Volume VI, Issue 3, Article 4 (October, 2000)

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Further Thoughts on the Neurobiology of EMDR:
The Role of the Cerebellum in Accelerated Information Processing*

Uri Bergmann, Ph.D.**

This discussion explores, briefly, the position that the repetitive redirecting of attention in EMDR is capable of turning on the brain's REM sleep system, leading to the activation of specific areas of the the anterior cortex of the cingulate gyrus, facilitating its function as a filter, thereby facilitating the integration of traumatic memory into general semantic networks. This integration is seen to lead to the subsequent reduction in both the strength of hippocampally mediated episodic memories of the traumatic event as well as the amygdaloid mediated negative affect of PTSD. The possibility is suggested that another underlying mechanisms of EMDR stimulation is the activation of the lateral cerebellum. The contribution of the cerebellum to cognitive and language functions is explored. The activation of the dentate nuclei in the lateral neocerebellum is shown to facilitate activation of the ventrolateral and central lateral thalamic nuclei. The activation of the ventrolateral nucleus is shown to lead to the activation of the left dorsolateral prefrontal cortex; further facilitating the integration of traumatic memory into general semantic and other neocortical networks.

Key words: EMDR, Cerebellum, REM-sleep

Presented at the 16th Annual Conference of the International Society for the Study of Dissociation, November, 1999, Miami, Florida

        Most forms of PTSD have been found to produce dramatic biological changes (Eberly et al., 1995; Rauch et al., 1996; Shin et al., 1997) that have been considered resistant to treatment (Solomon, Gerrity, & Muff, 1992) . However, for the past ten years a new approach, Eye Movement Desensitization and Reprocessing (EMDR), has shown itself to be dramatically effective and rapid.

        Four controlled studies examining the effectiveness of EMDR on single-trauma PTSD, have been carried out by independent research teams, using a total of 107 EMDR subjects (Marcus, Marquis, & Sakai, 1997; Rothbaum, 1997; Scheck, Schaeffer, & Gillette, 1998; Wilson, Becker, & Tinker, 1995,1997). In contrast, one controlled study of the use of flooding, or Stress Inoculation Therapy (SIT), with single-trauma PTSD victims, has been published in a peer-reviewed journal. It consisted of only 10 single-trauma PTSD victims, at posttest, in each of its two conditions (Foa, Olasov Rothbaum, Riggs, & Murdock, 1991). The only other published controlled studies of exposure with single-trauma PTSD victims examined a combination of in-vivo and imaginal exposure with 14 subjects (Richards, Lovell, & Marks, 1994). More recently, a similar protocol was tested with 20 subjects (Marks, Lovell, Noshirvani, Livanou & Thrasher, 1998). All of these exposure studies entailed 7 to10 treatment sessions and daily homework. The results of the Foa et al. (1991) study revealed that 55% of the subjects no longer met criteria for PTSD at posttest, after having received approximately 25 hours of exposure. In the study by Richards et al. (1994), 80% of the subjects no longer met criteria for PTSD after undergoing approximately 50 hours of exposure therapy. Similar results were reported at posttest by Marks et al. (1998) after approximately 100 hours of exposure. It should be noted that these studies utilized measures of compliance to exposure homework as a correlation of positive treatment effects (Marks et al., 1998; Richards et al., 1994;  Scott & Stradling, 1997).  In contrast, the four studies of EMDR, mentioned above, using comparable accepted standard measures (Strupp, Horowitz, & Lambert, 1997) and independent assessors, demonstrated that after the equivalent of three 90-minute sessions (i.e., 4.5 hours), without homework, 84 to100% of the single-trauma subjects no longer met criteria for PTSD, at posttest.

        EMDR is a complex and integrated form of therapy incorporating aspects of many traditional psychological orientations. In addition to its procedures, it utilizes a variety of bilateral stimuli (eye movements, audio and tactile). The inducement of alternating left-right attention, while recalling various aspects of a trauma (traumatic pictorial memories, negative self-beliefs, related affect and physical sensations), appears to produce a physiological effect that fosters accelerated reprocessing of dysfunctionally stored information about the trauma.

        Claims that EMDR leads to changes on a neurobiological level naturally give rise to questions as to neurobiological mechanisms that could underlie its effects. Indeed some research has begun to suggest that EMDR does produce significant specific neurobiological changes in brain function (Levin, Lazrove & van der Kolk, 1999; van der Kolk et al. 1997). As EMDR was developed primarily on empirical findings rather than on an accepted theoretical foundation, there are increasing demands for a theoretical model which can explain its robust effects. Shapiro (1989a, 1989b, 1991a, 1994, 1999), notes that the use of eye movements in EMDR was based upon an accidental discovery of their apparent ability to desensitize negative emotions and cognitions, rather than the logical outcome of a theoretical position. Her subsequent examination of the literature, however, revealed that this was not the first time such a role had been observed for oculomotor behavior. Years earlier, Antrobus and his colleagues (Antrobus, 1973; Antrobus, Antrobus, & Singer, 1964) had demonstrated, in systematic experiments, the association between spontaneous eye movements and changes in unpleasant emotions and cognitions. They noted, that characteristics of eye movements appeared to correspond significantly with certain cognitive responses (Antrobus, 1973; Antrobus et al.,1964). They reported, that "the attempt to break up a thought sequence when it is unpleasant or anxiety provoking may very well lead to a series of almost, desperate rapid shifts in cognitive activity with consequent ocular motility" (Antrobus et al., 1964, p. 251). Thus, Shapiro's observation that inhibition of unpleasant thoughts and cognitive content shifts are associated with spontaneous multiple saccades suggests that she had simply rediscovered a phenomenon that had already been documented in the laboratory (Shapiro, 1999).

        The only component analysis study claiming to test the effects of eye movement in the original "EMD" technique (Shapiro, 1989a) with a diagnosed PTSD population, was by Montgomery and Ayllon (1994). Eye Movement Desensitization (EMD) was the initial model in the evolution of EMDR. Montgomery and Ayllon tried to determine whether the addition of eye movements to exposure and cognitive restructuring was necessary for treatment gains. In their words, “The data indicate that with PTSD subjects the use of short duration repeated exposure and cognitive restructuring alone were insufficient for positive treatment gain." However, the addition of the eye movements in five of six subjects “resulted in the significant decreases in self-reports of distress previously addressed. These findings are reflected by decreases in psychopathological arousal" (p. 228).

        It is important to note that other kinds of stimulation (e.g., rhythmic, bilateral hand-taps, and auditory sound), in addition to eye movements, have also been shown to have clinical utility with EMDR (Shapiro, 1991b, 1994,1995). It is of great import, therefore, to find the common denominator among these various kinds of clinically effective stimuli. Recently, in a series of controlled studies Andrade, Kavanagh, & Baddeley, (1997) evaluated the effects of a variety of tasks (articulation, tapping, and eye movements) employed during mental imaging. The specific goal of this research was to test the hypothesis that the "eye-movements reduce the vividness of distressing images by disrupting the function of the visuospatial sketchpad (VSSP) of working memory, and that by doing so they reduce the intensity of the emotion associated with the image [and that other) visuospatial tasks may also be of therapeutic value" (Andrade et al. 1997, p. 209). Their hypothesis was supported for recollections of personal memories, indicating the presence of a direct physiological effect of the dual stimulation, which lessened both the vividness of the disturbing image and the attendant emotional distress (Shapiro, 1999). Interestingly, the various dual attention tasks used by these investigators appear to have shown differential efficacy. This may be explained by the fact that this was a dual attention task and, therefore, not the bilateral stimuli that are used in clinical practice

        As was stated above, since EMDR was developed primarily on empirical findings rather than on an accepted theoretical foundation, there are increasing demands for a theoretical model which can explain its robust effects. What follows is an attempt to speculate and construct such a model

The Role of REM Physiology in Memory Consolidation

        To date, the only detailed explanation of the underlying mechanisms of EMDR has come from Stickgold (1998b). He posits that EMDR facilitates the activation of the brain's REM sleep system. This will be detailed following a review of the function and anatomy of memory, REM sleep and their interrelationship.

The Formation, Transfer and Integration of Episodic Memory

        Very little of what we have experienced is remembered as episodic memory. Instead, the brain extracts, abstracts and stores critically useful information from the sum total of our experiences (Schacter & Tulving, 1994; Squire, 1992; Stickgold, 1998b). Information from the outside world passes first through sensory cortices which produce separate internal representations of a stimulus in each sensory modality. Visual, olfactory, tactile and auditory inputs are each processed by their respective regions of sensory cortex, and then passed on to higher processing regions (Stickgold, 1998a; 1998b). As the process of passing on information ensues, information from both perceptual and semantic representations flows into the hippocampal complex. The hippocampus serves two major functions (Brodal, 1980; Brodal, 1992; McClelland et al., 1995; Winson, 1985). Initially, the memory traces formed in the perceptual and semantic memory systems, in the cortex, are too weak for direct recall. In response, the hippocampus forms much stronger representations which can now be intentionally recalled. The creation of these hippocampal memories facilitates the ability to recall the events of the day and to remember and subsequently recall addresses, hotel room numbers and names heard only once. This is in part because of the second function of the hippocampus, which is to store memories contextually (Brodal, 1980; Brodal, 1992; Nadel & Moscovitch, 1998; Winson, 1985). Thus a hippocampal memory is both strong and integrated, storing together simultaneous inputs for all sensorimotor modalities as well as associated, amygdaloid mediated, affect. Additionally, it links together sequences of sensory perceptions which occur over time to produce a memory of sensations and actions over time, a movie-like memory of episodes from our lives (Stickgold, 1998a, 1998b).

The Formation of Semantic Memory

        In the neocortex, memories are stored in dense highly overlapping neural networks. By a process referred to as "interleaved replay," hippocampal memories are slowly and repetitively replayed from the hippocampal complex to the cortex where the memories are eventually incorporated and consolidated into the individual's general semantic knowledge (McClelland et al., 1995; Stickgold, 1998b). Thus, cortical memories, in contrast to hippocampal memories, which are sparse and quickly formed, are slowly formed and densely represented. Semantic memories are the extraction, abstraction and storage of critically useful information from the sum total of our experiences (Schacter & Tulving, 1994; Squire, 1992). As a result, hippocampal memories make us smart and factual, but semantic memories make us wise (Stickgold, 1998b).

        With respect to REM (also known as D and dream) sleep, it has been posited from decades of research that its presence suggests internal information processing and memory consolidation (Aserinsky & Kleitman, 1953; Aston-Jones & Bloom, 1981; Crick & Mitchison, 1983; Dement & Kleitman, 1957; Hobson & McCarley, 1977; Hobson, Stickgold & Pace-Schott, 1998; Jouvet & Delorme, 1965; Karni & Tanne, 1994; Kelly, 1991; Llinas & Ribary, 1993; Pavlidas & Winson, 1989; Reiser, 1994; Smith, Young & Young, 1980; Stickgold, 1998a; Stickgold et al., 1994; Stickgold et al., 1995; Stickgold et al., 1998; Stickgold et al., 1999; Wilson, & McNaughton, 1994; Winson, 1985,1993). It is beyond the scope of this discussion to detail these studies. The reader is referred to them for elaboration.

        Recent neuroimaging studies (Maquet et al., 1996; Braun et al., 1997; Nofzinger et al., 1997) have shown a consistent activation, in REM sleep, of the pontine brain-stem, the amygdaloid complexes and the anterior cortex of the cingulate gyrus; structures involved in the mediation of emotion. A concomitant deactivation was noted in the dorsolateral prefrontal cortical structures that are involved in the executive, and mnemonic aspects of cognition. Maquet et al. (1996) also observed increased activation of the left thalamus. Braun et al. (1997) also observed increased activation in the hippocampus, anterior hypothalamus and areas of the cerebellum. These studies confirm previous laboratory research which had assigned REM sleep a role in the processing of emotion in memory systems, by showing consistently that the cortical areas activated in REM are rich in afferentation from the amygdala, while those areas with sparse amygdalar afferentation were deactivated. They, therefore, inform and enrich the integrated picture of REM sleep as emotion-driven cognition, with a concomitant deficiency in memory, orientation, volition and analytic thinking vis-a-vis dreams, resulting from neocortical deactivation (Hobson, Stickgold & Pace-Schott, 1998).

Sleep and Memory Consolidation

        As was mentioned previously, numerous studies have shown that sleep plays a critical role in the process of memory transfer and consolidation. These studies are noted above and elegantly reviewed in Stickgold, 1998a. Evidence suggests that REM and non-REM sleep serve related but distinct functions in off-line memory reprocessing. Non-REM sleep appears most critical for strengthening of hippocampal memories and REM sleep most critical for neocortical memories (Plihal & Born, 1997). In rats, information flows out of the hippocampus and into the cortex during non-REM sleep; with the flow reversed during REM sleep, from the cortex into the hippocampus (Buzsaki, 1996). In addition, and as evidence of a parallel processing pattern in humans, semantic memory in humans preferentially activates weak associations in REM sleep, but strong ones in non-REM sleep (Stickgold, Scott, Rittenhouse, & Hobson, 1999). Regional brain activation is also dramatically different in the two sleep states, with limbic and sensory cortices preferentially activated in REM sleep (Braun et al., 1997; Hobson et al., 1998; Maquet et al., 1996; Nofzinger et al., 1997). This is most evident in the bizarre and hyperassociative quality of dreams, which appears to be the result of the preferential activation of semantic, cortical, networks, with their weak and loose associations, combined with the lack of hippocampal input, with it’s strong and linear associations (Stickgold et al., 1998, 1999). The preferential activation of limbic, and particularly amygdaloid, cortices can be seen in the hyper-emotional aspect of dreaming.

        The profound import of these processes for the understanding of, both, memory and PTSD is as follows: while hippocampal outflow to the cortex, during non-REM sleep, facilitates the reinforcement of old memories, the blocking of hippocampal outflow, during REM sleep, and the concomitant facilitation of neocortical semantic outflow to the hippocampus, facilitates the formation of new associative links which are profoundly necessary for understanding the meaning of events in our lives (Stickgold, 1998b).

        In PTSD this system breaks down (Ball et al., 1994; Lavie et al.,, 1979; Hefez, Metz, & Lavie, 1987; Claubman, Mikulincer, Porat, Wasserman, & Birger, 1990; Mellman et al., 1995), due to noradronergic and serotonergic surges. This is evidenced by the constant, intrusive, replay of hippocampal, episodic memories of the event(s), combined with the associated amygdaloid affect, without the necessary neocortical input as to the semantic meanings of the traumatic events.

The Role of REM Physiology in EMDR

        According to Stickgold (1998b) one of the physiological hallmarks of REM sleep are the waves of electrical activity that ensue in the pontine brainstem, the lateral geniculate nucleus of the thalamus and in the occipital cortex, collectively known as Pontine Geniculate Occipital (PGO) waves. This is consistent with previous observations that the Gigantocellular Tegmental Field (GTF) neurons, in the locus coeruleus (LC) and reticular formations of the pons, drive the PGO waves and generate REM sleep (Hobson & McCarley, 1977; Hobson, 1989; Reiser, 1994). He notes that the only other circumstance that allows for the generation of these PGO waves is the startle reflex. Stickgold proposes that when a startle occurs a brief surge of acetylcholine is required for the release and shifting of attention. He posits that EMDR stimulation (eye movements, auditory tones and tactile stimulation), with its constant alternating shifting of attention, drives a sustained surge of acetylcholine. He draws a parallel to the reciprocal interaction model (Hobson, McCarley & Wyzinski, 1975; McCarley & Hobson, 1975) and the inception of REM sleep, when serotonergic and noradronergic neuromodulation ceases and the production of acetylcholine is markedly upregulated. This cholinergic surge, produced by EMDR’s alternating stimulation, is seen to facilitate PGO wave activity, the activation of the brain's REM sleep systems and specific areas of the anterior cingulate gyrus.

        The anterior cingulate gyrus, one of the largest parts of the limbic lobe (Brodal, 1981), forms a large region around the rostrum of the corpus collosum that is termed the anterior executive region. The anterior executive region is further subdivided into affect and cognition areas. The affect area has extensive connections to the amygdala and parts of it project to the autonomic brainstem nuclei (Devinsky et al.,1995; Vogt,1993). This area is involved in conditioned emotional learning, vocalizations associated with expressing internal states, assessments of motivational content, assigning emotional valence to external and internal stimuli and regulating context-dependent behaviors. Devinsky et al. (1995) posit that the anterior cingulate cortex and its connections provide the mechanisms by which affect and intellect can be joined. They view the anterior cingulate gyrus as both an amplifier and filter, interconnecting the emotional and cognitive components of the mind.

        Stickgold (1998b) posits that EMDR stimulation jump-starts the REM sleep system, activates areas of the anterior cingulate, as a filter (Devinsky et al., 1995), opening the processing system that facilitates the flow of information from the neocortex back into the hippocampus, allowing for semantic neocortical input and, therefore, the reprocessing of information that is defective or dysfunctional. What is most fascinating is that, unlike natural REM sleep, when the neocortex is deactivated, EMDR appears able to activate REM systems and facilitate frontal cortical activation as well as the activation of areas of the anterior cingulate gyrus (Levin, Lazrove & van der Kolk, 1999; van der Kolk et al. 1997). The underlying mechanisms for this process will be the focus of the remainder of this discussion.

The Role of the Cerebellum

        When the human brain enlarged in the course of its phylogenetic evolution, the cerebellum enlarged more dramatically than any other part of the brain except the cerebral cortex (Brodal, 1981; Passingham, 1975). The phylogenetically new parts of the cerebellum developed in parallel, not with the cerebral cortex as a whole, but specifically in parallel with cerebral association areas (Leiner, Leiner & Dow, 1986, 1989, 1991).

        It has been noted that within the enlarged, multi-folded, cerebellum, the number of nerve cells apparently exceeds the population in the cerebral cortex (Noback & Demarest, 1981; Shepherd, 1983; Zagon et al., 1977), making it the largest structure in the human brain (Williams and Herrup, 1998). Containing billions of nerve cells, this cerebellar mechanism in the hindbrain is connected by millions of nerve fibers to many parts of the brainstem and forebrain, including all the lobes of the cerebral cortex (Brodal, 1981; Larsell & Jansen, 1972; Llinas and Sotelo, 1992).

        It is generally accepted that the language capabilities of humans are dependent on some phylogenetically new areas of the cerebral cortex, such as Broca's language area, but it is not generally appreciated that new areas in the cerebellum may be important as well (Leiner, Leiner & Dow, 1986, 1989, 1991). Leiner et al. posit that concomitant with the evolution of the new association areas in the cerebral cortex, new neural connections evolved that descend (via enlarged structures in the brainstem) to new areas in the lateral cerebellum, which can respond to linguistic signals received from the posterior lobes of the cerebral cortex. Such responses can be transmitted from the neocerebellum to Broca's language areas in the frontal lobe of the cerebral neocortex (Leiner, Leiner & Dow, 1989, 1991). In the newly evolved cerebro-cerebellar system of the human brain, therefore, the neocerebellum can serve as a link between the posterior and frontal language areas of the cerebral neocortex.

        In effect, the neocerebellum provides the cerebral cortex with an additional 'association area'. In serving as such an adjunct of the cerebral cortex, the human cerebellum seems able to contribute not only to the motor processes that produce fluent human speech, but also to the cognitive processes that generate the words to be expressed (Leiner, Leiner & Dow, 1986, 1991). Based on its physioanatomical position, allowing it to affect known attentional systems, it has been shown for the past decade that the cerebellum contributes to attention operations by allowing attention to be shifted rapidly, accurately, smoothly and effortlessly (Akshoomoff and Courchesne, 1992, 1994; Courchesne et al., 1994; Courchesne and Allen, 1997).

        Because the neural connectivity within the cerebellum is relatively straightforward in its geometrical organizations, this circuitry can serve as a favored site for examining the basic information-processing characteristics that are shared by living nervous systems and inanimate information-processing machines (Leiner, Leiner & Dow, 1991).

        Leise (1990) suggests that one characteristic that is shared by parts of vertebrate and invertebrate nervous systems as well as by information-processing machines is the modular organization of the processing components. The cortex of the neocerebellum is seen to be an example of such modular organization. It is constructed of neural modules called 'longitudinal microzones, which are arrayed perpendicular to the cortical surface and parallel to each other (Ito, 1984). The suggestion has been made that such micro-modules may be the biological equivalents of modern microprocessor chips, from which information-processing machines are constructed (Leise, 1990). Hopfield (1982) posits that even in machines, when modules with modest information-processing capabilities are assembled in large numbers in parallel, the resulting network can achieve remarkably powerful computing capabilities, which can be used for solving problems in a wide variety of fields.

        Supporting this view, is the recent behavioral and empirical evidence that the cerebellum participates in cognitive and language functions of the human brain, beyond the purely motor expression of speech or gesture (Cartford et al., 1997; Clark et al., 1997; Krupa & Thompson, 1997; Nakazawa et al., 1997; Yeo et al., 1997). Such evidence has, also, emerged as a result of advanced techniques for scanning and imaging the brain which have revealed that the lateral cerebellum is strikingly activated when an individual performs information-processing, semantic association, working memory, declarative and episodic memory tasks (Andreasen et al., 1995; Awh et al., 1995; Courchesne et al., 1989; Courchesne and Allen, 1997; Courtney et al., 1996; Decety et al., 1990; Parsons et al., 1997; Peterson et al., 1989; Raichle et al., 1987).

        To understand how the cerebellum participates in this wide variety of functions, the anatomical connections linking it to other parts of the brain must be considered. Through such connections, the cerebellum can communicate with different neural structures as they perform their different tasks - motor, vegetative, emotional, cognitive and linguistic.

Input to the Cerebellum

        From the cerebral cortex, the human cerebellum receives information via many different projections, some phylogenetically new and some phylogenetically older (Brodal, 1981; Crosby, 1969; Ito, 1984). The phylogenetically new projections, which enlarged enormously in the human brain, descend to structures in the brainstem that enlarged concomitantly with the cerebral cortex and cerebellum, namely: the pontine nuclei, the red nucleus, and the inferior olivary nucleus (Leiner, Leiner & Dow, 1991). The cerebellum receives not only visual, auditory and somatosensory information from the posterior lobes of the cerebral cortex, and not only motor information from the frontal lobe, but also highly processed multisensory information from some association areas. This multimodal information, which may be needed for carrying out high-level functions, is conveyed both to the pontine nuclei and to the red nucleus, in the mesencephalon. The pontine nuclei receive such information from the posterior/parietal, temporal and prefrontal cortex. The red nucleus is the recipient of projections from the parietal cortex and from the prefrontal cortex [Broca's area] (Leiner, Leiner & Dow, 1991).

        In addition to such projections from the cerebral neocortex, the phylogenically older limbic lobe and hypothalamus also project to the pontine nuclei (Dietrichs and Haines, 1989), which can, therefore, provide the cerebellum with some motivational and affective information that may be needed for regulating autonomic and emotional behavior. In addition to these direct thalamic and hypothalamic projections, the cerebellum is also connected to reticular structures in the brainstem. They provide another, but less direct route to the older limbic structures, which are concerned with autonomic, emotional, and motivational behavior (Haines and Dietrichs, 1987).

Output from the cerebellum

        Two direct routes from the cerebellum to the cerebrum have been traced anatomically. One route connects the cerebellum to the thalamus and, thence, to the prefrontal cortex. The other route connects the cerebellum to the hypothalamus and thence to the older, limbic, structures of the brain. In addition to these direct thalamic and hypothalamic projections, the cerebellum also is connected to reticular structures in the brainstem, providing a less direct, but additional, route to the older structures of the limbic brain, which are concerned with autonomic, emotional, and motivational behavior (Haines et al.,1984; (Haines and Dietrichs, 1987; Leiner, Leiner & Dow, 1991).

        It is generally agreed that each output nucleus of the cerebellum sends its output fibers to two main regions of the thalamus; to the ventrolateral nucleus and to the central lateral nucleus (Chan-Palay, 1977; Ilinsky & Kultas-Ilinsky, 1987; Leiner, Leiner & Dow, 1991; Steriade et al., 1990). These two nuclei of the thalamus differ in their projections to the cerebral cortex. The central lateral nucleus, which is an intralaminar nucleus has a more diffuse projection and may provide a substrate through which the cerebellum can contribute to cortical arousal, alertness. or attention (Leiner, Leiner & Dow, 1991; Saper, 1987). In contrast, the thalamic ventrolateral nucleus provides a more specific route for conveying information to particular columns of the cerebral cortex; most specifically, the frontal lobes (Leiner, Leiner & Dow, 1991; Steriade et al., 1990).

        Of particular interest, to this discussion, are the specific targets in the prefrontal cortex to which the ventrolateral thalamic nucleus can send signals. Leiner et al. (1991) posit that when hominoids evolved, the ventrolateral thalamus enlarged concomitantly with the enlargement of the cerebellar dentate nucleus. Just as a newly differentiated area evolved in the cerebellar dentate nucleus, so too in the ventrolateral thalamic nucleus, a newly differentiated area evolved (Van Buren, & Borke, 1972). These new areas could very well provide a new neural substrate for the evolution of cognitive and language skills through the transmission of information to the dorsolateral prefrontal cortex (Leiner, Leiner & Dow, 1989,1991).

        Evidence is available that the human ventrolateral thalamus is involved in cognitive and language functions as well as in motor function (Armstrong, 1980; Llinas & Pare, 1993; Ojemann, 1977; Ojemann & Creutzfeld, 1987). Also evident is its ability to send output to the prefrontal cortex as well as to the motor cortex (Freeman & Watts, 1947; Galaburda, 1984; Leiner, Leiner & Dow, 1989,1991; Van Buren, & Borke, 1972). It is beyond the scope of this discussion to detail these studies. The reader is referred to them for elaboration

        Leiner et al. (1991) posit that to a designer of information processing mechanisms, the phylogenically new part of the cerebro-cerebellar system seems ideally suited for carrying out high-level processing of information. They cite the rod-to-column arrangement by means of which the dentate nucleus of the cerebellum can transmit information through segregated channels of communication to the frontal neocortex. Because different modules of the cerebellum can send output fibers to different rods in the thalamus, and because each rod can send its output fibers, as a unit, to a small aggregate of cortical neurons, these segregated bundles of fibers provide an extremely powerful way of communicating information between the cerebellum and the dorsolateral prefrontal cortex and Broca's Area, specifically (p.122).

        The cerebellum receives input and is activated from virtually every sensory system (Brodal, 1981; Brodal, 1992; Parsons et al., 1997; Welker, 1987), including vestibular, proprioceptive, visual, auditory, tactile and somatosensory (Donga & Dessen, 1993; Naito et al., 1995; Snider & Stowell, 1944; Welker, 1987). Neuroimaging studies on tactile stimulation, with no movement, have shown a marked activation of the dentate nucleus, the lateral cerebellum's output nucleus (Fox et al., 1985; Parsons et al., 1997). This was seen bilaterally, but more prominently in the right dentate nucleus.

        I would, therefore, suggest that EMDR stimulation (visual, auditory and tactile), in addition to its constant alternating shifting of attention, noted above, also constitutes a constant and marked stimulation of the cerebellum. Output fibers to the hypothalamus and to reticular nuclei in the brainstem allow the cerebellum to transmit information to the limbic structures. Input fibers from the hypothalamus and from the reticular nuclei in the brainstem allow it to receive information from the limbic lobe. The concomitant activation of each output dentate nucleus of the cerebellum, then, sends its processed information through output fibers to two main regions of the thalamus; to the ventrolateral thalamic nucleus and to the central lateral thalamic nucleus. With respect to this discussion, the ventrolateral nucleus transmits its information and activates areas of the dorsolateral prefrontal cortex.

        In summary, the mechanisms that underlie EMDR appear to be extremely complex and multi-varied. We can, however, begin to speculate on the following: that EMDR stimulation (visual, auditory and tactile), with its constant alternating shifting of attention, facilitates a cholinergic surge, which jump-starts the REM sleep system, activating areas of the anterior cingulate, as a filter, thereby facilitating the integration of traumatic memory into general semantic networks. This integration leads to a reduction in strength of both hippocampally mediated episodic memories of the traumatic event as well as the amygdaloid mediated negative affect of PTSD.(Stickgold, 1989b); and that EMDR stimulation (visual, auditory and tactile), also constitutes a constant and marked stimulation of the cerebellum. This allows the cerebellum to act as another association area and information processing center, facilitating, through its extensive input and output fibers, outgoing and incoming information to the limbic area, directly activating areas in the dorsolateral cortex; further facilitating the integration of traumatic memory into general semantic and other neocortical networks.

        To date, the only neurobiological data regarding EMDR has been derived from an EMDR study, utilizing single photon emission computerized tomography (SPECT) scanning (Levin, Lazrove & van der Kolk, 1999; van der Kolk et al., 1997). The results showed the following: after three EMDR treatment sessions, subjects no longer met diagnostic criteria for PTSD; areas of the anterior cortex of the cingulate gyrus evidenced increased activity, bilaterally; and areas in the frontal lobe, evidenced increased activity. The speculations in this discussion, derived theoretically, appear to be generally consistent with van der Kolk's neuroimaging results.

        The neurobiological mechanisms of EMDR are, undoubtedly, complex and multi-faceted. Many issues have yet to be clarified. In particular, the cingulate gyrus and its functioning needs to be refined further, with respect to its many areas. For example, in the anterior executive region of the cingulate gyrus, the affect division has been defined (according to Brodman) as areas 24, 25 and 32. (Devinsky et al., 1995; Vogt, 1993). These areas are considered a projection site for the amygdaloid complexes (Vogt, 1993). Neuroimaging studies of PTSD have consistently shown activation of the anterior cingulate gyrus (Eberly et al., 1995; Rauch et al., 1996; Shin et al., 1997). Neuroimaging studies of REM sleep (Braun et al., 1997; Maquet et al., 1996; Nofzinger et al., 1997) have also consistently shown activation of the anterior cingulate. Indeed, van der Kolk's post EMDR neuroimaging study (Levin, Lazrove & van der Kolk, 1999; van der Kolk et al., 1997) also showed bilateral activation of the anterior cingulate.

        It would appear, then, that the anterior areas of the cingulate gyrus are involved in the generation of multi-varied levels of affect. In the neuroimaging studies of PTSD and REM-sleep, noted previously, the levels of activation in the anterior cingulate apeared to highlight it's function as an amplifier; facilitating increased affective levels. EMDR appears to change the level of activation in certain specific areas of the anterior cingulate, facilitating a more modulated and appropriate emotional valence and, therefore, a lessening of negative affect; thereby, promoting more of a filtering function. This issue should be refined by future imaging studies. I would suggest, speculatively, that future imaging studies may show EMDR to downregulate certain areas of the anterior cingulate, rather than an overall increase in activation. What is becoming clearer, however, is that the anterior portion of the cingulate gyrus is too large and complex a structure to be discussed as a whole, and needs to be better understood with respect to its specific, areas.

        What is most fascinating, though, is that EMDR stimulation and the protocol that anchors it, involves, comprehensively, the pontine brainstem, limbic area, lateral cerebellum, gyral cortical structures and the neocortex.

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**Correspondence concerning this paper or reprints should be addressed to the author via email at UBergmann@worldnet.att.net,  or at 353 Veterans Memorial Highway, 3rd Floor, Commack, New York 11725.
*** Translation into Farsi by Reza Bidhendi is available here.