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Table of Contents
1. The contribution of neuropsychology to psychiatry.......................................................................................... 1 2. Bibliography...................................................................................................................................................... 16

10 May 2012

ProQuest

Documento 1 de 1

The contribution of neuropsychology to psychiatry

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Autor: Keefe, Richard S E.

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Informacin de publicacin: The American Journal of Psychiatry 152. 1 (Jan 1995): 6-15.
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Resumen: Neuropsychological test data are applied with increasing frequency in research studies and clinical practice in psychiatry. This article addresses three popular assumptions about neuropsychological test data and describes the limitations and contributions of neuropsychological assessment of patients with psychiatric disorders. All research articles from major journals in psychiatry and clinical psychology since 1991 that focused on neuropsychological assessment of psychiatric patients were reviewed. Other journals and earlier studies were reviewed selectively. Neuropsychological test data have made significant contributions to the development of hypotheses about abnormal brain structure and function in patients with psychiatric disorders, yet many findings from neuropsychological assessments of psychiatric patients are misinterpreted. The extent to which neuropsychological test data in psychiatric populations can be interpreted to reflect abnormalities in brain structure and function is frequently exaggerated, as is the ability of neuropsychological measures to serve as specific cognitive probes in imaging studies of physiological activation. On the other hand, the utility of neuropsychological test batteries as measures of the patterns of cognitive strength and deficit in individuals with specific psychiatric disorders is frequently underestimated. In addition to testing models of regional brain dysfunction in psychiatric disorders, neuropsychological tests can provide researchers in psychiatry with an improved understanding of the relation between central cognitive impairments and symptoms and serve to identify cognitive predictors of course of illness, and they may provide a method for discriminating among heterogeneous forms of some psychiatric disorders. Clinically, neuropsychological test data can be used to develop treatment strategies tailored for an individual's specific cognitive strengths and deficits.
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Texto completo: Neuropsychology is generally understood to be the study of the relation between brain function and behavior (1). Neuropsychological assessment has traditionally focused on determining specific changes in mental processes in patients with discrete lesions following normal development. In this manner, neuropsychology in clinical practice has enabled practitioners to determine the locus of insult or disease as well as the functional capacities of patients in treatment. Neuroscientists have benefited from human neuropsychological data, since studies of the relation between brain lesions and specific patterns of functional deficit have made substantial contributions to understanding the role of specific neuroanatomic regions in normal mental processes. There are many applications of neuropsychology in psychiatry, including the identification of brain lesions in psychiatric patients, the evaluation of cognitive deterioration over time, and the advancement of theories regarding the neuroanatomic localization of the symptoms of various psychiatric disorders. The purpose of this article is to discuss the contributions that neuropsychology and neuropsychological assessment can make to psychiatry. It is based on a review of all research articles from major journals in psychiatry and clinical psychology since 1991 that focused on neuropsychological assessment of psychiatric patients. Other journals and earlier studies were reviewed selectively. The article considers the validity of three common assumptions in 10 May 2012 Page 1 of 16 ProQuest

which neuropsychological data are regarded as supportive of hypotheses about the specific regions of impairment in specific major psychiatric disorders. It also emphasizes underutilized practical applications of neuropsychological assessment in psychiatry. One of the most important contributions of neuropsychological assessment is that it makes possible an objective evaluation of behavior in the context of the ability to perform basic tasks. When applied properly, a battery of neuropsychological tests yields an understanding of the cognitive and behavioral abilities and weaknesses of an individual or group of individuals. It provides the clinician or investigator with an objective description of what areas of behavior and cognition are likely to be a problem for the psychiatric patient and what areas are not. In this manner, neuropsychological data serve as a window into the everyday mental processes of the psychiatric patient. ASSUMPTIONS ABOUT NEUROPSYCHOLOGICAL TEST PERFORMANCE DATA Neuropsychological test performance data have made significant contributions to the development of hypotheses about abnormalities of brain structure and function in patients with several major psychiatric disorders, including schizophrenia, major depressive disorder, and Alzheimer's disease. While these contributions have helped to reshape the focus of investigations into the etiology and pathophysiology of these disorders, findings in this area have often been either exaggerated or underemphasized, and frequent erroneous conclusions have been made about neuropsychological assessments. Three of the most common assumptions are addressed here. ASSUMPTION 1: Neuropsychological Tests Measure Specific Functions, and Poor Performance on a Single Test Indicates a Specific Neuropsychological Deficit A frequent conclusion of research reports in psychiatry and psychology is that performance on a particular neuropsychological test (or very small number of tests) in a particular group of patients is worse than normal, indicating impairment in the function that the test measures. This conclusion is drawn even in some of the best research studies (2-13). Neuropsychological test batteries, when constructed properly, assess a broad range of functions, including, among others, perception in all sensory modalities, attention, learning and memory, motor skills, verbal and nonverbal skills, comprehension and expression of language, spatial abilities, laterality, abstraction, and "executive" functions. There is great overlap among these categories, and many tasks include redundant features. For example, both abstraction, as measured by the interpretation of proverbs, and verbal memory require intact verbal comprehension. Almost all individual neuropsychological tests of higher mental processes, because of their inherent complexity, involve a number of different functions, and poor performance can be attributed to any variety of functional deficits. Formal neuropsychological test batteries, such as the Halstead-Reitan (14) and the Luria-Nebraska (15), are designed to measure a broad range of functions with a fixed set of tests. The Halstead-Reitan is based on a series of tests devised in the late 1940s to discriminate between patients with frontal lobe lesions and control subjects. The Luria-Nebraska is an attempt to standardize the assessment procedures used by Luria. These formal batteries are useful in making general conclusions about the presence of impairment in individuals without psychiatric disorder, but they are not flexible enough to allow the investigator to assess the variety of functions that may underlie a performance deficit on a complex cognitive task. The level of complexity of some tests of higher mental functions can be seen clearly in a consideration of the assessment of executive functions with the Wisconsin Card Sorting Test (16), which was originally developed by Grant and Berg in 1948 and is currently the most extensively used neuropsychological test in psychiatry research. The standard version of this task in clinical practice (17) requires patients to sort cards by a series of principles that they must deduce. The cards vary in the shape, color, and number of stimuli printed on them. There is an arbitrary correct sorting principle that patients must learn through feedback from the tester ("right" or "wrong" after each sorting trial). The subject demonstrates knowledge of the principle by placing each card under a set of "key" cards which differ in form, color, and number. The principle changes once the subject has responded correctly for 10 consecutive trials, indicating that she or he has learned the principle. To perform 10 May 2012 Page 2 of 16 ProQuest

normally on the Wisconsin Card Sorting Test, an individual must have normal capacities for at least the following functions: memory of the goal of the task, auditory attention to the description of the task demand and to the feedback from the tester, visual attention to the characteristics of the sorting cards and the key cards, adequate motor skills to allow placement of the cards where the subject intends, learning of the principles to be acquired, proper abstraction to allow learning of the principles, categorization of the cards, maintenance of the categorization in "working memory," and executive control of the many cognitive functions at work at the same time. This list is only partially complete, but it serves to emphasize the complexity of functions involved in the completion of many neuropsychological tests. Thus, conclusions about any single poor test performance must include a consideration of the possibility that any of a number of functions may be causing the deficit. While this reserve should be applied to any neuropsychological evaluation, it is particularly important that it be applied to the evaluation of patients with psychiatric disorders, since there are many nonspecific reasons that their performance may suffer. To address the many possibilities that can contribute to poor performance on a neuropsychological test, consider further the example of using the Wisconsin Card Sorting Test as a measure of executive functions in patients with schizophrenia. Schizophrenic patients make various types of errors on the Wisconsin Card Sorting Test (18). One of the key measures of impairment on this test is the number of perseverative errors committed. These are scored when a subject continues to sort according to a principle despite feedback indicating that this strategy is incorrect. This measure has been associated with frontal lesions in studies by Milner (19) and others (20-22), although not in all studies (23). A similarity in the number of perseverative errors made by patients with frontal lobe damage and patients with schizophrenia has contributed to the development of the notion that the frontal cortex is dysfunctional in schizophrenia (24, 25). Schizophrenic patients make more perseverative errors on the Wisconsin Card Sorting Test than comparison subjects, including patients with affective disorders, and these differences exist even when factors such as premorbid intelligence and symptom severity are controlled (6). However, there are many mechanisms by which schizophrenic patients can make perseverative errors on this test, even if they are cooperative and motivated to perform well. As a result of verbal information-processing or verbal learning deficits, they may never gain a proper understanding of the purpose of the test. Because of impaired short-term or working memory functions, they may lose their awareness of the purpose of the test. Impaired auditory attention may lead them to misunderstand the nature of the feedback they receive. Finally, the symptoms of psychosis may interfere with their ability to process the feedback. While any of these possible, and not unlikely, situations would lead to a great number of perseverative errors, none of the errors could be specifically attributable to impairment in executive functions. Thus, the conclusion that there is a specific deficit can rarely be made on the basis of poor performance on a single test. A neuropsychological deficit in a psychiatric patient should be determined through a broad assessment of the functions described above. Because of the increased likelihood of spurious poor performance on any test or set of tests by a single individual, this is especially important in a clinical evaluation. A clinical finding based on a single test performance can be useful in generating hypotheses about areas of impairment, but such a finding requires considerable substantiation from additional measures in the same area of functioning. Hence, one of the important considerations in the use of standard formal test batteries such as the Halstead-Reitan is that the clinical investigator should pursue important findings with tests outside of the limited formal battery. In research studies of a group of patients, the time required to complete a full battery for each subject is generally prohibitive. Any individual test performance of the patient group, however, should be compared to an estimate of how the general population performs, as determined in the process of test standardization. (This comparison can be problematic, however, if the standardization sample is not reflective of the general population. For example, users of the Heaton manual for the Wisconsin Card Sorting Test [17] may note that the average number of perseverative errors among "normal" individuals is 12.6, but since this standardization sample had an IQ of 114--about 1 SD above the mean--and Wisconsin Card Sorting Test performance is 10 May 2012 Page 3 of 16 ProQuest

correlated with IQ [17], this standardization sample is not reflective of the general population.) Ideally, patient and control groups will be shown to differ on a task that is identical to a control task with the exception of one feature, which is matched between tasks for difficulty, ceiling effects, and floor effects. In an optimal comparison, the scores in each group should be normally distributed, with perfect performance a rarity. This prevents results such as spurious between-group differences due to near-perfect performance by patients and control subjects on an extremely easy control task. A specific deficit identified in comparisons of groups' performance in this manner has been referred to as a "differential deficit" by Chapman and Chapman (26), since the difference between the two tests discriminates the performance of the two groups, enabling one to conclude that a group demonstrates a performance deficit which can be accounted for by a specific feature and not simply by general dysfunction. For example, a research finding that the performance of patients with major depression is impaired on a neuropsychological test with a timed motor component is not of interest, because these patients tend to perform worse than normal subjects on almost all relatively difficult tasks that are timed (27). This general deficit may be attributable to any number of problems, including, among others, lack of motivation, lethargy, distraction secondary to intrusive thoughts, and general motor retardation. Furthermore, it is often not correct to conclude that the "worst" deficit in a battery of tests reflects the most basic or central cognitive disturbance in a disorder, even if the scores on a series of tests are made statistically comparable to one another with a "standardized residualized scores" approach (28). It is more likely that the largest differences between a group with a disorder and a control group will occur on the most difficult tests. With the use of appropriate statistical procedures, attempts to replicate findings of specific deficits in psychiatric disorders have often resulted in finding that the disorders are attributable to generalized deficits (29). Control subjects may be able to summon the energy or motivation to perform well on particularly difficult tests, whereas psychiatric patients may not have this capacity. One of the more impressive findings in schizophrenia research is that while schizophrenic patients may demonstrate deficits on verbal recognition tests in comparison with normal control subjects, their verbal recall deficit is more severe (30, 31). This finding is impressive because the differential deficit persists even when the tasks are matched for difficulty in such a way that nonschizophrenic control subjects perform similarly on both tests (32). Finally, a strategy to match patients and control subjects on a specific measure must consider the impact of the psychiatric disorder on the variable chosen. For instance, since level of education and socioeconomic status can be reduced by disorders such as schizophrenia, a strategy to compare the cognitive performance of schizophrenic patients and control subjects matched on these variables would result in a group of schizophrenic patients who are likely to have exceeded the level of functioning expected of the average individual with schizophrenia, and they may thus perform better than the average schizophrenic patient on the test of interest (26). A better strategy is to match groups on variables not affected by the illness, such as the pronunciation of irregular words as measured by performance on the National Adult Reading Test (33), which has been found not to be compromised by schizophrenia (34) or Alzheimer's disease (35). Another alternative is to match patient and control groups on the level of education or socioeconomic status of the parents of the patients and control subjects, as long as the parents are unaffected by the disorder under study (26). The strategy of administering to patients and control subjects a battery of tests of similar difficulty, some of which do not differ between groups, makes possible not only a more accurate determination of changes in mental processes associated with psychiatric disorder but also the identification of preserved functions in the patient group. Determining normal abilities in individuals with severe psychiatric disorders can be as important as identifying deficits. While the finding that a patient or group of patients has impairment in a specific area of neuropsychological function but has other areas of normality may or may not lead to confirmation of a particular model of deficient mental processes, it certainly provides data about the experience of these patients and about which mental functions may be failing them and which are preserved. ASSUMPTION 2: Abnormal Neuropsychological Test Performance Indicates Specific Regional Brain 10 May 2012 Page 4 of 16 ProQuest

Dysfunction Possibly the most prevalent assumption made about neuropsychological test data is that if psychiatric patients' performance on a specific test is equivalent to the performance of patients with discrete lesions in a specific region, this suggests the presence of similar neuroanatomic abnormalities in the psychiatric patients. This assumption is found even in many of the best published papers involving the assessment of neuropsychological functions in psychiatric patients (2-5, 9-13, 36-40). It is very likely not to be true. Poor performance may be the result of a broad range of possibilities, including damage to one of several areas, the accumulative effect of mild deficits in multiple areas, or factors unrelated to specific brain dysfunction. As I have mentioned, any individual or group of individuals may perform poorly on a neuropsychological test or series of tests for many different reasons. The more complex the measure, the more likely it is that poor performance will result from nonspecific factors. The best example of this phenomenon is that psychiatric patients with reduced motivation will often demonstrate neuropsychological profiles consistent with frontal lobe disease, since in a battery of standard neuropsychological tests, the most highly complex tasks are generally chosen as measures of frontal lobe function. Thus, the complexity of functions involved in any single neuropsychological test almost always prohibits the conclusion, based solely on test performance, that a specific brain region is impaired. Even if patients are able to comprehend and maintain the concepts required for task completion and are motivated to perform well, poor performance on a test is not necessarily related to dysfunction of specific brain regions. Throughout the history of the study of regional brain function, attempts have been made to isolate specific functions of specific brain regions, but the success of these mapping efforts has been mixed with overestimations of the capacities of the map at any given time. In 1861 Broca proposed that the third frontal convolution of the left hemisphere, area 44, is associated with expressive speech, and damage to this region results in expressive language deficit. This disturbance, now termed "Broca's aphasia," continues to serve as a leading indicator of disease or insult in this region. Other findings, such as the laterality of motor perception and movement and the role of the occipital cortex in vision, have had a tremendous impact on our current understanding of regional brain function. In addition, data from animal studies suggest that some brain regions mediate very specific functions. In monkeys, for example, memory of the precise spatial location of visual stimuli has been found to be subserved by neural pathways leading to specific regions of the prefrontal cortex (41). However, most recent data support the notion that higher brain functions cannot be isolated to a specific region. Many important behavioral and cognitive functions are mediated by complex networks of neurons throughout the brain, and damage to an area does not always result in impairment of the function associated with that region, possibly due to the plasticity of regional brain function. Luria (42) described higher mental functions in terms of complex functional systems that "cannot be localized in narrow zones of the cortex or in isolated cell groups, but must be organized in systems of concertedly working zones, each of which performs its role in the complex functional system, and which may be located in completely different and often far distant areas of the brain" (p. 31). Studies of damaged cortical connectivity (43, 44), including commissurotomy (45), and physiological studies on "neural networks" in human and nonhuman primates (41, 46-49) have supported Luria's conceptualizations of higher cortical functions. They suggest that higher cortical functions may be impaired by damage to any aspect of the complex system that regulates them. These concepts have become particularly relevant for understanding brain dysfunction in psychiatric patients (50-53), since poor neuropsychological test performance is found in many psychiatric disorders without established regional brain dysfunction. Studies of the organization of relations among brain regions in psychiatric patients suggest that identifying the regional pattern of electrical activity may improve psychiatric diagnosis and treatment (46). An example of the complexity of the relation between brain structure and neuropsychological function in psychiatric patients can be seen in the strong positive correlation between hippocampal size and physiological activation of the dorsolateral 10 May 2012 Page 5 of 16 ProQuest

prefrontal cortex (but not other regions) during the Wisconsin Card Sorting Test in schizophrenic twins compared with their normal cotwins (54). Since activation of the dorsolateral prefrontal cortex during this test is related to task performance (55), it suggests that structural deficits may lead to performance deficits farther "downstream" in the neural circuitry associated with a complex task. Thus, the complexity of neural networks associated with a neuropsychological task suggests that damage to any part of the network has the potential to impair performance on the task. In considering the relation between neuropsychological deficit and brain impairment in psychiatric patients, it is also important to consider the ability of the brain to adapt to damage. According to Luria (56), higher mental functions result from a unified system of components with a complex and plastic, not concrete, structure in which the initial and final links of the system (the task and the effect) remain constant and unchanged, and the intermediate links (the means and the performance of the task) may be broadly modified. The functional capacities of different brain regions are quite flexible in humans and other animals. If one area is damaged, the functioning of different brain areas is altered to accommodate for the damage, which may lead to greater adaptive capacities in the individual or greater impairment (57-64). Thus, it seems unwarranted to draw the conclusion that there is specific regional damage in psychiatric patients on the basis of isolated neuropsychological deficit. The effect of insult to the brain may depend heavily on the stage of development at which the insult occurs (65), which may have important implications for developmental models of psychiatric illness (58, 66). In the early stages of development, basic functions such as visual perception depend heavily on "lower" areas of the cortex, but in the later stages of development, the activity starts to depend on a different neural network (67). For example, a lesion of the lower regions of the visual cortex in early childhood leads to systemic underdevelopment of the higher regions responsible for the integration of visual concepts. In contrast, a similar lesion in an adult causes only partial deficiencies of visual analysis and synthesis, leaving the more complex cognitive functions, formed at an earlier stage, unaffected (42). This developmental model of brain insult and adaptation may eventually be useful in accounting for psychiatric illnesses with developmental etiologies, since neural network models of psychiatric disorders propose that a variety of intrinsic and extrinsic factors, even early emotional experiences, may affect the course of brain development (68). In sum, the assumption that abnormal neuropsychological test performance indicates specific regional brain dysfunction is often not true in brain-injured patients with otherwise normal histories; it is even less likely to be true in the assessment of patients with psychiatric disorders. Most mental processes, especially the higher cognitive functions relevant to psychiatric disorders, are regulated by complex neural networks that connect various brain regions. Therefore, deficits on neuropsychological tests may derive not only from nonspecific factors, such as lack of motivation in psychiatric patients, but from dysfunction in any of the connected brain regions that form the neural networks that guide higher mental processes, and even in the connections themselves. Increasingly, research on the neuropsychology of psychiatric disorders needs to focus on the function and dysfunction of these neural networks. ASSUMPTION 3: "Hypoactivity" During Functional Imaging Procedures With Cognitive Activation Tasks Suggests Regional Brain Dysfunction Another frequent assumption about neuropsychological test performance and psychiatric disorders is that less than normal regional activation during a test, as measured by a variety of functional imaging technologies including regional cerebral blood flow, single photon emission computed tomography, and positron emission tomography, is an indication of pathology in that region in the disorder under examination (55, 69-73). This conclusion is viewed as bolstered by evidence that reduced metabolism is positively correlated with poor performance on the test used for activation. This assumption, although more subtle than assumption 2 discussed above, can also be erroneous. It is likely that patients who perform poorly on a neuropsychological test are not processing the task in the same manner as normal subjects who perform well on the task. There are 10 May 2012 Page 6 of 16 ProQuest

enormous differences between patient groups and normal subjects in the manner in which they approach tasks, and these differences are almost certain to result in different patterns of activation that are correlated with performance, especially since level of difficulty within a single task can greatly affect regional activation (74). Thus, the correlation between poor performance and reduced activation reported in numerous functional imaging studies may actually reflect the different approaches of patients and control subjects, possibly due to differences in task difficulty, rather than reflecting regional brain dysfunction in the patients. Particularly striking are reports of an absence in patient groups of the lateral asymmetry found in normal subjects. In general, among groups of normal control subjects with left-hemisphere dominance, verbal tasks are known to activate left-hemisphere regions in functional imaging studies, while nonverbal visual tasks activate right-hemisphere regions (75). Schizophrenic patients, who perform worse than normal subjects on both verbal and nonverbal visual tasks (28, 76, 77), have been reported to have less extreme laterality of physiological activation during execution of these tasks (73, 78, 79), including the Continuous Performance Test, a test of visual attention (78, 79). It seems most parsimonious to understand these findings in terms of the inability of the patients to approach the task in the same way as normal subjects who perform well. Specifically, if schizophrenic patients are not completing a task such as the Continuous Performance Test effectively, or are unable to attend to the task as well as normal subjects, it is not surprising that the brain regions that are activated during test performance are more randomly distributed, which would result in a statistical "regression to symmetry," since random signals would follow a symmetrical activation pattern. One method proposed for dealing with this type of problem is to teach patients to perform the activation task as well as normal subjects do before collecting imaging data, or to choose patients who perform as well as normal control subjects (unpublished 1993 paper by C.D. Frith). While this strategy may result in the selection of an atypical patient group, the findings of these studies could be compared to those from patients with more typical performance. Finally, as with studies of brain structure, the reduced activation of a brain region as assessed by physiological activation studies does not suggest that the underactivated region is impaired, but only that is it not activated normally. Since there are many components of a neural network that are activated to perform a specific task, the impairment of any of these components could lead to dysfunction and/or underactivation of the region under study. Additionally, with functional imaging, the usual method for identifying reduced activation in a group of patients is through calculation of the differences between activation patterns in two separate conditions. While this method is useful in identifying mean differences between conditions, and thus in identifying isolated areas of abnormal activity, it limits the conclusions that can be drawn from the data collected. Identification of specific abnormal patterns of activation may provide evidence of impaired neural networks associated with specific psychiatric disorders (73, 80). Statistical path analysis of the physiological activation of multiple areas corresponding to a putative neural circuit associated with task performance may provide more convincing support of a physiology-task relationship. This type of analysis can be applied to determine the functioning of this circuit in patients who are believed to have an abnormality. Another strategy for understanding patterns of regional brain activation in psychiatric patients is to use cognitive activation tasks that are simple enough so that the neural networks that mediate performance by normal subjects are understood. For example, data on nonhuman primates suggest that tests of visuospatial working memory activate neural networks connecting the primary visual centers, parietal cortex, premotor regions, and dorsolateral prefrontal cortex (41). Preliminary imaging data suggest that this function is regulated by a similar activation pattern in humans (81). Such a simple cognitive task may prove to be a useful probe for imaging studies assessing hypotheses of prefrontal dysfunction in psychiatric disorders. Performance data on tests of visuospatial working memory tasks under laboratory conditions (82) and typical clinical conditions (83) suggest that schizophrenic patients may have relatively specific deficits in this area of functioning. This type of task may help to refine models of specific neural network dysfunction in schizophrenia and other psychiatric disorders. PRACTICAL CONTRIBUTIONS OF NEUROPSYCHOLOGICAL EVALUATION 10 May 2012 Page 7 of 16 ProQuest

The greatest contribution of the neuropsychological evaluation of patients with psychiatric disorders may be that it provides important, objective data about the mental deficiencies that shape our patients' lives. While neuropsychological tests may serve to inform specific neuropathological models of psychiatric disorders by comparing the performance of psychiatric patients and patients with brain lesions, this role is likely to be usurped in the future because of the tremendous advances in imaging technologies (84). However, images of the structure and regional activation of the brains of our patients will not provide us with information about their difficulties with their mental processes or about their cognitive strengths that can be used to facilitate their treatment. The differential pattern of performance on tests of higher mental processes can be used to predict the course of psychiatric illnesses, reduce the diagnostic heterogeneity within disorders and thus improve diagnostic classifications, serve as an aid in the development of treatment options, and create individualized management of patient care. Three practical ways in which neuropsychological data may be used to serve these ends are described below. PREDICTORS OF COURSE OF ILLNESS. The identification of specific cognitive deficits in psychiatric disorders may be a powerful predictor of the course of illness. Naturally, patients of a particular diagnostic group who also have global cognitive impairment are likely to have worse outcomes than similarly diagnosed patients who perform normally on neuropsychological tests. In a group of patients assessed in a psychiatric emergency room, cognitive deficit was the single best predictor of referral for inpatient hospitalization; it was even superior to the patients' diagnoses (85). In some disorders, such as schizophrenia and Alzheimer's disease, cognitive deficits as assessed by a battery of neuropsychological tests may predict the onset of illness. It has been demonstrated that general impairment on tests assessing information, memory, and concentration (86) serves as a better tool for the prediction of the eventual development of Alzheimer's disease in normal elderly volunteers than prior head injury, age of the mother when the subject was born, smoking, or family history of Alzheimer's disease (87). While these studies indicate the value of determining cognitive impairment in general in psychiatric patients, the identification of specific cognitive deficits may be of even greater value. Patients with major depression and particularly severe memory deficits may be unable to sustain even simple medication regimens or may be unable to benefit from previous gains they made in psychotherapy. Schizophrenic patients with severe learning deficits may never gain the capacity to understand the goals of their treatment and thus may never be able to function independently. These factors may have a tremendous effect on the ability of patients to benefit from treatment and may thus lead to a substantially worse outcome. The ability to identify specific cognitive deficits in patients may allow better prediction of the course of illness, or, if possible, the identification of treatment strategies to improve the course of illness (88, 89). TOOLS FOR IMPROVING DIAGNOSTIC CLASSIFICATION. Similar to the phenomenology of many major psychiatric disorders, the pattern of cognitive deficits among patients in a single diagnostic group is heterogeneous. Not all schizophrenic patients perform poorly on tests of verbal memory or the Wisconsin Card Sorting Test, and not all depressed patients perform poorly on tests of psychomotor speed. Although the etiologies of the subtypes of different psychiatric disorders have been presumed to differ (90, 91), the success of attempts to validate these distinctions made on the basis of phenomenology has been limited (92, 93). The identification of stable patterns of deficit on neuropsychological tests within a disorder may contribute to the development of hypotheses about the differing etiologies of the disorder (94). A subtypology based on specific differences in cognitive functions among patients with the same diagnosis is more compelling than a scheme based on phenomenology, since it suggests that different mechanisms lead to the common end-state of disorder, while phenomenological distinctions are limited to differences in the appearance of a disorder. AIDS TO TREATMENT STRATEGIES. There are few empirical data on the relation between neuropsychological deficit and response to medication, psychotherapy, and treatment setting. However, baseline cognitive impairment may be an important predictor of eventual response to treatment (95, 96), and improvement in cognitive abilities during the very early stages of treatment may herald the amelioration of 10 May 2012 Page 8 of 16 ProQuest

symptoms weeks later (95). It seems plausible, and worthy of investigation, that the heterogeneity of response to treatment among patients with psychotic, affective, and anxiety disorders may be related to their pretreatment level of cognitive functioning, and that treatment regimens which are suited specifically to an individual's pattern of cognitive deficits and abilities may be more effective. Because of the centrality of cognitive processes in any psychotherapeutic treatment, this strategy may be particularly applicable for psychiatric disorders that might benefit from psychotherapy. Historically, psychotherapeutic treatment of many psychiatric disorders, including most notably schizophrenia, mania, and anorexia nervosa, has not reflected a consideration of the significance of cognitive deficits. Any attempts to treat schizophrenia with insight-related or even cognitive therapies that require advanced concept formation, verbal memory and learning, and normal attentional capacities were clearly not informed by data suggesting that schizophrenic patients are generally unable to perform these functions normally. A very basic understanding of the cognitive deficits of a patient can prevent similar future treatment failures. An example of an improved psychotherapeutic strategy based on data from cognitive studies can be found in the treatment of anorexia nervosa. Recent cognitive behavioral and family treatment approaches, informed by data suggesting that patients with severe forms of anorexia nervosa are unable to process emotionally laden and internally derived mental events, have been far more successful than earlier approaches (97). Recommendations regarding important environmental factors in psychiatric treatment, such as living arrangements, work schedules, and partial hospitalization programs, may also benefit from a consideration and assessment of cognitive deficits. This type of assessment is often performed in an informal manner, such as observing that a patient does not have sufficient attentional capacity to participate in structured group activity or to handle independent living circumstances. While these observations can result in improvements in patient care, a more formalized determination of a patient's profile of neuropsychological strengths and deficits may provide clinicians and staff members with a clearer picture of which treatments will be maximally beneficial to their patients. In this manner, neuropsychological assessment can improve the quality of individualized therapeutic management. One of the specific benefits of determining a pattern of cognitive strengths and deficits associated with a psychiatric disorder is that it may shed light for clinicians onto possible strategies of cognitive rehabilitation. Since the range of possible cognitive deficits in psychiatric patients is broad, it is necessary to make several determinations about the level of intervention that is most likely to be successful and the goals to be attained. Baseline neuropsychological assessment may contribute to the development of cognitive rehabilitation programs by laying out the specific deficits that most require treatment, and indicating whether the focus of rehabilitation should be at the level of elementary cognitive deficits (such as those in perceptual processes), moderately complex deficits (such as those in problem solving and verbal memory), or highly complex deficits (such as those in interpersonal interaction) (98). In addition, since profiles of neuropsychological performance can make possible a determination of which cognitive functions remain intact, they can point to the areas of capacity upon which innovative rehabilitation strategies can rely. For example, one of the primary symptoms of neurological or psychiatric disorders that involve the frontal cortex is impairment in the ability to develop alternative coping strategies. Thus, these patients need assistance in generating such strategies, which should be directed by cognitive rehabilitation specialists in such a manner that the utilization of identified cognitive strengths can be optimized. An even more specific application of neuropsychological assessment to cognitive rehabilitation programs is tailoring treatment to an individual's particular profile of cognitive deficits (99), which may eventually be keyed to a patient's phase of illness (98). CONCLUSIONS The importance of investigations of the possible neuroanatomic etiology and pathophysiology of major psychiatric disorders cannot be minimized. Findings generated from research that relate neuropsychological deficits to neuroanatomic and neurophysiological abnormalities determined by brain imaging procedures are 10 May 2012 Page 9 of 16 ProQuest

likely to be a part of these eventual insights into major psychiatric illness. The important findings in this research are likely to develop from an understanding of the neural networks that underlie specific cognitive functions and of how this circuitry can be impaired. If properly applied, neuropsychological tests may be useful in specifying the relation between brain function and cognitive performance in individuals with psychiatric disorders. The abnormal changes in mental processes suggested by the performance of psychiatric patients on standardized neuropsychological tests should also be considered as potential tools for improving currently available treatments, especially with regard to individualizing treatment strategies. Research evidence of abnormal brain metabolism or structure in groups of patients with a particular psychiatric disorder is a suggestion that something specific may be wrong with a patient which may be relevant to the patient's psychiatric disorder. Most importantly, however, cognitive deficits as revealed by impaired performance on neuropsychological tests are a direct indication that something quite specific and tangible is wrong with the patient, which is very relevant to the patient's disorder. REFERENCES 1. Kolb B, Whishaw IQ (eds): Fundamentals of Human Neuropsychology, 3rd ed. New York, WH Freeman, 1989 2. Gruzelier J, Seymour K, Wilson L, Jolley A, Hirsch S: Impairments of neuropsychological tests of temporohippocampal and frontohippocampal functions and word fluency in remitting schizophrenia and affective disorders. Arch Gen Psychiatry 1988; 45:623-629 3. Katsanis J, Iacono WG: Temporal lobe dysfunction and electrodermal nonresponding in schizophrenia. Biol Psychiatry 1992; 31:159-170 4. Perlick D, Mattis S, Stastny P, Silverstein B: Negative symptoms are related to both frontal and nonfrontal neuropsychological measures in chronic schizophrenia. Arch Gen Psychiatry 1992; 49:245-246 5. Sandman CA, Barron JL, Nackoul K, Goldstein J, Fidler F: Memory deficits associated with chronic fatigue immune dysfunction syndrome. Biol Psychiatry 1993; 33:618-623 6. Goldberg TE, Gold JM, Greenberg R, Griffin S, Schulz SC, Pickar D, Kleinman JE, Weinberger DR: Contrasts between patients with affective disorders and patients with schizophrenia on a neuropsychological test battery. Am J Psychiatry 1993; 150:1355-1362 7. Marcus JM, Hans SL, Auerbach JG, Auerbach AG: Children at risk for schizophrenia: the Jerusalem infant development study, II: neurobehavioral deficits at school age. Arch Gen Psychiatry 1993; 50:797-809 8. Hollander E, Cohen L, Richards M, Mullen L, DeCaria C, Stern Y: A pilot study of the neuropsychology of obsessive-compulsive disorder and Parkinson's disease: basal ganglia disorders. J Neuropsychiatry 1993; 5:104-107 9. Gambini O, Abbruzzese M, Scarone S: Smooth pursuit and saccadic eye movements and Wisconsin Card Sorting Test performance in obsessive-compulsive disorder. Psychiatry Res 1993; 48:191-200 10. Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner DJ, Heninger GR, Bowers MB, Charney DS: Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Arch Gen Psychiatry 1994; 51:199-214 11. Stolar N, Berenbaum H, Banich MT, Barch D: Neuropsychological correlates of alogia and affective flattening in schizophrenia. Biol Psychiatry 1994; 35:164-172 12. Seidman LJ, Yurgelun-Todd D, Kremen WS, Woods BT, Goldstein JM, Faraone SV, Tsuang MT: Relationship of prefrontal and temporal lobe MRI measures to neuropsychological performance in chronic schizophrenia. Biol Psychiatry 1994; 35: 235-246 13. Keefe RSE, Silverman J, Lees Roitman SE, Harvey PD, Duncan A, Alroy D, Siever LJ, Mohs RC, Davis KL: Performance of nonpsychotic relatives of schizophrenic patients on cognitive tests. Psychiatry Res 1994; 53:112 10 May 2012 Page 10 of 16 ProQuest

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63. Babb TL: Short-term and long-term modification of neurons and evoked potentials in the human hippocampal formation. Neurosciences Res Program Bull 1982; 20:729-739 64. Hubel DH, Wiesel TN, LeVay S: Plasticity of ocular dominance columns in monkey striate cortex. Philos Trans R Soc Lond Biol 1977; 278:377-409 65. Schneider GE: Is it really better to have your brain lesion early? a revision of the "Kennard principle." Neuropsychologia 1979; 17:557-583 66. Weinberger DR: Implications of normal brain development for the pathogenesis of schizophrenia. Arch Gen Psychiatry 1987; 44:660-669 67. Luria AR, Simernitskaya EG, Tubylevich B: The structure of psychological processes in relation to cerebral organization. Neuropsychologia 1970; 8:13-19 68. Edelman GM, Cunningham BA: Place-dependent cell adhesion, process retraction, and spatial signaling in neural morphogenesis. Cold Spring Harb Symp Quant Biol 1990; 55:303-318 69. Buchsbaum MS, Nuechterlein KH, Haier RJ, Wu J, Sicotte N, Hazlett E, Asarnow R, Potkin S, Guich S: Glucose metabolic rate in normals and schizophrenics during the Continuous Performance Test assessed by positron emission tomography. Br J Psychiatry 1990; 156:216-227 70. Busatto G, Kerwin RW, Costa DC, David AS, Pilowsky L, Ell PJ: Temporal lobe activation during verbal memory challenge: a SPET study (abstract). Schizophr Res 1992; 6:148-149 71. Gur RE, Skolnick BE, Gur RC, Caroff S, Rieger W, Walter DO, Younkin D, Reivich M: Brain function in psychiatric disorders, II: regional cerebral blood flow in medicated unipolar depressives. Arch Gen Psychiatry 1984; 41:695-699 72. Warren LR, Butler RW, Katholi CR, McFarland CE, Crews EL, Halsey JH Jr: Focal changes in cerebral blood flow produced by monetary incentive during a mental mathematics task in normal and depressed subjects. Brain Cogn 1984; 3:71-85 73. Gur RE, Jaggi JL, Shtasel DL, Tagland JD, Gur RC: Cerebral blood flow in schizophrenia: effects of memory processing on regional activation. Biol Psychiatry 1994; 35:3-15 74. Gur RC, Gur RE, Skolnick BE, Resnick SM, Silver FL, Chawluk JB, Muenz L, Obrist WD, Reivich M: Effects of task difficulty on regional cerebral blood flow: relationships with anxiety and performance. Psychophysiology 1988; 25:392-399 75. Allen M: Models of hemispheric specialization. Psychol Bull 1983; 93:73-104 76. Braff DL, Heaton R, Kuck J, Cullum M, Moranville J, Grant I, Zisook S: The generalized pattern of neuropsychological deficits in outpatients with chronic schizophrenia with heterogeneous Wisconsin Card Sorting Test results. Arch Gen Psychiatry 1991; 48:891-898 77. Hoff AL, Riordan H, O'Donnell DW, Morris L, DeLisi LE: Neuropsychological functioning of first-episode schizophreniform patients. Am J Psychiatry 1992; 149:898-903 78. Buchsbaum MS, Haier RJ, Potkin SG, Nuechterlein K, Bracha HS, Katz M, Lohr J, Wu J, Lottenberg S, Jerabeck PA, Trenary M, Tafalla R, Reynolds C, Bunney WE: Frontostriatal disorder of cerebral metabolism in never-medicated schizophrenics. Arch Gen Psychiatry 1992; 49:935-942 79. Cornblatt BA, Keilp JG: Impaired attention, genetics, and the pathophysiology of schizophrenia. Schizophr Bull 1994; 20:31-46 80. Sackeim HA, Prohovnik I, Moeller JR, Brown RP, Apter S, Prudic J, Devanand DP, Mukherjee S: Regional cerebral blood flow in in mood disorders, I: comparison of major depressives and normal controls at rest. Arch Gen Psychiatry 1990; 47:60-70 81. Jonides J, Smith EE, Koeppe RA, Awh E, Minoshima S, Mintun MA: Spatial working memory in humans as revealed by PET. Nature 1993; 363:623-625 82. Park S, Holzman PS: Schizophrenics show working memory deficits. Arch Gen Psychiatry 1992; 49:975-982

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83. Keefe RSE, Lees Roitman SE, Harvey PD, Blum C, DuPre RL, Davidson M, Davis KL: A pen-and-paper human analogue of a monkey prefrontal cortex activation task: spatial working memory in patients with schizophrenia. Schizophr Res (in press) 84. Keefe RSE, Harvey PD: Understanding Schizophrenia. New York, Free Press, 1994 85. Galankyer I, Harvey PD: Neuropsychological screening in the psychiatric emergency room. Compr Psychiatry 1992; 33:291-295 86. Blessed B, Tomlinson E, Roth M: The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. Br J Psychiatry 1968; 114:797-811 87. Katzman R, Aronson M, Fuld P, Kawas C, Brown T, Morgenstern H, Frishman W, Gidez L, Eder H, Ooi WL: Development of dementing illness in an 80-year-old volunteer cohort. Ann Neurol 1989; 25:317-324 88. Brenner HD, Hodel B, Roder V, Corrigan P: Treatment of cognitive dysfunctions and behavioral deficits in schizophrenia. Schizophr Bull 1992; 18:21-26 89. Bellack AS: Cognitive rehabilitation in schizophrenia: is it possible? is it necessary? Schizophr Bull 1992; 18:43-50 90. Bleuler E: Dementia Praecox or the Group of Schizophrenias (1908). Translated by Zinkin J. New York, International Universities Press, 1950 91. Zimmerman M, Coryell W, Pfohl B, Stangl D: The validity of four definitions of endogenous depression, II: clinical, demographic, familial, and psychosocial correlates. Arch Gen Psychiatry 1986; 43:234-244 92. Fenton WS, McGlashan TH: Natural history of schizophrenia subtypes, I: longitudinal study of paranoid, hebephrenic, and undifferentiated schizophrenia. Arch Gen Psychiatry 1991; 48: 969-977 93. Guscott R, Grof P: The clinical meaning of refractory depression: a review for the clinician. Am J Psychiatry 1991; 148:695-704 94. Shallice T, Burgess PW, Frith CD: Can the neuropsychological case-study approach be applied to schizophrenia Psychol Med 1991; 21:661-673 95. Serper MR, Davidson M, Harvey PD: Attentional predictors of clinical change in neuroleptic: treatment. Schizophr Res (in press) 96. Marder SR, Asarnow RF, Van Putten T: Information processing and neuroleptic response in acute and stabilized schizophrenic patients. Psychiatry Res 1984; 13:41-49 97. Garner DM, Garfinkel PE, Bemis KM: A multidimensional psychotherapy for anorexia nervosa. Int J Eating Disorders 1982; 1:3-46 98. Green MF: Cognitive rehabilitation in schizophrenia: is it time yet? Am J Psychiatry 1993; 150:178-187 99. Spaulding WD, Sullivan M: From the laboratory to the clinic: psychological methods and principles in psychiatric rehabilitation, in Handbook of Psychiatric Rehabilitation. Edited by Liberman RP. Elmsford, NY, Pergamon Press, 1991
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Materia: Psychological tests; Psychiatry; Neurology; Mental disorders;

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MeSH: Brain -- physiopathology, Cognition Disorders -- diagnosis, Cognition Disorders -- physiopathology, Cognition Disorders -- psychology, Diagnosis, Differential, Humans, Intelligence Tests,; (principal), Neuropsychological Tests (principal)
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Mental Disorders --

physiopathology, Mental Disorders -- psychology, Models, Neurological, Mental Disorders -- diagnosis

Ttulo: The contribution of neuropsychology to psychiatry

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Autor: Keefe, Richard S E

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Ttulo de publicacin: The American Journal of Psychiatry

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Tomo: 152
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Nmero: 1
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Pginas: 6-15
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Nmero de pginas: 10
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Ao de publicacin: 1995
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Fecha de publicacin: Jan 1995

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Ao: 1995
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Editorial: American Psychiatric Association

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Lugar de publicacin: Washington

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Pas de publicacin: United States

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Materia de la revista: Medical Sciences--Psychiatry And Neurology

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ISSN: 0002953X
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CODEN: AJPSAO
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Tipo de fuente: Scholarly Journals

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Idioma de la publicacin: English

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Tipo de documento: PERIODICAL

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Nmero de acceso: 7802121, 02204522

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ID del documentos de ProQuest: 220480304

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URL del documento: http://search.proquest.com/docview/220480304?accountid=14621

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Copyright: Copyright American Psychiatric Association Jan 1995

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ltima actualizacin: 2011-09-26

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Base de datos: 3 bases de datos; -ProQuest Psychology Journals; -ProQuest Research Library; -ProQuest Science Journals; ;
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Bibliography
Citation style: APA 6th - American Psychological Association, 6th Edition Keefe, R. S. E. (1995). The contribution of neuropsychology to psychiatry. The American Journal of Psychiatry, 152(1), 6-15. Retrieved from http://search.proquest.com/docview/220480304?accountid=14621

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