Brainstem

The effects of imposing helplessness

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This 2016 New York rodent study found:

“By using unbiased and whole-brain imaging techniques, we uncover a number of cortical and subcortical brain structures that have lower activity in the animals showing helplessness than in those showing resilience following the LH [learned helplessness] procedure. We also identified the LC [locus coeruleus] as the sole subcortical area that had enhanced activity in helpless animals compared with resilient ones.

Some of the brain areas identified in this study – such as areas in the mPFC [medial prefrontal cortex], hippocampus, and amygdala – have been previously implicated in clinical depression or depression-like behavior in animal models. We also identified novel brain regions previously not associated with helplessness. For example, the OT [olfactory tubercle], an area involved in odor processing as well as high cognitive functions including reward processing, and the Edinger–Westphal nucleus containing centrally projecting neurons implicated in stress adaptation.

The brains of helpless animals are locked in a highly stereotypic pathological state.”

Concerning the study’s young adult male subjects:

“To achieve a subsequent detection of neuronal activity related to distinct behavioral responses, we used the c-fosGFP transgenic mice expressing c-FosGFP under the control of a c-fos promoter. The expression of the c-fosGFP transgene has been previously validated to faithfully represent endogenous c-fos expression.

Similar to wild-type mice, approximately 22% (32 of 144) of the c-fosGFP mice showed helplessness.”

The final sentence of the Introduction section:

“Our study..supports the view that defining neuronal circuits underlying stress-induced depression-like behavior in animal models can help identify new targets for the treatment of depression.”

Helplessness is both a learned behavior and a cumulative set of experiences during every human’s early life. Therapeutic approaches to detrimental effects of helplessness can be different with humans than with rodents in that we can address causes.

The researchers categorized activity in brain circuits as causal in the Discussion section:

“Future studies aimed at manipulating these identified neural changes are required for determining whether they are causally related to the expression of helplessness or resilience.”

Studying whether or not activity in brain circuits induces helplessness in rodents may not inform us about causes of helplessness in humans. Our experiences are often the ultimate causes of helplessness effects. Many of our experiential “neural changes” are only effects, as demonstrated by this and other studies’ induced phenotypes such as “Learned Helplessness” and “Prenatally Restraint Stressed.”

Weren’t the researchers satisfied that the study confirmed what was known and made new findings? Why attempt to extend animal models that only treat effects to humans, as implied in the Introduction above and in the final sentence of the Discussion section:

“Future studies aimed at elucidating the specific roles of these regions in the pathophysiology of depression as well as serve as neural circuit-based targets for the development of novel therapeutics.”

http://journal.frontiersin.org/article/10.3389/fncir.2016.00003/full “Whole-Brain Mapping of Neuronal Activity in the Learned Helplessness Model of Depression” (Thanks to A Paper a Day Keeps the Scientist Okay)

Advance science by including emotion in research

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This 2015 analysis of emotion studies found:

“Emotion categories [fear, anger, disgust, sadness, and happiness] are not contained within any one region or system, but are represented as configurations across multiple brain networks.

For example, among other systems, information diagnostic of emotion category was found in both large, multi-functional cortical networks and in the thalamus, a small region composed of functionally dedicated sub-nuclei.

The dataset consists of activation foci from 397 fMRI and PET [positron emission tomography] studies of emotion published between 1990 and 2011.”

From the fascinating Limitations section:

“Our analyses reflect the composition of the studies available in the literature, and are subject to testing and reporting biases on the part of authors. This is particularly true for the amygdala (e.g., the activation intensity for negative emotions may be over-represented in the amygdala given the theoretical focus on fear and related negative states). Other interesting distinctions were encoded in the thalamus and cerebellum, which have not received the theoretical attention that the amygdala has and are likely to be bias-free.

Some regions—particularly the brainstem—are likely to be much more important for understanding and diagnosing emotion than is apparent in our findings, because neuroimaging methods are only now beginning to focus on the brainstem with sufficient spatial resolution and artifact-suppression techniques.

We should not be too quick to dismiss findings in ‘sensory processing’ areas, etc., as methodological artifacts. Emotional responses may be inherently linked to changes in sensory and motor cortical processes that contribute to the emotional response.

The results we present here provide a co-activation based view of emotion representation. Much of the information processing in the brain that creates co-activation may not relate to direct neural connectivity at all, but rather to diffuse modulatory actions (e.g., dopamine and neuropeptide release, much of which is extrasynaptic and results in volume transmission). Thus, the present results do not imply direct neural connectivity, and may be related to diffuse neuromodulatory actions as well as direct neural communication.”

Why did the researchers use only 397 fMRI and PET studies? Why weren’t there tens or hundreds of times more candidate studies from which to select?

The relative paucity of candidate emotion studies demonstrated the prevalence of other researchers’ biases for cortical brain areas. The lead researcher of the current study was a coauthor of the 2016 Empathy, value, pain, control: Psychological functions of the human striatum, whose researchers mentioned that even their analyses of 5,809 human imaging studies was hampered by other imaging-studies researchers’ cortical biases.

Functional MRI signals depend on the changes in blood flow that follow changes in brain activity. Study designers intentionally limit their findings when they scan brain areas and circuits that are possibly activated by human emotions, yet exclude emotional content that may activate these areas and circuits.

Here are a few examples of limited designs that led to limited findings when there was the potential for so much more:

It’s well past time to change these practices now in the current year.

This study provided many methodological tests that should be helpful for research that includes emotion. It showed that there aren’t impenetrable barriers – other than popular memes, beliefs, and ingrained dogmas – to including emotional content in studies.

Including emotional content may often be appropriate and informative, with the resultant findings advancing science. Here are a few recent studies that did so:

http://journals.plos.org/ploscompbiol/article?id=10.1371%2Fjournal.pcbi.1004066 “A Bayesian Model of Category-Specific Emotional Brain Responses”

State-dependent brain functions and adrenaline

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This 2015 German/Italian rodent study investigated:

“How a specific neuromodulatory input may influence the information content and the readout of cortical information representations of sensory stimuli.

The locus coeruleus (LC) is a brainstem neuromodulatory nucleus that likely plays a prominent role in shaping cortical states via a highly distributed noradrenaline release in the forebrain. In particular, the LC:

  • Contributes to regulation of arousal and sleep;
  • Is involved in cognitive functions such as vigilance, attention, and selective sensory processing; and
  • Modulates cortical sensory responses and cortical excitability.

An important addition of our work to previous models of state dependence was the inclusion of the contribution of an important neuromodulator – the noradrenergic system. Our results support the hypothesis that the temporal structure of LC firing causally influences cortical dynamics.

Our work highlights the importance of timing of LC burst: suitably timed LC burst (for example, triggered by an alerting stimulus) can very rapidly trigger transitions into excitable cortical states, which in turn decrease the threshold for cortical responses and thus dynamically facilitate the processing of salient or attended events.

State dependence may either:

  • Force neurons to transmit information only using codes that are robust to state fluctuations (e.g., relative firing rates), or may
  • Force downstream neurons to gain information about the state of the networks sending the sensory messages and then to use the knowledge of state to properly interpret neural responses.

Our results suggest that the latter information transmission scheme is feasible, because detecting state by either monitoring the dynamics of cortical ongoing activity alone or by also monitoring the dynamics of noradrenergic modulation substantially increased the amount of information about sensory stimuli in the late response components relevant for behavior.”

The study added to the evidence that state dependencies can’t be overlooked in explanations of brain function and resultant physical and mental activity. Locus coeruleus neural activity “can very rapidly trigger transitions into excitable cortical states..and thus dynamically facilitate the processing of salient or attended events.”

Adrenaline from the locus coeruleus produced a state of arousal in multiple brain and body areas tied into the subjects’ sympathetic nervous systems. Such internal state changes may be accompanied by state-dependent memories, following the findings of What can cause memories that are accessible only when returning to the original brain state?

The study highlighted the capability of a lower brain structure to influence other brain areas. Its findings should inform researchers in attention and behavior studies, especially when investigating causes of attention and behavior difficulties.

http://www.pnas.org/content/112/41/12834.full “Modeling the effect of locus coeruleus firing on cortical state dynamics and single-trial sensory processing”

A problematic study of beliefs and dopamine

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This 2015 Virginia Tech human study found:

“Dopamine fluctuations encode an integration of RPEs [reward prediction errors, the difference between actual and expected outcomes] with counterfactual prediction errors, the latter defined by how much better or worse the experienced outcome could have been.

How dopamine fluctuations combine the actual and counterfactual is unknown.”

From the study’s news coverage:

“The idea that “what could have been” is part of how people evaluate actual outcomes is not new. But no one expected that dopamine would be doing the job of combining this information in the human brain.”

Some caveats applied:

  • Measurements of dopamine were taken only from basal ganglia areas. These may not act the same as dopamine processes in other brain and nervous system areas.
  • The number of subjects was small (17), they all had Parkinson’s disease, and the experiment’s electrodes accompanied deep brain stimulation implantations.
  • Because there was no control group, findings of a study performed on a sample of people who all had dysfunctional brains and who were all being treated for neurodegenerative disease may not apply to a population of people who weren’t similarly afflicted.

The researchers didn’t provide evidence for the Significance section statement:

“The observed compositional encoding of “actual” and “possible” is consistent with how one should “feel” and may be one example of how the human brain translates computations over experience to embodied states of subjective feeling.”

The subjects weren’t asked for corroborating evidence about their feelings. Evidence for “embodied states of subjective feeling” wasn’t otherwise measured in studied brain areas. The primary argument for “embodied states of subjective feeling” was the second paragraph of the Discussion section where the researchers talked about their model and how they thought it incorporated what people should feel.

The study’s experimental evidence didn’t support the researchers’ assertion – allowed by the reviewer – that the study demonstrated something about “states of subjective feeling.” That the model inferred such “findings” along with the researchers’ statement that it “is consistent with how one should “feel” reminded me of a warning in The function of the dorsal ACC is to monitor pain in survival contexts:

“The more general message you should take away from this is that it’s probably a bad idea to infer any particular process on the basis of observed activity.”

The same researcher who hyped An agenda-driven study on beliefs, smoking and addiction that found nothing of substance was back again with statements such as:

“These precise, real-time measurements of dopamine-encoded events in the living human brain will help us understand the mechanisms of decision-making in health and disease.”

It’s likely that repeated hubris is one way researchers respond to their own history and feelings, such as their need to feel important as mentioned on my Welcome page.

The Parkinson’s patients were willing to become lab rats with extra electrodes that accompanied brain implantations to relieve their symptoms. Findings based on their playing a stock market game didn’t inform us about “mechanisms of decision-making in health and disease” in unafflicted humans. As one counter example, what evidence did the study provide that’s relevant to healthy humans’ decisions to remain healthy by taking actions to prevent disease?

The unwarranted extrapolations revealed a belief that the goal of research should be to explain human actions by explaining the actions of molecules. One problem caused by the preconceptions of this widespread belief is that it leads to study designs and models that omit relevant etiologic evidence embedded in each of the subjects’ historical experiences.

This belief may have factored into why the subjects weren’t asked about their feelings. Why didn’t the study’s design consider as relevant subject-provided evidence for feelings? Because the model already contrived explanations for feelings underlying the subjects’ actions.

http://www.pnas.org/content/113/1/200.full “Subsecond dopamine fluctuations in human striatum encode superposed error signals about actual and counterfactual reward”

Trapped, suffocating, unable to move – a Primal imprint

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“The malady of needing to move constantly: organizing trips, making reasons to go here and there, and in general, keeping on the move..below all that movement is a giant, silent scream.

The price we pay is never knowing our feelings or where they come from.

We have the mechanism for our own liberation inside of us, if we only knew it.

When we see constant motion we understand, but we never see the agony. Why no agony? Because it is busy being acted-out to relieve the agony before it is fully felt.”

http://cigognenews.blogspot.com/2015/11/epigenetics-and-primal-therapy-cure-for_30.html “The Miracle of Memory – Epigenetics and Primal Therapy: The Cure for Neurosis (Part 13/20)”

Leaky gates, anxiety, and grocery store trips without buying list items

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An interview with Jeff Link, the editor of Dr. Arthur Janov’s 2011 book “Life Before Birth: The Hidden Script that Rules Our Lives” with Ken Rose:

“Even further confirmation for some of the views of Janov, that maybe weren’t widely accepted for a time, it’s new research now being done into memory and what a lot of scientist are seeing, a lot of different studies is that memory reactivates the same neuroimpulses that were initially firing off when the event happened.

So a traumatic event when you remember it, the act of remembering it is actually creating a neuromirror of what went on initially.

In a lot of ways that is what Primal Therapy is attempting to do; is to go back to that place and reconnect, or as it’s sometimes referred to, reconsolidate the brain state so that real healing can take place.”

Transcript (part 4 of 6): http://cigognenews.blogspot.com/2015/09/ken-rose-on-life-before-birth-part-46.html

MP3: http://www.pantedmonkey.org/podcastgen/download.php?filename=2011-12-15_1300_what_now_jeff_link.mp3

Emotionless brain research that didn’t deal with human reality

gettingwell4 0-1 star Wasted resources, Amygdala, Anterior cingulate cortex, Brainstem, Cerebrum, Hippocampus, Limbic system, Lower brain, Thalamus

Are tasks you do at work and home never influenced by emotional content or contexts?

Does your ability to focus on a task always have nothing to do with your emotional state?

The researchers who designed this 2015 Boston human study acted as if both of your answers to these questions were “Yes” by stripping out any emotional content from their experiments. As a result, this study which purported to:

“Have the potential to provide additional insights into how inhibitory control may break down in a wide variety of individuals with neurological or psychiatric difficulties”

couldn’t achieve anything near its goal.

This study included fMRI scans of subjects’ entire brains. Limbic system areas were in 3 of the 5 modules, and lower brain areas were in one.

Functional MRI signals depend on changes in blood flow that follow changes in brain activity. Given this study’s goal, did it make sense for researchers to design experiments that didn’t actively engage scanned areas of subjects’ brains?

It wasn’t all that difficult to include emotional content that could potentially contribute to the purported goal. This 1996 review described studies that developed varieties of emotional content with the same test type (Stroop) used. Presumably these approaches had made progress since 1996 incorporating emotional content in Stroop tests given to normal people, who were subjects in this study.

http://www.pnas.org/content/112/32/10020.full “Flexible brain network reconfiguration supporting inhibitory control”

Are a child’s genes the causes for their anxiety?

gettingwell4 0-1 star Wasted resources, Amygdala, Brain development, Brainstem, Cerebrum, Epigenetics, Limbic system, Lower brain, Stress , , ,

This 2015 Wisconsin macaque study was another attempt to justify the school’s continuing captivity of thousands of monkeys. The researchers performed a study that – if its experimental design was truly informative for helping humans – could have been done with humans.

A problem I saw in the news coverage was that the finding of:

“35 percent of variation in anxiety-like tendencies is explained by family history”

was attributed to genetics, with headlines such as “Anxious Brains Are Inherited, Study Finds.” The lead researcher encouraged this misinterpretation with statements such as:

“Over-activity of these three brain regions are inherited brain alterations that are directly linked to the later life risk to develop anxiety and depression.”

However, the researchers produced this finding by running numbers on family trees, not by studying genetic samples to assess the contributions of genetic and epigenetic factors!

The study’s “family history” correlation was different than finding an inherited genetic causation that wasn’t influenced by the subjects’ caged environments!

The study found:

“Metabolism within a tripartite prefrontal-limbic-midbrain circuit mediates some of the inborn risk for developing anxiety and depression.

The brain circuit that was genetically correlated with individual differences in early-life anxiety involved three survival-related brain regions. These regions were located in the brain stem, the most primitive part of the brain; the amygdala, the limbic brain fear center; and the prefrontal cortex, which is responsible for higher-level reasoning and is fully developed only in humans and their primate cousins.”

The 592 subjects were the human-equivalent ages of 3 to 12 years old. Primate brainstems and limbic systems are fully-developed BEFORE these ages.

The researchers skipped over potential evidence for the important contributions of epigenetic factors to “the later life risk to develop anxiety and depression” that change the studied brain areas during womb-life, infancy, and early childhood. Studies such as:

show:

  1. A developing fetus adapts to being constantly stressed by an anxious mother.
  2. When these adaptations persist after birth, they may present as physiological and behavioral maladaptations of the infant and young child to a non-stressful environment.
  3. Later in life, these enduring changes may be among the causes of symptoms such as the anxious overreactions the current study found.

http://www.pnas.org/content/112/29/9118.full “Intergenerational neural mediators of early-life anxious temperament”

What is Primal Therapy by Dr. Arthur Janov

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“We have needs that we are all born with.

When those basic needs are not met, we hurt.

And when that hurt is big enough, it is imprinted into the system.

It changes the system, our whole physiologic system.

What our therapy does, it goes back to those early brains, those hurt brains, and relive the pain, and get it out of the system.

Because meanwhile, that pain is being held in storage, and just waiting for its exit, so to speak.

So Primal Therapy is a way of accessing our feeling brain, and down below even the feeling brain, to the brainstem, to get to all of the hurts that started very early in our lives.

And bring them up to consciousness for connection and integration.

It is a very systematic therapy, by the patient.

The patient decides when he comes and when he leaves and how long he stays.

There’s no 50-minute hour anymore.

It’s the feelings of the patient that determine when he stops.”

If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

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This 2014 rodent research reliably induced many disorders common to humans. Here are some post-birth problems the researchers caused, primarily by applying different types of stress, as detailed in the study’s supplementary material:

Yet the researchers’ goal was to identify a brain receptor for:

“Novel therapeutic targets for stress-related disorders.”

In other words, develop new drugs to treat the symptoms.

Where are the studies that have goals to prevent these common problems being caused in humans by humans?

Where is the research on treatments to reverse the enduring physiological impacts to stress by treating the causes?

What do you think of this excerpt?

“Accumulating evidence suggests that traumatic events particularly during early life (e.g., parental loss or neglect) coupled with genetic factors are important risk factors for the development of depression and anxiety disorders.

Moreover, the brain is particularly vulnerable to the effects of stress during this period.

Maternal separation in rodents is a useful model of early-life stress that results in enduring physiological and behavioral changes that persist into adulthood, including increased hypothalamic–pituitary–adrenal (HPA)–axis sensitivity, increased anxiety, and visceral hypersensitivity.”

http://www.pnas.org/content/111/42/15232.full “GABAB(1) receptor subunit isoforms differentially regulate stress resilience”

Why do researchers title their study the cortex vs. the limbic system or lower brain?

gettingwell4 2-3 stars Required further work, Brain development, Brainstem, Cerebrum, Limbic system, Lower brain, Stress ,

This 2012 review of 89 studies was ostensibly of the prefrontal cortex. The review title showed how researchers characterize their work as studying the cerebrum, even when they primarily deal with the limbic system and lower brains.

For example, the reviewer discussed rodent studies of the developing pup fetus regarding:

  • Sensory/motor – Paternal complex housing, maternal complex housing
  • Stress – Mild stress, bystander stress, moderate stress
  • Psychoactive drugs – Stimulants
  • Adult stimulants – Ethanol

The active brain areas of the rodent fetus are the brainstem and the limbic system, and those areas were primarily what was studied. The cerebrum of the developing pup is a tiny strip that has little cognitive function.

http://www.pnas.org/content/109/Supplement_2/17186.full “Experience and the developing prefrontal cortex”

Activation of brainstem neurons induces REM sleep

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This 2014 MIT/Harvard rodent study provided evidence that specific brainstem neurons (cholinergic, or containing acetylcholine) regulated dream sleep.

The researchers used a more exact technique that selectively activated just one neuron. They made the neurons in this study sensitive to light using an algae protein that responded to a specific light frequency. Once expressed in the neuron, the protein activated the neuron when that specific frequency of light was shown onto it.

“Interestingly, both manipulations resulted in a change in the number of REM [rapid eye movement] sleep episodes and did not change REM sleep episode duration, suggesting that the PPT [pedunculopontine tegmentumis part of the brainstem] involved in REM sleep initiation but not REM sleep maintenance.”

http://www.pnas.org/content/112/2/584.full “Optogenetic activation of cholinergic neurons in the PPT or LDT induces REM sleep”

The brainstem nucleus locus coeruleus is the primary source of norepinephrine

gettingwell4 4-5 stars Advanced knowledge, Brainstem, Cerebrum, Cortisol, Locus coeruleus, Lower brain, Neurochemicals

This 2014 rodent study provided further information on the locus coeruleus segment of the brainstem:

“The brainstem nucleus locus coeruleus is the primary source of norepinephrine to the mammalian neocortex.

Neurons in the locus coeruleus maintain segregated connections to brain regions with distinctly different functions. Specifically, cells that communicate with the prefrontal cortex, a region involved in cognition and executive function, are characterized by properties that allow for independent and asynchronous modulation of operations in this area, compared with those that project to the motor cortex and regulate movement generation.”

http://www.pnas.org/content/111/18/6816.full “Heterogeneous organization of the locus coeruleus projections to prefrontal and motor cortices”

The thalamus’ role in coordinating REM sleep stages

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This 2013 human study provided more details about dream sleep. The thalamus portion of the limbic system coordinates REM stages, which play critical roles in learning and memory.

This study also noted that science assigns no functions to dreams themselves, which was the first I’d heard of it.

http://www.pnas.org/content/110/25/10300.full “Rhythmic alternating patterns of brain activity distinguish rapid eye movement sleep from other states of consciousness”

Rebooting the brain with anesthesia: Implications for Primal Therapy and evolution

gettingwell4 4-5 stars Advanced knowledge, Anterior cingulate cortex, Brain development, Brainstem, Hypothalamus, Limbic system, Locus coeruleus, Lower brain, Memory, Primal Therapy, Thalamus , , ,

Here are some paragraphs from a 2013 summary article of 105 studies entitled Evolution of consciousness: Phylogeny, ontogeny, and emergence from general anesthesia:

“The emergence of consciousness (from anesthesia) (as judged by the return of a response to command) was correlated primarily with activity of the brainstem (locus coeruleus), hypothalamus, thalamus, and anterior cingulate (medial prefrontal area). Surprisingly, there was limited neocortical involvement that correlated with this primitive form of consciousness.

In the sleep study, midline arousal structures of the thalamus and brainstem also recovered function well before cortical connectivity resumed. Thus, the core of human consciousness appears to be associated primarily with phylogenetically ancient structures mediating arousal and activated by primitive emotions, in conjunction with limited connectivity patterns in frontal–parietal networks.

The emergence from general anesthesia may be of particular interest to evolutionary biology, as it is observed clinically to progress:

  1. from primitive homeostatic functions (such as breathing)
  2. to evidence of arousal (such as responsiveness to pain or eye opening)
  3. to consciousness of the environment (as evidenced by the ability to follow a command)
  4. to higher cognitive function.

Regarding ontogeny of H. sapiens, peripheral sensory receptors are thought to be present from 20 wk of gestation in utero. The developmental anlage of the thalamus is present from around day 22 or 23 postconception, and thalamocortical connections are thought to be formed by 26 wk of gestation. Around the same time of gestation (25–29 wk), electrical activity from the cerebral hemispheres shifts from an isolated to a more continuous pattern, with sleep–wake distinctions appreciable from 30 wk of gestation.

Both the structural and functional prerequisites for consciousness are in place by the third trimester, with implications for the experience of pain during in utero or neonatal surgery.“

I recently came out of anesthesia after being anesthetized for three hours during rotator cuff surgery. I felt pain, and went into a primal reliving of a painful memory.

I interpret the event as a reliving of my birth experience because of the following:

  • The beginning point was complete anesthetization as it was at my birth. My mother was completely anesthetized, so I, weighing less than one twentieth of her, was also completely anesthetized.
  • I felt a great urge and impulse to “get out” as it was at my birth. The attending nurse told me the next day that she called over another person to help her restrain me in the post-op chair.
  • I had a great need for oxygen and started breathing rapidly as it could have been at my birth. The nurse told me the next day that she was already giving me oxygen, and per the monitors, I didn’t need more oxygen.
  • I had to frequently “spit up” as it could have been at my birth. There was nothing in my current situation to cause me to expectorate.
  • My lower brain and limbic system were in control, as I thrashed, cried and moaned. I probably used primarily the same brain areas as what were the developed parts of my brain at birth.

The attending nurse told me the next day when I called her that she followed the established protocol, which was to get me out of the experience. She intentionally distracted me away from my pain. I was instructed to sit still, to think of some place pleasant, and to calm down.

I heard her as though she was at the other end of a tunnel at first, and then started to comply as I regained cognitive awareness.

I understand how such a powerful event could present a danger to a patient. It didn’t occur to me until the next day to tell the nurse of relevant history, that I’ve had relivings while in therapy, and wasn’t in the same danger that her regular patients may have been.

Even if I had said something, however:

  • Neither the anesthesiologist nor the attending nurse had a method of understanding how an evolutionary-determined sequential process – such as rebooting a person’s brain after prolonged anesthesia – may have therapeutic benefits.
  • They had no training to recognize aspects of neurobiologic therapeutic value in what was going on inside of me during this event, as a therapist in Dr. Arthur Janov’s Primal Therapy has.
  • The default response per medical protocol would be to shut down a patient’s expressions of their feelings.

As a result, my experience of this event was pretty much the opposite of what happens in Primal Therapy. Although I didn’t feel harmed, my reliving wasn’t therapeutic, as previous re-experiencings had been. The reliving’s progression through my levels of consciousness was purposely interrupted, and approached from a non-therapeutic direction.

Unlike my experience of coming out of anesthesia, Dr. Arthur Janov’s Primal Therapy isn’t something the patient is thrown into and potentially overwhelmed by their feelings. It’s a gradual process where the patient is in control.

This summary study showed that existing science is already in alignment with the background of Primal Therapy, that the core of human consciousness is in the limbic system and lower brain structures. My anesthesia experience showed that medical professionals are familiar with at least the outward signs of a primal reliving.

The challenge seems to be how to use this complementary knowledge for people’s benefit. What can be done with therapeutic re-experiencing so that people aren’t burdened with the continuing adverse effects of traumas?

How can scientists and medical professionals get the eyes to see what’s in front of them?