Havening has three components • Recall and activation of an emotional core • Distraction / other sensory input • Havening touch
THE EXTRASENSORY RESPONSE TO TOUCH • Touch modulates GABA release via serotonin • Increase in Delta wave production • Depotentiates activated glutamate receptors
Displacement of thought fromworking memory by distraction • Humming a tune • Counting • Visualizing movement
Extrasensory Responses of Sensory Input Can Change the brain • Smell • Sight • Touch • Taste • Auditory • Kinesthetic
THE PSYCHOSENSORY THERAPIES• INVOLVE THE APPLICATION OF SENSORY INPUT TO ALTER BIOLOGICAL FUNCTIONING• ARE SENSORY RECEPTOR DRIVEN• ARE ELECTROCHEMICAL IN NATURE• THE RESPONSE TO THE SENSORY INPUT CAN BE LEARNED OR INNATE• THE EFFECT DUE TO AN EXTRASENSORY RESPONSE
Fear is stimulated by our senses • Olfactory • Kinesthetic • Auditory • Visual • Gustatory
Fear Activates Physiologic Changes via the Amygdala-- increased heart rate-- pupil dilation-- heightened sensory awareness-- increased oxygen availability-- increased muscle strength-- inhibition of all non survival activities-- increases our ability to store and retrieve events
The Amygdala Activates our Emotions and Coordinates our Survival Responses
OUTFLOW FROM CENTRAL NUCLEUSEmotional StimulusThalamusLA/BLA/AB AmygdalaCe AmygdalaPhysiological Response RESPONSE BRAIN AREA Prepare us for Flight or Fight Sympathetic Activation Aid in Danger Evaluation Prefrontal Cortex Motivate us to Action Nucleus Accumbens Increase Salience Ventral Tegmentum Increase Vigilance Locus Coeruleus Cause Freezing Central Grey Mediate Pain Perception Insula and Amygdala
EVENT• Increases cortisol and norepinephrine, dopamine• Experienced personally or vicariously• Produces intense emotional response
MEANINGIs about ATTACHMENT • PHYSICAL • PERSONAL • PUBLIC
LANDSCAPEThe neurochemical state ofthe brain at any given time.
INESCAPABILITYA perceived inescapable threateningsituation has the potential to traumatize.The perception need not last long, nor isit necessary for this perception to reachconscious awareness. The prefrontalcortex does not inhibit amygdalaencoding.
A TRAUMATIC ENCODING MOMENT • Requires four conditions • Remains permanently biologically active • Stimulation activates a part or all of the original physiological response • Emotional component synaptically encoded in the amygdala
Mechanism of TraumatizationEvent sensed by thalamus as UFS Signal sent to LAActivation of Ce Release of NE and Cortisol Inhibition of mPFCContent and context enters amygdala via LA and hippocampusRequirements met Glutamate receptors in amygdala potentiatedBinding of components of event Traumatization occurs
Traumatization at the neural level is the processthat permanently encodes and synapticallyconsolidates linkages between the emotional,cognitive, autonomic, and somatosensorycomponents present during the traumatizingevent.
Any of the components recalled, eitherconsciously or subconsciously, activatesthe amygdala and causes the release ofstress hormones.
For each reactivation, we experiencesome or all of the components as ifthey were happening for the first time.
Traumatic Memory Conscious activation or inadvertentreminders lead to the recalling of theevent and its emotional content.
Components of a traumatic memory• Emotional – the affective response to an event• Autonomic – automatic brain functions that regulate body functions• Cognitive – both conscious and subconscious• Somatosensory – sensed throughout the body as in pain, tingling, numbness and other sensations
Dissociated Traumatic Memory Thoughts, feelings and sensations that are experienced when activated by subconscious stimuli that arise from abnormal retrieval.
POTENTIATION OF AMPA GLUTAMATE RECEPTORSAND THEIR STABILIZATION THAT MAKES THEM PERMANENT THE ABSENCE OF FORGETTING REQUIRES PHOSPHORYLATION OF RECEPTORS PROTEIN KINASE Mζ –EXPRESSED ONLY IN NEURAL TISSUE PROTEIN KINASE Mζ CONTINUALLY PHOSPORALATES AMPA RECEPTORS BECAUSE IT LACKS A REGULATORY DOMAIN DURING ELECTRICAL STIMULATION AT 100Hz THE TRANSLATION OF THE PROTEIN KINASE Mζ FROM RNA TO PROTEIN IS ACTIVATED PROTEIN KINASE Mζ STABLIZES AND MAKES PERMANENT POST- SYNAPTIC AMAPA RECPTORS.
Mechanism of TraumatizationStimulus [ unimodal and UFS ] pass through thalamus Signal toAmygdala Fear / defensive rage generated increases NE andCortisol in amygdala Inhibition of mPFC Complex content andContext enter amygdala Four requirements met AMPA GlutamateReceptors in BLC amygdala potentiated BLC modulates binding ofthe components of event A traumatic memory is stored
Thalamo-Amygdala Pathway Generated During Traumatization CORTEX Emotional Complex Content and Context (directly and via hippocampus) Somato- AMPA ReceptorThalamus Emotion Producing sensory Stimulus Lateral Nucleus of Amygdala Autonomic Electrochemical Transduction Cognitive Sensory Input Components
Recalling and activating of a traumaticmemory requires working memory • Cognitive conscious / subconscious (feelings) • Autonomic • Somatosensory • Emotional
Retrieval of cognitive and somatosensorycomponent into working memory • Limited storage focus on one thought • Short term usage • Part of the pre frontal cortex • Controlled by central executive which modulates attention • Phonological loop auditory and speech information i.e. Verbal commands • Visual spatial sketchpad visual and spatial information i.e. Ride a bike, imagine doing a physical task
EFFECT OF STIMULATION OF VARIOUS AREASDELTA WAVE POWER GENERATED AS MULTIPLE OF RESTING STATECHEEK 90XSHOULDER 5-38XPALMS OF HANDS 5XBACK OF HANDS 1.1XKNEE 1XVIBRATING PADS ON PALMS 3-4XLATERAL EYE MOVEMENT 12-20XGAMUT POINT 1.1XMERIDIAN POINTS VS NON MERIDIAN POINTS 1X
Amygdala Pathway Is Disrupted During Depotentiation Emotional AMPA Somato-STIMULUS Receptor sensory Internalized Lateral Nucleus of Amygdala Autonomic Cognitive
DE-POTENTIATION OF AMPA RECEPTORS BY LOW FREQUENCY WAVEACTIVATION OF POST-SYNATPTIC NEURON BY RECALLLOW FREQUENCY WAVE OPENS CALCIUM CHANNELS IN ACTIVATED NEURONSTHIS ACTIVATES CALCINEURIN FOR WHICH THE AMPARECEPTOR IS THE CRITICAL SUBSTRATEPARTS OF AMPA RECEPTOR DEPHOSPHORYLATEDREMOVAL FROM SURFACE AND THUS NO LONGER ABLE TOTRANSMIT… RECEPTOR IS DE-POTETNTIATEDCALCINEURIN INHIBITORS BLOCK THIS EFFECTTHE TIME COURSE IS IN MINUTES, CONSISTENT WITHCLINICAL OBSERVATIONS