The Hippocampus Release Event and Reset Process Technique – The Underlying Neuroscience.
These ideas are the outcome of my various musings on the neural physiology of my hippocampus release event. Their summary is that the closed loop feedback mechanism of the human fear cycle may have evolved from the anatomy and physiology of our ancestral venomous reptilian bite function. This mechanism may be controlled by a neural reflex in the human brainstem, which can malfunction in the event of localised soft tissue injury.
The emotion of fear is not an uncontrollable mental state, but rather only the temporary product of our physiological response to vital threat. Living in an apparently permanent state of fear despite the continued absence of such a threat could simply indicate a sustained physiological malfunction, which can be resolved by addressing its underlying anatomical injuries.
The Human Fear Cycle
The hypothesis is based on the engineering concept of a closed loop feedback mechanism. This is where an ordered and complete sequence of events takes place, initiated by a trigger signal. Theoretically, the cycle concludes by returning to its starting point. However, in the real world, anything physical can break or jam at will, and since we are talking about human anatomy and physiology here, the opportunities for mischievous malfunction are boundless – particularly when the subject under discussion is the closed loop feedback system of the human fear cycle.
This hypothesis is purely intuitive conjecture at the moment, but it is based on the fact that the two events which immediately preceded my hippocampus release event were the realignment of my dislocated jaw and the release of my partially restricted tongue root. These two events combined sequentially to trigger the immediate deactivation of my autonomic fear responses, the most evident of which was the return to normal dilation and responsivity to light intensity of my eye pupils, which had been invariantly fully dilated for as long as I could remember. They also set in train the neurology which triggered the hippocampus release event.
Over the millennia of the evolution of our species, we have developed our physical brain capacity by overlaying its original reptilian core with multiple additional layers of brain tissue, allegedly to enhance our cognitive functions. Since we have retained our reptilian brain core, it is possible that we could have also retained a vestigial venomous reptilian bite neural reflex.
This reflex would communicate with the brain’s reptilian core through the spinal cord, activating the autonomic sympathetic nervous system’s escalation of our fear responses when a vital threat is detected, and the parasympathetic nervous system’s de-escalation of the same responses when the threat has been vanquished. In other words, a neural reflex trigger could control the operation of the human fear cycle.
The release of my jaw dislocation restored my rear bite action evenly on both sides, thereby relieving associated muscular tension in the back of my neck. The release of my tongue root as the second part of the process was achieved by a speech therapy exercise which mimics the outward and downward flick of a snake’s tongue as it threatens to bite.
And a frightened snake will bite.
Consequently, the hypothesis is that the closed loop feedback mechanism of the human fear cycle may have evolved from the closed loop feedback mechanism of the venomous reptilian bite cycle. The trigger for the cycle could be a vestigial venomous reptilian bite reflex in the human mid brainstem, which would replicate the original position of the neural reflex in reptiles.
Since ancestral venom sacs may have evolved into human salivary glands, the closed loop feedback mechanism of the snakebite process would operate harmlessly enough in humans in terms of being unable to deliver a physical dose of venom in self defence. The normal resolution of the cycle could merely result in excess salivation.
However, the underlying neural pathways of this reflex could still be functional, and could have a catastrophic and long term physiological impact in the event of malfunction. An inability to close the jaw completely or to swallow properly could inhibit the oral neural signal to the trigger reflex in the mid brainstem that the human reptilian bite delivery process had been completed. This situation would leave the fear cycle active until the injury or injuries preventing its reset were resolved, and sadly this resolution might never happen if these injuries remain undetected over the course of a lifetime.
The Physiology of The Human Fear Cycle
The physiology of the human version of the venomous reptilian self-defence feedback loop mechanism could include the following sequence of events.
The involuntary compression of muscle tissue impacting the pathway of the reflex could stimulate the human vestigial reptilian bite reflex in the brainstem to activate, alerting the sympathetic nervous system to trigger normal fear responses such as quickened pulse rate, shallow breathing, eye pupil dilation, increased production of adrenaline, reduced salivation, the ‘fight or flight’ decision process, the activation of the hippocampus ‘dashcam’ memory function to record events as they develop and, in extreme terror, the urge to urinate and defaecate to facilitate a ‘flight’ response. This muscle tissue compression could also be triggered simply by the mental perception of danger, as a reflex physiological response to a moment of emotional terror.
With an ‘attack’ (fight) decision, the reptilian bite would be delivered, discharging the venom sacs. In human physiology the simulation of the physical ejection of venom could be the activation of the tongue root to discharge the contents of the salivary glands. A Māori hakke includes such a tongue gesture, and this ritual could offer ancient wisdom regarding the resetting of the human fear cycle.
The tongue root activation of the venom delivery, possibly combined with a neural impulse triggered by the contraction of the venom sacs on discharge, could send a nerve signal to the reptilian venomous bite reflex to confirm that the bite delivery process has been completed and it can now deactivate. In humans, this process could be mimicked by a rush of saliva which would be swallowed, and it could be this action which sends the neural signal to the bite reflex trigger to switch off. This could initiate the parasympathetic nervous system’s deactivation of the original sympathetic neural fear alert and its associated physiological responses.
The conclusive resolution of the cycle, under normal circumstances, would be both routine and undetectable. However, the bite reflex trigger could be trapped in its active state by a local soft tissue injury. Since this injury would have been sustained while the fear response cycle was active, and since the reflex trigger would now be incapable of being deactivated until the injury causing the impediment is resolved, we can be left in a constant and permanent state of fear alert. The reflex trigger reset may never happen over the course of a lifetime, since the indications of this need, including the malfunction of the eye pupils, are both almost imperceptible and are also open to misinterpretation.
This sequence of events could also suggest an explanation for the association between a long term anxiety state and an excoriatingly accurate memory, as the hippocampus ‘dashcam’ appears to record memory events continuously from the time it is first triggered until the moment that the bite reflex trigger is deactivated.
Once the human fear cycle has been turned off, the human reptilian brain begins to prepare for its heat-based hippocampus release event, if it needs one as the result of an extended period of activity from apparent ongoing trauma.
This is the summary of my personal technical interpretation of what happened during my hippocampus release event. As more people experience and document the same event, I am sure that the details of this physiology will be developed and established in more detail.