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Neuropsychiatric Practice and Opinion   |    
Cognitive NeuropsychiatryPotential for Progress
Anthony S. David, M.D.; Peter W. Halligan, Ph.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2000;12:506-510. doi:10.1176/appi.neuropsych.12.4.506
View Author and Article Information

Cognitive NeuropsychiatryNeuropsychologyNeuropsychiatric Practice and Opinion

From the Institute of Psychiatry, London, and the MRC Neuropsychology Unit, University Department of Clinical Neurology, Rivermead Rehabilitation Centre, Oxford, UK. Address correspondence to Dr. David, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, United Kingdom; e-mail: a.david@iop.kcl.ac.uk

The purpose of this article is to introduce the emerging specialization of "cognitive neuropsychiatry" to practicing neuropsychiatrists, and in particular those outside the United Kingdom. Cognitive neuropsychiatry is a new hybrid discipline that tries to apply some of the successful methodology of its sister discipline, cognitive neuropsychology, to (neuro-) psychiatric disorders.1,2

The main starting point is cognitive neuropsychology, or to go back even further, neuropsychology. In fact, the latter term is fairly modern, having been used initially in 1913 but only really becoming established after a publication by Donald Hebb in 1949 and the launch of the journal Neuropsychologia in 1963.3 There is a reciprocity to these neurological branches of medicine and psychology. In one direction, neuropsychology seeks to determine the relevance of brain damage or disease to changes in behavior and cognition. In the other direction, patients presenting with a set of behaviors or cognitive deficits, or even a specific deficit, may be studied and tested by the neuropsychologist in order to aid in diagnosis. It may be possible to say whether the behavior or deficit in question resembles those seen in circumstances where a lesion or disease is known to have had an effect.

The same reciprocity is inherent in cognitive neuropsychiatry, which takes full advantage of the established bedrock of knowledge about brain-behavior-cognition relationships. What marks the approach as distinctive within medical specialisms is the explicit move beyond diagnosis and classification, toward offering a cognitive explanation for the disorder and, as an important second, location of the brain systems responsible. The characteristic feature of cognitive neuropsychiatry, however, remains its theoretical approach: using patterns of impaired and intact cognitive performance found in patients to inform and revise current models of normal cognitive functioning. A few examples of this will be given below. The relative success or failure of these examples rests on their heuristic value, their testability, and the degree to which they are supported by converging evidence from clinical neuropsychology and cognitive neuroscience.

The remit of cognitive neuropsychiatry is broad—arguably broader than neuropsychiatry or behavioral neurology, although firm boundaries have yet to be drawn. For example, schizophrenia is not normally regarded as falling within the ambit of the neuropsychiatrist,4 despite the increasing evidence of its neurological basis. The reason for this is in part a matter of pragmatism; with a lifetime prevalence of approximately 1%, the disorder will always be part of mainstream psychiatry. Furthermore, there are no psychiatric disorders that cannot, in principle, be conceived to have a neurophysiological basis, and many that are associated (albeit subtly) with altered neuroanatomy. Nevertheless, schizophrenia is a core interest in cognitive neuropsychiatry, as we shall discuss below.

Another important disorder is Alzheimer's disease. In the United Kingdom, presenile cases tend to be managed by neurologists, occasionally with assistance from a neuropsychiatrist—especially where diagnosis is obscure and comorbid depression and alcohol misuse complicate the picture. After age 65, patients may be managed mostly by geriatricians, internists, and psychogeriatricians, as well as, of course, family practitioners. Again, the neuropsychiatrist in his or her hospital base does not usually have the community and social resources to manage such patients, who at this age may be classed as having a common disorder. However, here too the neuropsychiatrist may be called upon to assist with diagnostic and some management issues.

So what of cognitive neuropsychiatry? It is the phenomenological manifestations of schizophrenia, Alzheimer's, and the rest that comprise the "bread and butter" of cognitive neuropsychiatry—delusions, hallucinations, misidentifications, and apparently extraordinary behaviors. By seeking analogies from less complicated and better understood neurological disorders, cognitive neuropsychiatry tries to formulate a functional model or context of the symptom. Note the insistence on symptoms (occasionally symptom clusters) rather than diagnoses per se. This is another departure from mainstream neuropsychiatry. The argument here is that "causal" cognitive explanations are not, and indeed cannot be, relevant to all the manifestations of disorders and diseases—such as cerebral atrophy or hemiparesis—although such manifestations may be important for the diagnostic process.

Given the reliance on analogy, it is hardly surprising that the psychiatric phenomena that to date have proved most amenable to the cognitive neuropsychiatric approach are those demonstrating the greatest "organicity"—for example, the delusional misidentification syndromes.5 Indeed, Ellis summarizes work in this area as "an exemplary vindication of the new discipline."6 This work was partly experimental and partly theoretical, and was able to place such phenomena as the Capgras delusion (where the patient believes that a relative has been replaced by impostors), and the Fregoli delusion (where the patient believes that a certain person has assumed different physical appearances) within the cognitive framework of normal face processing, of which the anatomical counterpart is fairly well understood. Out of this framework it was formulated that such patients, although able to recognize faces, have an abnormal sense of familiarity. This sense is normally conveyed via a ventral brain pathway in the form of an orienting or arousal response. Conventional tests of facial recognition were relatively intact in such patients, offering supporting evidence, but a more critical test was that autonomic responses to familiar and unfamiliar faces were no different.7 Hence if a patient is confronted by a person whom he or she perceptually recognizes and yet does not experience the usual reassuring feeling of familiarity, this can lead to an interpretation that assumes the person is an impostor. This last step of attribution requires further explanation and may have its roots in reasoning and judgment processes or in individual biases.

Although it is unlikely that a unified theory of all delusions will be forthcoming in the near future, it is desirable that theories of normal belief formation should eventually cast light on both the content of delusions and the processes whereby beliefs are formed.

Hallucinations are common to both "functional" and "organic" disorders. Hence one place to begin the search for an underlying mechanism is in conditions with known pathophysiology. In the case of auditory hallucinations, such conditions are less apparent, although studies of epilepsy and brain stimulation8 form a reasonable point of departure. The notion that "irritation" of auditory association areas may produce such experiences has now been put to the test with the advent of functional neuroimaging techniques, and indeed finds support.912 Further work is still required to explain the particular grammatical construction and emotional content constituting most auditory hallucinations.

Visual hallucinations have been seen as the province of neuropsychiatry ever since the discipline emerged. Why visual experiences should be induced more often than auditory experiences by brain perturbation remains an intriguing question.13 We are now well on the way to a comprehensive explanation of the phenomena that takes into account the role of the sleep-wake cycle, neurotransmitter imbalance, degradation of sensory input, and the constructive capacity of the human visual system.14,15 Further work contrasting neuropsychological deficits in people with neuropsychiatric conditions with and without hallucinations is awaited with interest. The extent to which discrete psychopathologies such as hallucinations can be mapped onto physiological processes remains an active area of investigation.

Insight and awareness is a crucial area with theoretical as well as practical implications. Several authors have proposed an analogy with anosognosia, the lack of awareness of physical deficits sometimes observed in patients following right hemisphere lesions.1618 Lack of awareness of behavioral and personality change following brain injury and degenerative disorders can put a huge burden on caregivers and pose major challenges to clinical management. Careful content analysis of statements made by patients recovering from anosognosia can be used to test hypotheses about the origin of the deficit.19 In tandem with this effort, fractionation of the hitherto vague general psychiatric concept of "poor insight" into components that may be more likely to have a neurocognitive basis (such as the ability to relabel certain symptoms as pathological) and those whose basis may lie in cultural and social models of disease (such as whether or not one is suffering from an illness) is likely to render the problem tractable.20

The disjointed, and at times incomprehensible, speech of patients with schizophrenic thought disorder has long intrigued neuropsychiatrists who saw similarities with certain kinds of fluent aphasia.21 Similarly, the poverty of speech commonly observed in patients with negative symptoms brings to mind the lack of spontaneity and alogia of the frontal lobe patient. Linguistic analysis of schizophrenic speech has attracted polarized opinions.22 However, the distinctions between phonology, lexical-semantics, and pragmatics of language have been applied to schizophrenic thought disorder and suggest problems in making use of context online to understand, and by inference plan, utterances.23 Others have concentrated more on semantics and have taken the techniques of semantic priming from the experimental psychology laboratory into the clinic. The work is based on the view that our storage of word meanings is in the form of a network of nodes, whose proximity is determined by the degree to which they share meaning.24 The exposure to a given word leads to the automatic spread of activation through the network, from one node to its neighbors. Spitzer25 has argued that in schizophrenic thought disorder this spread is broader and leads to activation of words of only indirect semantic relatedness. This "spills out" into conversation as thought disorder.

Psychologist Martin Harrow once quipped that patients don't get admitted to the hospital because of bad grammar! It is the content—as well as the form—of the thought disorder that leads to concern. Indeed, the discussion of emotive personal themes has recently been shown to exacerbate thought disorder.26

A crude distinction between the subject matter of neuropsychology and neuropsychiatry used to be made on the basis of affect. That is to say, the deficits (and excesses) of neurological patients were seen as value- free and content-neutral. The disorders of psychiatry, on the other hand, were viewed as essentially about topics involving personal investment, beliefs, and desires. The advent of "affective neuroscience"27,28 has swept such distinctions away. Thanks to the work of Le Doux29 and Damasio,30 emotions are once again a legitimate topic for research. Again neuroimaging has boosted this reappraisal with specific neural substrates for different (basic) emotions being mapped out: the amygdala for fear,31 the insula for disgust,32 and possibly the orbitofrontal cortex for anger.33,34

The neurobiology of affective disorder has, of course, always been a major focus of research, as have the behavioral manifestations of lesions of the limbic system. This is outside the scope of the current article. Interest has now broadened to encompass disorders such as autism, now regarded as being a disorder of social cognition in which the natural ability to infer an other's mental state is impaired.35 Depersonalization disorder is another neglected condition, which has long had its "organic" and "functional" proponents.36,37 Advances in the understanding of the neurobiology of emotional controls, and the way in which affect colors cognition, have led to suggestions that such patients fail to experience (as opposed to recognizing) emotional arousal.34,38,39 A model comprising reduced subcortical activation in the face of emotional stimuli and reduced physiological arousal, combined with intact frontal subsystems that are in inhibitory mode, can be pieced together from the growing body of evidence. The interaction of similar networks has been proposed to account for certain cases of psychopathy.40 The additional element appears to be damaged frontal subsystems, which lack inhibitory tone. While it is foolish and undesirable to seek to "explain away" complex biopsychosocial phenomena, advances in the cognitive neuropsychiatric understanding of the whole range of disorders add an important perspective.41

Conversion hysteria is a famous battleground for the proponents of exclusively psychological versus physiological modes of mental states. The crux of the problem lies in the philosophical conundrum of having to explain how psychological or mental states (caused, in this case, purportedly by a reaction to an excessive emotional state) can produce specific long-term motor, sensory, and cognitive effects in subjects who claim not to be consciously responsible.42 In terms of the history of ideas, "hysteria" is an object lesson. Although Freud's work drew attention to the clinical disorder over a century ago, there has been little or no empirical research concerning the neural and psychological mechanisms. Freudian formulations have not endured, and the view that all hysterical conversion is undiagnosed neurology43 has suffered a similar fate.44 Into this void, cognitive neuropsychiatry has begun to take its first tentative steps. This is not so brave (or foolish) as it might appear. Conceptual advances in implicit and explicit cognitive influences,45 the understanding of mechanisms of dissociated awareness,46 and evidence provided by functional neuroimaging on the brain areas for willed intentions47 have all made such a venture feasible.

Although only a handful of reports have previously attempted to explain hysterical behaviors in terms of neuropsychological disorders, the nature of the condition and the brain structures responsible have not been significantly elucidated beyond views expressed at the end of the nineteenth century in the work of Janet (1889), and Freud (1894). Given that hysterical paralysis, like normal voluntary movement, must express itself through the structural medium of normal brain functioning, the emergence and availability of noninvasive neuroscience methodologies such as functional imaging has provided researchers with the possibility of finding out which areas of the brain are involved. A recent case study employing PET provides some insights as to the abnormal physiological brain activations in hysterical motor conversion.49

Another phenomenon that has been classed both as a conversion disorder and a neurological deficit is pure retrograde amnesia. The careful analysis of certain cases of "fugue" has shown that it is just as possible to uncover positive evidence of intractable social and personal dilemmas as it is to uncover a neurological lesion, provided the effort is made. The weakness of cognitive neuropsychiatric explanations for this syndrome has been the lack of a convincing cognitive account of retrograde amnesia, given current theories of memory. This weakness is beginning to be addressed50 as such theories (rooted in functional neuroanatomy51) begin to accommodate such case material.52

We have discussed above just a few examples of the territory in which cognitive neuropsychiatry is beginning to apply itself successfully. Many other conditions and topics have benefited from this approach (e.g., posttraumatic stress disorder53 and obsessive-compulsive disorder54), and no doubt more will benefit in the future. Evidence of the growing interest in this field can be seen from the growing numbers of recent books,35,55,56 together with the launch in 1996 of the new quarterly journal Cognitive Neuropsychiatry. We would like to see more activity in developmental disorders and more cognitively motivated applications to rehabilitation. Also, there is a need to take stock of functional and structural neuroimaging so that these powerful technologies can be put to the service of theoretical understanding and not merely cerebral localization.57 As we leave the "Decade of the Brain," we predict that it will be the combined use of multimodal technologies and careful clinical observation that will provide the greatest advances in theoretical and practical neuropsychiatry.

David AS: Cognitive neuropsychiatry? Psychol Med  1993; 23:1— 5
 
David A, Halligan P: Cognitive neuropsychiatry (editorial). Cognitive Neuropsychiatry  1996; 1:1—3
[CrossRef] | [PubMed]
 
David AS, Cutting JC: The Neuropsychology of Schizophrenia, 1st edition. Hove, East Sussex, UK, Lawrence Erlbaum, 1994
 
Lishman WA: Organic Psychiatry: The Psychological Consequences of Cerebral Disorder, 3rd edition. Oxford and London, Blackwell Scientific, 1998
 
Benson DF, Gardner H, Meadows JC: Reduplicative paramnesia. Neurology  1976; 26:147—151
[PubMed]
 
Ellis HD: Cognitive neuropsychiatry and delusional misidentification syndromes: an exemplary vindication of the new disciplines. Cognitive Neuropsychiatry  1998; 3:81—90
[CrossRef] | [PubMed]
 
Ellis HD, Young AW, Quayle AH, et al.: Reduced autonomic responses to faces in Capgras delusion. Proc R Soc London B Biol Sci 1997; 264:1085—  1092
 
Penfield W, Perot P: The brain's record of auditory and visual experience: a final summary and conclusion. Brain  1963; 86:568— 693
 
Suzucki M, Yuasa S, Minabe Y, et al: Left superior temporal blood flow increases in schizophrenic and schizophreniform patients with auditory hallucinations: a longitudinal case study using 123I-IMP SPET. Eur Arch Psychiatry Clin Neurosci  1993; 242:257—261
[CrossRef] | [PubMed]
 
David A, Woodruff PWR, Howard R, et al: Auditory hallucinations inhibit exogenous activation of auditory association cortex. Neuroreport  1996; 7:932—936
[CrossRef] | [PubMed]
 
Woodruff PWR, Wright IC, Bullmore ET, et al: Auditory hallucinations and the temporal cortical response to speech in schizophrenia: a functional magnetic resonance imaging study. Am J Psychiatry 1997; 154:1676—  1682
 
Dierks T, Linden DEJ, Jandl M, et al: Activation of Heschl's gyrus during auditory hallucinations. Neuron  1999; 22:615—621
[CrossRef] | [PubMed]
 
David AS, Busatto G: The hallucinations: a disorder of brain and mind, in Disorders of Brain and Mind, edited by Ron MA, David AS. Cambridge, UK, Cambridge University Press, 1998; 336—362
 
Manford M, Andermann F: Complex visual hallucinations: clinical and neurobiological insights. Brain 1998; 121:1819—  1840
 
ffytche DH, Howard RJ, Brammer MJ, et al: The anatomy of conscious vision: an fMRI study of visual hallucinations. Nature Neuroscience  1998; 1:738—742
[CrossRef] | [PubMed]
 
Prigatano GP, Schacter DL: Awareness of Deficit after Brain Injury: Clinical and Theoretical Issues. New York, Oxford University Press, 1991
 
Keefe RSE: The neurobiology of disturbances of the self: autonoetic agnosia in schizophrenia, in Insight and Psychosis, edited by Amador XF, David AS. New York, Oxford University Press, 1998, pp 142—173
 
Barr WB: Neurobehavioral disorders of awareness and their relevance to schizophrenia, in Insight and Psychosis, edited by Amador XF, David AS. New York, Oxford University Press, 1998, pp 107—141
 
Berti A, Làdavas E, Stracciari A, et al: Anosognosia for motor impairment and dissociations with patients' evaluation of the disorder: theoretical considerations. Cognitive Neuropsychiatry  1998; 3:21—44
[CrossRef]
 
David AS: "To see oursels as others see us." Aubrey Lewis's insight. Br J Psychiatry  1999; 174:210—216
 
Faber R, Abrams R, Taylor MA, et al: Comparison of schizophrenic patients with formal thought disorder and neurologically impaired patients with aphasia. Am J Psychiatry 1983; 140:1348—  1351
 
McKenna P: The psychology of schizophrenic thought; the neuropsychology of schizophrenic speech. Speech and Language Disorders in Psychiatry: Proceedings of the Fifth Leeds Psychopathology Symposium, 1995
 
Kuperberg G, McGuire P, David AS: Reduced sensitivity to linguistic context in schizophrenic thought disorder: evidence from on-line monitoring for words in linguistically anomalous sentences. J Abnorm Psychol  1998; 107:423—434
[CrossRef] | [PubMed]
 
Goldberg TE, Weinberger DR: Thought disorder in schizophrenia: a reappraisal of older formulations and an overview of some recent studies. Cognitive Neuropsychiatry  2000; 5:1—19
[CrossRef]
 
Spitzer M: A cognitive neuroscience view of schizophrenic thought disorder. Schizophr Bull  1997; 23:29—50
[PubMed]
 
Haddock G, Wolfenden M, Lowens I, et al: Effect of emotional salience on thought disorder in patients with schizophrenia. Br J Psychiatry  1995; 167:618—620
[CrossRef] | [PubMed]
 
Davidson RJ, Sutton K: Affective neuroscience: the emergence of a discipline. Curr Opin Neurobiol  1995; 5:217—224
[CrossRef] | [PubMed]
 
Lane RD, Nadel L: Cognitive Neuroscience of Emotion. New York, Oxford University Press, 1999
 
LeDoux JE: The Emotional Brain. New York, Simon and Schuster, 1996
 
Damasio AR: Descartes' Error: Emotion, Reason and the Human Brain. New York, GP Putnam and Sons, 1994
 
Adolphs R, Tranel D, Damasio H, et al: Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature  1994; 372:669—672
[CrossRef] | [PubMed]
 
Phillips ML, Bullmore E, Howard R, et al: Investigation of facial recognition memory and happy and sad facial expression perception: an fMRI study. Psychiatr Res: Neuroimaging  1998; 83:127—138
[CrossRef]
 
Blair RJ, Morris JS, Frith CD, Perrett DI, Dolan RJ: Dissociable neural responses to facial expressions of sadness and anger. Brain  1999; 122:883—893
[CrossRef] | [PubMed]
 
Phillips ML, Williams L, Senior C, et al: A differential neural response to threatening and non-threatening negative facial expressions in paranoid and non-paranoid schizophrenics. Psychiatry Res Neuroimaging  1999; 92:11—31
[CrossRef]
 
Frith C: Cognitive Neuropsychology of Schizophrenia. Hove, East Sussex, UK, Lawrence Erlbaum, 1992
 
Mayer-Gross W: On depersonalization. Br J Med Psychol 1935; 15(2):103—126
 
Kenna JC, Sedman G: Depersonalization in temporal lobe epilepsy and the organic psychoses. Br J Psychiatry  1965; 111:293— 299
[CrossRef] | [PubMed]
 
Sierra M, Berrios GE: Depersonalization: neurobiological perspectives. Biol Psychiatry  1998; 44:898—908
[CrossRef] | [PubMed]
 
Simeon D, Gross S, Guralnik O, et al: Feeling unreal:30 cases of DSM-III-R depersonalization disorder. Am J Psychiatr 1997; 154:1107—  1113
 
Anderson SW, Bechara A, Damasio H, et al: Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience 1999; 2:1032—  1037
 
Dolan R: On the neurology of morals. Nature Neuroscience  1999; 2:927—929
[CrossRef] | [PubMed]
 
Marsden CD: Hysteria: a neurologist's viewpoint. Psychol Med  1986; 16:277—288
[CrossRef] | [PubMed]
 
Slater E: Diagnosis of hysteria. British Medical Journal 1965; 1:1395—  1399
 
Crimlisk H, Bhatia K, Cope H, et al: Slater revisited:6 year follow-up of patients with medically unexplained motor symptoms. BMJ  1998; 316:582—586
 
Bryant RA, McConkey KM: Functional blindness: a construction of cognitive and social influences. Cognitive Neuropsychiatry  1999; 4:227—241
[CrossRef]
 
Oakley DA: Hypnosis and conversion hysteria: a unifying model. Cognitive Neuropsychiatry  1999; 4:243—265
[CrossRef] | [PubMed]
 
Spence SA: Hysterical paralyses as disorders of action. Cognitive Neuropsychiatry  1999; 4:203—226
[CrossRef] | [PubMed]
 
Charcot JM: Clinical Lectures on Diseases of the Nervous System Delivered at Salpétrière, vol 3. London, The New Sydenham Society, 1872
 
Marshall JC, Halligan PW, Fink GR, et al: The functional anatomy of a hysterical paralysis. Cognition 1997; 64:B1—B8
 
Lucchelli F, Muggia S, Spinnler H: The syndrome of pure retrograde amnesia. Cognitive Neuropsychiatry  1998; 3:91—118
[CrossRef]
 
Markowitsch HJ, Fink GR, Thöne A, et al: A PET study of persistent psychogenic amnesia covering the whole life span. Cognitive Neuropsychiatry  1997; 2:135—158
[CrossRef]
 
Kapur N: Syndromes of retrograde amnesia: a conceptual and empirical synthesis. Psychol Bull  1999; 125:800—825
[CrossRef] | [PubMed]
 
Rauch SL, van der Kolk BA, Fisler RE, et al.: A symptom provocation study of post-traumatic stress disorder using positron emission tomography and script-driven imagery. Arch Gen Psychiatry  1996; 53:380—387
[PubMed]
 
McGuire PK, Bench CJ, Frith CD, et al: Functional anatomy of obsessive-compulsive phenomena. Br J Psychiatry  1994; 164:459—468
[CrossRef] | [PubMed]
 
David AS, Cutting JC: The neuropsychological origins of auditory hallucinations, in The Neuropsychology of Schizophrenia, edited by David AS, Cutting JC, 1st edition. Hove, East Sussex, UK, Lawrence Erlbaum, 1994, pp 269—313
 
Halligan PW, Marshall JC: Method of Madness: Case Studies in Cognitive Neuropsychiatry. Hove, East Sussex, UK, Psychology Press, 1996
 
Kosslyn SM: If neuroimaging is the answer: what is the question? Proc R Soc London B Biol Sci 1999; 354:1283—  1294
 
+

References

David AS: Cognitive neuropsychiatry? Psychol Med  1993; 23:1— 5
 
David A, Halligan P: Cognitive neuropsychiatry (editorial). Cognitive Neuropsychiatry  1996; 1:1—3
[CrossRef] | [PubMed]
 
David AS, Cutting JC: The Neuropsychology of Schizophrenia, 1st edition. Hove, East Sussex, UK, Lawrence Erlbaum, 1994
 
Lishman WA: Organic Psychiatry: The Psychological Consequences of Cerebral Disorder, 3rd edition. Oxford and London, Blackwell Scientific, 1998
 
Benson DF, Gardner H, Meadows JC: Reduplicative paramnesia. Neurology  1976; 26:147—151
[PubMed]
 
Ellis HD: Cognitive neuropsychiatry and delusional misidentification syndromes: an exemplary vindication of the new disciplines. Cognitive Neuropsychiatry  1998; 3:81—90
[CrossRef] | [PubMed]
 
Ellis HD, Young AW, Quayle AH, et al.: Reduced autonomic responses to faces in Capgras delusion. Proc R Soc London B Biol Sci 1997; 264:1085—  1092
 
Penfield W, Perot P: The brain's record of auditory and visual experience: a final summary and conclusion. Brain  1963; 86:568— 693
 
Suzucki M, Yuasa S, Minabe Y, et al: Left superior temporal blood flow increases in schizophrenic and schizophreniform patients with auditory hallucinations: a longitudinal case study using 123I-IMP SPET. Eur Arch Psychiatry Clin Neurosci  1993; 242:257—261
[CrossRef] | [PubMed]
 
David A, Woodruff PWR, Howard R, et al: Auditory hallucinations inhibit exogenous activation of auditory association cortex. Neuroreport  1996; 7:932—936
[CrossRef] | [PubMed]
 
Woodruff PWR, Wright IC, Bullmore ET, et al: Auditory hallucinations and the temporal cortical response to speech in schizophrenia: a functional magnetic resonance imaging study. Am J Psychiatry 1997; 154:1676—  1682
 
Dierks T, Linden DEJ, Jandl M, et al: Activation of Heschl's gyrus during auditory hallucinations. Neuron  1999; 22:615—621
[CrossRef] | [PubMed]
 
David AS, Busatto G: The hallucinations: a disorder of brain and mind, in Disorders of Brain and Mind, edited by Ron MA, David AS. Cambridge, UK, Cambridge University Press, 1998; 336—362
 
Manford M, Andermann F: Complex visual hallucinations: clinical and neurobiological insights. Brain 1998; 121:1819—  1840
 
ffytche DH, Howard RJ, Brammer MJ, et al: The anatomy of conscious vision: an fMRI study of visual hallucinations. Nature Neuroscience  1998; 1:738—742
[CrossRef] | [PubMed]
 
Prigatano GP, Schacter DL: Awareness of Deficit after Brain Injury: Clinical and Theoretical Issues. New York, Oxford University Press, 1991
 
Keefe RSE: The neurobiology of disturbances of the self: autonoetic agnosia in schizophrenia, in Insight and Psychosis, edited by Amador XF, David AS. New York, Oxford University Press, 1998, pp 142—173
 
Barr WB: Neurobehavioral disorders of awareness and their relevance to schizophrenia, in Insight and Psychosis, edited by Amador XF, David AS. New York, Oxford University Press, 1998, pp 107—141
 
Berti A, Làdavas E, Stracciari A, et al: Anosognosia for motor impairment and dissociations with patients' evaluation of the disorder: theoretical considerations. Cognitive Neuropsychiatry  1998; 3:21—44
[CrossRef]
 
David AS: "To see oursels as others see us." Aubrey Lewis's insight. Br J Psychiatry  1999; 174:210—216
 
Faber R, Abrams R, Taylor MA, et al: Comparison of schizophrenic patients with formal thought disorder and neurologically impaired patients with aphasia. Am J Psychiatry 1983; 140:1348—  1351
 
McKenna P: The psychology of schizophrenic thought; the neuropsychology of schizophrenic speech. Speech and Language Disorders in Psychiatry: Proceedings of the Fifth Leeds Psychopathology Symposium, 1995
 
Kuperberg G, McGuire P, David AS: Reduced sensitivity to linguistic context in schizophrenic thought disorder: evidence from on-line monitoring for words in linguistically anomalous sentences. J Abnorm Psychol  1998; 107:423—434
[CrossRef] | [PubMed]
 
Goldberg TE, Weinberger DR: Thought disorder in schizophrenia: a reappraisal of older formulations and an overview of some recent studies. Cognitive Neuropsychiatry  2000; 5:1—19
[CrossRef]
 
Spitzer M: A cognitive neuroscience view of schizophrenic thought disorder. Schizophr Bull  1997; 23:29—50
[PubMed]
 
Haddock G, Wolfenden M, Lowens I, et al: Effect of emotional salience on thought disorder in patients with schizophrenia. Br J Psychiatry  1995; 167:618—620
[CrossRef] | [PubMed]
 
Davidson RJ, Sutton K: Affective neuroscience: the emergence of a discipline. Curr Opin Neurobiol  1995; 5:217—224
[CrossRef] | [PubMed]
 
Lane RD, Nadel L: Cognitive Neuroscience of Emotion. New York, Oxford University Press, 1999
 
LeDoux JE: The Emotional Brain. New York, Simon and Schuster, 1996
 
Damasio AR: Descartes' Error: Emotion, Reason and the Human Brain. New York, GP Putnam and Sons, 1994
 
Adolphs R, Tranel D, Damasio H, et al: Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature  1994; 372:669—672
[CrossRef] | [PubMed]
 
Phillips ML, Bullmore E, Howard R, et al: Investigation of facial recognition memory and happy and sad facial expression perception: an fMRI study. Psychiatr Res: Neuroimaging  1998; 83:127—138
[CrossRef]
 
Blair RJ, Morris JS, Frith CD, Perrett DI, Dolan RJ: Dissociable neural responses to facial expressions of sadness and anger. Brain  1999; 122:883—893
[CrossRef] | [PubMed]
 
Phillips ML, Williams L, Senior C, et al: A differential neural response to threatening and non-threatening negative facial expressions in paranoid and non-paranoid schizophrenics. Psychiatry Res Neuroimaging  1999; 92:11—31
[CrossRef]
 
Frith C: Cognitive Neuropsychology of Schizophrenia. Hove, East Sussex, UK, Lawrence Erlbaum, 1992
 
Mayer-Gross W: On depersonalization. Br J Med Psychol 1935; 15(2):103—126
 
Kenna JC, Sedman G: Depersonalization in temporal lobe epilepsy and the organic psychoses. Br J Psychiatry  1965; 111:293— 299
[CrossRef] | [PubMed]
 
Sierra M, Berrios GE: Depersonalization: neurobiological perspectives. Biol Psychiatry  1998; 44:898—908
[CrossRef] | [PubMed]
 
Simeon D, Gross S, Guralnik O, et al: Feeling unreal:30 cases of DSM-III-R depersonalization disorder. Am J Psychiatr 1997; 154:1107—  1113
 
Anderson SW, Bechara A, Damasio H, et al: Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience 1999; 2:1032—  1037
 
Dolan R: On the neurology of morals. Nature Neuroscience  1999; 2:927—929
[CrossRef] | [PubMed]
 
Marsden CD: Hysteria: a neurologist's viewpoint. Psychol Med  1986; 16:277—288
[CrossRef] | [PubMed]
 
Slater E: Diagnosis of hysteria. British Medical Journal 1965; 1:1395—  1399
 
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