Correspondence concerning this paper should be addressed to the author
via email at UBergmann@worldnet.att.net,
or 77 Grassy Pond Drive, Smithtown, New York 11787, USA
The speculations considered in this paper
are submitted to stimulate further discussion and research about the underlying
mechanisms of EMDR. These speculations are derived from recent empirical
findings in the areas of the limbic system, the neurobiology of trauma
and of REM-sleep. This discussion explores the possibility that EMDR
processing gradually enables the capacity of higher, cortical, brain functions
to override the input from the limbic structures, thereby facilitating
limbic downregulation, reduced kindling and, consequently, an enhanced
integration of thalamic, amygadaloid, hippocampal and cortical functioning.
This appears to correct hemispheric laterality and allows the brain to
maintain balanced inter- hemispheric functioning on its own.
Francine Shapiro posits that one of the simplest ways of describing integrative EMDR effects is to say that the target event has remained unprocessed because the immediate biological responses to, the trauma have left it isolated in neurobiological stasis. The processing mechanism of EMDR is physiologically configured to take misprocessed information to an adaptive level (Shapiro, 1994, 1995). To comprehend how this takes place at a neurobiological level, I believe that it is imperative to understand the relationship between the amygdala and the following: the other limbic structures; the neocortex; the mediating anatomy, physiology and function of dream sleep; and the specific neurotransmitters that impact on these anatomical connections and functions.
The concept of the limbic system is, today, an issue of controversy in the fields of neuroanatomy and neuroscience. Those who object to viewing the limbic structures as a system cite the lack of objective structural and functional criteria that are needed to define it as an anatomical entity (Brodal, 1980; Brodal, 1992; LeDoux, 1992; Walsh, 1987). However, it is beyond the scope of this paper to discuss this. For the purposes of this presentation, the term limbic system will be used to indicate a group of limbic structures and will be defined as composed of, collectively, portions of the thalamus, hypothalamus, hippocampus, amygdala, caudate nucleus, septum, mesencephalon and cingulate gyrus. This paper will address the particular limbic structures essential to this current discussion.
The amygdala is an almond-shaped cluster of interconnected structures perched above the brainstem, near the bottom of the limbic ring. The amygdala is composed of two structures (the corticomedial and basolateral nuclear groups), one on each side of the brain, nestled in the temporal lobe, underneath the uncus. The corticomedial nuclei are connected primarily with the olfactory bulb, the hypothalamus and the visceral nuclei of the brain stem. The basolateral nuclei are connected with the thalamus and parts of the cerebral cortex. The hippocampus is also located in the temporal lobe. It forms an elongated bulge in the temporal horn of the lateral ventricle. The thalamus, the largest part of the diencephalon, is situated in the temporal lobe on each side of the third ventricle. The thalamus is composed of many smaller nuclei and is a relay station for almost all information transmitted from the lower parts of the central nervous system to the cerebral cortex. Below the thalamus, also in the temporal lobe, lies the hypothalamus, the smaller part of the diencephalon, which is primarily involved with the central control of the autonomic nervous system (Brodal, 1992). The septum, also located in the temporal lobe, receives neural input from the hippocampus and sends neural input to the hypothalamus (Bloom & Lazerson, 1988; Brodal, 1992). Encircling the limbic structures, forming the major part of the limbus, is the cingulate gyrus. It’s anterior cortex appears to be involved in conditioned emotional learning, assigning emotional valence to internal and external stimuli and facilitating a more realistic differentiation between real and perceived threat (Devinsky et al, 1995).
The hippocampus and the amygdala were the two key parts of the primitive "nose brain" (rhinencephalon) that evolved and gave rise to the cortex and then to the neocortex (Brodal, 1992; Goleman, 1995). These limbic structures are necessary for the onset of learning and remembering (Brodal, 1980; Brodal, 1992; Goleman, 1995; LeDoux, 1986, 1992, 1994; Walsh, 1987).
The amygdala provides the central crossroads junction where information from all senses is tied together and endowed with emotional meaning. It is here that the sights, sounds, smells, tastes, proprioceptive and touch sensations of an experience are brought together and remembered (Reiser, 1994). The hippocampus has been referred to as the "gateway" to the limbic system (Winson, 1985). It is here that information from the neocortex is processed and transmitted to the limbic system, where memory and emotion are integrated (Reiser, 1994). This is accomplished through extensive, two-way connections with various cortical association areas and, second, the direct and indirect connections with other limbic structures such as the septal nuclei and the hypothalamus (Brodal, 1992). This complex structure is known to play a central role in memory, particularly the retrieval of memories for approximately three years following the the registration of the experience (Brodal, 1992; Reiser, 1994).
Observations indicate that the hippocampus is particularly important for the memory of events, objects, words and other types of information.The observations of patients in whom the hippocampus has been destroyed by disease or trauma indicate that they suffer from global amnesia. They cannot remember anything that happened during the three years preceding the onset of the disorder (retrograde amnesia), although, they can remember things that happened prior to it. Moreover, they cannot lay down any new memories at all (anterograde amnesia). Anything that happens to them now cannot, without rehearsal, be remembered for more than a few minutes (Bloom & Lazerson, 1988; Brodal, 1992; Reiser, 1994; Walsh, 1987). While the amygdala retains the emotional flavor of memory, the hippocampus retains the dry facts. It appears to process memory in terms of perceptual patterns and contexts (LeDoux, 1992; van der Kolk, 1994). It is the hippocampus that recognizes the different significance of a bear in the zoo versus one in your backyard (Goleman, 1995 ). It also differentiates the significance of events that happened long ago from those that are recent.
The brain’s damper switch for the amygdala appears to lie at the other end of a major circuit to the neocortex, in the left prefrontal lobe, just behind the forehead. Some of this circuitry is also found in the temporal lobe. This neocortical part of the brain brings a more analytic and appropriate response to our emotional impulses, modulating the amygdala and other limbic areas (Goleman, 1995; LeDoux, 1986).
The prefrontal cortex is the brain region responsible for working memory. Beside the structural bridge between these areas, there is also a biochemical one. Both contain areas that have a high concentration of serotonin receptor sites. The presence of circuits connecting the limbic brain to the prefrontal lobes implies that the signals of emotion; anxiety, anger and terror, generated in the amygdala, can create neural static, sabotaging the ability of the prefrontal lobe to maintain working memory and homeostasis (Selemon et al, 1995). Similar observations have been made by van der Kolk (1994). He notes that external and internal stimuli, including stress-induced corticotropin-releasing factor (CRF) production, decrease hippocampal activity. When stress interferes with "hippocampally mediated memory storage and categorization, some mental representation of the experience is probably laid down by means of a system that records affective experience but has no capacity for symbolic processing or placement in space and time (p. 261)."
Recent studies of the amygdala have discovered a role that is pivotal in the understanding of trauma, as well as in shedding new light on maturation and development (`LeDoux, 1986, 1992, 1994). In the brain’s architecture, the amygdala is poised like an alarm. Incomplete or confusing signals from the senses let the amygdala scan experiences for danger. Sensory signals from the eyes, nose, mouth, skin and ears travel first in the brain to the thalamus, and then across a single synapse, to the amygdala. A second signal from the thalamus is routed to the neocortex - the thinking brain. This branching allows the amygdala to respond before the neocortex, which mulls information through several layers of brain circuits before it fully perceives and initiates a response (LeDoux, 1986). Prior to LeDoux’s observations, it was thought that the limbic system had to wait for the neocortex to give permission for the amygdala to react. LeDoux’s studies have shown that anatomically the "emotional" amygdala can act independently of the neocortex. He posits that some emotional reactions and memories can be formed with no cognitive conscious participation.
The amygdala can store memories and initiate response repertoires that we enact without consciousness, because the shortcut from the thalamus to the amygdala bypasses the neocortex. As the amygdala becomes aroused, either from external stress or internal anxiety, a nerve running from the brain to the adrenal gland triggers a secretion of epinephrine and norepinephrine, which then surge through the body, eliciting alertness. These neurotransmitters activate the receptors on the vagus nerve. While the vagus nerve carries messages from the brain to regulate the heart, it also carries signals back into the brain, triggered by epinephrine and norepinephrine. The amygdala is the main site in the brain where these signals are carried. They activate neurons within the amygdala to signal other brain regions to strengthen the memory of what just happened. This amygdaloid arousal seems to imprint in memory most moments of emotional arousal with an added degree of strength (Goleman, 1994). The more intense the amygdaloid arousal, the stronger the imprint (LeDoux, 1986).
Similar observations have been made by van der Kolk (1994). He cites that when people are under severe stress, they secrete endogenous stress hormones that effect the strength of memory consolidation. He posits that "massive secretion of neurohormones at the time of the trauma plays a role in the long-term potentiation (and thus the overconsolidation) of traumatic memories (p.259)." He cites LeDoux’s work in noting that this phenomenon is largely mediated by the input of norepinephrine to the amygdala. This excessive stimulation of the amygdala interferes with hippocampal functioning, inhibiting cognitive evaluation of experience and semantic representation. Memories are then stored in sensorimotor modalities, somatic sensations and visual images (van der Kolk & van der Hart, 1989). From an evolutionary perspective, this is adaptive and allows animals to react quickly and protect themselves. Overreacting is, obviously, more adaptive for survival than underreacting (LeDoux, 1994). For humans, this method of allowing past, highly charged emotionally imprinted memories to control our present day functioning and relations is maladaptive.
Turning, now, to dream (also known as D and REM) sleep, it has been posited that its presence suggests some sort of internal information processing (Aston-Jones & Bloom, 1981;(Kelly, 1991; Jouvet & Delorme, 1965; Winson, 1993; Henry, 1994). Another hypothesis states that a necessary aspect of mammalian memory processing is the integration of individual experience into a strategy for future use (Winson, 1985, 1993). Experience gained during species-specific waking behavior is reaccessed and integrated into an animal’s behavior strategy during D-sleep. The integrative memory process that occurs in humans is the same as in lower species, with one modification. In humans, the information integrated is no longer confined to specific behaviors but consists of all waking experience that pertain to psychological survival (Winson, 1993).
Winson’s (1985) studies of a variety of mammalian species found certain behavioral states (important for survival) and physiological conditions in which a particular rhythm of brain electrical activity (theta rhythm) can be regularly observed in parts of the hippocampus. He also noted that theta rhythm always appears in one other state in all the species studied, namely REM sleep. Since theta rhythm (during REM) occurs when there is no sensory input from the outside world, Winson posits that "it is as if certain information gathered during the day, information associated with survival behavior, was being dealt with again by structures in which theta rhythm is generated: the entorrhinal cortex and the hippocampus (pp.190-91)."
In a study utilizing positron emission tomography (PET) scanning and statistical parametric mapping, Maquet et al (1996) studied REM sleep in humans, using regional cerebral blood flow (rCBF) as a measure of specific anatomic involvement and mediation. The results showed the following: rCBF was positively corrolated with REM sleep in the pontine tegmentum, left thalamus, both amygdaloid complexes, anterior cingulate cortex and right parietal operculum. Negative correlations between rCBF and REM sleep were observed bilaterally in a vast area of the dorsolateral prefrontal cortex, the parietal cortex, as well as in the posterior cingulate cortex. Given the role of the amygdaloid complexes in the acquisition of emotionally influenced memories, Maquet et al (1996) posit that " the pattern of activation in the amygdala and the cortical areas provides a biological basis for the processing of some types of memory during REM sleep (p. 163)."
During sleep, a number of mid and hind brain structures and mechanisms become involved; they include the ascending reticular activating system (ARAS), the pons and the locus coeruleus (LC). The ARAS can be activated by any sensory stimulus and, subsequently, diffusely activates the entire cerebral cortex. The LC is extremely important to REM sleep. A major contribution of the LC to REM sleep is the activation of another set of neurons, the Gigantocellular Tegmental Field (GTF) neurons. These are very large cells located in the LC and in the reticular formations of the pons. They are thought to provide executive control of dream sleep (Henry, 1994; Reiser, 1994).
An important mechanism during REM sleep involves a distinct pattern of high amplitude electrical potentials in three areas: the reticular formations of the pons (P), the lateral geniculate nucleus (G) of the thalamus, and the occipital cortex (O); collectively known as Pontine Geniculate Occipital (PGO) waves (Henry, 1994; Reiser, 1994). They appear to originate in the GTF neurons of the pons, occur just before the start of REM and continue during the REM period.
Observations have shown that a relationship exists between PGO spikes and rapid eye movement (REM) (Kelly, 1991; Reiser, 1994). The conclusion that PGO spikes represent a primary triggering process for phasic ocular movements is supported by findings that, in cats, the first derivative of the electrooculargram, during episodes of REM, is perfectly corrolated with PGO spike activity (Kelly, 1991). The conclusion is that the GTF cells drive the PGO waves and generate REM sleep. (Henry, 1994; Hobson & McCarley, 1977; Hobson, 1989; Reiser, 1994). In order for GTF cells to become activated and for REM sleep to ensue, the noradronergic cells of the locus coeruleus must be quiescent, facilitating the suppression of norepinephrine (NE) (Winson, 1993).
Siegel and McGinty (1977) found that GTF cells are activated at two times. First, they are highly active during D-sleep, a time of intense activation of motor systems. Second, they are also activated when there are certain phasic muscle and eye movements during wakefulness.
A good way to try to understand how EMDR appears to work is to outline the pathways of processing trauma.
A traumatic event ensues. The amygdala sounds the alarm and sends urgent messages to every major part of the brain: it triggers the secretion of the body’s fight or flight hormones and the hypothalamus is signaled to order the pituitary gland to produce corticotropin-releasing factor (CRF). It mobilizes the cerebellum for movement and signals the medulla to activate the cardiovascular system, the muscles and other systems. Other circuits signal the locus coeruleus (LC) for the secretion of norepinephrine (NE) to heighten the reactivity of the brain centers, suffusing the brainstem, limbic system and the neocortex. The hippocampus is signaled for the release of dopamine, to allow for the riveting of attention (Goleman, 1995; van der Kolk, 1994). In most cases, the traumatic event wanes and the systems return to baseline.
If the trauma continues unabating, a feeling of loss of control and helplessness begins. The brain undergoes allostatic reequilibration and enters a state that we know as post-traumatic stress disorder (Goleman, 1995, Kolb, 1987).
The LC becomes hyperactive, secreting extra-large doses of NE in situations that hold no danger, but are, somehow, reminiscent of the trauma. The hypothalamus becomes hyperactive, continuing to signal the pituitary gland to secrete CRF, alerting the body to an emergency that isn’t there. The aroused amygdala signals opioid centers in the cortex to release endorphins. This triggers the numbing and anhedonia (van der Kolk, 1994). In effect, the neocortex is taken out of the loop. The left prefrontal cortex is unable to shut the emergency systems down.
Since NE levels are extremely high, GTF and PGO activities decrease or fail. REM sleep is disturbed or fully inhibited. The information that should be processed for a more adaptive tomorrow is misprocessed. As this continues for days, REM deprivation ensues. The emotional and cognitive interpretations of the event are distorted. The event is locked in the amygdala, and the neocortex is unavailable to mediate.
In a study utilizing positron emission tomography (PET) scanning Rauch et al (1996) sought to explore the mediating neuroanatomy of PTSD symptoms by measuring changes in relative regional cerebral blood flow (rCBF) associated with the PTSD symptomatic state This study entailed a within-subject design and did not include a control group. All the subjects suffered from PTSD. Baseline scans were performed prior to being subjected to recordings of scripts describing the subjects’ past personal experiences, including the traumatic experiences that caused their PTSD. The script- driven scans revealed a marked lateralization of activity in the right hemisphere, evidenced by increases in normalized rCBF in the right-sided limbic, paralymbic and visual cortex. No significant changes were found in the hippocampus or the thalamus. Decreases in rCBF were found in the left inferior frontal (Broca’s area) and middle temporal cortex.
These results suggest that emotions associated with PTSD symptoms are mediated by the limbic and paralimbic areas within the right hemisphere. Activation of the visual cortex may correspond to the visual component of PTSD reexperiencing phenomena.
The above presents limitations with respect to the lack of a true control group. Therefore, it is not possible to conclude that the observed pattern of activation is unique to PTSD. However, it may be that the results reflect the normal mediating anatomy of intense emotions or emotional memories. The preponderance of right-sided brain findings is consistent with literature supporting the preferential role of the right hemisphere in evaluating the emotional significance of incoming information and in regulating autonomic and hormonal responses to these incoming signals. It is also consistent with its role in anxiety, panic and phobic disorders. It may also support the speculation that one of the roles of the left frontal lobe is to mediate or inhibit the activity of the right frontal lobe and right-sided limbic structures (particularly, the amygdala).
Schiffer et al (1997), utilizing electroencephalography (EEG) with a focus on probe auditory evoked potentials, studied patterns of hemispheric lateralization in control versus traumatized (abused) groups. The finding in the traumatized group showed right hemispheric evoked potential suppression, causing a marked laterality in favor of the right hemisphere and a concomitant diminished left hemispheric functioning, during recall of distressing memories. Interestingly, during the neutral memory task evoked potentials were strongly suppressed over the left cortex, indicative of enhanced left cortical activity. The controls showed no significant laterality during the recall of distressing memories. The authors suggest that the two hemispheres function more autonomously (less synchronized) in patients with childhood abuse.
Teicher et al (1997) used EEG coherence to study lateralization in fifteen hospitalized children with histories of intense physical or sexual abuse. These were compared to fifteen "normal" volunteers of equal age. EEG coherence was used to ascertain the degree of connectivity between different brain regions. Abused children differed significantly from the controls. They evidenced higher levels of left hemisphere coherence and a reversed asymmetry, with left hemisphere coherence significantly exceeding right hemisphere coherence. Detailed analyses suggested that the increased left coherence stemmed from a deficit in left cortical functioning.
Nicosia (1994) noted that the examination of EMDR clients by qualitative analysis of electroencephalography (QEEG) has shown a normalization in the slower brain wave activity in the two cortical hemispheres. He posits that the phase relationship of the two hemispheres is disrupted by the failure of NE suppression. Like Winson (1993), Nicosia posits that high amounts of NE, released in the forebrain during trauma, account for the suppression of REM sleep and a disruption of pacemaker activity in the cells of the septum. He theorizes that this is due to a localized decoupling of one area of the cortex from the pacemaker. This asynchrony prevents integrative memory processing. Nicosia suggests that EMDR resynchronizes the activity of the two hemispheres, because the repetitive alternating stimulation mimics the activity of the pacemaker mechanism which was suppressed. He notes that his QEEG study of a patient receiving EMDR treatment showed that a nearly 5 standard deviation hypocoherence, interhemispherically, had been resolved by the EMDR therapy’s intervention in a period of less than ninety minutes.
The observations by Winson (1993) of pacemaker cells, in the septum, and their function appear to corroborate Nicosia’s position. Kelly (1991) posits that pontine generated phasic activity is thought to be the pacemaker that drives many of the phasic events of REM sleep, including middle ear muscle activity, muscle twitches, changes in respiration, heart rate and coronary flow, in addition to eye movements.
In a recent study, utilizing single photon emission computerized tomography (SPECT), van der Kolk et al (1997) performed scans to determine the mediating neuroanatomy of traumatic emotions and the effects of three EMDR treatment sessions on the brain. Baseline scans were performed prior to the EMDR treatment. The results showed the following: after three EMDR treatment sessions, the anterior cortex of the cingulate gyrus evidenced increased activity, bilaterally; and the prefrontal lobe, evidenced increased activity. .
Given the fact that the study lacked a control group and only six subjects were tested, the findings are considered as preliminary (van der Kolk, 1997, personal communication). However, they begin to shed light on the following hypotheses: hat EMDR does appear to correct the marked asymmetry in lateralization, evidenced by the increased activation of the prefrontal area; that the lateralization may be further corrected by the increased bilateral activation of the anterior cingulate cortex, facilitating a more realistic differentiation between real and perceived threat and a concomitant reduction in hypervigilence; and that EMDR processing, in general, gradually enables "the capacity of higher brain functions to override the input from the limbic structures charged with the initial appraisal of the degree of threat posed by incoming stimuli (p. 106)."
The mechanisms of EMDR’s efficacy are as yet unknown to us. However some questions come to mind that need to be answered. Does the GTF activity seen during wakeful eye and muscle movement facilitate the same PGO activity and concomitant memory processing that appears to occur as a result of spontaneous sleep GTF activity? The issue of eye movements, themselves, needs to be examined. For years, now, EMDR stimulation has also been facilitated by the use of alternating hand taps as well as alternating audio tones. Hundreds of practitioners, this author included, have found no difference in the efficacy of one over the other. Neurologically, lateral eye movements, alternating hand taps and alternating audio tones appear to have one characteristic in-common; they produce a constant shifting of attention in the brain.. This could very well be the essence of EMDR stimulation, rather than the eye movements, themselves.
Does the alternating bilateral stimulation of EMDR act as a pacemaker, inducing, artificially, the correct inter-hemispheric activity, until, through an impact on gating properties in neural networks (Hopenwasser, 1997) it allows for enhanced integration of thalamic, amygdaloid, hippocampal and cortical functioning? Does this then allow the brain to maintain balanced inter-hemispheric functioning on its own?
Is it possible that attending to the negative affect and body sensations brings the amygdala on line for EMDR stimulation and processing? This is probably most profoundly relevant to body sensations, since so much response is observed when processing them. Does focusing on affect and somatic sensations target dissociated mental representations of the experience that are not symbolically processed or placed in space and time? Can we view the reprocessing of the positive cognition (PC) as a stimulation of cells in the left prefrontal lobe of the neocortex?
It may be that EMDR stimulates or emulates the pacemaker cells in the septum and/or the pontine saccade generator, in the midbrain, and resynchronizes the hemispheres. It is my opinion, that if true, this might facilitate an integration of neocortical and amygdaloid activity. Stated more specifically, EMDR processing gradually allows for the downregulation of the sensitized pontine and limbic area, facilitating the integration of higher cortical function. In other situations, where no cognitions are available, a predominant focus on body sensations leads to the amelioration of symptoms by apparently facilitating LC and amygdaloid inhibition. Once noradronergic firing is diminished, "self-perception is altered and individuals are able to interpret and self-reinforce, cognitively, more adaptive explanations of their traumatic experiences (Hopenwasser, 1997, p. 19)."
If the above is accurate, it has great implications for our understanding and treatment of trauma, both chronic and acute. It has long been known that many potent emotional memories date from the first few years of life. During this early period brain structures, like the hippocampus, which is crucial for forming consciously accessible memories and, therefore, narrative memory, as well as the neocortex, have yet to fully develop. The hippocampus is not fully myelinated until the third or fourth year of life. The amygdala, by contrast, matures very early in the infant’s brain development (LeDoux, 1994; van der Kolk, 1994 ). As the central nervous system matures, memory storage shifts from primarily sensorimotor and perceptual representations to symbolic and linguistic organization of mental experience (Piaget, 1962; van der Kolk, 1994).
LeDoux posits this as support for the position that psychodynamic psychology has taken; that the experience of life’s earliest years lays down a set of emotional lessons based on the level of atunement between infant and caretaker. This sheds light on the difficulty traditional psychotherapy has had in ameliorating neuroses and character disorders. These early interactions are so potent and difficult to understand and work through from the vantage point of adult life, because they are stored in the amygdala as rough, wordless blueprints for emotional life (LeDoux, 1992, 1994).
A multitude of questions remain to be answered.
The hypotheses contained in this discussion need to be verified and operationalized.
The neurophysiological meaning of the chronicity of these brain changes
versus their acuteness remains to be understood. The neurophysiological
understanding of the brain and of EMDR is not just for those who are so
inclined or curious. It is crucial because it informs practice.
If EMDR is used to treat chronic neuroses and personality disorders, and
we understand that we are dealing with preverbal material, the above information
may direct us to focus more on processing body sensations; using
them as a language. What appears to be evident, is that EMDR
may be the first clinical tool that interfaces directly with the amygdala
and the other limbic structures.
Allostatic - Derived from allostasis. Like homeostasis, it is the brain’s attempt to maintain an equilibrium despite continued trauma and/or the anticipation of continued trauma. Allostatic equilibrium, though, is the price paid by the rest of the systems, i.e. increases in adronergic functions, gluccocorticoid secretion, endorphin secretion, etc. These changes, in turn, facilitate the classic symptoms of PTSD.
Anterior - Situated in front of, or in the front part of an organ or structure.
Broca’s area - The region of the left prefrontal cortex responsible for the generation of words that are to be attached to internal experiences, allowing one to translate ersonal experiences into communicable language.
Dopamine - A neurotransmitter. Lack of dopamine is a cause of Parkinson’s disease, in which a person loses the ability to initiate controlled movements. Dopamine moves into the frontal lobe regulating the flow of information coming in from other areas of the brain. Compromise in the flow of dopamine may cause disrupted or incoherent thought as in schizophrenia. In milder disorders, too much dopamine in the limbic system and not enough in the cortex may produce an overly suspicious personality, leading to bouts of paranoia or an inhibition of social interaction. A shortage of Dopamine in the frontal lobes may contribute to poor working memory. Dopamine is also thought to produce feelings of bliss (the pleasure chemical). More dopamine into the frontal lobe lessens pain and increases pleasure.
Dorsal - denoting a position toward the back of a surface. Similar to the posterior of the human anatomy.
Downregulation: The reduction of activity in a process or a system.
Electrical potentials - Electrical activity in neural pathways which drives a process.
Endorphins - mediate pain at receptor sites. In an injury, receptors in the skin make electrical signals that go up the spinal cord to the brain. The brain then evaluates the pain by releasing pain killers called endorphins which bind at opiate receptor sites of neurons to mediate pain. Endorphins effect the dopamine pathway that feeds into the frontal lobe. These pathways inhibit the flow of dopamine. Vast quantities of endorphins are released and nerves are shut off so more dopamine flows through pathway to get to frontal lobe therefore replacing pain with pleasure.
Epinephrine - Another name for Adrenaline. Secreted by the adrenal medulla. A potent stimulator, similar to norepinephrine of sympathetic nervous activity.
Gating - The opening and closing of neural channels, facilitated by the interaction of receptors and neurotransmitters, proteins and enzymes.
GTF neurons - Gigantocellular Tegmental Field (GTF) neurons. These are very large cells located in the locus coeruleus (LC) and in the reticular formations of the pons. They are thought to provide executive control of dream sleep.
Kindling: a lowering of seizure threshold after repeated electrical stimulation of the brain at a level that is initially insufficient to produce a seizure. By analogy, some intrusive PTSD symptoms develop through a kindling-like process (hyperarousal and excessive emotional stimulation induce limbic activation and kindling) in which long-term changes in excitability occur, rendering the victim increasingly likely to develop certain symptoms; thereby, lowering the excitability threshold. The analogy has been drawn from the observations of the effects of anticonvulsant medications on PTSD.
Lateralization - The dominance of one cerebral hemisphere over the other vis-a-vis a certain function.
Locus coeruleus (LC) - Within the pons, a concentrated set of neural cell bodies whose axons secrete the neurotransmitter norepinephrine.
Neurotransmitters - the substance that is released when the axon terminal of a presynaptic neuron is excited. The substance then travels across the synapse to act on the target cell to either inhibit or excite it. Disorders in the brain physiology of neurotransmitters have been implicated in the pathogenesis of a variety of psychiatric illnesses.
Norepinephrine - a hormone produced by the locus coeruleus, similar in chemical and pharmacological properties to epinephrine ( a hormone secreted by the adrenal medulla in response to stimulation of the sympathetic nervous system). Norepinephrine and epinephrine are the two active hormones that cause some of the physiological expressions of fear and anxiety and have been found to be in excess in some anxiety disorders when a disturbance in their metabolism occurs.
Parietal lobe - The top (dorsal) aspect of the cortex, in contrast to the frontal (front), temporal (side) and occipital (rear).
Parietal operculum - A region in the parietal lobe of the brain
P.E.T. - Positron emission tomography. A technique of functional imaging.
PGO spikes - combined electrical activity in the pons, the lateral geniculate nucleus of the thalamus and the occipital lobe; collectively known as pontine-geniculate-occipital (P.G.O.) spikes.
Pons - a part of the brain-stem, along with the medulla and cerebellum, which contains a large number of neurons that relay information from the cerebral hemispheres to the cerebellum.
Posterior - Situated in back of, or in the rear part of an organ or structure.
Proprioceptive - Receiving stimuli within the tissues of the body, as within muscles and tendons.
Receptor - the terminal structure of a neuron, specialized to receive stimuli and transmit them to the spinal cord and brain.
Reequilibration - a recalibration aimed at achieving a new equilibrium.
R.E.M. - Rapid eye movement. A direct result of the combined electrical activity in the pons, the lateral geniculate nucleus of the thalamus and the occipital lobe; known as pontine-geniculate-occipital (P.G.O.) spikes.
Serotonin - a chemical, 5-hydrozytryptamine (5-HT), present in
blood platelets, the
gastrointestinal tract, and certain regions of the brain. It
plays an important role in initiating sleep and fighting depression (prescription
drugs that treat depression raise the brain's levels of serotonin).
Serotonin is synthesized from the amino acid L-tryptophan. Serotonin (and,
therefore, L-tryptophan) also serves as a precursor for the pineal hormone
melatonin, which regulates the body's clock.
S.P.E.C.T. - Single photon emission tomography. A technique of functional imaging.
Synapse - The point of junction between two neurons in a neural pathway, where the termination of the axon of one neuron comes into close proximity with the cell body or dendrites of another. At this point, where the relationship of the two neurons is one of contact only, the impulse traveling in the first neuron initiates an impulse in the second neuron.
Uncus - A well defined, hooked shaped, part of the cortex found at the upper and medial parts of the temporal lobe.
Ventral - denoting to a position more toward the underside of a structure
Working-memory - Temporarily stored information, used to guide a future action. The ability to hold in mind all information relevant to the task at hand. The executive function of the left prefrontal cortex .
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