Brody et al (2001) studied 24 untreated patients with major depressive disorder (MDD). Positron Emission Tomography (PET) brain imaging was used to provide images of the patients before and after 12 weeks of either interpersonal psychotherapy treatment or pharmacologically with Paroxetin (an SSRI). A control group of non-depressive patients were also evaluated.
Subjects with depressive symptoms at the baseline had higher metabolism than the control group in the prefrontal cortex (PFF), and lower metabolism in the temporal lobe (TL).
With treatment, the depressive subjects showed metabolic changes. Their brain scans changed to match those belonging to the normal group.
The Hamilton Depression Rating scale was used to access the experience of depression in the subjects. In both treatment groups the subjects saw decrease in depression experience. However theparoxetine-treated subjects had a greater mean decrease in Hamilton Depression Rating Scale score (61.4%) than did subjects treated with interpersonal psychotherapy (38.0%).
Both subgroups showed decreases in normalized PFF and left anterior cingulate gyrus metabolism and increases in normalized left temporal lobe metabolism; the paroxetine-treated bilaterally, while interpersonal psychotherapy-treated on the right.
This study showed that inter-personal therapy treatment effected change in the metabolic activity in the brain. The effect of the treatment is also moderately different as that from pharmacological treatment.
Further study by Martin et al. (2001), using Single-Photon-Emission Computer Tomography (SPECT), comparing 28 depressive patients treated with 6 weeks of interpersonal psychotherapy and depressive patients treated with Venlafaxin(a SSNRI).
The researchers discovered, after 6 weeks of treatment, both groups of patients showed increased cerebral blood flow in the right basal ganglia. However, when they tested the patients again on the 12th week (this means 6 weeks after treatment has completed), only the psychotherapeutically treated patients retained the increased blood flow in the right posterior cingulum.
Conclusion
What the studies tell us is that the treatment of depression with inter-personal psychotherapy and pharmaceuticals do alleviate depressive symptoms.
Biologically, however there is a difference in how both types of treatment work.
The significant point of the studies is, that although pharmaceutical treatment seem to work as well as psychotherapy, the effect of interpersonal psychotherapy is lasting. 6 weeks after treatment has ended, the client keeps the benefits of the psychotherapeutic treatment. Pharmaceutical treatment was shown, however, to be transient, setting the patient back to original condition when the drugs are discontinued.
Bibliography
Brody, A. L., Saxena, S., Stoessel, P., Gillies, L. A., Fairbanks, L. A., Alborzian, S., … & Ho, M. K. (2001). Regional brain metabolic changes in patients with major depression treated with either paroxetine or interpersonal therapy: preliminary findings. Archives of general psychiatry, 58(7), 631-640.
Martin, S. D., Martin, E., Rai, S. S., Richardson, M. A., & Royall, R. (2001). Brain blood flow changes in depressed patients treated with interpersonal psychotherapy or venlafaxine hydrochloride: preliminary findings. Archives of General Psychiatry, 58(7), 641-648.
Functional Neuroimaging (fMRI) studies of fear, specific phobia, social anxiety and PTSD are compared in the article by Etkin & Wager (2007) indicates to us how the different kinds of fear- and anxiety-related disorders differ in activation in the brain.
Etkin & Wager, 2007
As therapists we learn to treat each patient’s symptoms as individual. Language to describe fear-type emotions can be limited to a few adjectives. The experiences of different patients are different. fMRI studies show that biologically, these symptoms are also not similar.
The findings mentioned in this paper also accentuates the point that no anti-anxiety drug can remove the symptoms for all fear-based disorders. This often leads the medical professionals to prescribe cocktails of drugs as a measure.
Bibliography
Etkin, A. & Wager, T. D. (2007). Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. American Journal of Psychiatry, 164(10), 1476-1488.
This is a presentation on how the world of neuroscience conceptualizes emotions. Many neuroscientists have managed to co-relate modern neuro-scientific understandings with psychoanalytic theories (of Freud and Co.). Neurobiology is not complete without psychology and vice versa. Knowing both the biological/ molecular biological aspect of brain function and the psycho-social aspect of the mind provides us with a holistic picture of mental life. Treatment methods are more effective with holistic attitude of the practitioners.
While these ideas are not new, there is much more information that can be inferred from this knowledge in the profession of psychotherapy. What I am currently interested in is in the individual differences of patients suffering from psychopathologic symptoms that are given blanket descriptions in the DSM namely:
Anxiety Disorders: is the anxiety derived from “panic” (as in the experience of loss?)? “Fear” (as in post traumatic disorders o phobias?
Depression: is this a derivative of loss, grief and lack of mourning? is this the reason why we are seeing clients who suffer both anxiety and depression?
Anger management: is it anger due to frustration (Rage), or anger due to appetite (predatory, seeking)?
Shame: where does this come in? it is not basic emotion? Do we not see it in animals? How does shame in animals look like? Human can articulate shame? is shame only a human phenomenon?
Solm’s lecture
How this concept compares to other theories in neuroscience
Bibliography
Solms, M. (2015). The animal within us. Source: Youtube URL https://www.youtube.com/watch?v=JfqVIG9bejU.
Solms, M., & Turnbull, O. (2002). The brain and the inner world: An introduction to the neuroscience of subjective experience. Karnac Books.
►Negative symptoms: affect and speech impoverishment, apathy, disturbed vigilance and concentration
►Affective disturbances dominate in almost 100%, followed by formal thinking disturbances (90%), drive disturbance (85%), diminished attention (84%) and delusions (70%).
Several clinical types:
►Paranoid (hallucinatory) type (ICD 10: F 20.0. DSM-IV 295,30)
►Hebephrenic S. (F 20.1)
►Catatonic S. (F 20.2)
►Undifferentiated S. (F 20.3)
►S. simplex (F 20.6)
►Other S.’s (F 20.8) (e.g. jealousy delusions)
Types of Schizophrenia Symptoms
Paranoid Type:
►Delusional ideas, mostly accompanied by acoustic hallucinations and other S. symptoms.
►Examples of delusional ideas are: persecution, megalomania, particular (religious or other) mission, particular connections.
►Hallucinations consist of commenting or commanding voices (possibly driving to suicide)
► Olfactory or coenesthetic hallucinations may occur
Hebephrenic Type:
►Affective disturbances are predominant
►Inappropriate mood, with affectation, smiling or laughing, grimaces, mannerisms
►Thinking disturbed, speech longwinded, often ridiculous behavior.
►Delusions and hallucinations are short and less severe
Catatonic Type:
►Mainly psychomotor disturbances between stupor and excitement
►Behavior is often characterized by robot-like automatism, rigid and bizarre bodily positions are kept for long time
►Rare in Western countries.
►Often intensive scenic hallucinations
►Severe state with high lethality, emergency state
Other Types:
►Undifferentiated type: Characteristic schizophrenic symptoms without fitting into one of the specific types.
►S. simplex: rare form with only few symptoms, strange behavior, cognitive faculties progressively disturbed, apparently less psychotic than the previously described types. As a rule no delusions or hallucinations. Diagnosis often difficult.
►Postschizophrenic depression (ICD 10: 20.4) consists of mainly negative symptoms, depression, lack of initiative, low level functioning.
Epidemiology of Schizophrenia
►Prevalence: 0.5 – 1% (about the same all over the world)
►Yearly incidence: 0.01%
►Life prevalence: 0.6
►males = females
►Illness begin on average at 21 years (males) and 26 years (females). Hebephrenic form begins with puberty, paranoid-hallucinatory form in about the 4th decade. “Late schizophrenia” begins after 40.
Etiology
►Genetic
Higher familial occurence (Häfner 1993)
Family and twin studies: concordance rate in monozygotic twins reaches 44-50%, in heterozygotic twins 10-12%, in siblings 7%.
However, no single gene is related to the aetiology of S.;
Polygenetic heredity seems to cause the illness.
►Adoption studies (Tienari 1991)
“Multifactorial” aetiology
Certain neurophysiological or biochemical changes may take place in the brain, leading to higher vulnerability and predisposition.
Unfavorable social conditions heighten the chances to develop S. in vulnerable individuals.
Coping strategies or protective factors favor better prognosis or subclinical illness.
►Association studies
Searching for a gene, genotype, an allele, or a certain DNA sequence variant occuring more frequently than expected in S. populations as risk factor.
“Candidate genes” as genetic risk carriers: genes for various dopamine-receptor constellations, e.g. on chromosome 6.
►Morphological and neuropathological findings
S. patients have larger brain ventricles than normal population. Atrophic process concentrates mainly on the temporal lobe and the limbic system (thalamus, pallidum, s. nigra, temporal lobe, corpus callosum etc.), diminishing the amount and the arrangement of neurons.
Such atrophic processes seem to begin at an early age
Brain imaging makes it possible not only to find morphological correlations to S., but also to “observe” dynamic processes occuring in the brain of “normal” and psychotic individuals. Reduced blood perfusion and metabolism could be located in the frontal area
Findings are heterogeneous and show great variability.
►Biological hypotheses
Dopamine hypothesis: (Experience through dopaminergic drugs: neuroleptics as dopamine-D²-antagonists. Dopamine agonists cause psychotic symptoms) Dopaminergic hypoactivity in the frontal area (leading to “negative symptoms”) and dopaminergic hyperactivity in the mesolimbic system (® “positive symptoms”)
Cholinergic hypothesis: also based on the mechanism of cholinergic side-effects of neuroleptics
Glutamate hypothesis: Hypofunction of the glutamatergic receptor system (narrowly associated with dopaminergic system)
Serotonergic system: Receptor Serotonin-5HT-2a (atypical neuroleptic drugs inhibit these receptors)
Complex receptor systems involved (dopaminergic, glutamatergic, serotonergic, gabaergic): balance and interactions between the different systems disturbed
Thalamus function disturbance: striato-thalamic pathways filter sensory stimuli reaching the brain cortex. Through disturbance of this mechanism the cortex is poorly protected and thus overstimulated
Immunological hypothesis: changes affecting the immune system may follow viral infections. Inconstant findings involving higher antibody titers to cytomegalic, herpes, influenza or measles viruses.
►Psychosocial hypotheses
“Schizophrenogenic mother” (Fromm-Reichmann 1950): dominant, possessive, overprotective, rigid and emotionally cold mother “driving” child into “madness” (S.)
Double bind hypothesis (Bateson et al. 1956): pathological (double bind) communication between mother and infant, which lead to intellectual and emotional confusion. Lack or passivity of father increases helplessness and frustration of the child, who reacts with withdrawal into psychosis. First group dynamic hypotheses.
“Expressed emotions” hypothesis (EE): High emotional level and overprotective-hostile behavior could be found in the families of s. patients, which may lead to frequent s. episodes. Relapse risk predictable by high EE-score (Vaugh & Leff 1976). No specific theory for S., but for all psychiatric conditions
“Life Event” hypothesis (Brown & Birley 1970): In about 50% of cases, important life events were found three weeks prior to the beginning of a s. episode. LE are considered as precipitating factors, but not involved in the genesis of the disease
Multifactorial theory: Genetic and familial factors concurring (Tienari 1991). At present, multifactorial theory is favorized in all psychiatric and psychosomatic conditions
Group dynamic hypothesis (Ammon 1971): Destructive dynamics of the primary group (hostile, manipulative, parentifying, abusive, emotionally traumatizing and confusing atmosphere provoking guilt feelings) interiorized by the child and later enhanced by and acted out in other significant groups (school, work etc.)
Detailed information is found in this lecture:
Schizophrenia is not one disease (in some cases the term disease is not appropriate). There are subtypes of schizophrenia syndromes and it also occurs in a spectrum.
What Neuroscience has uncovered and theorized so far:
1. Imaging: reduction of brain tissue and dysconnectivity (Gruber, Meisenzahl, Koutsouleris),
These are results from Magnetic encephalography (MEG) studies. “In this study, we found that coupled local and global feedback (CLGF) circuits in the cortical functional network are related to the abnormal synchronization and also correlated to the negative symptom of schizophrenia.”
The differences in the excitation-inhibition balance in patients with normal and schizophrenic symptoms can be explained by observing these:
Smaller & fewer dendritic spines, reduced GABA synthesis, increased suppression of GABA release, fewer GABA a1 receptors, reduced GABA re-uptake and more GABA 2 receptors.
a) Working memory task induces lower change in activation in schizophrenia compared to healthy subjects.
b) NMDA-receptor antagonist ketamine evokes similar patterns
c) A computational model of working memory, comprised of task-activated (top) and task-deactivated (bottom) modules highlighting a possible mechanism for deactivation, followed by results. We tested whether ‘disinhibition’ via reduced NMDA receptor conductance onto GABA cells (E–I) (small red arrow) would resemble activation/deactivation BOLD findings under ketamine and observations in schizophrenia.
Synaptic specifities: D2R / D1R predominance e.g. PFC (signal / noise ratio in information processing; Voit)
7. Genes:for enzymes, receptors … susceptibility genes, including neuregulin-1, ErbB4, nNOS, PICK1, and DISC1, (Rujescu, Schmitt)
References:
Ammon, G. (1971): Auf dem Wege zu einer Psychotherapie der Schizophrenie (Towards a psychotherapy of schizophrenia). Dyn. Psychiat. 4: 9-28 (English summary)
Bateson, G. et al. (1956): Toward a theory of schizophrenia. Behav. Science 1: 251-264
Fromm-Reichmann, F. (1950): Principles of intensive psychotherapy. Chicago: Univ. Chicago Press
Gaebel, W. (2005): New developments and treatment issues in schizophrenia. In: Christodoulou, G. N. (Ed.): Advances in Psychiatry, Vol. 2. World Psychiatric Association, 45-52
Kaplan & Sadock’s Synopsis of Psychiatry (2003) (KSSP). Philadelphia: Lippincott Williams & Wilkins, 471-504
Kaplan & Sadock’s Comprehensive Textbook of Psychiatry, 2 Vol. (2000) (KSCT). Philadelphia: Lippincott Williams & Wilkins, 1096-1231
Vaugh, C., Leff, J (1976): The measurement of expressed emotions in the families of psychiatric patients. Brit. J. Soc. Psychol. 15: 157-165
Drawing much inspiration from a lecture given by Sapolsky (2011), an expert in the neuro- and biological field, I would like to discuss the use of language, or — more accurately put– communication, as a cure for psychological pain.
The profession of Psychotherapy, at its formation, was termed the “talking cure” (Freud & Breuer, 1895). This literally means talk as a means of relieving one of symptoms or psychical and often also somatic nature. What the term “talking” does not describe is the “listening” from the other person. In psychotherapy it is the talking to someone who is actively listening that cures. Read also: The Psychotherapeutic Alliance.
Language is in verbal and non-verbal communication
Talking and listening is communication. When we think of communication, we think of dialogue, and language. Language, according to Sapolsky is more than speaking or writing verbally. Neuroscience has indicated, especially through studying the neurobiology of sign language learning of completely deaf individuals, that whether it is verbal or non-verbal, the communication process is the same. This means that language is not merely a motoric process (i.e. about moving lips and tongue), but rather a cognitive process.
Language is unique to humans
Human communication has universal qualities. All forms of human languages have semanticity, embedded clauses, all human language can “talk about things”, can talk strategy. There is arbitrariness of language, in which words are not tied to meaning. People are able to tell lies, and say one thing and mean/feel another. Language is also invented and re-invented. Human children have innate ability to coin phrases and say things they have never heard before (N. Chompsky).
Unlike animals that have specific vocals for specific emotions, human language is not tied to specific emotions. This explains why in therapy we notice a quality of communication in which there is a “content-affect split”.
Non-verbal aspect of language
We do not communicate with words alone, there is also verbal tone, sounds, body movement, hand gestures, facial expression. Gestalt therapists look out for these during therapy as well, since the non-verbal language reveal often much of the emotional content of the communication. Certainly emailing does not allow for non-verbal communication. Perhaps that is why many of us feel more secure communication over messenger apps to even talking on the phone.
Neuro-centers of the brain that affect language
Ninety percent of humans process verbal language in the left hemisphere of the brain. The other (right) hemisphere, process the non-verbal and emotional content of the communication. The Broca’s area is connected to the motoric nature of language production. The Wernicke’s center is responsible for language comprehensibility. The connection between these two centers connect the two functions.
Through studies of biological brain disfunction due to disease, degeneration or injury, scientists have managed to identify which part of the brain is utilized for which function. Through neuro-imaging, we know that in tourettes syndrome, for example, where the sufferer curses uncontrollably, the limbic system is hyperactive. The limbic system is not known to be responsible for emotions and not language production, but language is connected to the formation of emotions.
Many have also proven that singing is a way for people who suffer damage to the Broca’s area (and hence have problems talking). Singing activates the right hemisphere and emotional centers of the brain.
Hence the phenomenon of the talking cure; an emotional weight off the shoulders when on talks emotionally to someone who is willing to listen. One can also see how verbal language is only a part of communication. Clients who have problems with speech (in particular in Alzheimers patients) respond to communication with music.
This is a simple article to explain highly complex subjects: neuroscience, psychopathology and genetics. The question is, why, despite decades of progressive molecular biological research, we cannot exclusively answer psychopathology / mental disorders not caused entirely by organic conditions, by looking at genes alone. Although there are numerous twin studies for mental disorder, the results are inconclusive.
The diagram below describes the simplistic idea to a comprehensive concept of genetics linking to mental disorder (psychopathology).
It would have been easy if we could identify a gene for each disorder, as in (a). With issues of the psyche, it is much more complex. The nature of genes is that genes switch on and off, and what gets transcribed from genes into proteins are very dependent on the environment in which the individual lives in and the experiences (consequence of time / relationships / fate).
The image below describes how the environment / perceptions and social interactions affect gene expression and the condition of the neurocircuits in the brain.
The graphic below explains how multiple experiences and the type of life experiences affect gene expression and hence the severity of a psychological symptom.
The diagram below further illustrates the effects of stress on gene expression leading to neurological consequences that lead to setting up of psychiatric disorders.
The image below shows that the genotype (and hence the quality of certain essential proteins) plays a role in susceptibility to disorder. No man is created equal, in other words.
Which genes are responsible for what disorder? The diagram below is an illustration that disorders are complex and involve the expression of different genes. These genes affect different biochemical pathways. In order to put a finger on which pathway leads to what consequence is complex and may not hold true for all persons suffering the same symptoms.
That said, the type of genetic make-up leads to susceptibility to a disorder. This is because the proteins that are involved in neuro circuitry, may differ in structure in different individuals (are polymorphic) even if these have the same function. The polymorphism explains why some people are more likely to get the disorder. The graphic below also explains to us that environmental factors play important role.
The diagram below repeats the same message as the previous diagram.
In conclusion, genes are simply there to be coded. The coding, however does not tell us a whole lot about the individual because the expression of the genes are regulated. Not all genes are expressed at all times, and how they are regulated is dependent on the experience of the individual’s environment / social situation and structure / family history, health, etc. Furthermore psychopathology is very complex, and in the molecular sense involves complicated biochemical pathways which are constantly being regulated. It is however true that some people are predisposed to certain conditions, however the severity of the symptoms (or if there are symptoms at all) is dependent on the environment.
With regard to neuro-imaging studies, the table below presents us with a summary of what neuroscience has mapped out, and this is what it can tell us about the various parts of the brain and it’s functions.
Bibliography
Tretter, F., Winterer, G., Gebicke-Haerter, P. J., & Mendoza, E. R. (Eds.). (2010). Systems biology in psychiatric research: from high-throughput data to mathematical modeling. John Wiley & Sons.
The field of Neuroscience faces continued challenges because of the reductionistic nature of the natural sciences in the first place. In my field of psychotherapy, we tend view the concept of mental states in a holistic manner and this article may seem out of place in this blog. However, a little bit of reductionism can lead us to better visualization of observed phenomena.
How do neuroscientists categorize elements that make up our understanding of what mental state is?
Consciousness:
the wakeness, disorder in the organic brain process (caused by disease/accident or drugs) affect the wakefulness of a person.
The qualitative nature of the wakefulness, like one’s orientation to place, time, situation, and other persons / self. In dementia, for example, the quality of consciousness is affected.
Attention:
extension, duration, control of attention span. Deficits in attention are seen in psychosis, or when affected by substance. There are also other organic disorders.
Perception:
psychopathologic conditions involve inability to percieve reality: illusions, hallucinations or delusious perceptions
Thinking:
the ability to form thoughts. Whether normal or subnormal is relative to cultural norms and a person’s ability as a result to function in socientx. There is usually a formal flow and content (otherwise ther is delusion).
Memory:
short-term, long-term memory; storage, recall
Affects:
Intensity and Modulation of emotions, especially of anxiety, depression and aggression; control of effect and impulses
Drives:
general level of motivation, physical / sexual needs, interests.
Expectations:
concerns and wishes (significant factor in studying addiction) and delusions.
Behavioural planning:
Structure of the intentions, reality in relation to plans, action regulation (disorder in depression and schizophrenia)
Motor behaviour :
This domain is evaluated in relation to occuring motor patterns that are observed during the communication („Psychomotorics“; reduced in depression, elevated in Mania).
Ego-functions:
ability to decide (ambivalence in schizophrenia), judgement, idealization / ideals, have the will to do something (feeling of being controlled externally in schizophrenia).
Self-concept:
Realism and balance of self image (e.g. strong polarization in addiction, neuroses and Personality disorders).
References
Tretter, F., Winterer, G., Gebicke-Haerter, P. J., & Mendoza, E. R. (Eds.). (2010). Systems biology in psychiatric research: from high-throughput data to mathematical modeling. John Wiley & Sons.
Here are some notes taken off an interesting article, entitled “The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas” that can be downloaded online. See bibliography below.
Researchers developed a strategy of comparing Freudian concepts of primary and secondary processing of cognition with fMRI neuroimaging, by studying brain activity under psychedelic- induced altered states.
The ego and the secondary process
1. Default energy store or reservoir, which possesses the property of being spontaneously or tonically active.
2. Receives and ‘contains’ or ‘represses’ endogenous excitation.
3. Minimizes free-energy.
4. Integrates or binds the primary process and its representational system (the id) into a broader, more cohesive, composite organization (the ego).
5. Specific ontogenetic development.
6. Supports reality-testing and perceptual processing.
7. Supports conscious awareness, cognition and directed attention.
8. Possesses internally and externally-focused components, which are inversely related (anti-correlated).
9. Excessive-engagement of internally-focused component and impoverished engagement of externally-focused network during pathological withdrawal; e.g. in depression and schizophrenia.
10. Failure of systems to minimize free-energy (suppress endogenous excitation) results in disturbed affect, cognition and perception; as seen in non-ordinary states such as dreaming and psychosis.
The id and primary process thinking
11. Characteristics of the system unconscious/the id and primary process thinking: i.e. a primitive, ‘magical’ or animisitic style of thinking, characterized neurophysiologically by ‘free’ movement of energy. One can think of primary process thinking in evolutionary terms as a ‘protoconsciousness’.
Psychopathology and Neuroscience
Studies and papers written of the DMN through neuro-imaging are producing data to show the activity level differences in brain activity of individuals with Alzheimer’s disease (Royall et.al 2012), Bipolar Disorder and Schizophrenia (Öngür et.al 2010), Post traumatic Stress disorder (Lanius et.al. 2010).
Bibliography
Buckner, R. L., Andrews-Hanna, J. R., & Schacter, D. L. The brain’s default network: anatomy, function, and relevance to disease Ann NY Acad Sci 2008; 1124: 1-38.
Carhart-Harris, R. L., & Friston, K. J. (2010). The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas. Brain, 133(4), https://academic.oup.com/brain/article/133/4/1265/307446#main-content, 1265-1283.
Lanius, R. A., Bluhm, R. L., Coupland, N. J., Hegadoren, K. M., Rowe, B., Theberge, J., … & Brimson, M. (2010). Default mode network connectivity as a predictor of post‐traumatic stress disorder symptom severity in acutely traumatized subjects. Acta Psychiatrica Scandinavica, 121(1), 33-40.
Öngür, D., Lundy, M., Greenhouse, I., Shinn, A. K., Menon, V., Cohen, B. M., & Renshaw, P. F. (2010). Default mode network abnormalities in bipolar disorder and schizophrenia. Psychiatry Research: Neuroimaging, 183(1), 59-68.
Royall, D. R., Palmer, R. F., Vidoni, E. D., Honea, R. A., & Burns, J. M. (2012). The default mode network and related right hemisphere structures may be the key substrates of dementia. Journal of Alzheimer’s Disease, 32(2), 467-478.
This is my presentation on this topic, “Psychedelics and Psychotherapy”. ONe can also download a pdf version of this assignment here. References:
Blewett, D., Chwelos, N (1959). Handbook for the Therapeutic use of Lysergic Acid Diethylamide-25 individual and group procedures. Erowid.org Ed. 2012 OCR version.
Bruckner, R, Andrews-Hanna, J & Schacter, D. (2008). The brains default network: Anatomy, function, and relevance to disease. Annals of the New York Academy of Sciences 1124, pp.1-38.
Buoso, J., & Riba, J. (2014). Ayahuasca and the treatment of drug addiction. In B.C. Labate & C. Cavnar (Eds). The Therapeutic Use of Ayahuasca. NY:Springer. pp. 95-109.
Carhart-Harris, R. L., & Friston, K. J. (2010). The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas. Brain, awq010.
Carhart-Harris, R. L., et al. (2011). Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. . Proceedings of the National Academy of Sciences of the USA. Vol 109 no. 6. 2138-2143.
Conway M., Pleydell-Pearce C. (2000) The construction of autobiographical memories in the self-memory system. Psychol Rev. 2000;107:261–88.
Drevets WC, Price JL, Furey ML (2008) Brain structural and functional abnormalities in mood disorders: Implications for neurocircuitry models of depression. Brain Struct Funct 213:93–118.
Fischer, F. (2015). Therapy and Substance: Psycholytic psychotherapy in the twenty first century. UK: Muswell Hill Press.
Freud, S. (1933). New Introductory Lectures on Psychoanalysis. Vol 22. London: Vintage.
Friston K. (2010) The free-energy principle: A unified brain theory? Nat Rev Neurosci11:127–138.
Griffiths, R., Richards, W., McCann, U., Jesse, R. (2006). Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance. Psychopharmacology. Vol 187,3, pp. 268-283.
Grof, S. (1980). LSD Psychotherapy (The healing potential of psychedelic medicine.). pp. 28.
Grob CS, et al. (2011) Pilot study of psilocybin treatment for anxiety in patients with advanced-stage cancer. Arch Gen Psychiatry 68:71–78.
Huxley A., (1954) The Doors of Perception and Heaven and Hell. Harper & Brothers: London.
ICEERS (International Center for Ethnobotanicals Education Research & Service) (2014) Ayahuasca Conference 2014. http://www.aya2014.com/).
Ino, T., Nakai, R., Azuma, T., Kimura, T., & Fukuyama, H. (2011). Brain Activation During Autobiographical Memory Retrieval with Special Reference to Default Mode Network. The Open Neuroimaging Journal, 5, 14–23.
Mithoefer, M. (2012). Durability of improvement in posttraumatic stress disorder symptoms and absence of harmful effects or drug dependency fter MDMA assisted psychotherapy. Journal of Psychopharmacology Nov 20 2012 , Vol. 7, 2 pp. 101-116.
Nielson J., & Megler J. (2014). Ayahuasca as a candidate Therapy for PTSD . In B.C. Labate & C. Cavnar (Eds). The Therapeutic Use of Ayahuasca. NY:Springer. pp. 41-58.
Northoff, G., Heinzel, A., Greck, M., Bennoihl, F., Dobrowolny, H. & Panksepp, J. (2006). Self referential processing in our brain: A meta-analysis of imaging studies on the self. Neuroimage, 31(1), 440-457.
Palhano-Fontes, F. et al. (2014). The therapeutic potentials of Ayahuasca in the treatment of depression . In B.C. Labate & C. Cavnar (Eds). The Therapeutic Use of Ayahuasca. NY:Springer. pp. 41-58.
Prickett, J., & Leister, B. (2014). Hypothesses regarding Ayahuasca’s potential Mechanisms of action in the treatment of addiction. In B.C. Labate & C. Cavnar (Eds). The Therapeutic Use of Ayahuasca. NY:Springer. pp. 111-130.
Raichl,e M., et.al. (200). A default mode of brain function ProcNatlAcad of Sci USA 98:676-82.
Sessa B. (2005) Can psychedelics have a role in psychiatry once again? Br J Psychiatry186:457–458.
Sheline YI, Price JL, Yan Z, Mintun MA. (2010) Resting-state functional MRI in depression unmasks increased connectivity between networks via the dorsal nexus. Proc Natl Acad Sci USA107:11020–11025. Holtzheimer PE, Mayberg HS (2011) Stuck in a rut: Rethinking depression and its treatment. Trends Neurosci 34:1–9.
Springer, A. (2015). Psychopharmacology. Lecture series at the Sigmund Freud University, Vienna. Unpublished.
Winkelman, M. (2014). Psychedelics as Medicines for Substance Abuse Rehabilitation: Evaluating Treatments with LSD, Peyote, Ibogaine and Ayahuasca. Current Drug Abuse Reviews, Vol. 7, 2 pp. 101-116.
. SE 2.
References: