Excerpts from Hobson, J. Allan, Pace-Schott, E. and Stickgold, R. (2000), DREAMING and the BRAIN: Toward a Cognitive Neuroscience of Conscious States, Behavioral and Brain Sciences 23 (6): XXX-XXX.

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4. The Activation Synthesis Model

a. The Original Activation Synthesis Model

Abundant studies in the 1960s and 1970s on the cellular neurophysiology of the sleep cycle as well as the functional reorganization of the visual system during sleep suggested a new conceptual approach to brain-mind states. First expressed as the Activation-Synthesis hypothesis of dreaming (Hobson & McCarley 1977), this model proposed the global mapping of brain states to mind states. This was the position taken by Freud in his famous Project for a Scientific Psychology (1895) but ostensibly abandoned in the Interpretation of Dreams (1900). For a detailed discussion of this subject, see McCarley & Hobson (1977).

Enunciating the general principle of brain-mind isomorphism, the activation-synthesis model placed emphasis on such aspects of the form of dreams which might be expected to have their roots traced to isomorphic forms of brain activity. In so doing, the new theory proposed some of the cellular and molecular mechanisms by which changes in activation, in stimulus origin and in neuromodulation could explain the state-dependent changes in perception, thinking and memory seen in shifts from waking to NREM and REM sleep (Flicker et al. 1981). The Activation-Synthesis hypothesis proposed that formal aspects of dream mentation reflected the outcome of attempts by sensorimotor and limbic regions of the forebrain to produce a coherent experience from the incomplete and chaotic inputs received from the brain stem. The specific formal features of dream mentation, it was proposed, could best be explained by examining the unique configuration of brain activity that occurs during REM sleep.

To illustrate how this global brain-to-mind mapping concept is articulated, we considered the probable consequences of a shift in visual system input source from the formed visual images on the retina in waking to the chaotic brain stem stimulation of REM sleep (Bizzi 1966a,b; Callaway et al. 1987; Nelson et al. 1983; Pivik et al. 1977). This shift in input source occurs in the context of a concurrent cessation of activity in brain stem noradrenergic and serotonergic neurons (Hobson & Steriade 1986; Steriade & McCarley 1990). The quiescence seen in these aminergic modulatory neurons results in the demodulation and disinhibition of the visual cortex (Evarts 1962), the lateral geniculate bodies (Bizzi 1966b) and brain stem oculomotor networks (Mouret et al. 1963).

As a result of the aminergic disinhibition, cholinoceptive peribrachial neurons become hyperexcitable and fire in bursts, causing phasic activation of the lateral geniculate bodies and visual cortex. This phasic activation is recordable in the REM sleep of cats as the PGO waves which, in turn, correlate with the direction of the rapid eye movements (Monaco et al. 1984; Nelson et al. 1983). We have speculated that this cholinergically mediated stimulation conveys information to the visual system about the direction of the eye movements which have become, in REM sleep, uncoupled from external sensory stimuli (Calloway et al. 1987).

The net result of these shifts is an activated brain stem and visual system which are 1) deafferentated, 2) aminergically demodulated, and 3) cholinergically auto-stimulated. But the brain stem signals still convey information about the direction of rapid eye movements to the deafferentated, demodulated forebrain. According to the Activation-Synthesis hypothesis, these changes in sensory input source and neuromodulation could contribute to such cognitive features of dreaming as 1) the hallucinatory visual imagery, 2) the frequent shifts and reorientations of attention, 3) the loss of voluntary control of both motor action and internal attention, 4) the emotional intensification especially of anxiety, elation and anger, and 5) the memory loss within and after dreaming (Mamelak & Hobson 1989a).

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As the Activation-Synthesis model has evolved, it has metamorphosed into the three-dimensional framework of the AIM model. We now update the Activation-Synthesis concept as follows: 1) high levels of cortical activation (high values of "A") are a correlate of the mind's ability to access and manipulate significant amounts of stored information from the brain during dream synthesis; 2) the blockade of external sensory input and its functional replacement by internally generated REM sleep events such as PGO waves (internal sources of "I") provide the specific activation of sensory and affective centers which prime the cortex for dream construction; and 3) the shift of the brain from aminergic to cholinergic neuromodulation (low ratios of aminergic to cholinergic neuromodulation, "M") alters the mnemonic capacity of the brain-mind and reduces the reliability of cortical circuits, increasing the likelihood of bizarre temporal sequences and associations which are uncritically accepted as waking reality when we are dreaming.

As the brain shifts from alert waking through drowsiness to NREM and REM sleep, a concerted set of physiological and chemical changes occur in the brain and periphery. Global changes are seen in all major physiological systems, including the nervous, respiratory, cardiac, renal, immunological, endocrine and motor systems (Gottesmann 1997; Hobson 1989; Orem 1980). The changes in central neurophysiology include changes in gating of sensory input, inhibition of motor output and neuromodulation of widespread regions of the cortex (Gottesmann 1997; Hobson 1988b; Hobson & Steriade 1986; Steriade & McCarley 1990). More specific neurophysiological changes involve both tonic and phasic activation of numerous brain regions, including, but not limited to, the medullary bulbar reticular formation, the pontine reticular formation, the lateral geniculate nucleus, the amygdala, the hippocampus, and the limbic and unimodal visual associative cortex, as well as regional deactivation of the dorsal raphe, locus coeruleus and multimodal association cortices (Amzica & Steriade 1996; Braun et al., 1997; Hobson & Steriade 1986; Maquet et al. 1996; Nofzinger et al., 1997; Steriade & McCarley 1990). (See Table 2 and Figure 7.) Not surprisingly, these changes are accompanied by dramatic shifts in the activity of the mind.

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AIM makes three major claims:

1) AIM proposes that conscious states are in large part determined by three interdependent processes, namely the level of brain activation ("A"), the origin of inputs ("I") to the activated areas, and the relative levels of activation of aminergic (noradrenergic and serotonergic) and cholinergic neuromodulators ("M"). While these variables tend to vary in concert with one another, many paradoxical and dissociated mental states, both normal and abnormal, arise from the sometimes strikingly independent variation of these parameters as we will shortly illustrate.

2) The AIM Model proposes that the universe of possible brain-mind states can be construed as a three-dimensional state space, with axes A, I and M (activation, input and mode), and that the state of the brain-mind at any given instant of time can be described as a point in this space. Since the AIM model represents brain-mind state as a sequence of points, time is a fourth dimension of the model.

3) The AIM model proposes that while stable and reproducible mental states reflect the tendency of the brain-mind to occupy a small number of fixed locations in this state space, corresponding to such identified brain-mind states as alert wake or vivid REM sleep dreaming (see Kahn et al. 1997) , all three parameters defining the state space are continuous variables, and any point in the state space can in theory be occupied. In the remainder of this section, we will discuss each of these three claims in detail.

A. The Three Dimensions of the State Space

Experimental testing of the AIM Model requires that each of the three parametric axes of the brain-mind state space be directly measured and, ideally, manipulated. Toward this end, we have attempted to define the underlying parameters as well as to indicate how they can best be measured (see again Figure 1). As we shall show below, reasonable measures of A and I can be readily obtained in both humans and animals. At the present time, M can only be measured directly in animals, but because its value can be manipulated experimentally in humans with pharmacological agents, its role in human conscious state determination can be indirectly assessed.

1. Activation

Conscious states show a clear-cut dependence on brain activation level. The production of conscious experience, as reflected in the length, intensity and complexity of subjective reports of mental activity, as well as in levels of arousal and alertness, is generally greater in waking and in REM sleep than it is in deep NREM sleep and greater in alert waking than in quiet resting. The AIM model predicts that this physiological measure, "A," reflects the rate at which the brain-mind can process information regardless of its source (measured as "I") or its mode of processing ("M"). This activation parameter is based upon Moruzzi & Magoun's concept of a reticular activating system (Moruzzi & Magoun 1949; Steriade et al. 1980). Broad consensus already exists for the importance of this first dimension of the AIM Model.

In its simplest form, brain activation is defined as the mean firing frequency of brain stem neurons. It can be approximated in both humans and animals from the EEG spectrum, with increasing activation reflected in relatively high power in the high frequency range and relatively low power at low frequencies. In animals, the activity of the reticular activating system can be precisely quantified from the frequency of firing of neurons in the midbrain reticular formation (Huttenlocher 1961; Kasamatsu 1970; Steriade et al. 1980).

In humans, an alternative measure of overall brain activation might be the level of gamma frequency (30-70 Hz) oscillation in the brain (Llinas & Ribary 1993; Llinas et al. 1994). Although some recent work questions the association of gamma oscillation with REM sleep (Germain & Nielsen 1996), other work appears to confirm it (Uchida et al. 1997). Such gamma activity in humans has been shown to correlate with discrete cognitive events (Lutzenberger et al. 1995; Muller et al. 1996; Tallon-Baudry & Bertrand 1999; Tallon-Baudry et al. 1996, 1997, 1998) and to be measurable with depth electrodes in the human medial temporal lobe (Hirai et al. 1999).

2. Input Source

Waking, NREM sleep and REM sleep represent states in which the sources of information processed by the brain differ dramatically. The second parameter of our AIM Model, input source (I), is a measure of the extent to which the brain-mind is processing external sensory data impinging upon receptors (as it is in waking) or from internal data sources (as in day dreaming or REM sleep). Since one component of sensory input is proprioceptive feedback reflecting the extent of motor activity, we also include the efficacy of such feedback in parameter I. Internally generated pseudosensory data can be produced by brain stem mechanisms (e.g., via PGO stimulation of visual cortex in REM sleep), it can be recalled from memory, or it can be intentionally created by directed mental imagery.

In alert waking, the contents of our conscious experience (e.g., our thoughts and our feelings) tend to be driven by external stimuli and are predictive of subsequent motor behavior. During sleep, in contrast, conscious experience is normally driven by internally generated stimuli and has no apparent behavioral consequence. In the AIM Model, waking is characterized as both more exteroceptive and exteroeffective than either NREM or REM sleep, while REM sleep is markedly more interoceptive than NREM sleep but less exteroeffective than either waking or NREM sleep.

This second dimension of our AIM Model, though robust, has not been specified by many cognitive theorists who tend to regard internally generated signals as simply the phasic intensification of activation level. Such a view ignores what to us are very significant differences in such mental functions as vision, visual imagery and visual hallucination. But while some seem to consider it an irrelevant factor, Llinas & Pare (1991) have suggested that this dimension by itself could be an adequate explanation of the phenomenological differences between such high activation states as waking and REM sleep (Llinas & Pare 1991). We agree with Llinas & Pare that both in waking and in sleeping, input source represents a major determinant of the nature of conscious experience. However, we do not regard the differences in input source to be an adequate explanation of the phenomenological distinction between waking and dreaming. How, for example, could it account for dream forgetting or the relatively low visual intensity and bizarreness of daydreams?

Physiologically, the input source axis of the AIM Model reflects both input-output gating and non-sensory activation of sensorimotor cortices. The activation of these cortical regions by external sensory stimuli can be directly measured in humans using evoked potential (ERP) techniques (e.g., Niiyama et al. 1997; Sallinen et al. 1996) or using stimulus threshold studies (see Arkin & Antrobus 1978 and Price & Kremen 1980 for reviews). In this regard, it is notable that Price & Kremen (1980) measured a rise in auditory stimulus threshold and Sallinen et al. (1996) observed a decreased ERP response in human phasic compared to tonic REM sleep. Similarly, the H-reflex can be used to measure motor blockade (Hodes & Dement 1964). In animals these same measures can be obtained and complemented by more refined assessments. For example, the amount of presynaptic inhibition of 1A afferent terminals (Bizzi & Brooks 1963; Pompeiano 1967b) specifically measures the sensory gate function while the amount of motoneuronal hyperpolarization (Chase & Morales 1990; Pompeiano, 1967a) measures gating of motor activity. (For a recent review of such measurements see Gottesmann 1997.)

In humans and animals, eye movement density in REM sleep provides an estimate of the amount of internally generated pseudosensory data because eye movement density reflects brain stem PGO and motor pattern generator activity. In addition, the frequency of PGO waves (or the burst intensity of PGO waves) can be measured in animals to determine this parameter more directly. Currently, PGO waves cannot be easily or confidently recorded from humans although numerous suggestive EEG findings have been reported (McCarley et al. 1983; Miyauchi et al. 1987, 1990; Niiyama et al. 1988; Salzarulo et al. 1975 ) and new dipole tracing techniques show promise in identifying human PGO waves (Inoue et al. 1999a).

3. Modulation

The third major and clear-cut physiological difference among waking, REM and NREM is in the neuromodulation of the brain. In the AIM Model, we focus on the marked shift in modulatory balance seen from aminergic (noradrenergic and serotonergic) predominance in waking to cholinergic predominance in the REM sleep of animals. We call this modulatory factor M and define it as the ratio of aminergic to cholinergic chemical influence upon the brain.

It is our contention that this shift of neuromodulatory balance underlies the similar modal shifts in information processing (data processing, storage and retrieval) seen as the brain shifts from one wake-sleep state to another. We propose that this modulatory factor M is involved in the regulation of such conscious state functions as directed attention, deliberate thought, self reflective awareness, orientation, emotion, memory and insight. All of these functions are altered in the transition from waking to NREM sleep as a function of the diminished activation and sensory input level. But their even more marked dramatic alteration in dreaming, when the activation level is as high as in waking, must have another brain basis, which we think the changes in input-output gating alone are inadequate to explain. This element of our model has found little support among sleep psychologists who, we believe, either have failed to fully appreciate the extent of the alteration of cognitive features (such as the defective memory of REM sleep) or have simply rejected the concept of a neurophysiological description of psychological phenomenology (for one exception see Hartmann 1982).

Measurement of "M" is based on comparing the rates of firing or amounts of transmitter released by norepinephrine-containing locus coeruleus neurons and serotonin-containing raphe neurons to that of putatatively cholinergic, PGO burst cells in the peribrachial region. State-dependent shifts in this parameter have been extensively documented in animal models (Datta 1995, 1997b; Foote et al. 1983; Hobson 1992b; Hobson & Steriade 1986; Hobson et al. 1986; Jacobs & Azmita 1992; Lin et al. 1994; Sanford et al. 1995b; Sherin et al. 1996; Steriade & Biesold 1990; Steriade & Hobson 1976; Steriade & McCarley 1990; Szymusiak 1995). A more accurate measure of this parameter may be obtained by the simultaneous measure of release of the two classes of modulator using microdialysis techniques (e.g., Kodama & Honda 1996; Lydic et al. 1991a; Portas et al. 1998; Williams et al. 1994). Unfortunately, methodological constraints have so far largely prevented the measurement of this parameter in humans (although see Sudo et al. 1999 and Wilson et al. 1997). Evidence that such changes occur, and are significant, in humans is indirect but consistently confirmatory.

The role of this parameter in human conscious experience has been extensively studied in waking experiments using drugs known to alter neuromodulatory balance (see Perry & Perry 1995; Perry et al. 1999). In addition, cholinergic stimulation has been found to potentiate REM sleep (Berger et al. 1989; Gillin et al. 1991; Sitaram et al. 1976, 1978b) and dreaming (Sitaram et al. 1978a) while many serotonergic and noradrenergic agents are known to have REM suppressive as well as alerting effects (Nicholson et al. 1989; Gaillard et al. 1994). Reviews of psychopharmacological evidence suggests that the role of modulation in humans is homologous to that in experimental animals (e.g., Hasselmo 1999; Perry & Perry 1995).

An important aspect of the AIM model is its effort to mirror cognition's psychological features in its three physiological dimensions. Thus, "Activation" has a specific meaning at both the neurobiological and cognitive levels [see Anderson's ACT* model (Anderson 1983)]. Cognitivists also speak of information processing and thus share the concept of "input source" with neurobiologists, who express this dimension in terms of sensory thresholds, the excitability of motor pattern and efferent copy circuits, and the threshold for motor output. Finally, the mode concept is important to cognitivists as a memory/amnesia dimension (as well as, possibly, an attention/inattention axis) while neurobiologists represent mode as the ratio of aminergic to cholinergic neuromodulator release. It is by these formal homologies between neurobiology and the cognitive sciences that the AIM model attempts to produce an integrated picture of the brain-mind.

An initial attempt to model the neuroanatomical structures participating in REM-state-dependent changes in activation, input source and neuromodulation is illustrated in Figure 8.

B. The AIM State Space

The AIM model proposes that conscious states can be defined and distinguished from one another by the values of three parameters. These parameters can be considered as the axes of a three-dimensional state space. This state space can be represented visually as a cube where normal values for the parameters range along the three axes (Figures 1 and 10). The model is not only useful in representing normal states but is also helpful as a heuristic tool to illustrate several critical issues in sleep research.

In quantitative renditions of the model (Hobson 1990, 1992a) the activation parameter (A) was derived from either the mean rate of firing of reticular formation neuronal populations which varies in animals from a low of 25/s in NREM sleep to 50/s in REM or from the inverse of the voltage amplitude of the EEG which varies from 25-50 mV in waking to 150-200 mV in stage IV NREM sleep in humans. A four-fold range of values is assumed in visual representations of the model. The input source parameter can be derived from arousal threshold or H-reflex amplitude in humans or PGO wave frequency in animals. The range of these values is roughly the same order of magnitude as factor A. The modulatory parameter, M, is derived from the mean rate of neuronal population discharge of the aminergic populations (2-4 c/s in waking, 1-2 c/s in NREM, 0.01-0.1 c/s in REM) or from the concentration of norepinephrine, serotonin or acetylcholine in microdialysis studies which vary over a range of about 10 fold (Steriade & Hobson 1976; Hobson & Steriade 1986; McCarley & Steriade 1990).

All the parameters of the model are known to vary over the sleep cycle in a non-linear manner. For example, factor M has a clearly exponential deceleration in the NREM-REM transition. Some aspects of this non-linearity are embodied in earlier mathematical modeling of the reciprocal interaction model using the Volterra-Lotka equations (McCarley & Hobson 1975, McCarley & Massaquoi 1986) which yield ellipses as the graphical representation of the sleep cycle.

We acknowledge the tentative and necessarily speculative nature of our assumption of homology across mammalian sleep mechanisms but point out that it is supported by abundant indirect evidence. And we recognize one important exception to this homology assumption: the relative complexity of the human forebrain gives rise to a greater complexity of EEG patterns in human NREM sleep compared to animals. We believe that this complexity is underestimated by currently available measures and that activation models of cognition likewise underestimate the differences between NREM states.

We do not pretend to have solved the problem of modeling conscious states, only to have proposed more realistic and heuristically valuable approaches to this problem. AIM constitutes only a simplified framework for modeling the physiology underlying changes of behavioral state and we in no way claim that it can fully account for the wide variety of human subjective experience which includes thought, imagery, fantasy, and altered or pathological states as well as dreaming. Moreover, we recognize that the axes of the AIM state space are not independent. For example, at sleep onset a declining in general activation is likely to parallel a decline in aminergic modulation and a decline in the strength of external stimulus drive. Likewise at REM sleep onset the steep rise in cholinergic activity is likely to parallel the rise in internal stimulus drive and a rise in general activation level. But the axes of the model are uniquely capable of accounting for just the kinds of paradoxes that arise from an interactive system that changes its states paradoxically: i.e., has high levels of activation in both waking and sleep; shifts from external to internal stimulus processing; and processes information differently in two equally activated states.

Current developments in basic and clinical neurobiology suggest the exciting possibility that the M dimension may become measurable in behaving (i.e., waking, thinking, performing, sleeping, dreaming) human beings. Already, microdialysis techniques with depth electrodes implanted to localize epileptic foci have shown fluctuations in serotonin across the wake-NREM-REM cycle paralleling those seen in animals (Wilson et al. 1997). Moreover, the newest PET techniques for radiolabeling receptor ligands as well as magnetic resonance spectroscopy (Rauch & Renshaw 1995) may yield further possibilities for the localization and quantitation of neuromodulatory dynamics in the human CNS.

One use of the AIM model is to depict the highly dynamic and variable nature of human consciousness, and thus to visually plot specific "states" of consciousness within the state space. As an example, normal consciousness, at the coarsest level, can be divided into the states of waking, REM and NREM sleep. Each of these states can be characterized both by distinct physiologies and by distinct differences in mentation. To help the reader orient to the AIM state space, the positions of these three states in the AIM state space, as well as the trajectory from waking through NREM into REM sleep, are shown in Figure 9.

In this figure, the fully alert, wake state is depicted in the upper-right corner of the back plane of the cube. This corresponds to maximal levels of brain activation (right surface of cube), maximal external input sources with minimal internal sources (back surface), and maximal aminergic and minimal cholinergic neuromodulation (top surface). Cognitively, this corresponds to alertness with attention focused on the outside world.

In the center of the cube lies deep NREM sleep, with low levels of brain activation, intermediate levels of both aminergic and cholinergic neuromodulation, and minimal levels of both external and internal input. In this state, the mind tends towards perseverative, non-progressive thinking with minimal hallucinatory activity, and this is reflected in the brevity and poverty of NREM sleep reports.

As cholinergic modulation increases and aminergic modulation decreases, the modulatory function falls to its low point. The brain-mind, however, regains waking levels of activation and moves from NREM into REM sleep. AIM (here referring to the brain's location in the AIM state space) moves to the bottom front edge of the cube, with input now internally driven (front surface) and neuromodulation predominantly cholinergic (bottom surface). We emphasize the paradox that instead of moving to the left surface of the cube - to a position diametrically opposed to waking - brain activation returns to waking level. This forces AIM to the right surface of the cube. As a result the mind is alert, but because it is demodulated and driven by powerful internal stimuli, it becomes both hallucinatory and unfocused. REM sleep's deviation from the main diagonal axis provides a visual representation of the distinctively unique phenomenology of REM sleep and shows why that state favors dreaming.

A second function of the AIM state-space model is as a tool to clarify the concept of substates. While consciousness can be coarsely divided into waking, REM and NREM sleep, these are only a few of many possible brain-mind states. For example, NREM sleep can be subdivided on physiological bases into substates: sleep onset, stage II of NREM sleep, and deep stages III and IV NREM sleep. Presumably, sleep mentation changes in concert with these physiological changes. Similarly, REM sleep can be subdivided physiologically into phasic and tonic REM or psychologically into lucid and non-lucid dreaming substates. Finally, the waking state can be subdivided into a vast multiplicity of substates, defined by attentive parameters (alert, attentive, vigilant vs. drowsy, inattentive, day dreaming), emotional parameters (calm, angry, sad, afraid), or even by information processing strategies (focused and goal directed vs. creative and freely associating). Other substates of waking can be produced by specific induction procedures, such as trance, hypnosis, sleep deprivation, and by the ingestion of psychoactive drugs.

For each of these substates, a subregion of AIM state space could, in theory, be defined which would characterize its physiological and psychological nature. However, as the distinctions between states become more subtle, these regions necessarily begin to overlap and blur. At the same time, the three dimensions of the AIM model quickly become inadequate. For example, the model is strained to account for differences between various emotional substates of waking. This could be partially resolved by adding a regional activation dimension to our model, such as the ratio of limbic to neocortical activation as suggested by neuroimaging studies (e.g. Maquet et al. 1996; Nofzinger et al. 1997).

Could the changes in regional activation of the brain be related to the shift in neuromodulatory balance that we have described? It seems likely to us that the changes in regional activation (AR) are a combined function of changes in I and M such that, for example, it is the cholinergic pathway from pons to amygdala that is responsible for the selective activation of the limbic brain in REM sleep. Similarly, it could be that the deactivation of the frontal lobe is caused by the withdrawal of aminergic inputs to that region in REM sleep. These suggestions are not simply ways of saving the model's relative simplicity. Rather they demonstrate the capacity of the model to generate new, testable hypotheses about the cellular and molecular basis of regional brain activations.
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Hypnagogic and Hypnopompic Hallucination: From the perspective of the AIM model, hypnagogic and hypnopompic hallucinations, associated with transitions into and out of sleep respectively, result from the REM-like enhancement of internal stimuli coupled with an activated, aminergically modulated waking brain.

With internal and external inputs in an unstable balance, AIM moves to a position half-way between the front and back surfaces of the cube. But unlike NREM sleep, which is also at this midpoint of input source (with minimal internal and external inputs), both sources are being powerfully driven in hallucinosis. It is this unexpected combination of high internal and high external inputs which defines the functional dissociation of these hallucinoid states. The frequency of this combination may be elevated by the abnormal physiology of narcolepsy, a condition in which the frequency of hypnagogic hallucinations is likewise elevated (Broughton et al. 1982; Mignot & Nishino 1999).

We can approximate a representation of this state by hypothesizing that while the brainstem signals continue to evoke internal representations in the cortex, the blockade of external stimuli has broken down. As a result, the dissociated state results from a dissociation of the forebrain from the brainstem. This dissociation is represented in the AIM model by splitting the cube representing the brain-mind into forebrain (F) and brainstem (B) sections and showing their relative positions in AIM space.

A more extreme example of this kind of dissociation is temporal lobe epilepsy in which abnormal phasic activation signals of limbic origin commandeer the cortex and force it to process external world data on limbic terms (e.g., Rabinowicz et al. 1997). Given the new findings on selective limbic activation in REM sleep (Braun et al. 1997, 1998; Maquet et al. 1996; Nofzinger et al. 1997), it seems reasonable to suppose that a similar, though normal, process may also drive the dreaming brain. By this we mean that the cortex of the dreaming brain is compelled to process internal signals arising from the pons and amygdala, as was originally suggested by the activation synthesis hypothesis. This epilepsy analogy is also cogent because the internal signals of REM sleep are spike and wave complexes arising in the pons and amygdala (Elazer & Hobson 1985). The limbic lobe may then direct the forebrain to construct dreams in a manner similar to that by which it creates the dreamy states of temporal lobe epilepsy (see Epstein 1995). Indeed, a recent study has shown more unpleasant and higher intensity emotions in the dreams of epileptics as compared to normals (Gruen et al. 1997).