About the Book

• The Lady and the Unicorn: A Psychological Metaphor



• Dreaming…With Eyes Wide Open: Schizophrenic Hallucinations



• Information Processing in Schizophrenia



• Clarification of our Clinical versus Forensic Function: Dual Relationship



• Art Psychotherapy



• Lord of the Rings: A Psychological Metaphor



• Aviation Psychology



• So, You have just been Passed by a Girl! A Holley Carborator may help



• Approaches in Memory Rehabilitation



• Memory Enhancement Module



• Negaunee Center



• The Final Transition



• Is Deinstitution- alzation a Misnomer



• Token System: a Psychiatric Case Study



• A Token Economy System: Inpatient Psychiatric Population



• Insight: An Aspect of Neurocognition

Dreaming… With Eyes Wide Open: Schizophrenic Hallucinations

Clearly, one of the hallmarks of an organic brain disorders is that of visual hallucinations (i.e., infections, tumors, lesions of the amygdale, hippocampus, diencephatic nuclei, limbic periventricular & occipital lobe). The etiology has been hypotheses as dynamic changes in the neural transmitters within the cerebral cortex. One avenue of study has proposed a premise which has resulted primarily from the research into various sensory deprivation states. In support of this contention, Bentall (1990) stated that "there can be no doubt that hallucinations are sometimes associated with physical disorders such as progressive sensory loss (causing "release hallucinations") (Hammeke, McQuillen, & Cohen, 1983; T. Miller & Crosby, 1979; Ross, 1978) and a variety of medical and neurological conditions (Asaad & Shapiro, 1986; Slade & Bentall, 1988)" (p. 82).This perspective may be view as distinctly different at this stage from the path of functional disorders (Freud, 1956).

Unfortunately, the discussion here is more speculative and antidotal versus deeply rooted in empirical science. The anecdotal evidence for schizophrenic hallucinations as well as from other neurological disorders is abundant and comes from a variety of sources ( Gloor et. al., 1982; Davison et. al., 1969) That being said, descriptions of visual hallucinations by patients appears too differ in a myriad ways in terms of content (Micro-macropsia, Lilliputian, Metamorphopsia) (Cadet et. al, 1986). Although it is often striking to me that a fairly consistent factor in the study of visual hallucinations is that the structure of the reality context remains fixed.

The groundwork has been established to suggest that these visual hallucinations experiences by schizophrenics may in fact be waking dream projections. For instance, patients can describe their hallucinations as to what they perceive but it appears against the visual backdrop of a room or situations they actually know. A great many dreams have often vivid projections of images and situations. It has been also suggested that we have more then one dream episode per night although some times being unable to recall the event (Aserinsky and Klectman, 1953). Understanding the basic mechanisms the dreaming phenomena may be helpful in examining the hallucinatory event. Dreams themselves are visual projections within our sleep cycles and most occur during the Rapid Eye Movement (REM) phase of sleep. “Because of their distinguishing character, those periods are seen as constituting a separate state of sleep. This distinct state of sleep is referred to as D-Sleep (desynchronized or dream sleep).” In contrast, to the awake state that activates noradrenaline, REM activates acetylcholine which produces activity more diffusely within the brain. Associations areas are more active in the visual, motor and emotional subsystems. (Gershaw, 1995). But Gershaw stated that “like a window for viewing the world, it allows us to see some things through the glass very clearly, while the frame (of reference) itself blocks other things from our awareness (p. 30).

The phenomena of psycho-motor sleep paralysis provides a fertile ground for hallucinations. Thus “hypnopompic state, the brain cannot instantaneously switch from dreaming to a waking state, and the dream extends into the waking period. The brain circuits activated during dreams then send signals-such as an image of the succubus- to the cerebral cortex, where they are processed as if they came from the outside world. Thus, dream images extend into waking and the sleeper sees visual images (or has sensations in other modalities) within the context of the real bedroom.” (Siegel 1992, p. 88) Although the exact source of our dreams remains unknown, with many distinguished researcher exploring this territory. Various authors have proposed that hallucinations are a direct response to an emergence of normally preconscious material into conscious awareness.

Now brings us to the conceptualization of the role that sensory stimulation and neurotransmitter activations lays within the subcortical processes in the production of visual hallucinations. Pribram (1971) has suggested that the midbrain is sensitive to serotonin within ordinary sleep where as the locus ceruleus is sensitive to norepinephrine in paradoxical sleep in which dreaming occurs. People experience excitement and euphoria during the initial stages these intermittent synchronous wave are the signpost of hallucinations. “The result is a failure in the brain’s ability to modulate incoming signals, thus permitting all signals to enter with full power.” (Siegel 1992, p. 49) The gate controlling the brain’s sensory systems swing open so to speak, giving full access to many more inputs than the individual is able to sort through. This state of irregular of high frequency, low-voltage activity in the cerebral cortex, creates an overwhelming process of sensory confusion. As this electrical wave surge through the brain’s circuits, the individual will fluctuate between states of relatively lucid perception and ones marked by hallucinations and illusions. In terms of schizophrenia, Pelez (2000) has hypothesized result from a blockade afferent impulses traveling from prefrontal cortical regions through the thalamus subcortical areas which may play a role in filtering stimulation.

The perceptual release theory of West (1955, 1962, and 1975) considers the etiology of hallucinatory phenomena. He has proposed that the brain continually receives sensory stimuli from both external as well as from internal sources simultaneously (West, 1975). In normal functioning, the brain is capable of selective attention, which excludes from consciousness sensory input, which is either irrelevant or not necessary for adaptation. It has been pointed out by Aizenberg (1986) that the assumption upon which the theory is based is that "a sustained and varied level of sensory input is usually necessary to inhibit the emergence of percepts or memory traces within the brain itself. When levels of attention-commanding sensory stimuli decrease below a certain threshold, as might be the case in acquired hearing loss, previously recorded perceptions may be released into awareness through the disinhibition of the brain circuitry that represents them" (p. 310). The censorship mechanism (filter, switch) seems to need a constant flow of sensory impulses to operate effectively to inhibit earlier perceptions from emerging into consciousness.

Thus, Asaad (1986) hypothesized that: If the sensory input is disturbed or absent, as in the case of excessive affect during "functional" psychosis, faulty synaptic transmission during toxic states, or prolonged periods of sensory deprivation, then the censorship mechanism is impaired. Such impairment allows the emergence of earlier perceptions or "traces" into consciousness, which the individual re-experiences as hallucinations. Increased cortical arousal, induced by a diminution of sensory impact, is essential for this process to take place. (p. 1088) In this regard, West (1980) argued that conscious sensory scanning would be impaired by abnormally high or low levels of cortical arousal (regulated by the ascending reticular activating system). Therefore, West was able to draw parallels between hallucinations and the dream state while simultaneously hypothesizing those psychotic hallucinations might result from over-arousal systems (Bentall, 1990).

In conclusion, it is appreciated that visual hallucinations are more infrequent then auditory hallucinations with schizophrenia. The study of visual hallucinations does occur in many other neurological states, which warrants further scientific inquire. Examining only one of the possible etiologies that of sensory filtering offer a prospective towards our understanding of how the visual hallucinations seep into consciousness. More research into the visual productions of dreams is important and possible a workable hypothesis for understanding vivid visual hallucinations. Further research may take a path towards the memory association’s process with the occipital lobe visual cortex.

References