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Reprinted from Neuropsychiatry, Neuropsychology,
Clinical Neuroscience, 3rd Edition
(Academic Press),

By Rhawn Joseph, Ph.D.

CHAPTER 3

BLIND SIGHT & DISCONNECTION SYNDROMES
by Rhawn Joseph, Ph.D.

Blind Sight & Disconnection Syndromes:

BLINDSIGHT

Following damage to the primary visual neocortex patients will become "blind" (cortically blind) and will be unable to see, name or describe complex visual stimuli, though they may perceive motion or gradations in lighting (Holmes, 1918; Scharli, Harman & Hogben, 1999; Weiskrantz, 1986, 1996). Although blind, these patients may avoid obstacles, and correctly retrieve desired objects, and thus appear to have some residual visual functions even though they verbally claim no conscious awareness of the visual stimulus and thus have no verbal awareness that they can see (Poppel, Held & Frost, 1973). Nevertheless, although the verbal aspects of consciousness have been disconnected from the visual cortex and claims it cannot see, the patient continues to behave as if visual input is still being received; hence the term "blind sight."

Specifically, those who are "cortically" blind but demonstrate "blind sight" accomplish these acts apparently because undamaged midbrain, thalamic, and neocortical tissues (e.g. temporal/parietal lobe) involved in visual functioning continue to function normally (Milner & Goodale, 1995; Stoerig, 1996; Ziki, 1997), although completely dissociated from the "dominant" stream of verbal consciousness mediated by the left hemisphere.

For example, although "cortically blind" the eyes are functional, and visual impressions are transmitted via the optic nerve directly to the midbrain visual colliculus, and via the optic tracts and optic radiations to the lateral geniculate nucleus of the thalamus and other forebrain structures including the visual areas in the temporal and parietal lobe (Milner & Goodale, 1995; Stoerig, 1996). In some cases, this residual visual input may be transmitted to those islands of striate cortex which remain intact (Wessinger et al., 1997). However, in other cases, there is no evidence for functional activity in the primary visual receiving areas as residual vision appears to be due to the preservation of a visual area located in the temporal occipital border and which responds to visual motion (Barbou, et al., 1993; Zeki, 1997); and/or the midbrain visual colliculus (see chapter 17).

Nevertheless, in cases of "blindi sight" these intact areas are unable to communicate with the language areas of the brain, which, in failing to receive visual signals, claims to have no knowledge of the visual world, other than "non-visual feelings" (Scharli, et al., 1999). However, although disconnected form the language axis, which reports only "non-visual feelings" these isolated visual areas may continue to mediate behavior, perhaps via connections with the midbrain--a structure which responds to visual motion, and which can direct head and orienting movements (Blessing, 1997, Klemm & Vertes, 1990)

Consider, for example, the classic cases of blindsight first described by Riddoch (1917). According to Riddoch (1917) although these patients had suffered extensive destruction of the primary visual areas, they remained "conscious of something moving when the object oscillate... and that.... the consciousness of something moving kept up a continual desire to turn the head."

The fact that these and other patients with blind sight may have a feeling of seeing movement (Scharli et al., 1999; Zeki, 1997), are/or experience a desire to turn the head (Riddoch, 1917), and/or correctly reach out and grasp or move around objects, directly implicates the midbrain visual colliculus as this structure is able to detect movement and different gradations of light and shadow (Davidson & Bender, 1991), and (via the lower brainstem) can direct head turning, groping and grasping, and even walking (Blessing, 1997; Klemm & Vertes, 1990).

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For example, because the midbrain visual colliculus is able to detect movement and different gradations of light and shadow (Davidson & Bender, 1991), and (via the lower brainstem) can direct head turning, groping and grasping, and even walking (Blessing, 1997; Joseph, 1999c; Klemm & Vertes, 1990), this may explain why patients with blindsight can still motorically respond to visual stimuli. Indeed, one does not need language or a neocortex in order to perform complex movements, which is why creatures such as reptiles, frogs, etc., are capable of complex visually guided behaviors even though they never evolved language or neocortex.

Humans, however, have evolved neocortex, and the primary visual receiving areas hierarchically analyze these subcortical visual signals which are then transferred to the adjoining visual association areas thereby forming complex visual associations (Kaas & Krubitzer, 1991; Milner & Goodale, 1995; Sereno, Dale, & Reppas, 1995). These complex associations are then transmitted to the language axis which then names and verbally describes what the individual sees (Critchley, 1964; Geschwind, 1965; Joseph, 1982). These visual impressions come to be associated with language and thus with linguistic consciousness. However, with massive injuries to the primary visual cortex, the language axis no longer receives visual input, and the patient reports that he or she is blind and cannot see, though they avoid obstacles and can reach for desired objects and or report non-visual "feelings."

Thus patients with "blind sight" demonstrate at least two disconnected streams of mental activity, one of which utilizes language to deny visual experience other than through the experience of "feelings", and a second non-verbal form of subcortical or isolated neocortical mental activity that is capable of seeing and/or controlling movements of the body in response to certain visual stimuli. Moreover, these multiple modes of conscious-awareness, including those supporting blindsight may wax and wane, "resulting in blindsight in some test sessions and in conscious awareness of the same stimuli in others... which raises the interesting question of whether the brain switches from one neural system to another during the waxing and waning of consciousness (Zeki, 1997, p. 175).

DENIAL OF BLINDNESS

In contrast to those who display blindsight, in some cases immediately following massive injury to the visual neocortex and the surrounding visual association areas, although cortically blind, patients may initially deny blindness (Redlich & Dorsey, 1945; Joseph, 1986a) --a condition referred to as Anton's syndrome. For example, a number of patients described by Redlich and Dorsey (1945), refused to acknowledge blindness, even when they bumped into furniture, tripped and fell to the floor, and were unable to describe or name objects shown to them. Rather, when told of their disability by doctors and family, they instead invented elaborate excuses for their errors; e.g. claiming that it is a little dark and they need their glasses, or conversely, that they see better at home. That is, these patients confabulate due to disconnection of the language axis and its propensity to fill the gaps in the information received with related ideations (Joseph, 1982, 1986a, 1988a,b).

Specifically, because all visual cortices including the association areas have been destroyed, the language axis is completely disconnected and receives absolutely no information regarding the visual status of the brain and cannot be informed that it no longer sees (Critchley, 1964; Geschwind, 1965). The intact (non-visual) portion of the brain does not know it is blind (due to the destruction of all neocortical visual areas), just as the brain of a creature that never evolved sight does not know that it cannot see--a condition also referred to agnosagnosia (not knowing that they do not know). Instead, the language area fills the gaps and discrepancies in the information available by confabulating an explanation as to why they cannot see, i.e. "I see better at home." By contrast, those who admit to blindness receive signals form the still intact visual association areas which inform the language axis that no visual signals are being received from the damaged primary visual cortex.

BLIND SIGHT & DISCONNECTION SYNDROMES

The brain is organized such that four distinct, albeit overlapping mental systems, are essentially localized one on top (brainstem/limbic system) and one beside the other (right/left hemisphere). However, because the "mental systems" of the brain are hierarchically organized and lateralized, they are not always able to fully communicate as they speak different languages. Indeed, given the newly evolved ability to employ language and logic, and the fact that half of the brain is depending on language for understanding whereas older social-emotional mental systems are lateralized to the right half of the cerebrum, this lateralized system of mental activity often predisposes humans to developing intra-psychic conflicts and to sometimes ignore or suppress "warning signs" and "alarm bells" when interacting with others, members of the opposite sex and business and political opponents in particular. Often the left fails to attend to or acknowledge what the right hemisphere is fully aware of, a consequence of functional disconnection secondary to functional lateralization.

The brain and the mind can also become fractured and disconnected from yet other regions of the brain and mind due to head injury, stroke, tumor, or epilepsy. In some cases, the neocortex may be disconnected from limbic sources of input, the right hemisphere may be disconnected from the left hemisphere and the language dependent mind, and in some cases the language axis itself may be fractured such that Broca's area may be unable to communicate with Wernicke's area.

For example, if Broca's area is disconnected from Wernicke's area and the IPL due to a lesion of the arcuate fasciculus, the patient will suffer an extreme "tip of the tongue" word finding difficulty, and might completely lose the ability to produce speech altogether, though they still "know" what they wish to say; referred to as conduction aphasia, or in the less extreme, anomia (Goodglass & Kaplan 1999). However, in some instances the linguistic aspects of consciousness may remain intact, but become disconnected and thus dissociated from a non-verbal region of the mind (Bogen, 1993; Critchley, 1964; Freud, 1891; Geschwind, 1965; Joseph, 1986a,b, 1988a,b; Sperry, 1966, 1982). If that occurs, the disconnected aspect of non-verbal awareness may act independently of that portion of the mind associated with language and verbal thought.

AGNOSIA: "THE PATIENT WHO SPEAKS IS NOT THE PATIENT WHO IS PERCEIVING"

In some instances of cerebral trauma, the language axis may become disconnected from yet another region of the brain that remains intact and which subserves a different aspect of consciousness. That is, conscious awareness may be split and fragmented. However, the broken off portions of consciousness may retain the ability to engage in complex actions as well as store these experiences in memory (Bogen, 1969, 1993; Geschwind, 1965; Joseph, 1986b, 1988b; Sperry, 1966, 1982). For example, if a patient suffers a discrete lesion in the left occipital-temporal visual associations areas, although vision is preserved and the patient can see (due to preservation of the primary visual cortex), they will be unable to verbally recognize, describe, or name objects that are shown to them, even if encouraged to guess or if provided multiple choices. This is because the language axis is disconnected from the visual association areas and cannot receive complex visual associations. It cannot name what it sees because it cannot match an auditory equivalent with the visual image due to disconnection. Instead, the language axis may confabulate and call a "glass of water" a "clock" or a "comb" a "harmonica" or "toothbrush," and so on, and they may fail to realize an error has been made (Freud, 1891; Geschwind, 1965). Although unable to name or identify a glass of water, or explain its function or utility, once they became thirsty they might pick up the glass and drink from it (Geschwind 1965). Nevertheless they may remain unable to name the item even during the course of utilizing it (depending on the extent of disconnection).

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If instead the lesion disconnected the Language Axis from the left superior parietal lobule and the primary receiving areas for somesthesis, although able to correct name what they see, the patient would be unable to name whatever object might be secretly placed in their right hand, e.g. a "comb;" for example, if they were blindfolded, a condition referred to as stereoagnosia. In fact, they may not consciously (verbally) realize something was placed in their hand. They cannot name objects explored by touch alone because that aspect of consciousness associated with language is disconnected from that portion of consciousness that recognizes objects by touch. However, although unable to name, for example, a comb that had been placed in their hand, they can still demonstrate its use by combing their hair (Freud, 1891; Geschwind, 1965).

These unusual disturbances are not due to "word finding" difficulties for if provided mutliple choices they may still fail to pick the right word (Geschwind 1965). The object cannot be verbally identified because the Language Axis and verbal-consciousness have been disconnected and thus dissociated from the area of perception; a result of a lesion that destroys the axonal interconnections that normally link these neocortical tissues. Hence, if provided the correct word or descriptive phrase; i.e. "Is it a comb or a toothbrush?" the patient may still chose the wrong word or confabulate (Joseph 1982, 1986ab, 1988ab). They are unable to match the word with the visual or somesthetic image due to disconnection.

As demonstrated above, the dissociated area of perception can sometimes continue to act in isolation and can maintain a fragmentary non-verbal awareness which "it" may act on independently (Geschwind 1965). That is, the disconnected brain area that has been isolated from the Language Axis, may respond "normally". Hence, if asked to draw the object, or to show how it is used, they can do so, even though consciously, they cannot verbally describe or recognize what the object is. Thus, under these conditions, that aspect of the mind and personality that drinks from the glass or demonstrates the use of a comb, represents a broken off and disconnected fragment of the "mind" that is no longer attached to the dominant verbal stream of consciousness. However, this broken-off fragment of consciousness remains fully capable of acting independently and in a purposeful and intelligent manner. As stated by Geschwind (1965), under these conditions "we are dealing with more than one patient. The patient that speaks to you is not the patient who is perceiving--they are, in fact separate."

It is noteworthy that some academics claim that there is no evidence that consciousness can be fragmented or split apart following a brain lesion or as a consequence of emotional trauma. Nevertheless, as should be evident, those who make those claims are woefully uninformed. Indeed, not only does emotional trauma induce dissociative abnormalities, but all forms of dissociation are directly related to neurological abnormalities. If the brain is injured it is not uncommon for different mental systems to become disconnected and to act independently, as is the case with blind sight, and following split-brain surgery or medial frontal injuries.


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