The Pathology Of Consciousness
Blindsight results from unilateral damage caused by stroke or by surgical intervention to area V1 in the striate cortex, where signals from the optic nerve reach the cortex, affecting one side of the brain – the condition is called hemianopia. The result is that the subject loses conscious vision on the side opposite to the damaged side (input from the left eye goes to V1 on the right side and vice versa), but retains a limited ability to describe objects placed in the blind field, when prompted. The subject will strenuously deny being able to see the object, yet is able to describe it. If V1 is only partly damaged, different types of visual function may be affected.
Lawrence Weiskrantz at Oxford University has been prominent in investigating blindsight. One subject he investigated (Weiskrantz, Warrington, Sanders and Marshall, 1974) was able to discriminate horizontal from vertical stripes on 30 out of 30 occasions although he could not see them. Says Velmans (1995):
In a classical set of studies Weiskrantz (1986) tracked a patient for ten years who had a small non-malignant tumour removed which involved the destruction of V1 on one side of the brain, leaving him blind on the opposite side. This subject showed a capacity to detect, to discriminate orientation, movement and form under a variety of conditions. The subject reported that rapid transient events, eg, rapid movement or sudden onset/offsets, produced a 'feeling' or 'knowing' that some event had occurred even though it was not 'seen'.
An even more remarkable example of blindsight was reported by De Gelder et al (2008). A patient with bilateral damage to the primary visual (striated) cortex causing clinical blindness over his whole visual field can successfully navigate down the extent of a long corridor in which various barriers were placed. A video recording shows him skillfully avoiding and turning around the blockages. This demonstrates that extra-striate pathways in humans can sustain sophisticated visuo-spatial skills in the absence of perceptual awareness, akin to what has been previously reported in monkeys.
Weiskrantz (1997) also described 'deaf hearing', 'blindsmell' and 'numbsense', the equivalents of blindsight for other sensory modalities, resulting from damage to A1, the auditory cortical gateway, and S1, the somatosensory gateway.
From a strictly neurological standpoint, the phenomenon of blindsight can be explained by the fact that not all of the nerve fibres leaving the eye go to V1 in the striate cortex. Weiskrantz has pointed out that at least ten 'minor' pathways have been found going from the eyes to the cortex in addition to the main route towards V1. About 85% of cells go via the lateral geniculate from the eye to V1; the other 15% go via the superior colliculus to various cortical and sub-cortical areas (Blackmore, Consciousness: An Introduction).
Morris, De Gelder, Weiskrantz and Dolan (2001) described a subject who can discriminate different facial expressions presented in her blind field; this ability was shown to depend on information in the minor pathway running through the superior colliculus and amygdala.
The relationship between damage to V1 and consciousness is not so simple, however. Two main paths project from V1 to further on parts of the visual processing system, known as the ventral and dorsal pathways, and if V1 is only partially destroyed, then loss of visual function depends in a complex way on the extent of damage. Milner and Goodale (1995) conclude that the ventral pathway supports (often conscious) cognitive representations of objects and events, and is phylogenetically more recent, while the dorsal pathway supports the (largely unconscious) control of motor responses, and is phylogenetically older. This would of course fit with Libet's (1996) results, showing a substantial delay before knowledge of motor behaviour reaches consciousness (self-awareness).
V1 is at an early stage of visual processing; if regions involved in the later stages of visual processing are damaged, visual consciousness is often retained, but there can be partial failures of perception called visual agnosia, in which, for instance, a subject might be able to read type-matter but cannot recognize objects visually – other senses may still allow recognition, however.
Baars (In the Theater of Consciousness) suggests that V1, apart from the detailed visual processing that it does, acts as a spatial co-ordinating map, 'binding' together the forty or so cortical areas which have been identified as playing a part in visual processing, and it would thus be the loss of that co-ordination that disables visual consciousness (awareness). However this may be, it doesn't seem surprising that the loss of V1 would disable later stages of visual processing, since they are deprived of data. On this subject, see also Posner and Raichle (Images of Mind).
The phenomenon of blindsight seems to weigh so heavily on notions of consciousness that it has been very thoroughly tested and verified in numerous studies, and has been used by many writers to support their theories of consciousness (see eg Block, 1997, and a reply from Dennett, 1997).
Something that seems to deny the partial identity of consciousness with the visual processing areas downstream of V1 is the phenomenon of sensory substitution, which has been used to restore a kind of vision to people who have lost their sight through disease, or even to congenitally blind people. The most often used modality for this is touch. Bach-y-Rita and Gonzales (2002) used the tongue, which has a particularly high density of tactile receptors, to act as a channel for signals from a high-resolution video camera. Subjects who learn with practice to 'see' in this way indeed describe the experience as 'seeing', which supports the idea that it is the co-ordinating role of the primary sensory processing areas (V1 etc) that is important to conscious seeing, but not the identity of consciousness with the activity of sensory processing areas as such.
Churchland (Brain-Wise – Studies In Neurophilosophy) sums up:
In the terminology used in this book, the 'visual consciousness' being spoken about by the various authors would be at the level of what has been termed responsiveness, rather than consciousness, which arises as a social phenomenon: of course 'seeing' is integrated into self-awareness when that came along, but there seems no good reason to suppose that animals with eyes and visual processing systems cannot 'see' as we do, in their various ways; they just don't 'know' that they are seeing. Blindsight should therefore be as capable as occurring in a shark or a squirrel as it is in a human. Blindsight, or at least neural behaviours that correspond to blindsight, appears to have been demonstrated in macaque monkeys (Yoshida, Takaura and Isa, 2008) but no work appears to have been done in relation to 'lower' animals.
The word agnosia is a generic term for a range of conditions in which sufferers lose (or never had) the ability to gain conscious recognition of objects, persons, sounds, shapes, or smells. Typically, the sensory equipment itself is undamaged; agnosia results from damage to specific brain areas in the occipital or parietal lobes of the brain caused by strokes, dementia, developmental problems, surgical intervention or other neurological disorders.
Usually, but not always, agnosia affects only one sensory modality, and it frequently happens that patients can substitute for the cognitive deficit by using other senses which remain intact. It also is sometimes the case that only the part of the particular sensory processing stream which is directed towards consciousness is disabled, so that unconscious knowledge of the missing data is actually still present and being used by other parts of the brain. Naturally, such phenomena are extremely interesting and valuable in terms of understanding the neural workings of consciousness (NCC), and in general militate against any concept of consciousness as an all-pervasive function of the brain. Instead, consciousness seems more and more to be built up on the foundation of a certain number of quite specific modules and processes in the brain.
There are many types of agnosia, including semantic agnosia (inability to recognize objects), anosognosia (denial of bodily problems), simultanagnosia (inability to combine the individual elements of a scene), prosopagnosia (inability to recognize faces), agnosia alexia (inability to recognize text), color agnosia (inability to recognize colours), auditory agnosia (inability to recognize speech), somatosensory agnosia (astereognosia, or inability to recognize objects by touch).
Some types of agnosia have been much more thoroughly studied than others; also there is considerable similarity in the techniques used to identify the neural pathways which are and are not damaged in agnosias, and the conclusions which may be drawn as regards the building blocks of consciousness. Two particular types only of agnosia will therefore be described here: anosognosia and prosopognosia.
Literally, 'not knowing'. In anosognosia, a patient is consciously unaware of and denies physical impairment. Often it arises in sufferers from a stroke that partially or wholly disables the right hemisphere of the brain, thus paralyzing the left-hand side of the body. This hemiplegia is accompanied by transitory or permanent anosognosia in 20-30% of cases. Alzheimer's patients often display a comparable syndrome.
There is a close connection between anosognosia and unilateral neglect, a condition in which brain injury to (usually) the right cerebral hemisphere results in visual or, less commonly, other types of neglect of the left-hand side of space. Stroke patients who have suffered damage to the right parietal lobe of the brain can behave as if the left side of sensory space is nonexistent. A neglect patient may shave or add make-up only to the non-neglected side of their face.
Anosognosia affects approximately 50% of individuals with schizophrenia and 40% of individuals with bipolar disorder. It often leads patients to avoid taking medication, since they don't believe themselves to need it.
In another similar case, a man
Says Baars: 'Such neurological cases are not rare. They show the desperate creativity with which humans maintain as much coherence and stability in their conscious experience as they can, even when the brain itself has gone awry.'
Although not all researchers would go along with Baars's account, there does seem to be general agreement that anosopognosia is not directly related to sensory loss, but is caused by damage to higher level neurocognitive processes which are involved in integrating sensory information with processes which support spatial or bodily representations (including the somatosensory system). Bisiach and Geminiani point out that any explanation has to account for the facts that anosopognosia is far more frequently associated with right-brain than with left-brain lesions, and that it can be temporarily ameliorated by vestibular stimulation (just something as simple as pouring ice-cold water into the ear – Cappa, Sterzi, Vallar and Bisiach, 1987).
Anosognosia is often associated with other neurological/neuropsychological disorders, but Berti (2000) asserts that denial of hemiplegia in right-brain-damaged patients cannot thus be explained away; rather it has to be considered a specific neuropsychological disorder that calls for a proper explanation. Reviewing the literature on the neural basis of anosognosia for hemiplegia, Pia, Neppi-Mòdona, Ricci and Berti (2004) showed that its occurrence is related to damage to the frontal and parietal lobes, and suggested that the condition could be conceived as a disorder of motor awareness. But Berti, Bottini et al (2005) showed that denial is related to lesions mainly involving regions devoted to motor control. Says Berti:
This is all one more proof that consciousness, or awareness as it should better be called, is a very partial participator in motor sequences. Consciousness informs the anosognosic that the limb is working based on its observation of just one stage or section of the whole motor process, which is very parsimonious of nature, but leads to wrong conclusions when much of the rest of the machinery of movement is disabled!
Stoney (2000) proposes that it was the requisitioning by language of left-brain motor processing capacity that has led to the possibility for anosognosia:
It is irresistibly tempting to associate the symptoms of anosognosia with Jaynes's theory of the bicameral man. With the right brain, specialized into a role of leadership and guidance, incapacitated, the left brain has desperately to make up a story as it goes along, and uses its linguistic facility to do just that. The fact that the left brain has stopped hearing 'voices' from the right brain doesn't alter its historical dependence on the right brain.
Usually known as 'face-blindness', prosopagnosia is characterized by inability to recognize the faces even of very close relatives, although sufferers are often able to use other clues such as voice or particular remembered characteristics in order to establish the identity of a person. In its standard form, known as 'apperceptive prosopagnosia', the condition is usually due to damage in the right cortical hemisphere to the fusiform gyrus and/or to the inferior occipital gyrus, both being parts of the visual processing system in the extrastriate cortex (Hadjikhani and de Gelder, 2002, and Damasio, Damasio and Van Hoesen, 1982). Other types of prosopagnosia also exist, associated with other types of cortical damage; and congenital prosopagnosia has been described. In associative prosopagnosia, sufferers can recognize faces, but cannot associate them with semantic data such as the name of the owner of the face. Up to 10% of the population may suffer from mild forms of prosopagnosia (Duchaine and Nakayama, 2006).
Prosopagnosia is similar to blindsight in that sufferers appear to recognize faces at an unconscious level (known as 'covert recognition'), as demonstrated by experiments involving fMRI which show neural activity in prosopagnosics in brain areas known to be implicated in the face recognition process, and also by galvanic skin response tests in which prosopagnosics manifest changes in skin response which match those of normal people, albeit more weakly, when meeting people they recognize (see Barton, Cherkasova and O'Connor, 2001, Tranel and Damasio, 1985 and Hardcastle, Locating Consciousness).
Theories of neural processing to account for prosopagnosia are not as well developed as they are for blindsight, which has received much more attention. Nonetheless, Bauer (1984) described an approach based on differential functioning of the ventral and dorsal pathways projecting from V1 (see Milner and Goodale, ibid): the ventral pathway is damaged, and prevents conscious face recognition; but the dorsal pathway is undamaged and continues to mediate affective responses to recognized faces. De Haan, Bauer and Greve (1992) put forward a more worked-out version of this theory involving a somewhat different structure of pathways.
At any rate, the conclusion for prosopagnosia is the same as it is for blindsight, that consciousness is built upon the cognitive state of certain modules and processes in the brain, and not others. And as with blindsight, it is necessary to point out that in the terminology used in this book, the 'consciousness' being spoken about by the various authors would be at the level of what has been termed responsiveness, rather than consciousness, which arises as a social phenomenon. There is no reason to suppose that prosopagnosia would not arise in animals capable of face recognition if they suffer comparable lesions to human prosopagnosics, but this is even less testable in animals than blindsight. Face recognition certainly exists in primates, and has recently been demonstrated in horses (Proops, McComb and Reby, 2008) but not much work seems to have been done on the neural basis of recognition in animals such as dogs and cats, which can clearly recognize human individuals known to them, but may or may not use comparable neural techniques to do so.
Split-brain people are those who have undergone total or partial commissurotomy, ie the surgical separation of the two hemispheres of the brain, by cutting of the corpus callosum and its associated commissures (bridges of nerve tissue) which join the hemispheres, usually as a last resort in cases of epilepsy or schizophrenia. Many of these individuals, who have often appeared to benefit from the surgical procedure, have been studied. Wallace and Fisher (1999) contains a thorough analysis of research on split-brain subjects.
Sperry (1966) studied 24 patients whose epilepsy had been cured or much improved by partial commissurotomies (the anterior, hippocampal, habenular and posterior commissures were left intact). The operation appeared to leave the patients' personality, intelligence and general behaviour unaffected, although Sperry found some behavioural differences on closer investigation, for instance a strong tendency to favour the right side of the body (controlled of course by the left hemisphere); the left hemisphere showed superiority in verbal and mathematical tasks; the right hemisphere showed superiority in spatial tasks. Both hemispheres seemed equally capable of generating affective reactions.
Gazzaniga (1995) gives an example of left-brain/right-brain divergence in a split-brain subject:
Although Gazzaniga has demonstrated that the right hemisphere of the normal brain is normally non-linguistic, Le Doux, Wilson and Gazzaniga (1977) reported that in one subject, who had suffered damage to the left hemisphere in youth, the right hemisphere had taken over many linguistic functions and was able to reply linguistically to questions as well or better than the left hemisphere. The two hemispheres sometimes agreed, and sometimes not, and the patient appeared to be in a better mood when they agreed. Asked about President Nixon after Watergate, the right hemisphere expressed 'dislike' while the left hemisphere expressed 'like'.
There have been studies of dreaming in split-brain subjects: initially, it was reported that subjects with damage to the right hemisphere did not dream, and it was supposed that split-brain subjects probably did not dream (Humphrey and Zangwill, 1951) but Greenwood, Wilson and Gazzaniga (1977), by monitoring REM activity and awakening subjects immediately after it was displayed, found that split-brain subjects do indeed dream. Hoppe (1977) analyzed the content of dreams of split-brain patients, finding that they reported fewer dreams than normal, and that the content of the dreams was comparatively utilitarian and unimaginative, leading him to suppose that the lack of communication with the right hemisphere accounted for the poverty of the dream material.
Wegner (The Illusion of Conscious Will) reviews the evidence against the primacy of conscious intention presented by split-brain studies, concluding that the conscious left brain narrator interprets behaviour in normal adults rather than originating it. He quotes Gazzaniga (1988), who explains how the left-brain narrator compiles and presents a coherent story to self-awareness for use by the social agent:
MacLennan (1996) notes that in split-brain subjects each hemisphere is unconscious of what the other is experiencing, but that commissurotomies do not completely separate the hemispheres; at the very least the brain-stem is left intact. He quotes Gregory (1987), who observed that in split-brain patients the the right hemisphere forms a kind of unconscious mind for the left. Of course, the right hemisphere is as conscious as the left, and has ways of manifesting its consciousness, says Gregory; but its experience is not part of the left hemisphere's experience (or vice versa). One hemisphere may communicate with the other through transactions with the external world, for example, twitching the skin on one side of the face so that it can be felt on the other. (The patient is unconscious of doing this.) Split-brain patients experience these communications as inexplicable 'hunches', just like those from the unconscious.
Baars (1996) notes that:
Apart from confirming the detachment of consciousness (self-awareness) from much of the workings of the brain, and thus supporting the idea that consciousness exists as an outward-pointing social agent, to which consistency and continuity matter more than veracity, all this evidence raises – as discussed in the Note on Terminology – serious questions about the unsatisfactory nature of the word 'consciousness'. Writers speak of there being 'consciousness' in both hemispheres, and they can perhaps hardly do otherwise when the right brain behaves as sentiently – in its own terms – as does the left brain. Yet it cannot report its self-awareness, which according to Nagel (What Is It Like To Be A Bat?) is the defining hallmark of consciousness. Or perhaps it can, as in the case of Le Doux's split-brain subject who had acquired linguistic skill in the right hemisphere. So the reportability test breaks down, it would seem. The right brain is self-aware, but cannot communicate – is this what it is like to be a bat?
In this syndrome, one of the sufferer's hands acts autonomously and 'wilfully' without any sense of control on the owner's part; indeed the owner may even not know about the errant hand's behaviour until it is pointed out (Wegner, The Illusion of Conscious Will). Very often it is the left hand that behaves in this way, under the control of the right brain, evidently.
Banks et al (1989) report a patient whose ' left hand would tenaciously grope for and grasp any nearby object, pick and pull at her clothes, and even grasp her throat during sleep'. Banks also described another patient:
There are different types of alien hand syndrome (Scepkowski and Cronin-Golomb, 2003; Biran and Chatterjee, 2004). The classical variety, famously imitated by Peter Sellers as Dr Strangelove (but using the wrong hand, it would seem) is often due to damage in the medial motor frontal region on the side of the brain opposite the affected hand (Gasquoine 1993). The neural mechanisms lying behind the behaviour are quite complex (Goldberg, 2000). Utilization Behaviour, first described by French neurologist François L'hermitte (Cambier, 1999), in which the sufferer compulsively grabs and uses objects in their immediate environment, is most often associated with extensive bilateral frontal lobe damage.
In its most severe form it is called Environmental Dependency Syndrome. 'Posterior' alien hand syndrome involves 'pulling away' by the affected hand rather than reaching and grasping, and is associated with damage to the parietal lobe and/or occipital lobe of the brain.
Evidently alien hand syndrome results from a dysfunction in the complex interaction between causative (intentional) motor systems and matching inhibitory systems, sometimes aggravated by a failure in hemispherical communication. Sumner and Husain (2008) propose that the conventional distinction between the supposedly separate brain processes mediating voluntary conscious acts and automatic behavior may be undermined by the alien hand evidence among other disruptions of normal behaviour caused by brain lesions. They argue that: 'automatic motor activation forms an intrinsic part of all behavior, rather than being categorically different from voluntary actions. A crucial issue is how such automatic mechanisms are controlled so that the most appropriate responses are made and unwanted responses inhibited.' The authors discuss some of the brain areas involved, including the supplementary motor area and the parietal cortex and review evidence that some control may actually be achieved by automatically triggered inhibition as well as modulation of unconscious processes by attention and task goals.
What all types of alien hand syndrome have in common is that they involve perfectly co-ordinated and purposeful movements; but these are outside the volitional control and consciousness of the sufferers. As with blind-sight and the various agnosias, alien hand syndrome underlines the isolation, if that is not too strong a word, of consciousness (self-awareness) from the intentional and motor process in the brain. Patients are often so frustrated and disoriented by their experiences that they ascribe the behaviour of their hand to outside agency.
The word aphasia covers a variety of conditions in which sufferers experience linguistic disabilities, being variously unable to speak, unable to write, unable to comprehend language, unable to sing, etc. The causative factors often include injury to the brain areas specialized for language, such as Broca's area, which governs language production, or Wernicke's area, which governs the interpretation of language, as a result of stroke, neurological disease or remedial surgery. Except in rare individuals, these areas are in the left hemisphere of the brain. See Saffran (Aphasia and the Relationship of Language and Brain). However, Lieberman (2003) sums up evidence that cortical damage on its own is insufficient to produce long-lasting aphasias, and that sub-cortical damage, often to the basal ganglia, is invariably involved.
The focus of these notes will be on global aphasia, whose sufferers have very limited or no ability to speak or comprehend language. Their only means of communication may be via facial expressions, gestures and body language. Damasio (The Feeling of What Happens) says that however severe the symptoms of an aphasic, their thought processes and consciousness remain intact. He accounts for this by asserting that the language facility was added to the human brain at a time when it had already acquired a sense of self and the other accoutrements of a social agent.
To the extent that the brain lesions causing global aphasia are strictly limited to language-production areas, it can perhaps be assumed that global aphasics might yet be able to communicate with gestures, drawings, symbols and facial expressions, and the more this is the case, the more such evidence would support Damasio's observation that global aphasics are normal apart from their linguistic deficit. It's a problem obviously that no two cases are the same in terms of brain lesions, so that studies based on larger numbers of subjects are unlikely to yield worthwhile results. Having said that, there are a good number of reports involving one or a few global aphasics which do tend to support Damasio's position.
One distinction that might be highly relevant is between concepts or objects or feelings that can be represented non-verbally (which might be assumed to have been around before language came along) and those concepts for which no adequate non-verbal representation could be thought to exist – such as philosophical terms like the word metaphysics. It could be that the brain handles these two classes of concept in different ways and for that matter in different locations. Thus the study of communication in global aphasics might yield valuable insights into the ways in which the brain handles verbal and non-verbal concepts. There are many such studies; but two will be enough to indicate both the reality of non-verbal communication in global aphasics and the methodological difficulties that beset any attempt to draw firm conclusions. And there seem to have been few studies of the differences between aphasics' ability to handle verbally representable and verbally non-representable concepts.
Helm-Estabrooks, Fitzpatrick and Barresi (1982) worked with eight globally aphasic patients who had not responded to traditional treatment, using Visual Action Therapy (VAT), a nonvocal approach which ultimately trains patients to produce symbolic gestures for visually absent stimuli. Statistical analyses of pre and post VAT scores earned on the Porch Index of Communicative Ability (PICA) showed highly significant improvement on those subtests which measure pantomimic and auditory comprehension skills.
Naeser et al (1998) established that it was possible to predict success with treatment of chronic, severe aphasics with a nonverbal, icon-based computer-assisted visual communication (C-ViC) program based on the particular lesions suffered in individual cases. Out of seventeen patients with stroke and severe aphasia who began treatment with C-ViC from 3 months to 10 years after onset of stroke, the research was successful in predicting a more or less successful outcome for a majority of the subjects, and also accurately identified most of those subjects who would not benefit from treatment. 'Success' was defined in terms of level of ability to communicate using C-ViC on a personal computer, and about half of the cohort were judged to be successful on that basis.
The difficulties in filletting out conclusions about the brain's non-linguistic semantic capabilities from the complex and inevitably incomplete data of such studies are extreme. But if even one global aphasic is able to communicate semantically with a reasonable degree of accuracy then it at least appears established that language is an 'add-on' to a pre-existing, or anyway parallel non-verbal communication channel.
Symptoms thought particularly indicative of schizophrenia, as listed by Kurt Schneider (1887–1967), include the delusion of being controlled by an external force, the belief that an external agency is inserting or withdrawing thoughts from the mind, the belief that thoughts are being broadcast to other people, and the hearing of hallucinatory voices.
Naudin et al (1999) quote a patient, JP:
Jaynes (1990) says schizophrenia is a relapse into the bicameral mind, the state of the human psyche before the self-aware 'I' with its narrative 'remembered present' arose in the left hemisphere. Jaynes's theories, which are controversial more in terms of their historical timing than their substantive content, have been mentioned often enough earlier in the book; here the focus is on the similarity of the human psyche with a schizophrenic state prior to the emergence of the self-aware 'I'. Jaynes points out that insanity is not mentioned in the Iliad, written late in the second millennium BC, whereas by 400 BC when the bicameral mind had already broken down, a young Plato in Phaedrus (244A) describes insanity as 'a divine gift, and the source of the chiefest blessings granted to men'. Later in life Plato began to see insanity as something less desirable (Theaetetus, 158), and in his Laws (934) says that mad people should be kept at home.
The symptoms of florid, unmedicated schizophrenia include hallucinations (absent only in exceptional cases) which are predominantly voices, persecuting, helping, advising, criticizing or threatening, the deterioration of consciousness (self-awareness), the loss of the analog 'I' (the model of the self of which we are aware) and the accompanying inability to narratize.
Jaynes says that auditory hallucinations are strongly influenced by collective cognitive imperatives associated with the patient's total social environment. Weingaertner (1971) reported research in which three groups of hallucinating schizophrenics were given different instructions regarding aversion therapy – one group had boxes which gave them self-administered shocks when hallucinations began, one group had similar boxes but which did not administer shocks, and a third group did not have boxes at all. All groups were led to expect that the frequency of hallucinations would diminish, and indeed it did, and contrary to expectations it diminished by the same amount in each of the three groups. Jaynes also points out the importance of childhood training; in societies where there is a strong emphasis on guidance by God, subsequently-developing schizophrenics tend to hear commands from God by preference (Weinstein, 1962).
Schizophrenics often say that their voices seem to have access to more memories and knowledge than they do themselves, and complain that their voices anticipate their thoughts; as they read, the voices read in advance to them (Storring, 1907). This is technically known as Gedankenlautwerden, and Jaynes says it is close to how the bicameral mind would have operated.
Jaynes hypothesizes that schizophrenic hallucinatory behaviour is caused by the assertion of right-brain dominance in combination with impaired left-brain function and has anatomical evidence to support this. For instance, Flor-Henry (1969) reported that when temporal lobe epilepsy is caused by a lesion on the left temporal lobe, 90% of patients develop paranoid schizophrenia with massive auditory hallucinations, whereas when the lesion is on the right temporal lobe alone, fewer than 10% develop such symptoms.
The loss of the analog 'I' (the 'remembered present') is one of the most frequently described and awful of the symptoms of schizophrenia. Here is one such description, quoted by Jaynes, from Meyer and Covi (1960):
This can be expressed in Jaynes's words as a failure of narratization: 'with the erosion of the analog 'I' and its mind-space, narratization becomes impossible . . . behaviour is either responding to hallucinated directions, or continues on by habit. The remnant of the self feels like a commanded automaton, as if someone were moving the body about.' The failure of narratization goes along with a diminished or absent sense of time.
A very significant deficit that is frequently displayed by schizophrenics is an inability to pretend, to make believe or to imagine 'what if' scenarios, something that results from the loss of the analog 'I', to continue using Jaynes's term. Or at least, that ability is lost consciously, obviously undermining the ability of the social agent to interact with other individuals in a normal way. It doesn't follow that the unconscious mind has become incapable of imagining 'not now' scenarios.
Another view of the connection of language with schizophrenia, not necessarily conflicting with Jaynes's position, comes from Crow (1997, 2000) who argues that schizophrenia may be the result of left brain specialization for language, which has caused potential instability in the hemispherical balance, so that when the left brain fails to perform the complex tasks demanded of it, the right brain takes over and starts delivering the hallucinations typical of schizophrenia. Jaynes would have said that this was exactly the outcome intended by social evolution, to misuse the term slightly.
Schizophrenia is a complex disease, with no commonly agreed set of neurological causes. Edelman (The Remembered Present) offers a possibility in line with his Theory of Neuronal Group Selection – he doesn't put it any more strongly – that it could be a disease of re-entry (re-entry being the very marked tendency of the human brain to use recursive feedback loops). Edelman suggests that malfunctions at the synaptic level could lead to:
Indeed, the onrush of unfiltered sensory impression which is often described by schizophrenics could easily result from failure of mapping and categorization systems which are then bypassed by the sensory data.
Greenfield (The Private Life of the Brain) is one of many writers who have surveyed the possible role of neurotransmitter imbalances in schizophrenic brains, and particularly the association with dopamine (Strange, 1992). While admitting the probable role of dopamine in schizophrenia, Greenfield says it is more likely that:
Greenfield notes that dopamine is distributed mostly to the inner regions below the outer layer of cortex, but also reaches the prefrontal cortex, which she thinks may therefore play an important role in schizophrenia. Indeed the prefrontal cortex is particularly associated with working memory, and fMRI scans have shown that while schizophrenics are engaged in tasks which make demands on working memory, the pre-frontal cortex shows less activity than there is in the brains of non-schizophrenics (Weinberger and Berman, 1998). Greenfield goes on to note the similarity between dream states and schizophrenia, although dopamine levels are reported to be low during dreaming, the opposite of the situation with schizophrenia (Hobson, 1994). But Penfield and Perot (1963) succeeded in provoking 'dream-like' experiences by stimulating the temporal cortex; Greenfield's hypothesis would therefore be that reduced function in the prefrontal cortex would affect the sense of time, the construction of narrative memory (the autobiographical self) and therefore the analog 'I', reducing individual experience to a dream-like level, comparable to the situation that obtained before self-awareness developed (bicameral man, adds Jaynes from the sidelines), and also comparable to the experience of depersonalization experienced by schizophrenics.
Frith and Done (1989) compared the short-term memory skill of schizophrenics suffering from 'alien control' (the belief that their actions are controlled by an external agency) with that of other patients. The subjects played a video game, using a joy stick to shoot birds which might come from the left or the right; they had 2.8 seconds to correct an incorrect bullet. When the subjects could see the trajectory of the bullet for the full 2.8 seconds, there was no difference in the performance of the two groups; when the first two seconds of the trajectory were covered up, the 'alien control' group performed significantly worse than the control group.
The picture that emerges from this and much other evidence is that the central problem of schizophrenics is the loss of the autobiographical or narrative self, for which full operation of the prefrontal cortex appears necessary, and that this may be caused by chemical imbalances. Consciousness (self-awareness) doesn't reside in any one particular place, of course, but the prefrontal cortex seems to be a good candidate for one of its main loci. This is where the social agent has her roots.
While not resulting from brain lesions, these aberrant mental states offer some useful lessons to aid an understanding of consciousness.
Hypnosis is too well known as a phenomenon to require description; but it is interesting to note that it was first described only in the 18th century when Mesmer conducted his famous experiments. Like some other 'non-standard' states of the human mind, the mere fact of hypnosis raises some questions about consciousness and its relationship to the normal functioning of the brain.
Hysteria, unlike hypnosis, has a long history, having been first described by the ancient Greeks, but is now tending towards extinction as a useful scientific designation, becoming parcelled up into various more specific states or diseases. Anyway, it may still be said to mean a state of uncontrollable emotional excess, often of fear. Psychiatrists distinguish dissociative hysteria (involving loss of consciousness) from somatoform hysteria (in which consciousness is retained).
Multiple Personality Disorder, often nowadays called Dissociative Identity Disorder (DID), was put on a sound footing by Putnam (1984). There are many famous cases of DID, not least the fictional Dr Jekyll and Mr Hyde, but Christine Beauchamp may stand for them all (Prince, 1906). Christine may have been abused as a child, and arrived for treatment complaining of various physical and nervous ailments, which today might be called psychosomatic. During treatment a series of alter personalities emerged, including 'Sally', who was childish, selfish and naughty, unlike Christine, who was an upright, religious and controlled person. Sally delighted in putting Christine in difficult situations, shocking her friends, and making her smoke cigarettes, which she hated. Sally was the only one of Christine's personalities which claimed to know all of the others, and also to be fully conscious even while Christine or other personalities were in control. Prince was eventually successful in reintegrating Christine's various personalities.
DID sufferers often have ten or more separated personalities, which may or may not have knowledge of each other, or communication between themselves. Childhood abuse is sometimes said to be at the root of many cases of DID; Putnam and Spiegel (1988) speculate that abused children take refuge in a dissociated state of mind which develops over time into a differentiated self.
Many instances of supposed DID are supposed to have been faked either by the subject (often a suggestible young woman) or by the almost invariably male psychiatrist, and it was not until Putnam's work, which demonstrated a uniform set of characteristics over a large number of cases, that the condition was again given mainstream consideration. Many commentators still regard DID as a figment of the imagination at one level or another. There appears to be no convincing evidence to date of differential neural processing to go with the various personalities on offer.
James (The Principles of Psychology) was only one of many writers who reflected on consciousness in the light of hypnotism, pondering:
James is happy enough to suppose that during hypnosis there is a parallel, conscious self:
Hilgard (1977, 1987) was prominent in research into the cognitive state of hypnotized subjects:
Hypnotism is frequently used (perhaps less often now than before the arrival of chemical anaesthetics) to control pain. Hilgard and Hilgard (1994) consider that pain is felt at two levels of consciousness: a hypnotized subject will report the absence of pain in speech, but if asked to write down an answer to the same question will report the experience of pain. Sarbin and Coe, 1972, however, explain the effectiveness of hypnosis against pain with reference to the social context. This theory suggests that 'hypnotized subjects behave as they do because they are striving to enact the role of a hypnotized subject as it is defined by the hypnotist and society in general.' There is a possible link between this explanation and the phenomenon of self-deception, which has been fully described in the bulk of the book.
Gur and Gur (1974) argued that hypnotizability is correlated to right-brain processing. This conclusion was reached from a body of evidence that has indicated, for example, that hypnotizable subjects are more likely than low-susceptibility subjects to show reflective eye movements to the left. MacLeod-Morgan and Lack 1982 reported an apparent shift in cortical activation, as measured by alpha EEG activity, from the left to the right hemisphere when individuals are hypnotized.
Barber, 1969, suggested that hypnosis does not require a trance as such, but that it is sufficient for a subject to believe in her own suggestibility, in effect. Is there a difference? Maybe that just means a voluntary switch to right-brain processing?
Wegner (ibid) emphasizes the absence of will in the experience of hypnotism:
Wegner reports studies on the brain state of hypnotized subjects which revealed states different both from those of the waking self and from those of sleep. In one such study (Szechtman et al, 1998) PET scans were used to compare brain states when subjects were actually hearing a line, imagining that they were hearing it, or believing while hypnotized that they were hearing it (a hallucination, in other words). The PET scan showed that the right anterior cingulate cortex was active both when the subjects actually heard the line and when they hallucinated hearing it – but not when they imagined hearing it. For Wegner, such evidence tends to contradict 'faking' theories such as that of Sarbin and Coe and the socially-induced behavioural approach posited by Barber (supra).
Studies of brain activity during hysterical episodes using functional imaging techniques have detected reduced activity in frontal and sub-cortical circuits involved in motor control during hysterical paralysis, in somato-sensory cortices during hysterical anaesthesia, and in the visual cortex during hysterical blindness, along with increased activity in some limbic regions, such as the cingulate or orbito-frontal cortex, which may point to a role for affective and stress factors in hysteria (Vuilleumier, 2005). Vuilleumier also points out that hysterical paralysis is much more frequently encountered on the left side of the body (right-hemisphere involvement) than on the right side.
Wegner ends up by accepting a social backdrop for hypnotism: 'the way in which groups and cultures move along, changing their expectations of each other and themselves, produces an odd situation we might call the 'suggested society'. People become what they think they are, or what they find that others think they are, in a process of negotiation that snowballs constantly.'
Many types of hysteria are also thought to have social origins (Schapira, The Cassandra Complex), and there is certainly very often a degree of suggestibility in hysterics. James (ibid) describes hysterical anaesthesias, in which sensibility of the affected parts is retained in the form of a 'secondary consciousness', as is the case with hypnotic insensibility to pain, and he too allows a social element in many hysterias. Needless to say, mass hysteria owes much to human groupishness.
Miller, Galanter and Pribram (Plans and the Structure of Behaviour) note that much of our mental planning takes the form of talking to ourselves, out loud or silently, and compare this to the experience of the hypnotized person, who 'is not really doing anything different, with this exception: the voice he listens to for his plan is not his own, but the hypnotist's. The subject gives up his inner speech to the hypnotist.'
Cue Jaynes (ibid), who has been listening to this discussion with increasing impatience. For Jaynes, hypnosis, which can cause or enable fantastical behaviour on the part of subjects, is a clinching demonstration, if one was required, that consciousness (self-awareness) is a kind of decorative icing on the cake of the bicameral man:
Jaynes charts changes in the nature of hypnosis during the period since it was 'invented'. With Mesmer, subjects twisted and convulsed; within a few decades they began to speak and reply to questions during hypnosis; early in the 19th century they began to forget what had passed during the trance (Chastenet, 1809); then phrenology became merged with hypnosis, and finally at the end of the century hypnosis developed three states – catalepsy, lethargy and somnambulism (Binet and Frere, Le Magnetisme Animale). Jaynes gives modern examples of the tendency of hypnotic subjects to behave as they have been told they will behave, especially in group situations; he calls this the 'collective conscious imperative', and it clearly has its roots in the groupishness of human nature as explained in this book.
In the hypnotic trance, Jaynes points out, narratization by the analog 'I' is more or less brought to a halt; the subject does not introspect, and is not constantly monitoring himself as in the normal conscious state (see Hilgard, supra). The lack of narratization in the hypnotic subject goes along, as might be expected, with absence of a sense of time.
Apart from assimilating the phenomena of hypnosis to the nature of his 'bicameral man' (and he did not have the benefit of Szechtman's observations on cognitive laterality during hypnosis, which would have further strengthened his platform), Jaynes concludes:
And on the relationship of hypnosis to group imperatives, Jaynes's language is just too delicious not to be quoted:
As usual, it is necessary to qualify the use of the word 'consciousness' by Jaynes. His 'culturally learned' consciousness is the self-awareness of the social agent, and his ideas are perfectly consistent with the gradual building-up of responsiveness and awareness that has been charted in this book, as long as they are not called consciousness!
The state of brain activity during dreaming has been shown to be not dissimilar to that in a waking, conscious brain, although the dreamer is not normally self-aware of being in a dream state.
Vaas (1999) describes some of the neural correlates of different aspects of the dream state, as compared with a normal, waking state:
Vaas hypothesizes that dreaming is therefore a result of a functionally isolated loop between the extrastriate cortices and the (para)limbic system including the amygdala, largely disconnected from sensory input and motor output due to inhibition of the striatum and frontal cortex respectively, a chaotic autoactivation process within the extrastriate cortices and the (para)limbic system, triggered by an increased input from the brainstem and the basal forebrain, and the absence of top-down control because of an inhibited frontal cortex.
These results are based on PET scanning during REM periods, so it cannot be denied that these neural events take place; the problem is that the subject who then reports the dream activity does so with her conscious mind, and we all know how much confabulation, obfuscation, distortion and general misrepresentation that can involve. There are plenty of stories about dreamers who awake in response to an external noise which is perfectly synchronized with an event in their dream; but this may just be tacked on by consciousness as it 'wakes up' and reports the dream that had taken place while it was 'off duty'.
The phenomenon known as 'lucid dreaming', in which the dreamer experiences self-awareness during the dream, and can control its course, may help to explain what is going on. LaBerge et al (1981) proved that lucid dreaming coincided with periods of REM sleep, and that the onset of lucid dreaming as indicated by signals given by the dreamer could be matched to changes in 'polysomnograms' recorded during the REM period. In later research, LaBerge (1990) asked subjects to respond to a tone while dreaming by moving their eyes around, voluntarily suspending breathing or moving a finger – all of these turned out to be possible. Baars (ibid) points out that this requires skepticism, itself a product of self-awareness, and which is an aspect of meta-cognition (LaBerge and Kahan, 1994).
That is all very well, but again it is possible to explain the lucid dreaming as a result of the waking-up of consciousness at the moment of the onset of lucid dreaming or the external stimulus.
Erlacher and Schred (2008) assessed the literature on REM dreaming, showing very substantial similarity between the neural substrates of dreamed and executed actions, ie that dreamed action is equivalent to real action as far as the underlying brain mechanisms are concerned:
Erlacher and Schred look forward to the results of neuro-imaging studies of lucid dreaming – but these have yet to take place because of the mechanical difficulties associated with such testing.
The jury is still out, therefore, on whether the lucid dreamer is fully conscious and self-aware, or whether some kind of limited version of self-aware consciousness is involved.
It is not particularly surprising that self-awareness (generated within the frontal cortex?) should be switched off during dreaming – there is no need for the social agent to be 'on duty' during sleep, since social interaction doesn't take place, so that the sensory input needed to fuel the ongoing analog 'I' is not being received. Dreamers' interactions with other people would in that case have to be constructed from memory rather than being informed by the autobiographical self, which seems reasonable. One then wants to ask whether lucid dreamers can influence social interactions, and if the answer is yes, then one would want to know (and one would expect) that the frontal cortex is behaving as if the dreamer is awake and fully conscious.
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