas Publisher. In: Gazzaniga MS. Therapy and Addiction. Reis DJ. Thorburn GD.37(1-2):255-262. Int J Psychophysiol. 35. 18 Woerlee GM. Basar E. Brain Res. Stahl K. Cerebellum. Kogure K. ketamine and nicardipine on the hippocampal theta waves produced by cerebral ischemia in cats [in Japanese]. EAAT4. Choi DW. 2004:95. Hermann J. Jacobs WJ. 80. Increased proliferation of neural progenitor cells but reduced survival of newborn cells in the contralateral hippocampus after focal cerebral ischemia in rats. Gabrielsen G. 77. Benson H. 1994. 22. Jourdan JP. Brain Topogr. 78. Heim C. 1981. J Neurosci. Trans Assoc Am Physicians. Protection of rat hippocampus against ischemic neuronal damage by pretreatment with sublethal ischemia. The internal mystery plays: the role and physiology of the visual system in contemplative practices. 1998 May 30. Dev Psychopathol. Porges SW. Ann Neurol. Biol Psychiatry. 31. Depoortere H. Music and Altered States. 15. 1999. 2002. The near death experience as a product of isolated subcortical brain function. Alper KR. Ibogaine neurotoxicity: a re-evaluation. Maisonneuve IM. Nonlinear. Driessen M. 1999. Nakata N. ed. De Bellis MD. Clinical interventions with near-death experiencers. Comparison of the “mammal machine” and the “reptile machine”: energy production. Fundam Clin Pharmacol. Pereda E. The effects of stress on memory and the hippocampus throughout the life cycle: implications for childhood development and aging. 65. In: Lundahl C. Depersonalization in the face of life-threatening danger: a description. Am J Physiol. et al. 43. 81.36(2):233-237. Wettach G.29(2-3):169-195. Hippocampal volume in adolescent-onset alcohol use disorders. Welsh JP. Topographic EEG in brain ischemia—correlation with blood ﬂow and metabolism. 1995. Schutter DJ. Strubelt S. Love: an emergent property of the mammalian autonomic nervous system. Saito Y. Nature.89:331-359. With the Eyes of the Mind: An Empirical Analysis of Out-of-Body States. 2002.11(Suppl. 1997. 2001. Alkaloids Chem Biol.52(1):5-11. Int J Psychophysiol. de Vera L. Ann N Y Acad Sci. et al. Electrical stimulation of cerebellar fastigial nucleus protects rat brain. Treschow A. Grifﬁths PA. Shalev AY. et al. Biol Psychiatry. Kato H. Galea E. 2004. Nadel L. 1986.39(2-3):197-212. Pablo J. Molinari HH. 1995. Kobylarz KA. Reis DJ. Childhood trauma associated with smaller hippocampal volume in women with major depression. IL: Charles C. Gamundi A. Kanwisher N.48(3):247-261.tor. Kammers MP.” Percept Mot Skills. Die Iboga-Heilungszeremonie im Gabun: Gelenkte Nah-Todes-Erfahrung als Psychotherapie. Am J Psychiatry. A Collection of Near-Death Research Readings. EEG alpha and theta oscillations reﬂect cognitive and memory performance: a review and analysis. Nicolau MC.und Jugendalters. Cerebellum.19(2):105-111. Psychoneuroendocrinology. Alkaloids Chem Biol. 1999:139-148. Xu F. Glutamate neurotoxicity in cortical cell culture.92(4):512-531. spindles and evoked potentials. 71. Qian L.211(4483):717-719. Frontal midline theta rhythm and mental activity. 73. Frazier DT. 1985. 2001. Beaudoin M. 37. Reis DJ. Flynn CP. González J.1(4):54-63. van Honk J. 63.86(6):777-784. Madsen TM. Glickstein SB. 61. 2002. 1986. Orienting in a defensive world: mammalian modiﬁcations of our evolutionary heritage. In: Aldridge D. 24. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. Wang T.586(1):121-124. Wolf S. The selectively distributed theta-system functions. Kocsis B. Ein Vergleich afrikanischen Wissens mit internationalen Forschungsergebnissen [master’s thesis].20(24):9104-9110. et al. Kletti R. The effects of thiamylal. 34 ALTERNATIVE THERAPIES. 2002.77(3):1073-1080.12(3):177-200. 2000. Kosaka Y. J Near-death Stud. Gallotia galloti. jan/feb 2008. Syncope: a videometric analysis of 56 episodes of transient cerebral ischemia. 76. Ann N Y Acad Sci. Ohio: Chandler and Sharp. Zhou P. Yagita Y.269(2):251-257. Tirsch WS. 1994. Masui. 2001. Taylor T. 47.844:265-273. Galea E. 36.49(7):637-643. deprivation.56:1-38. 1998. Am J Psychiatry. Yuen G. Science. Barnes CD. Knoblauch H. Persinger MA. A case of illusory own-body perceptions after transcranial magnetic stimulation of the cerebellum. The Near-Death Experience. 2000.914:394-401. eds. et al. Stress-induced recovery of fears and phobias. Germany: University of Bielefeld. Seeck M. Bielefeld. Publishers.57(12):1115-1122.1(2):97-106. from staurosporine-induced apoptosis. Porges SW. Kanwisher JW. 1994. 74. Narayan M. Altern Ther Health Med. Fenwick P. 84. Brain Res. An electrophysiological link between the cerebellum. The New Cognitive Neurosciences. 17.1):39-43. 58. 21. Neuropsychobiology. Vythilingam M. Clark DB. Bauer M. Gould E. Klimesch W. trans-synaptic excitotoxicity. Kasaba T. 32. Blanke O. Arch Gen Psychiatry.5(3):238-240. Resuscitation. Am J Physiol. Neuroprotective electrical stimulation of cerebellar fastigial nucleus attenuates expression of periinfarction depolarizing waves (PIDs) and inhibits cortical spreading depression.17(22):8828-8841. Adv Neurol. Kriegstein AR. Nagata K. ed. 54. Electroencephalogr Clin Neurophysiol. 1975. Psychophysiologic correlates of unconsciousness and near-death experiences. Schutter DJ. et al. Am J Physiol. J Cereb Blood Flow Metab. Glickstein SR. 16. Beers SR. Ibogaine: complex pharmacokinetics. 69. 75. 2006.159(7):1112-1128. 1997. O’Hearn E. et al.62(6):796-803. 2001. 1984. Fachner J. Dormer KJ. 23. Praag H van. Ortigue S. Clark. Goldman RF. Music in the Iboga Initiation Ceremony in Gabon. 1998. Golanov EV. The inﬂuence of acute hypoxia and sleep states on the electrical activity of the cerebellum in the sheep fetus. Thorn B.79(2):328-338. Glick SD. Feinstein DL. Separation of hippocampal theta dipoles by partial coherence analysis in the rat. 2004. 29. 1994. Parry TJ. Chicago: Nelson-Hall Inc. Brain Res Brain Res Rev. Kuhl B. Neurogenesis in the adult mammalian brain. Reader AL 3rd.90(4):298-303.16(2):90-95. Schneider RA. Cerebellar modulation of ventilatory response to progressive hypercapnia.39(7):870-876.23(8):837-861. 2000 Sep. 30. 33. Anderson MC. Exp Physiol. 46. 1983.159(12):2072-2080. Why do Purkinje cells die so easily after global brain ischemia? Aldolase C. Inﬂuences on the defecation and micturition reﬂexes by the cerebellar fastigial nucleus. Maisonneuve IM. Three case reports of the metabolic and electroencephalographic changes during advanced Buddhist meditation techniques. Electroencephalogr Clin Neurophysiol. Szumlinski KK. 67. J Appl Physiol. Feinstein DL. ed. 70. 1994. Thinschmidt JS. Sakowitz O. Schürmann M. and the cerebellar contribution to posthypoxic myoclonus. Ibogaine: a review. Knyazev GG.47(12):1043-1049. Glutamate and the pathophysiology of hypoxic-ischemic brain damage. 39. De Vera L. Neuroimage. Lempert T.7(2):357-368. 56. 59. 44. eds. J Near-death Stud. 34. Hughes JW. fractal and spectral analysis of the EEG of lizard. 1 Lessons From the Iboga Healing Ceremony in Gabon . Science. Stoney CM. Possession. 1992. Slobodskaya HR. Pickel VM. Kitagawa K. Porges SW. Psychophysiology.22(4):235-249. A Polyvagal Theory. Berlin: Springer. 2002. Different kinds of near-death experience: a report on a survey of near-death experiences in Germany. Tingström A. Vertes RP. Behav Med. Philadelphia: Jessica Kingsley Publishers. Eisch AJ.277(1 Pt 2):R86-R93. Reptilian waking EEG: slow waves. Owen J. Noyes R. Stimulating illusory own-body perceptions. Role of the cerebellar deep nuclei in respiratory modulation. Janssen HF. Mechanisms of action of ibogaine: relevance to putative therapeutic effects and development of a safer iboga alkaloid congener. Springﬁeld. Parnia S. 50. C. J Near-death Stud.303(5655):232-235. 1982:51-64.32(4):301-318. 19. Relative right temporal-lobe theta activity correlates with Vingiano`s hemispheric quotient and the “sensed presence. 72. et al. 27. 82. Munro C. Harding R. and adult neurogenesis.240(1):R3-R9. Liu Y. 20. 14. 1999:127-137. 2003. Massachusetts: Bradford Books.19(2):71-90. 1981. 20(1):15-29. The New Cognitive Neurosciences. 1988. 1990. Binienda Z. Zetzsche T. 2000. Xu F. 41. In: Greyson B. 2001. Olney JW. Vagal modulation of responses to mental challenge in posttraumatic stress disorder. Maas U. Maulucci-Gedde M.57(2):166-173. Bourguignon E. Further studies on the circulatory and metabolic alterations of the oxygen-conserving (diving) reflex in man. Psychosom Med. 2006:101-124. Rial RV. Psychol Rev. Gage FH. Enter D. Bolwig TG. Massachusetts: Bradford Books.157(5):737-344. 1997. Jacobs GD. Psychiatry Clin Neurosci. Duman RS. Rothman SM. Malberg JE. Rial R. Rawson JA. 1992. 48. Lindvall O. 14. McElligott JG. Kainic acid administration in the fastigial nucleus produces differential cardiovascular effects in awake and anesthetized rats. 1990. J Near-death Stud. Bilateral lesions of the fastigial nucleus prevent the recovery of blood pressure following hypotension induced by hemorrhage or administration of endotoxin.15(4):231-258. Inanaga K. 64. Malhotra MS.56:39-53. Landis T. 1984:242-255. J Neurosci. New York: Praeger Publishers. Frodl T. 52. and preliminary efﬁcacy measures.
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.