Lower brain

Active areas of the brain when making decisions in stressful conditions

gettingwell4 2-3 stars Required further work, Cerebrum, Cortisol, Limbic system, Lower brain, Memory, Neurochemicals, Stress

This 2013 human study was of decision making under stressful conditions.

Acute stress (ice water immersion) evoked habitual behavior rather than deliberative behavior. In my view, the subjects’ behaviors when under stress were driven more by their limbic system and lower brain areas than their cerebrum.

This finding wasn’t a big surprise. However, the researchers went on to state:

“Subjects with more executive resources to spare find themselves less susceptible to the behavioral changes brought about by stress response.”

I interpreted this statement to mean that when stressed, the more-capable subjects didn’t act out as much as the less-capable subjects acted out their respective feelings, instincts and impulses.

I felt that to understand this statement called for more investigation into the individual histories of the subjects:

  • What happened in their lives that enabled each person to acquire “more executive resources” or not?
  • What happened in their lives that made each person more or less sensitive to stress?
  • How are these two avenues of investigation related?

http://www.pnas.org/content/110/52/20941.full “Working-memory capacity protects model-based learning from stress”

Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects

gettingwell4 < 0 Detracted from science, Amygdala, Brain development, Epigenetics, Hippocampus, Limbic system, Lower brain, Memory, Stress ,

This 2013 Wisconsin human study’s goal was to assess effects of childhood trauma using both functional MRI scans and self-reported answers to a questionnaire. The families of the study’s subjects (64 18-year-olds) participated with researchers before some of the teenagers were born.

How could the teenagers give answers that described events that may have taken place early in their lives, before their cerebrums were developed, around age 4? Even if the subjects were old enough to remember, would they give accurate answers to statements such as:

“My parents were too drunk or high to take care of the family.

Somebody in my family hit me so hard that it left me with bruises or marks.”

knowing that affirmative answers would prompt a visit to their family from a government employee?

Although some data may have been available, data from the teenagers’ prenatal, birth term, infancy, and early childhood wasn’t part of the study design. Intentional dismissal of early influencing factors ignored applicable research!

No

Was the study’s limited window due to the political incorrectness of placing importance in the development environment provided by the subjects’ mothers? The evidence was there for those willing to see.

One clue of ignored early traumatic events was provided by the lead researcher’s quote in news coverage:

“These kids seem to be afraid everywhere,” he says. “It’s like they’ve lost the ability to put a contextual limit on when they’re going to be afraid and when they’re not.”

This finding of “fear without context” possibly described the later-life effects of traumas that were encountered in utero and during infancy. A pregnant woman’s terror and fear can register on the fetus’ lower brain and the amygdala from the third trimester onward.

Storing a memory’s context is one of the functions that the hippocampus performs. Because the hippocampus develops later than the amygdala, though, it would be unable to provide a context for any earlier feelings and sensations such as fear and terror.

The researchers attempted to place the finding of unfocused fear into later stages of child development without doing the necessary research. They tried to force this finding into the subjects’ later development years by citing rat fear-extinction and other marginally related studies.

But citing these studies didn’t make them applicable to the current study. Cause and effect wasn’t demonstrated by noting various “is associated with” findings.

Was this science? Was it part of furthering an agenda like protecting publicly funded jobs?

Was this study published to make a contribution to science? Were the peer reviewers even interested in advancing science?

And what about the 64 18-year-old subjects? If the lead researcher’s statement was accurate, did these teenagers receive help that addressed what they really needed?

http://www.pnas.org/content/110/47/19119.full “Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence”

This page has somehow become a target for spammers, and I’ve disabled comments. Readers can comment on other pages or posts and indicate that they want their comment to apply here, and I’ll re-enable comments.

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?

Are 50 Shades of Grey behaviors learned in infancy?

gettingwell4 5+ stars Premium, Amygdala, Brain development, Cerebrum, Cortisol, Epigenetics, Hypothalamus, Limbic system, Lower brain, Memory, Neurochemicals, Primal Therapy, Serotonin, Stress , , , , , ,

Ever wonder how someone could become attached to their early childhood abuser?

Ever wonder what underlying neurobiological conditions may account for the popularity of Fifty Shades of Grey?

This 2014 rodent study “Enduring good memories of infant trauma” linked below showed how trauma changed infants’ limbic system and lower brains. As adults, they derived a neurochemical benefit from re-experiencing the traumatic conditions:

“Trauma and pain experienced in infancy clearly led to higher rates of adult rat depression-like behavior..(but) the infant brain has limited ability to link trauma to fear areas in the brain, such as the amygdala.

These results are surprising because cues associated with trauma experienced as adults provoke fear and do not rescue depressive behavior.

It is possible that giving SSRI medications to children could be detrimental to mental health in adulthood,” Dr. Sullivan says. “We believe that our research offers the first evidence for the impact of serotonin pathways.

The infant trauma increases serotonin to produce brain programming of later life depression, and the infant trauma cue increases serotonin to alleviate the adult depressive like symptoms.”

As the study may apply to humans, let’s say that as an infant, someone was traumatized by a caregiver who, for example, bound them too tightly and left them alone for too long. What adult behaviors and other symptoms may develop as results? The person may:

  • Show depression-like symptoms that would strangely be alleviated by being bound tightly and left alone for an extended period.
  • Develop attachments to people who treated them poorly in a way that triggered them to re-experience their early childhood traumas.
  • Feel their mood lift when their infancy traumas were cued.
  • Be unable to explain and integrate with their cerebrum what was going on with their limbic system and lower brains.
  • Be caught in a circle of acting out their feelings and impulses, with unfulfilling results.

Isn’t it curious that this acting-out behavior – driven by unconscious memories of traumatic conditions – is a subject for popular entertainment? It may have resonated with personal experiences of the people who read the books and watched the movie.

What about people who want to be relieved of their symptomatic behavior? Is it a justifiable practice:

  • To pass affected people over to talk therapies that aren’t interested in directly treating the cause – a neurobiological condition that exists in the limbic system and lower brains – only the symptoms?
  • To drug affected people with the neurochemicals that their condition makes scarce – the symptoms – instead of addressing the source?

A principle of Dr. Arthur Janov’s Primal Therapy is that people are capable of treating their own originating neurobiological conditions. One of the therapeutic results is that the patient is relieved of being caught in endless circles of acting-out behavior.

That way we can have our own lives, and not be driven by what happened during early stages of our lives.

http://www.pnas.org/content/112/3/881.full “Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction”