Go to Semiotic Review of Books Home Page
Go to SRB Highlights
Go to SRB Archives
This review appeared in Volume 4 (1) of The Semiotic Review of Books.
Awareness of Deficit After Brain Injury: Clinical and Theoretical Issues. Edited by George E Prigatano and Daniel L. Schacter. New York: Oxford University Press. l991. 271 p. ISBN 0-l9505941 7.
Trevarthen (1992) describes "the infinitely ambitious programme of semiotics" as uniting "all forms of communication, from physical communion among atoms and molecules, to the most fundamental and most profound of human symbolism in one hierarchy of information transfers." However what happens when the information transferred from one level of processing to another in the human nervous system is disrupted due to trauma or disease? Prigatano and Schacter have brought together authors from the fields of neurology, psychology and psychiatry to discuss how such breakdowns in communication can affect our experience of ourselves and of our world. The type of disorders described in the various chapters involve patients who have suffered some form of neurological impairment that has interfered either with vision, hearing, movement, speech, memory or attentional control That neurological impairment should give rise to such deficiencies is, in itself, not surprising. What is surprising is that many individuals, thus afflicted, seem unaware that they have sustained a loss of function. The issues raised by the anomalous experience of such patients will be of interest to scholars well beyond the fields represented in this volume. These issues have important implications for our understanding of the human mind and what it means to know about ourselves with respect to our internal experience of reality and with respect to our relationship to our physical and social enviroment.
The failure to know or appreciate the existence of a primary motor or sensory impairment is usually referred to as anosognosia. The term anosognosia was first used in 1914 by Babinski. Babinski, considered one of the founders of neurology, used it to describe a patient's apparent inability to perceive a significant paralysis of the left side of his body. However, while Babinski provided the term, he was not the first to describe the phenomenon. Bisiach and Geminiani report that over 2000 years ago Seneca, in a letter he had written to his friend Lucilius, reported that his wife's female companion, Harpastes, had lost her sight but that, incredible as it may seem, "She does not know she is blind". As is common with her more recent counterparts, Harpastes complained that her surroundings were simply too dark.
Given that such dissociations in awareness have been documented as long as 2000 years ago, the reader may wonder why it would be necessary to direct scholars' attention to anosognosia at this time. Prigatano and Schacter in their introduction and Bisiach and Geminiani in their chapter provide an account of the history of science that allows us to view the study of anosognosia from a sociological perspective. They point out that, prior to the turn of the century, most observers would have attributed a failure to appreciate one's condition to a general dementia or to a problem of character (this was indeed Seneca's interpretation of the hapless Harpastes with her entreaties to be taken to another house than his, one that was not so dark). It was not until 1885 that Constantine von Monakow described the case of a patient with a lack of awareness of severe loss of sight. Von Monakow was careful to underscore the difference between this case and those for whom one can not gauge the level of awareness for a specific disability due to more general cognitive impairment. This report was followed by others documenting anosognosia for cortical blindness, which has come to be known as Anton's Syndrome, as well as anosognosia for paralysis on the left side of the body following stroke.
The neuropsychological study of such phenomena that may have followed was eclipsed by another important development that occurred about the same time. There was a growing appreciation of how one could manipulate a person's conscious perceptions through hypnosis. Charcot was able to produce transient paralysis in a single limb that mimicked the atypical (assumed to be psychogenic) paralyses observed in some patients. These observations, along with the growing appreciation of psychodynamic sources of motivated denial allowed the anosognosias to be appropriated into the realm of psychiatry. Denial was thought to emerge from the self-protective filtering mechanisms that reside in the human psyche and was, therefore, not part of the mind-brain question. Thus, the accepted view by the middle of this century (Weinstein & Kahn, 1955) was that a neurological lesion could account for the nature of the dysfunction that was denied, but that such lesions could not explain the mechanism of denial .
We are now in a new stage in the understanding of mind-brain relationships. We are beginning to appreciate the levels of processing involved in even "simple perception. There is a growing awareness of how the relatively unique contributions of functionally distinguishable neural systems can interact to subserve various psychological and or cognitive functions. In this environment, many researchers find it more reasonable to entertain issues of dissociation of conscious awareness than during the time, not that long ago, when those interested in neuropsychological questions were debating the issue of whether language could or could not be localized in the brain.
Another factor is that experimental psychology as a field has moved away from rigid behaviourism giving questions of consciousness a renewed legitimacy. At the same time, clinical researchers are likely to approach the clinical case study in a more scientifically rigorous fashion. This has allowed even the sceptic to view these dissociations in conscious awareness as researchable phenomena. As well, the availability of brain imaging techniques has further allowed forthcoming documentation of lesion site in patients who demonstrate these associations
The authors describe a number of neurological disorders for which anosognosia can occur. These include cortically-based loss of vision (as in Anton's syndrome) or partial loss of vision (hemianopia), loss of language production or comprehension (the aphasias), a loss of the ability to attend to one side of space (hemineglect), and the loss of movement on one side of the body (hemiparesis). Described as well are amnesic patients who seem unaware of their inability to store or retrieve information. As well, patients suffering from multiple cognitive deficits can show a remarkable lack of awareness or concern. Such patients may be experiencing (or not experiencing!)the sequelae of traumatic brain injury, or progressive disease of the central nervous system such as Alzheimer's Disease or Huntington's Disease, and schizophrenia.
Presented as well are related conditions that imply a loss of communication between levels of information processing. These include blindsight, a condition in which the individual has suffered damage to the primary visual cortex that produces either total or partial loss of vision. As opposed to the denial that occurs in Anton's Syndrome, the patient with blindsight does report a lack of visual input but, nonetheless, shows an uncanny ability to detect objects in the world. These patients do not bump into things and, if encouraged to guess, can point correctly to stimuli that they protest they are unable to see. Analogous dissociations occur in patients with amnesia who show the effect on their behaviour of previous experience while having no conscious recollection of having had the experience. Similarly, patients who lose their ability to recognize familiar faces (prosopagnosics) can demonstrate some differential levels of familiarity on the basis of galvanic skin response.
While this increased rigor in the study of neurologically based cognitive dysfunction has been important in garnering the interest of experimental psychology in the study of clinical syndromes, there was a surprising lack of stringent case study evidence provided by authors in their description of anosognosia in its various forms. Authors would refer to papers describing case studies (e.g. Anton's paper describing the patient who was unaware of her blindness) and important reviews of the literature (e.g. McGlynn & Schacter's review of studies in anosognosia) but not bother to describe the clinical evidence themselves. There were some group studies of patients who have suffered traumatic brain injury (TBI), Huntington's Disease, and amnesia, but in general I found myself longing for at least one chapter that gave the kind of careful analysis of anosognosia that Humphries and Riddoch (1987) have provided for visual agnosia or that Weiskrantz (1986, 1989) has provided for blindsight.
While somewhat short on well controlled case study data on anosognosia, the book is not short on models developed to explain the phenomena along with the other disorders of conscious awareness. The models range from those based on the functioning of the nervous system to those that stay solidly within the bounds of cognitive or psychodynamic theory. I was hoping that the editors, in their final chapter, would have evaluated their enterprise by comparing and contrasting their models. One would assume that their goal would be to determine whether the formulations presented provide similar viewpoints, contrasting viewpoints or testable hypotheses. While the editors did provide a summary of the authors' views, they did not attempt a real discussion or integration of the material presented. The following is my attempt at such an integration.
Neuropsychological models. Bisiach and Geminiani and Heilman describe what they feel must happen within the nervous system for disassociations in awareness to occur. These are idealized models and while they are compatible with what has been demonstrated to be true of neural function they are not confirmed. The central theme is that there are areas within the central nervous system that are responsible for processing stimuli at various levels of complexity. These areas can be activated either by primary sensory stimulation or by internally generated or "top down" stimulation. In the absence of primary sensory stimulation (e.g., during sleep or during states of sensory deprivation), cellular groupings within a representational network may become activated on their own. This would account for the experience of events such as hypnagogic images, hallucinations and dreams. However, once external stimulation re-occurs, there is an inhibition of top down activation so that the experience produced by the topologically corresponding cellular groups are recognized as imagistic.
Basiach and Geminiani propose that in the case of hemineglect, parts of an internal representational system corresponding to one side of the body are destroyed or inactivated. The subsequent processing of information relevant to that internal representational system no longer occurs. One's internal experience of the world would be limited to the systems capable of producing that experience. Moreover, the patient would not experience the lack of sensation because the missing information cannot even be conceived. Hence, those patients suffering from hemineglect do not compensate by turning their head to take in a larger portion of their visual field as they would for a simple sensory deficit like hemianopsia. Thus, the degree to which this hemineglect can be considered anosognosic depends on the degree to which the internal representation of one side of the body and the associated perceptual experiences have been lost.
Heilman's model for why anosognosias in general occur is similar to Bisiach's but somewhat more dynamic. He postulates intentional-preparatory systems that initiate movement or perhaps some other activity like the observation of one's environment. If the motor system or the visual system alone were damaged, then one would experience a discrepancy between what one had intended to do and what had, in fact, happened. In order for anosognosia to occur the impairment would have to occur at the level of the motor intentional systems so that the individual is unlikely to experience any incongruity when the action that he or she has been asked to perform has not taken place.
Heilman focusses as well on the apparent lack of awareness that occurs in Wernicke's aphasia. He claims that such patients typically do not try to correct themselves when they produce streams of unintelligible speech because they have lost the "internal representation of word sounds". There is always, of course, the difficulty of how one would distinguish the loss of internal representations of knowledge from disrupted access to those internal representations. One can never observe internal representational systems at rest. In order to tap into those representations they have to be activated and, in a sense, re-perceived. Neither Bisiach and Geminiani nor Heilman deal with this issue.
Goldberg and Barr argue, in a similar vein, that for disorders of awareness to occur one requires 1)damage or loss of internal representations, 2) the disruption of feedback, and 3) the loss of some form of intentional representation against which action can be compared. As well, they suggest that the degree to which we are able to appreciate the loss of a function is proportional to the degree that the function is codifiable. They mean by this that the product of the process in question can be transformed into some form of symbol system which includes but would not be limited to language. Goldberg and Barr point out that many of the processes that we attribute to right hemisphere functioning are less codifiable than those we attribute to the left hemisphere and as such would be less accessible to conscious representation even in the normal state. The loss of these right hemisphere based functions would be less easily appreciated or reported upon. This argument, while not entirely convincing, is presented by Goldberg and Barr to explain the greater likelihood of anosognosia in right as opposed to left hemisphere lesions.
At a less abstract level, a number of authors attempted to integrate the idealized models of what must go on in the nervous system to produce disorders of awareness with what is known about the actual physiology of the nervous system. Prigatano, in describing the disorders of self-awareness that occur after head injury, gives the most complete description of how the nervous system might be able to integrate or fail to integrate the information necessary for conscious awareness to occur. He refers almost entirely to the work of Mesulam (1981, 1985) and, although presented from somewhat different perspectives, Mesulam's work forms the basis for theorizing in many other chapters. So, although Mesulam did not contribute a chapter, his work is well represented.
What we learn from Mesulam's formulation is that the cerebral cortex can be divided into distinct areas on the basis of the degree of association the neurons in that area have with other areas of the brain. Some areas respond primarily to one type of stimuli and these are the primary sensory cortical areas, i.e.,the areas where some of the initial sensory processes occur. Traditionally the rest of the cortex is referred to as the association cortex because of the more complex integration of sensory input that occurs there.
What is interesting for our understanding of how communication takes place within the brain is that these association areas can be further subdivided into unimodal and heteromodal association areas. Unimodal association cortex deals with stimuli at a more complex level than the primary sensory areas. However, these association areas are referred to as unimodal because they deal only with stimuli for which they are specialized and do not communicate with other specialized processing modules. The rest of the association cortex is considered to be heteromodal. These areas develop later from a phylogenetic point of view and are important for integrating information in two different ways: 1)information can be integrated from different types of stimuli (e.g.,different modalities), and 2) information that comes to us through our senses (e.g.,that which gets processed in the sensory and unimodal association areas) can be integrated with information that is generated internally (e.g.,that which arises within the paralimbic regions and which provides information about internal drive states). The paralimbic regions are also involved in arousal and attentional control. The heteromodal areas in which this integration becomes possible are in the prefrontal cortex, the inferior parietal lobule, the supra marginal gyrus, and the angular gyrus.
Disturbance in self-awareness may reflect damage to association areas that allow for this type of integration. While damage to the frontal cortex is often involved in a diminished self-awareness, Mesulam's model would suggest that a disturbance of awareness could result from damage to other heteromodal areas as well. It may be, as our neuromodelers have suggested, that whenever the neural substrate underlying the highest level of processing for a particular modality is damaged, the awareness of modality-specific deficits is diminished. It may not be because the representation for that function is lost, as suggested by Bisiach and Geminiani and others but that a failure to integrate information from one processing system to another prevents us from experiencing the information that was processed. Perhaps this transfer across processing systems is necessary for consciousness to occur.
How consistent is this model with the documented localization of damage in the various cases of dissociation presented here? We have learned that Wernicke's syndrome usually results from damage to the posterior portion of the superior temporal gyrus of the left temporal lobe. According to Heilman, damaged areas can also include the left inferior parietal lobe, as well as the supramarginal and the angular gyri. Much of this area would be considered part of the heteromodal cortex which would be consistent with the apparent inability of Wernicke's patients to appreciate the degree to which their linguistic production and comprehension is impaired. Patients suffering from Anton's syndrome usually have damage in the primary occipital areas, i.e.,those involved in the early processing of visual information. However, those who have persistent dissociations of awareness have usually sustained damage to portions of the heteromodal cortex which includes the angular gyrus and the superior temporal gyri.
Distortions in the awareness of self or in awareness of deficit across a broad range of abilities is often seen when damage has occurred in the prefrontal cortex. A number of authors have described the kinds of dissociations of awareness that can occur when the frontal lobes are damaged. These include disturbance of selfawareness and personal monitoring (Stuss), the disturbance of social behaviour (Prigatano), the failure to appreciate memory impairment (Schacter), and the failure to appreciate the loss of living skills (McGlynn and Kazniak).The frontal lobes are clearly part of the heteromodal system and since the work of the frontal system is integrative, a disturbance at the highest levels of association for that system should result in a disturbance at the highest levels of integration which would include concepts of the self.
With respect to the further instantiation of the neural substrate underlying dislocations in conscious awareness, we learn that thalamic stimulation can result in a physical movement that the patient experiences as voluntary. This demonstrates that the experience of volition can occur after the fact, as a misattribution about a neural event that was clearly not set into motion by the patient. We also learn that excision of the cingulate gyrus can result in the intensification of self-generated imagery so that it is harder to distinguish from real experience. This, it seems, is the reverse of the thalamically-based misattribution and may stem from an imbalance in top-down vs sensory-driven processes. It is also reported that damage to the anterior poles of the temporal lobes, areas of the brain especially at risk in the acceleration/deceleration of motor vehicle accidents, will result in difficulty moderating emotional drive states on the basis of external social demands. All of these areas (the thalamus, the cingulate gyrus, and the anterior poles of the temporal lobes) are considered part of the paralimbic system. Damage to these areas could lead to dissociations in awareness or disorders in self-monitoring through alterations in the intensity with which stimuli are experienced, increased variability in levels of arousal, or through alternations in the control of attentional processes.
Cognitive models.Kihistrom and Tobias present an historical introduction to cognitive models and discuss dissociations of awareness that occur in everyday life. They also present some computer models of information processing. It is clear that dissociations in conscious awareness would require a model at least as complex as the parallel distributed process models (PDP) because, as just discussed, one has to assume multiple processing systems, each with its hierarchy of complexity in order to produce the dissociations we have been dealing with.
Both Schacter and Johnson provide us with an information processing viewpoint regarding the general topic of reality monitoring. The strength of Schacter's chapter is that he describes how different types of processing have implications for our understanding of aware and unaware forms of memory. That is, Schacter concerns himself with how information can get learned and remembered without the individual having any conscious appreciation of what has been learned. The strength of Johnson's chapter is that she provides us with a well articulated discussion of how confusions arise about the source and the mnemonic status of information that we encounter during recall and recognition. Both Schacter and Johnson also provide us with their cognitively based models of information processing and describe how these models would operate to disrupt awareness of deficit or awareness of knowledge.
Schacter calls his model Dissociable Interactions and Conscious Experience (DICE). DICE is made up of structures which include a Conscious Awareness System (CAS) which has an output link to an executive system. This executive system is similar to the Supervisory Attentional System (SAS) proposed by Norman and Shallice (1986). According to this model, activation that occurs during early sensory processes (modular level processes) typically interact with CAS but can function indepedently. This means that activation at the modular level alone can produce a change in behaviour or performance but this is not sufficient to result in awareness of this activated information. Schacter uses this model to explain how learning can go on outside of conscious awareness and it is very consistent with the divisions proposed by Mesulam in describing informational linkages in the brain. CAS would represent the kind of functioning that goes on at higher stages of integration relevant to each processing system. In earlier work (Schacter, 1989), he does acknowledge Mesulam (1985a) along with Dimond (1976) as having provided inspiration for the development of DICE.
Johnson presents us with MEM, a Multiple Entry Modular Memory System. MEM consists of 2 hypothetical structures. One is referred to as the perceptual system which sounds roughly equivalent to the early sensory processing systems described by Mesulam. Johnson divides these further into 2 levels, P1 and P2, which would be roughly equivalent to early sensory and unimodal processing. The second construct in Johnson's model is the reflective system. This is divided in R1 and R2 which represent different levels of control and monitoring. These would correspond with the kinds of processing described as going on in the heteromodal association areas. She proposes that this reflectivity can go on at 2 levels so that she, like Schacter, and like Stuss in his chapter on awareness of the self, makes finer discriminations with respect to the workings of this heteromodal area.
These researchers have important things to say about information processing, but it is not clear to me what is gained by turning the processes they propose into formal structures. It is true that positing structures can at times capture something that would otherwise be difficult to conceptualize. Nonetheless, it behooves those who postulate such structures, complete with acronyms, to explain how they will further our conceptualization over and above that which is possible by sticking with functional descriptions of the processes being considered. I also think it behooves anyone who presents a new set of mental structures to present them in the context of models that are currently available and demonstrate why the model that they propose is different from those that came before. In fact, the models presented here are so alike in terms of their general thrust that it is not clear why we needed DICE when we have had MEM since at least 1983 (Johnson, 1983). It is true that DICE has allowed for differential input as a function of modality but could these not have been presented simply as friendly amendments to MEM?
Affectively driven models. Mesulam's model of neurophysiological function incorporates the drives and arousal that are usually mediated by the limbic system. This was not present at all in the cognitive models described by Schacter, Johnson, Kihistrom and Tobias and probably for good reason. While memory for affective associations has been studied by Johnson, the study of affect, arousal or drive states rarely makes its way into the cool and orderly study of cognition. Clinicians are much less able to ignore this factor. See for example Stuss' comprehensive overview of what it would mean experientially to suffer dissociations in the awareness of the self within and across time. See also Prigatano's description of patients' struggle to maintain control over their drive states and their struggle to understand and appreciate their altered sense of self in complex social interaction.
Lewis, in her chapter, presents a psychodynamic perspective on dissociations in awareness, a perspective rarely seen in the cognitive neuropsychology context. Lewis notes that denial can have adaptive and negative consequences, something to be noted by McGlynn and Kazniak and by Schacter who describe the methods they have used to try and promote awareness of deficit in amnesic and dementing individuals. While it is true that denial can get in the way of therapeutic programs, it is also true that sometimes one must carefully consider the ethics of promoting awareness in individuals for whom no treatment or demonstrably successful rehabilitation program currently exists.
Weinstein follows Lewis' general theme but describes how the situations and emotional concerns of the patient, while not necessarily causal, can define the nature of dissociated perceptions and beliefs. Considering the complex mixture of physiological and experiential factors at work for any individual who has suffered debilitating brain damage, one is reminded that we are dealing with persons, not syndromes. While Lewis and Weinstein do not speak to the neuropsychological underpinnings of disordered awareness, I hope their chapters are read, along with the chapters by Prigatano and by Stuss, by anyone who is studying, or is intending to study, the disorders of dissociation with which some individuals must cope.
In their concluding chapter, the editors suggest that the next step is to develop a taxonomy of disturbances in conscious awareness which will serve as a basis for real advances in the study of anosognosia. I hope this does not mean we will spend years demonstrating how condition X is really distinct from condition Y rather than X being some variant of condition Y. I envision this leading to a continually updated "discussions- of-conscious-awareness" edition of a diagnostic manual such as the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders. I would hope that as much attention will be paid to associations as to dissociations between these disturbances when they occur. I expect that much can be learned by examining how disorders of conscious awareness are alike, and we should postulate different categories only with reluctance.
I would also suggest that we think long and hard about postulating cognitive structures as opposed to refining our description of cognitive processes. A focus on the processes involved in cognition might facilitate the integration of cognitive and neurophysiological models. While it is not clear what level of description will ultimately be most appropriate, I do not believe we can have a complete theory of conscious awareness without that integration. Much could be gained by more collaborative work between those who develop theories of what must happen in order for dissociations of consciousness to occur and those who examine neurophysiological systems and what they are capable of. This is where the refinement of models can occur.
Awareness of Deficit after Brain Injury will, I am sure, fulfil the editors' goal of raising the profile of disorders of conscious awareness. The chapters are, on the whole, well written and would be quite accessible to readers from a wide range of disciplines. Even though the book contains a richer array of issues than I have been able to deal with in this review, there are, nonetheless, a few more that need to be considered with respect to the questions raised here. First, I suspect we will have to give far more consideration to the multiple roles that limbic processes play in moderating conscious awareness (see, for example, Mesulam, 1985b). Much could be gained, as well, by attending to the developmental literature, currently a very rich source of information about the emergence of levels of awareness (see, for example, Diamond, 1990). Another area missing from this review is the role of attention and attentional resources in the enhancement or inhibition of what we are able to process at any one time. In fact, it may be that to understand consciousness we must come to understand attention (see, for example, Posner & Rothbart, 1991). It is my belief that following up on these issues can add important perspectives to those presented by the contributors to this volume. There is much, as yet, to learn about how we come to know what we know and know that we know it.
Diamond, A. (Ed.). (1990). "The development and neural bases of higher cognitive functions." Annals of the New York Academy of Sciences, Vol.608. New York: The New York Academy of Sciences.
Dimond, S. J. (1976). "Brain circuits for consciousness." Brain, Behaviour and Evolution, 13. 376-395.
Humphreys, G.W. & Riddoch, M.J. (1987). To see but not to see: A case of visual agnosia. Hillsdale, New Jersey: Lawrence Erlbaum.
Johnson, M.K.(1983). "A multiple-entry, modular memory system." In G. H. Bowers (Ed.), The psychology of learning and motivation, Vol.17 (pp. 81-123). New York: Academic Press.
Mesulam, M.-M. (1981). "A cortical network of directed attention and unilateral neglect." Annals of Neurology, 10, 309-325.
---. (1985a). "Attention, confusional states, and neglect." In M.-M. Mesulam (Ed.), Principles of behaviourial neurology (pp.125-168). Philadelphia: F.A.Davis Co.
---. (1985b). "Patterns in behaviourial neuroanatomy: Association areas, the limbic system, and hemispheric specialization." In M.-M Mesulam (Ed.) Principles of behaviourial neurology (pp.1-70). Philadelphia: F.A.Davis
Norman, D.A. & Shallice, T. (1986). "Attention to action: Willed and automatic control of behaviour." In R.J. Davidson, G.E. Schwarz, & D. Shapiro (Eds.), Consciousness and self regulation Vol.4 (pp. 1-18), New York: Plenum Press.
Posner, M.l. & Rothbart, M.K. (1991). "Attentional mechanisms and conscious experience." In A.D. Milner & M.D. Rugg (Eds.), The neuropsychology of consciousness (pp. 91-111). New York: Academic Press.
Schacter, D.L. (1989). "On the relation between memory and consciousness: Dissociable interactions and conscious experience." In H.L. Roediger, lII & F.l.M. Craik (Eds.) Varieties of memory and consciousness: Essays in honour of Endel Tulving (pp.355-389). Hillsdale, NJ: Erlbaum.
Trevarthen, C. (1992). "Natural semiotics." In The Semiotic Review of Books, 3, 1-2.
Weinstein, E.A. & KLahn, R.L. (1955). Denial of illness: Symbolic and physiological aspects. Springfield, IL: Charles C. Thomas.
Weiskrantz, L. (1986). Blindsight: A casestudy and implications. Oxford: Oxford University Press.
Weiskrantz, L. (1989). "Blindsight." In F. Boller & J. Graflman (Eds.), Handbook of Neuropsychology, Vol.2, (pp.375-385). New York: Elsevier.
Jane Dywan is Assistant Professor in the Department of Psychology at Brock University. Her recent publications include: "Speed of information processing, health, and cognitive performance in older adults". Developmental Psychology 1992. 8 (4), 473-490 (with S. Segalowitz and A. Unsal), and "Memory for source after traumatic brain injury" Brain and Cognition 1993, 21, 20-43 (with S. Segalowitz, D. Henderson and L.Jacoby). She also coedited with R.D.Kaplan and F.J. Pirozzolo Neuropsychology and the Law. (1992)