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Informed Consent and Neuroanatomic Correlates of Intentionality and Voluntariness Among Psychiatric Patients
Anna L. Grimes, M.D.; Laurence B. McCullough, Ph.D.; Mark E. Kunik, M.D.; Victor Molinari, Ph.D.; Richard H. Workman, Jr., M.D.
Psychiatric Services 2000; doi: 10.1176/appi.ps.51.12.1561
Abstract

The authors examine the less-studied components of patients' autonomous decision making, or decisional autonomy, in the light of current research in psychiatry and neuropsychology and developments in the construct of informed consent. The three components of decisional autonomy—understanding, intentionality, and noncontrol or voluntariness—are related to clinical constructs in psychiatry and neuropsychology, in particular to executive control functions. The authors review studies that examine deficits in prefrontal cerebral function in schizophrenia, depression, and some anxiety disorders that are related to intentionality and voluntariness. Assessment of decisional autonomy should encompass evaluation of impaired intentionality and voluntariness, not simply impaired understanding. The main response to finding such impairments should be to provide treatment to ameliorate them. New strategies for psychiatric care should be developed to address the clinical challenges of an increasingly complex view of decisional autonomy.

Abstract Teaser
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Over the past several decades the concept of informed consent has evolved into a sophisticated and far-reaching construct as a result of ethical and legal developments in a health care system increasingly focused on patient rights (1). Whereas simple disclosure of medical information to patients formerly was considered adequate, today the need for a more rigorous standard has been recognized by ethicists and supported in the courts, particularly when the treatment or procedure carries significant risks (2,3,4,5,6,7).

Advances in neurobiological research and technology have added to this complexity by linking medical and psychiatric diagnoses with subtle neurological deficits, particularly executive dyscontrol, that may impair a patient's ability to participate adequately in the informed consent process. This problem is particularly relevant in psychiatric disorders, in which mental capacity is often neither clearly intact nor clearly impaired, and in which mental status may fluctuate as a function of time and therapy. Hence traditional tests of competency, which offer only a crude screening of cognitive function, are now recognized in many cases as inadequate to assess informed consent for research or treatment (6,8,9,10,11,12,13,14).

In previous reports Workman and associates (7,8) emphasized the clinical and ethical implications of impaired executive control for the autonomy of those suffering from the more classical "frontal lobe" syndromes. In this study we turn our attention to some of the traditional psychiatric disorders. We examine the less-studied components of autonomous decision making—voluntariness and intentionality—in the light of current research in psychiatry and neuropsychology to create a heuristic springboard for further research. We use clinical rather than research-based terminology in this discussion in the belief that there are few substantive differences in components of autonomous decision making between research and therapeutic settings.

In their seminal work, Faden and Beauchamp (1) identified three components of autonomous decision making, or decisional autonomy, in the informed consent process: understanding, intentionality, and voluntariness.

Understanding is a fairly straightforward concept that includes a recognition of the condition requiring treatment, a basic grasp of the fact that the patient is being asked to authorize intervention and of the intervention itself and its purpose, and comprehension of the risks and benefits associated with accepting as well as with declining the intervention. Underpinning successful understanding is the ability to process new data in a rational manner and to reach a decision within the context of personal values and goals (3,4,15,16,17). Because understanding has been explored extensively (3,4,15,16,18,19,20,21), in this review we focus on the other two components of autonomy, which have received less attention in the bioethics and psychiatric literature.

Intentionality entails initiating actions or decisions with forethought and conscious will, which requires that the person have goals, motivation, and an organized plan (1). In the clinical setting, patients should be able to process information provided by the physician on the basis of their values and preferences and to participate actively in developing an outpatient care plan. They should also be able to implement and monitor the plan and to make adjustments as necessary—for example, in response to a change in their condition or to a caregiving spouse's becoming ill.

Clearly, evaluative judgments also play a role in this component of autonomy, highlighting the need for the physician to assess, if possible, the patient's enduring goals and values. This may require discussions with the family and might include questions such as "How does [the patient] feel about treatment when he is not acutely ill? Does he generally feel that the benefits of this treatment outweigh the risks and side effects? What were his plans (for living, working, and so on) before he became ill?" (22).

The third element of decisional autonomy, noncontrol or voluntariness, is perhaps the most difficult to define and measure. Faden and Beauchamp (1) described influences that may affect a patient's control over the decision-making process on a continuum from substantially controlling to substantially noncontrolling. They specify that a voluntary decision is made without coercion or "substantially controlling manipulation."

Thus while real-life circumstance leaves little doubt that patients will be influenced in some way by external or internal forces, autonomy requires that the decision be essentially their own, with the threshold set low to protect patients from unwarranted paternalism. The difficulty lies in quantifying and measuring substantial manipulation, particularly when the controlling force is internal, such as in the case of a psychotic patient suffering from paranoid delusions. As will be discussed below, impairments of voluntariness may occur in a variety of psychiatric disorders.

In any attempt to integrate information from several fields of research, selection and use of vocabulary is of primary concern. The ethical terms delineated above may not be generally familiar to persons in the mental health professions, but they are related to constructs in the fields of psychiatry and neuropsychology. The correspondence is not one-to-one, because particular psychological abilities may be required to satisfy a minimum threshold for either or both intentionality and voluntariness, and psychiatric illnesses may affect one or more of these abilities.

Understanding is related to skills such as basic verbal and auditory communication, memory, assimilation of data, reasoning, and insight. Intentionality encompasses the psychological concepts of initiation, attention, planning, and cognitive set-switching—moving flexibly from one type of cognitive problem to another—which are necessary for decisional autonomy and executive autonomy—that is, ability to carry out one's decisions—as well as for adapting to change.

Voluntariness is concerned with the emotive side of decision making and is associated with motivation—more the desire than the ability to initiate—and choice: what does the patient want to do? It is also related to the ability to inhibit or control responses, to be sufficiently independent of external stimuli. Finally, it requires freedom from external and internal coercion—that is, it requires the absence of psychosis.

With the exception of freedom from coercion, the above aspects of cognition are subsumed collectively by neuropsychologists under the rubric "executive functions." In the next section, we discuss the specific neuroanatomic pathways or neural networks where executive functions are generated. After that, we review current research on the effects of specific psychiatric disorders on those neural networks and how those deficits are reflected in performance on current neuropsychological tests. Finally, we provide a preliminary framework to aid the clinician in approaching these types of impairments in decisional autonomy in the informed consent process.

Executive control functions are thought to be generated by the prefrontal cortex, and they have been most extensively studied in patients with frontal lobe lesions, typically resulting from tumor, trauma, or infarction. Salloway (23) and Lhermitte (24) have provided case descriptions of various "frontal lobe" syndromes. Although there is some controversy over anatomic division and nomenclature, three main prefrontal areas have been identified: the dorsolateral, mesiofrontal, and orbitofrontal pathways (25,26,27). These pathways are part of the multimodal association cortex, which integrates primary sensory inputs and indirectly regulates both perception and action via extensive cortical and subcortical connections (27,28,29).

The dorsolateral prefrontal cortex is crucial for initiation, planning, and problem solving, particularly in novel or changing circumstances. Lesions in this pathway may produce a "dysexecutive" syndrome, in which thinking becomes disorganized and concrete and the patient has difficulty with abstraction and with multistep tasks.

The mesiofrontal prefrontal or anterior cingulate cortex, which is often grouped with the dorsolateral prefrontal cortex, is the main mediator of motivation. Lesions in this pathway, particularly in the anterior cingulate gyrus, result in an "apathetic" syndrome, in which patients become passive and often lose all interest in their financial and personal affairs. Extensive bilateral damage may result in "akinetic mutism"—complete absence of movement and speech without apparent mood disorder—and indifference to pain.

The orbitofrontal prefrontal cortex mediates emotion, empathy, and impulse control. Deficits in this area produce a "disinhibited" syndrome with affective lability, insensitivity, tactlessness, and in some cases, unpredictable aggressive outbursts. The classic example of this syndrome is that of Phineas Gage, a railroad worker who suffered left orbital frontal damage when a tamping rod went through his skull (30). According to family and coworkers, his personality completely changed; formerly hardworking and temperate, he became "profane," "disrespectful," and lazy, with little regard for responsibilities.

With both lesions of the dorsolateral prefrontal cortex and of the orbitofrontal prefrontal cortex, patients may show "stimulus-bound" behavior, in which they are overly affected by environmental cues. On this subject Lhermitte (24) has provided a useful discussion of environmental dependency and imitation-utilization behavior. In lesions of dorsolateral prefrontal cortex, the dependence is due to a lack of internal initiation and planning. With lesions of the orbitofrontal prefrontal cortex, the problem is impaired restraint. Lesions in any of these areas will interfere with intentionality and voluntariness via their effects on executive control functions (7,8). However, it is important to keep in mind that psychiatric illnesses rarely present in as stark and clear-cut a fashion as direct neurological lesions. Subtle deficits in executive control functions may be overlooked in the presence of more florid symptoms, such as agitation and psychosis.

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Schizophrenia

Although the specific findings have varied, there is rich evidence that prefrontal abnormalities are present in patients with schizophrenia. Executive dysfunction is commonly assessed with instruments such as the Wisconsin Card Sorting Test (WCST), the Halstead Category Test, and the Trail Making Test-Part B (31,32,33). Impairment on these measures has been widely documented in patients with schizophrenia (12,34,35). However, such findings are tempered by heterogeneity of performance, with some patients demonstrating essentially no deficits and others showing severe impairment across a wide range of neuropsychological tests (34,36).

Functional neuroimaging has been more consistent in demonstrating frontal system dysfunction, perhaps because of its greater sensitivity. Many of the findings from neuroimaging studies are consistent with Weinberger's developmental "hypofrontality" theory of schizophrenia (37), whereby negative symptoms, which include executive dysfunction, are explained by a relative decrease in mesocortical dopaminergic projections and positive symptoms by an increase in mesolimbic projections of dopamine. Both single photon emission computed tomography (SPECT) and positron-emission tomography (PET) studies have shown a decrease in perfusion in the prefrontal cortex, particularly the dorsolateral prefrontal cortex, when patients perform an executive function task, compared with normal controls (38,39,40,41,42).

Studies with patients at rest—that is, in the absence of involvement in a task—have been less reliable but may differentiate between positive and negative symptoms of schizophrenia. In most studies negative symptoms are strongly correlated with decreased blood flow, especially to the anterior cingulate gyrus and the dorsolateral prefrontal cortex (43,44,45). Positive symptoms such as hallucinations and delusions have been associated with multiple abnormalities of the parietal, temporal, and frontal lobes, sometimes with an increase in metabolism in the anterior cingulate and orbitofrontal prefrontal cortex (44,46,47,48,49).

Newer technology such as magnetic resonance spectroscopy also supports the thesis that patients with schizophrenia have an abnormality in the dorsolateral prefrontal cortex. Schizophrenic patients of all types—acute, drug naïve, or chronic—show a decrease in membrane precursors in that area, and patients at an early stage in the disease also show an increase in membrane breakdown products (50,51). There also appears to be a decrease in the ratio of N-acetyl aspartate, a marker of neuronal integrity, to creatine or choline in the dorsolateral prefrontal cortex and hippocampus of medicated and unmedicated patients with schizophrenia (52,53,54,55). Taken together these findings provide strong support for the theory that executive functions, and therefore intentionality and voluntariness, are impaired in some schizophrenia patients.

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Affective disorders

In general, patients with unipolar or bipolar depression perform better on neuropsychological tests than patients with schizophrenia, and reports of deficits are not as well substantiated in patients with depression. However, subtle deficits are found in executive functions, as tested by the Category Test and the WCST (56,57). Sackeim and colleagues (58) used another measure of executive function, the performance subsections of the Wechsler Adult Intelligence Scale-Revised IQ test, to test inpatients with moderate to severe depression. These patients did show a decrease in performance scores that was not accounted for by psychomotor retardation. However, these results are somewhat confounded by the fact that approximately one-third of the patients met criteria for probable or definite psychosis at the time of testing.

Again, neuroimaging has proved helpful in investigating deficits not well assessed by present testing instruments. SPECT and PET studies show a decrease in cerebral blood flow to the prefrontal cortices and the limbic and paralimbic areas (48,59,60,61). Recent studies have also shown a normalization in the blood flow of patients with major depression in remission, a phenomenon not seen among patients with schizophrenia (62,63). Hence there appears to be some level of prefrontal deficit in depression, and it may be reversible with treatment.

Almost all research on affective disorders and frontal dysfunction has focused on depression, perhaps because of the difficulty patients with mania have in maintaining attention and cooperation for prolonged testing. However, among manic patients who have been included in a few SPECT studies, abnormalities in both the frontal and the temporal lobes have been shown (64,65). As far as executive control function testing is concerned, one might speculate from the clinical findings in mania that these patients would have difficulty with tasks of attention and concentration, which would impair performance on the higher-order functions of planning and cognitive set-switching. Obviously these postulations must be regarded cautiously until supported by clinical data.

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Anxiety

The anxiety disorders appear to be heterogeneous in their origin and neurobehavioral manifestations, and none except obsessive-compulsive disorder have been shown to consistently impair performance on neuropsychological testing. Specifically, frontal lobe dysfunction with impaired set-shifting and performance IQ has been detected in patients with obsessive-compulsive disorder as well as deficits in memory and visuospatial skills (66,67). In patients with other diagnoses in the anxiety spectrum, some researchers have found mild deficits on tasks of memory and attention, including the Trail Making test (68,69,70), but these results have not been well replicated.

Unfortunately, the literature in this area is sparse, and relatively few neuroimaging studies of patients with anxiety have been conducted, compared with studies of patients with psychotic and mood disorders (71). However, the PET and SPECT studies that have been done suggest increased activity ("hyperactivity") of the orbitofrontal and cingulate cortices in patients in anxious states (72,73,74). Again, this hyperactivity is most well documented in the specific case of obsessive-compulsive disorder (75,76,77,78). As in the case of depression, these abnormalities in blood flow have been shown to normalize with effective treatment (79). Deficits in attention can impair intentionality, and deficits in memory can impair both intentionality and voluntariness.

Although neuroimaging is still in the experimental stage and not yet reliable enough for diagnostic testing of individual patients (80), it has helped tremendously in demonstrating the definite presence of abnormalities in the prefrontal neural pathways of patients with schizophrenia, mood disorders, and some anxiety disorders. To make use of this burgeoning crop of data, one must be able to extrapolate the results to the individual patient. What signs and symptoms indicate to the health professional that the patient has prefrontal deficits? How are these signs and symptoms related specifically to impairment of intentionality and voluntariness?

As discussed above, the prefrontal area, with its myriad connections, is the seat of executive control functioning, which may be tapped—albeit imperfectly—by certain neuropsychological tests. Using these tools along with careful clinical observation and a detailed history, the clinician may collect valuable data to aid in assessing patients' level of decisional autonomy and therefore of their capacity to participate in the informed consent process.

The skills that are required for adequate intentionality can be moderately well tested by current instruments, but the clinical interview is crucial. Patients with depression or schizophrenia with prominent apathy often have difficulty initiating detailed plans. They may be able to understand that they have a disease—and even to delineate the specifics of their illness—and express a desire to "get better" and leave the hospital. However, they are less likely to have a coherent idea of what specifically they will do when they are discharged, how they will prevent relapse, and how they might cope with an unstable external environment.

Acutely psychotic and manic patients, in contrast, might express numerous ideas and "plans" for the future but not be able to maintain attention and remember their ideas from one moment to the next. Patients with anxiety can suffer from confusion and difficulties with short-term memory, which can also impede effective execution of a plan. In all of these cases, the intentionality aspect of decisional autonomy is impaired, and the patients' ability to participate in the informed consent process should be questioned.

Voluntariness also may be diminished by apathy, as when patients with depression feel hopeless and do not care what is done to them. Some patients may even make choices contrary to their values and "nondepressed" desires, out of a feeling that they are guilty and deserve punishment. Actively psychotic patients may have clear and enduring desires but suffer from auditory command hallucinations. If these commands contradict their own choices, fear of reprisal may prevent a voluntary decision.

Apathetic, psychotic, and manic patients all may exhibit stimulus-bound behavior, as tested by the WCST and other tests, reflecting undue influence by external cues. Patients with anxiety may perform well on tests but still be dependent on outside opinions because of overwhelming fear and low self-esteem. Thus the clinician may unwittingly control response by verbal and nonverbal suggestion. The responses of these patients should be probed to determine why they are making specific choices and how their choices correspond to their own values and goals. Great care must be taken to avoid the paternalistic assumption that an agreeable patient is a competent patient.

We believe that intentionality and voluntariness, along with understanding, should be requirements for decisional autonomy. We realize that this is a controversial stance and that some would argue that by taking a comprehensive conceptual and clinical approach, we are unjustifiably limiting the autonomy of psychiatric patients. However, we would respond that it is the disease itself that limits a patient's autonomy and that to ignore these deficits is to do a disservice to the patient.

Consider, for instance, the case of a patient with chronic schizophrenia, repeatedly admitted in a state of florid psychosis to an inpatient unit and known to be noncompliant with his medications on the outside. By the end of each admission, he is stable enough to understand his illness and to meet all the current criteria for legal competency. Hence he is released, despite the staff's knowing full well that he will soon be returned to the emergency service in great distress from his delusions and hallucinations. Our claim is that this patient continues to have prefrontal deficits and would ultimately enjoy greater autonomy if it were recognized that he cannot cope with the stresses of a completely independent existence but requires some level of continuous support and supervision.

This line of reasoning leads to three main conclusions. First, assessment of competency to participate in the informed consent process must be a much more rigorous procedure than is currently considered acceptable. Kitamura and associates (6) reviewed multiple instruments—and offered their own—for this purpose, but none of these instruments can adequately assess the subtle skills required for intentionality and voluntariness. More recently, Moore (81) developed a guide that begins to address these issues, but the focus remains on understanding.

Because it may not be possible in the emergent setting to perform in-depth testing before obtaining consent, we agree with the recommendations of the American Psychiatric Association (APA) that provisional treatment, either voluntary or involuntary, should be implemented as necessary, with a delay of formal adjudication procedures until a full assessment can be made (82). Even on inpatient units, a full neuropsychological battery often is not feasible, but the inclusion of brief objective executive control function testing and an interview that probes prefrontal function would not be an unreasonable demand on the clinician's time.

Royall and associates (83) developed the Executive Interview (EXIT) for older patients whose general incapacities preclude use of more intensive instruments such as the WCST. Because of the primary importance of avoiding false-positive tests of diminished decision-making capacity, patients should be assessed at several times in different modalities—written and oral, using the aid of family members, and so on (4). The goal is to avoid cursory assessments in which superficial deficits may be mistaken for cerebral impairments.

This testing should occur only after patients have been thoroughly educated about their disease process and treatment options and given any other information they need to participate in the development of their treatment plan. As suggested in the APA resource document on informed consent, disclosure should proceed in stages, giving the patient time to understand, assimilate, and accept the information (82).

Second, when capacity to participate in the informed consent process is found to be diminished, the next logical step is to restore that capacity. This is where the greatest burden of research lies—in the development of cognitive and behavioral strategies as well as psychodynamic and family-support-based techniques that will increase the patient's autonomy.

Again, interim measures may be necessary so that urgent treatment can proceed while the restoration is attempted. Adequate decisional and executive autonomy can be quickly restored to many patients with proper treatment, particularly those with acute, nonchronic conditions. Under these circumstances, interval testing and reevaluation are essential, and the medical community may do well to discern more precisely the line between "state" and "trait" illnesses. Because some research suggests that impairment of executive control function in patients with schizophrenia is developmentally "locked in"—trait rather than state—by the time of first diagnosis (36,84), another focus of investigation should be earlier diagnosis of these patients.

Finally, new strategies for psychiatric care must be developed to meet the challenges of an increasingly complex view of autonomy. The dichotomous view must be abandoned in favor of a tiered, sliding-scale approach both to the informed consent process and to treatment modalities. At present, personal care homes and skilled nursing facilities provide some middle ground, but they are inadequate to meet the needs of a psychiatric population consisting mainly of patients in the gray zone of decisional autonomy. Outpatient facilities cannot provide the required support and follow-up monitoring, so these patients often end up bouncing in and out of emergency rooms and locked units at great emotional and financial expense. The emotional distress is also felt by health care workers, who are frustrated by their lack of alternatives in treating such patients.

In public facilities, the financial expense is transmitted to society. Changes in the health care system that actively address the complex decisional autonomy needs of patients and provide nuanced environmental supports may at first be costly and time consuming, but the result will be a streamlined mental health care system that more efficiently provides the greatest benefit of care with the least restrictive treatment alternative. In this way we hope to preserve and increase rather than diminish the autonomy of patients with psychiatric illnesses.

The work in this paper was supported by grant R01-NR-04736 from the National Institutes of Health, the Department of Energy, and the Veterans Affairs Consortium on Informed Consent and by a Veterans Affairs Health Services Research and Development Service Advanced Research Career Development Award.

Dr. Grimes, who was a medical student at Baylor College of Medicine in Houston when this study was completed, is a resident in the department of psychiatry at the University of California, San Diego. Dr. McCullough is with the Center for Medical Ethics and Health Policy at Baylor College of Medicine, and Dr. Kunik, Dr. Molinari, and Dr. Workman are with the department of psychiatry and behavioral sciences. All except Dr. Grimes are also affiliated with the Huffington Center on Aging at Baylor and the Veterans Integrated Service Network 16 Mental Illness Research Education and Clinical Center. Send correspondence to Dr. Kunik, Houston Center for Quality of Care and Utilization Studies, Houston Veterans Affairs Medical Center, 2002 Holcombe Boulevard (152), Houston, Texas 77030 (e-mail, mkunik@bcm.tmc.edu).

Faden RR, Beauchamp TL: A History and Theory of Informed Consent. New York, Oxford University Press, 1986
 
Dyer AR, Bloch S: Informed consent and the psychiatric patient. Journal of Medical Ethics 13:12-16,  1987
[PubMed]
[CrossRef]
 
Grisso T, Appelbaum PS: Assessing Competence to Consent to Treatment: A Guide for Physicians and Other Health Professionals. New York, Oxford University Press, 1998
 
Grisso T, Appelbaum PS: Comparison of standards for assessing patients' capacities to make treatment decisions. American Journal of Psychiatry 152:1033-1037,  1995
[PubMed]
 
Kitamura T, Kitamura F, Mitsuhashi T, et al: Image of psychiatric patients' competency to give informed consent to treatment in Japan. International Journal of Law and Psychiatry 22:45-54,  1999
[PubMed]
[CrossRef]
 
Kitamura F, Tomoda A, Tsukada K, et al: Method for assessment of competency to consent in the mentally ill: rationale, development, and comparison with the medically ill. International Journal of Law and Psychiatry 21:223-244,  1998
[PubMed]
[CrossRef]
 
Workman RH, McCullough LB, Molinari V, et al: Clinical and ethical implications of impaired executive control functions for patient autonomy. Psychiatric Services 51:359-363,  2000
[PubMed]
[CrossRef]
 
Workman RH, Molinari V, Rezabek P, et al: An ethical framework for understanding patients with antisocial personality disorder who develop dementia. Journal of Ethics, Law, and Aging 3:79-90,  1997
[PubMed]
 
Appelbaum PS: Missing the boat: competence and consent in psychiatric research. American Journal of Psychiatry 155:1486-1488,  1998
[PubMed]
 
Bonnie RJ: Research with cognitively impaired subjects: unfinished business in the regulation of human research. Archives of General Psychiatry 54:105-111,  1997
[PubMed]
 
Elliott C: Caring about risks: are severely depressed patients competent to consent to research? Archives of General Psychiatry 54:113-116,  1997
 
Jones GH: Informed consent in chronic schizophrenia? British Journal of Psychiatry 167:565-568,  1995
 
Melamed Y, Kimchi Y, Shnit D, et al: Clinical assessment of competency to consent to psychiatric hospitalization. International Journal of Law and Psychiatry 22:55-64,  1999
[PubMed]
[CrossRef]
 
Royall DR, Cordes J, Polk M: Executive control and the comprehension of medical information by elderly retirees. Experimental Aging Research 23:301-313,  1997
[PubMed]
[CrossRef]
 
Appelbaum BC, Appelbaum PS, Grisso T: Competence to consent to voluntary psychiatric hospitalization: a test of a standard proposed by APA. Psychiatric Services 49:1193-1196,  1998
[PubMed]
 
Grisso T, Appelbaum PS: Assessing patients' capacities to consent to treatment. New England Journal of Medicine 319:1635-1638,  1988
[PubMed]
[CrossRef]
 
Marson DC, Chatterjee MD, Ingram KK, et al: Toward a neurologic model of competency: cognitive predictors of capacity to consent in Alzheimer's disease using three different legal standards. Neurology 46:666-672,  1996
[PubMed]
 
Bean G, Nishisato S, Rector NA, et al: The psychometric properties of the Competency Interview Schedule. Canadian Journal of Psychiatry 39:368-376,  1994
 
Coverdale JH, Chervenak FA, McCullough LB, et al: Ethically justified clinically comprehensive guidelines for the management of the depressed pregnant patient. American Journal of Obstetrics and Gynecology 175:496-500,  1996
[PubMed]
[CrossRef]
 
Stanley B, Stanley M: Psychiatric patients' comprehension of consent information. Psychopharmacology Bulletin 23:375-378,  1987
[PubMed]
 
Wirshing DA, Wirshing WC, Marder SR, et al: Informed consent: assessment of comprehension. American Journal of Psychiatry 155:1508-1511,  1998
[PubMed]
 
White BC: Competence to Consent. Washington, DC, Georgetown University Press, 1994
 
Salloway SP: Diagnosis and treatment of patients with "frontal lobe" syndromes. Journal of Neuropsychiatry and Clinical Neurosciences 6:388-398,  1994
[PubMed]
 
Lhermitte F: Human autonomy and the frontal lobes: II. patient behavior in complex and social situations: the "environmental dependency syndrome." Annals of Neurology 19:335-343,  1986
[PubMed]
[CrossRef]
 
Alexander GE, Crutcher MD, DeLong MR: Basal ganglia-thalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal," and "limbic" functions. Progress in Brain Research 85:119-146,  1990
[PubMed]
 
Cummings JL: Frontal-subcortical circuits and human behavior. Archives of Neurology 50:17-24,  1993
[PubMed]
 
Mega MS, Cummings JL: Frontal-subcortical circuits and neuropsychiatric disorders. Journal of Neuropsychiatry and Clinical Neurosciences 6:358-370,  1994
[PubMed]
 
Damasio AR. The time-locked multiregional retroactiviation: a systems level proposal for the neural substrates of recall and recognition. Cognition 33:25,  1989
[PubMed]
[CrossRef]
 
Fuster JM: The Prefrontal Cortex: Anatomy, Physiology, and Neuropsychiatry of the Frontal Lobe, 2nd ed. New York, Raven, 1989
 
Harlow JM: Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society 2:327-347,  1868
 
Halstead WC: Brain and Intelligence: A Quantitative Study of the Frontal Lobes. Chicago, University of Chicago Press, 1947
 
Heaton RK, Chelune GJ, Talley JL, et al: Wisconsin Card Sorting Test Manual: Revised and Expanded. Odessa, Fla, Psychological Assessment Resources, 1993
 
Reitan RM, Davison LA: Clinical Neuropsychology: Current Status and Applications. New York, Wiley, 1974
 
Braff DL, Heaton R, Kuck J, et al: The generalized pattern of neuropsychological deficits in outpatients with chronic schizophrenia with heterogeneous Wisconsin Card Sorting Test results. Archives of General Psychiatry 48:891-898,  1991
[PubMed]
 
Daniel DG, Weinberger DR, Jones DW, et al: The effect of amphetamine on regional cerebral blood flow during cognitive activation in schizophrenia. Journal of Neuroscience 11:1907-1917,  1991
[PubMed]
 
Goldstein G: Neuropsychological heterogeneity in schizophrenia: a consideration of abstraction and problem-solving abilities. Archives of Clinical Neuropsychology 5:251-264,  1990
[PubMed]
 
Weinberger D: Implications of normal brain development for the pathogenesis of schizophrenia. Archives of General Psychiatry 44:660-669,  1987
[PubMed]
 
Berman KF, Ostrem JL, Randolph C, et al: Physiological activation of a cortical network during performance of the Wisconsin Card Sorting Test: a positron emission tomography study. Neuropsychologia 33:1027-1046,  1995
[PubMed]
[CrossRef]
 
Berman KF, Torrey EF, Daniel DG, et al: Regional cerebral blood flow in monozygotic twins discordant and concordant for schizophrenia. Archives of General Psychiatry 49:927-934,  1992
[PubMed]
 
Carter CS, Perlstein W, Ganguli R, et al: Functional hypofrontality and working memory dysfunction in schizophrenia. American Journal of Psychiatry 155:1285-1287,  1998
[PubMed]
 
Parellada E, Catafau AM, Bernardo M, et al: The resting and activation issue of hypofrontality: a single-photon emission computed tomography study in neuroleptic-naïve and neuroleptic-free schizophrenic female patients. Biological Psychiatry 44:787-790,  1998
[PubMed]
[CrossRef]
 
Rubin P, Holm S, Friberg L, et al: Altered modulation of prefrontal and subcortical brain activity in newly diagnosed schizophrenia and schizophreniform disorder. Archives of General Psychiatry 48:987-995,  1991
[PubMed]
 
Ebmeier KP, Blackwood DHR, Murray C, et al: Single-photon emission computed tomography with 99mTc-exametazime in unmedicated schizophrenic patients. Biological Psychiatry 33:487-495,  1993
[PubMed]
[CrossRef]
 
Liddle PF, Friston KJ, Frith CD, et al: Patterns of cerebral blood flow in schizophrenia. British Journal of Psychiatry 160:179-186,  1992
[PubMed]
[CrossRef]
 
Wolkin A, Sanfilipo M, Wolf AP, et al: Negative symptoms and hypofrontality in chronic schizophrenia. Archives of General Psychiatry 49:959-965,  1992
[PubMed]
 
Cleghorn JM, Franco S, Szechtman B, et al: Toward a brain map of auditory hallucinations. American Journal of Psychiatry 149:1062-1069,  1992
[PubMed]
 
Cleghorn JM, Garnett ES, Nahmias C, et al: Increased frontal and reduced parietal glucose metabolism in acute untreated schizophrenia. Psychiatry Research 28:119-133,  1989
[PubMed]
[CrossRef]
 
Kishimoto H, Yamada K, Iseki E, et al: Brain imaging of affective disorders and schizophrenia. Psychiatry and Clinical Neurosciences 52(suppl):S212-S214, 1998
 
Silbersweig DA, Stern E, Frith C, et al: A functional neuroanatomy of hallucinations in schizophrenia. Nature 378:176-179,  1995
[PubMed]
[CrossRef]
 
Pettegrew JW, Keshavan MS, Panchalingam K, et al: Alterations in brain high-energy phosphate and membrane phospholipid metabolism in first-episode, drug-naïve schizophrenics: a pilot study of the dorsoprefrontal cortex by in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Archives of General Psychiatry 48:563-568,  1991
[PubMed]
 
Stanley JA, Williamson PC, Drost DJ, et al: An in vivo study of the prefrontal cortex of schizophrenic patients at different stages of illness via phosphorus magnetic resonance spectroscopy. Archives of General Psychiatry 52:399-406,  1995
[PubMed]
 
Bertolino A, Callicott JH, Elman I, et al: Regionally specific neuronal pathology in untreated patients with schizophrenia: a proton magnetic resonance spectroscopic imaging study. Biological Psychiatry 43:641-648,  1998
[PubMed]
[CrossRef]
 
Bertolino A, Callicott JH, Nawroz S, et al: Reproducibility of proton magnetic resonance spectroscopic imaging in patients with schizophrenia. Neuropsychopharmacology 18:1-9,  1998
[PubMed]
[CrossRef]
 
Bertolino A, Nawroz S, Mattay VS, et al: Regionally specific pattern of neurochemical pathology in schizophrenia as assessed by multislice proton magnetic resonance spectroscopic imaging. American Journal of Psychiatry 153:1554-1563,  1996
[PubMed]
 
Deicken RF, Zhou L, Schuff N, et al: Hippocampal neuronal dysfunction in schizophrenia as measured by proton magnetic resonance spectroscopy. Biological Psychiatry 43:483-488,  1998
[PubMed]
[CrossRef]
 
Goldman R, Axelrod B, Tompkins L: Effect of instructional cues on schizophrenic patients' performance on the Wisconsin Card Sorting Test. American Journal of Psychiatry 149:1718-1722,  1992
[PubMed]
 
Savard R, Rey A, Post R: Halstead-Reitan Category Test in bipolar and unipolar affective disorders. Journal of Nervous and Mental Disease 168:297-304,  1980
[PubMed]
[CrossRef]
 
Sackeim HA, Freeman J, McElhiney M, et al: Effects of major depression on estimates of intelligence. Journal of Clinical and Experimental Neuropsychology 14:268-288,  1992
[PubMed]
[CrossRef]
 
Ebmeier KP, Prentice N, Ryman A, et al: Temporal lobe abnormalities in dementia and depression: a study using high resolution single photon emission tomography and magnetic resonance imaging. Journal of Neurology, Neurosurgery, and Psychiatry 63:597-604,  1997
[PubMed]
[CrossRef]
 
Galynker II, Cai J, Ongseng F, et al: Hypofrontality and negative symptoms in major depressive disorder. Journal of Nuclear Medicine 39:608-612,  1998
[PubMed]
 
Ito H, Kawashima R, Awata S, et al: Hypoperfusion in the limbic system and prefrontal cortex in depression: SPECT with anatomic standardization technique. Journal of Nuclear Medicine 37:410-414,  1996
[PubMed]
 
Mayberg HS, Liotti M, Brannan SK, et al: Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness. American Journal of Psychiatry 156:675-682,  1999
[PubMed]
 
Ogura A, Morinobu S, Kawakatsu S, et al: Changes in regional brain activity in major depression after successful treatment with antidepressant drugs. Acta Psychiatrica Scandinavica 98:54-59,  1998
[PubMed]
[CrossRef]
 
Goodwin GM, Cavanagh JT, Glabus MF, et al: Uptake of 99mTc-exametazime shown by single photon emission computed tomography before and after lithium withdrawal in bipolar patients: associations with mania. British Journal of Psychiatry 170:426-430,  1997
[PubMed]
[CrossRef]
 
O'Connell RA, Vantleertum RL, Luck D, et al: Single-photon emission computed tomography of the brain in acute mania and schizophrenia. Journal of Neuroimaging 5:101-104,  1995
[PubMed]
 
Behar D, Rapoport JL, Berg CJ, et al: Computerized tomograph and neuropsychological test measures in adolescents with obsessive-compulsive disorder. American Journal of Psychiatry 145:363-369,  1984
[CrossRef]
 
Head D, Bolton D, Hymas N: Deficit in cognitive shifting ability in patients with obsessive-compulsive disorder. Biological Psychiatry 25:929-937,  1989
[PubMed]
[CrossRef]
 
King G, Hannay J, Masek B, et al: Effects of anxiety and sex on neuropsychological tests. Journal of Consulting and Clinical Psychology 46:375-376,  1978
[PubMed]
[CrossRef]
 
Martin N, Franzen M: The effect of anxiety on neuropsychological function. International Journal of Clinical Neuropsychology 11:1-8,  1989
[CrossRef]
 
Tyler S, Tucker D: Anxiety and perceptual structure: individual differences in neuropsychological function. Journal of Abnormal Psychology 91:210-220,  1982
[PubMed]
[CrossRef]
 
Charney DS, Nagy LM, Bremer JD, et al: Neurobiological mechanisms of human anxiety, in Neuropsychiatry. Edited by Fogel BS, Schiffer RB, Rao SM. Baltimore, Williams & Wilkins, 1996
 
Gur RC: Measurement and imaging of regional brain function: implications for neuropsychiatry, in Laterality in Psychopathology. Edited by Flor-Henry P, Gruzelier J. Amsterdam, Elsevier, 1983
 
Johanson AM, Risberg J, Silfverskiold P, et al: Regional changes of cerebral blood flow during increased anxiety in patients with anxiety neurosis, in The Roots of Perception. Edited by Hentsche U, Smith G, Draguns JG. Amsterdam, Elsevier, 1986
 
Wu JC, Buchsbaum MS, Hershey TG, et al: PET in generalized anxiety disorder. Biological Psychiatry 29:1181-1199,  1991
[PubMed]
[CrossRef]
 
Baxter LR, Schwartz JM, Phelps ME, et al: Cerebral glucose metabolic rates in nondepressed patients with obsessive-compulsive disorder. American Journal of Psychiatry 145:1560-1563,  1988
[PubMed]
 
Baxter LR, Phelps ME, Mazziotta JC, et al: Local cerebral glucose metabolic rates in obsessive-compulsive disorder: a comparison with rates in unipolar depression and in normal controls. Archives of General Psychiatry 44:211-218,  1987
[PubMed]
 
Insel T: Toward a neuroanatomy of obsessive-compulsive disorder. Archives of General Psychiatry 49:739-744,  1992
[PubMed]
 
Swedo SE, Schapiro MB, Grady CL, et al: Cerebral glucose metabolism in childhood-onset obsessive-compulsive disorder. Archives of General Psychiatry 46:518-523,  1989
[PubMed]
 
Benkelfat C, Nordahal TE, Semple WE, et al: Local cerebral glucose metabolic rates in obsessive-compulsive disorder: patients treated with clomipramine. Archives of General Psychiatry 47:840-848,  1990
[PubMed]
 
Nemeroff CB, Kilts CD, Berns GS: Functional brain imaging: twenty-first-century phrenology or psychobiological advance for the millennium? American Journal of Psychiatry 156:671-673,  1999
 
Moore RF: A guide to the assessment and care of the patient whose medical decision-making capacity is in question. Medscape General Medicine [online serial], Nov 10, 1999. Available at http://psychiatry.medscape.com/medscape/generalmedicine/journal/1999/v01.n11/mgm1110.moor/mgm1110.moor-01.html
 
American Psychiatric Association resource document on the principles of informed consent in psychiatry. Journal of the American Academy of Psychiatry and Law 25:121-125,  1997
 
Royall DR, Mahurin RK, Gray KF: Bedside assessment of executive cognitive impairment: the Executive Interview. Journal of the American Geriatrics Society 40:1221-1226,  1992
[PubMed]
 
Scully PJ, Coakley G, Kinsella A, et al: Psychopathology, executive (frontal), and general cognitive impairment in relation to duration of initially treated versus subsequently treated psychosis in chronic schizophrenia. Psychological Medicine 27:1303-1310,  1997
[PubMed]
[CrossRef]
 
+

References

Faden RR, Beauchamp TL: A History and Theory of Informed Consent. New York, Oxford University Press, 1986
 
Dyer AR, Bloch S: Informed consent and the psychiatric patient. Journal of Medical Ethics 13:12-16,  1987
[PubMed]
[CrossRef]
 
Grisso T, Appelbaum PS: Assessing Competence to Consent to Treatment: A Guide for Physicians and Other Health Professionals. New York, Oxford University Press, 1998
 
Grisso T, Appelbaum PS: Comparison of standards for assessing patients' capacities to make treatment decisions. American Journal of Psychiatry 152:1033-1037,  1995
[PubMed]
 
Kitamura T, Kitamura F, Mitsuhashi T, et al: Image of psychiatric patients' competency to give informed consent to treatment in Japan. International Journal of Law and Psychiatry 22:45-54,  1999
[PubMed]
[CrossRef]
 
Kitamura F, Tomoda A, Tsukada K, et al: Method for assessment of competency to consent in the mentally ill: rationale, development, and comparison with the medically ill. International Journal of Law and Psychiatry 21:223-244,  1998
[PubMed]
[CrossRef]
 
Workman RH, McCullough LB, Molinari V, et al: Clinical and ethical implications of impaired executive control functions for patient autonomy. Psychiatric Services 51:359-363,  2000
[PubMed]
[CrossRef]
 
Workman RH, Molinari V, Rezabek P, et al: An ethical framework for understanding patients with antisocial personality disorder who develop dementia. Journal of Ethics, Law, and Aging 3:79-90,  1997
[PubMed]
 
Appelbaum PS: Missing the boat: competence and consent in psychiatric research. American Journal of Psychiatry 155:1486-1488,  1998
[PubMed]
 
Bonnie RJ: Research with cognitively impaired subjects: unfinished business in the regulation of human research. Archives of General Psychiatry 54:105-111,  1997
[PubMed]
 
Elliott C: Caring about risks: are severely depressed patients competent to consent to research? Archives of General Psychiatry 54:113-116,  1997
 
Jones GH: Informed consent in chronic schizophrenia? British Journal of Psychiatry 167:565-568,  1995
 
Melamed Y, Kimchi Y, Shnit D, et al: Clinical assessment of competency to consent to psychiatric hospitalization. International Journal of Law and Psychiatry 22:55-64,  1999
[PubMed]
[CrossRef]
 
Royall DR, Cordes J, Polk M: Executive control and the comprehension of medical information by elderly retirees. Experimental Aging Research 23:301-313,  1997
[PubMed]
[CrossRef]
 
Appelbaum BC, Appelbaum PS, Grisso T: Competence to consent to voluntary psychiatric hospitalization: a test of a standard proposed by APA. Psychiatric Services 49:1193-1196,  1998
[PubMed]
 
Grisso T, Appelbaum PS: Assessing patients' capacities to consent to treatment. New England Journal of Medicine 319:1635-1638,  1988
[PubMed]
[CrossRef]
 
Marson DC, Chatterjee MD, Ingram KK, et al: Toward a neurologic model of competency: cognitive predictors of capacity to consent in Alzheimer's disease using three different legal standards. Neurology 46:666-672,  1996
[PubMed]
 
Bean G, Nishisato S, Rector NA, et al: The psychometric properties of the Competency Interview Schedule. Canadian Journal of Psychiatry 39:368-376,  1994
 
Coverdale JH, Chervenak FA, McCullough LB, et al: Ethically justified clinically comprehensive guidelines for the management of the depressed pregnant patient. American Journal of Obstetrics and Gynecology 175:496-500,  1996
[PubMed]
[CrossRef]
 
Stanley B, Stanley M: Psychiatric patients' comprehension of consent information. Psychopharmacology Bulletin 23:375-378,  1987
[PubMed]
 
Wirshing DA, Wirshing WC, Marder SR, et al: Informed consent: assessment of comprehension. American Journal of Psychiatry 155:1508-1511,  1998
[PubMed]
 
White BC: Competence to Consent. Washington, DC, Georgetown University Press, 1994
 
Salloway SP: Diagnosis and treatment of patients with "frontal lobe" syndromes. Journal of Neuropsychiatry and Clinical Neurosciences 6:388-398,  1994
[PubMed]
 
Lhermitte F: Human autonomy and the frontal lobes: II. patient behavior in complex and social situations: the "environmental dependency syndrome." Annals of Neurology 19:335-343,  1986
[PubMed]
[CrossRef]
 
Alexander GE, Crutcher MD, DeLong MR: Basal ganglia-thalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal," and "limbic" functions. Progress in Brain Research 85:119-146,  1990
[PubMed]
 
Cummings JL: Frontal-subcortical circuits and human behavior. Archives of Neurology 50:17-24,  1993
[PubMed]
 
Mega MS, Cummings JL: Frontal-subcortical circuits and neuropsychiatric disorders. Journal of Neuropsychiatry and Clinical Neurosciences 6:358-370,  1994
[PubMed]
 
Damasio AR. The time-locked multiregional retroactiviation: a systems level proposal for the neural substrates of recall and recognition. Cognition 33:25,  1989
[PubMed]
[CrossRef]
 
Fuster JM: The Prefrontal Cortex: Anatomy, Physiology, and Neuropsychiatry of the Frontal Lobe, 2nd ed. New York, Raven, 1989
 
Harlow JM: Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society 2:327-347,  1868
 
Halstead WC: Brain and Intelligence: A Quantitative Study of the Frontal Lobes. Chicago, University of Chicago Press, 1947
 
Heaton RK, Chelune GJ, Talley JL, et al: Wisconsin Card Sorting Test Manual: Revised and Expanded. Odessa, Fla, Psychological Assessment Resources, 1993
 
Reitan RM, Davison LA: Clinical Neuropsychology: Current Status and Applications. New York, Wiley, 1974
 
Braff DL, Heaton R, Kuck J, et al: The generalized pattern of neuropsychological deficits in outpatients with chronic schizophrenia with heterogeneous Wisconsin Card Sorting Test results. Archives of General Psychiatry 48:891-898,  1991
[PubMed]
 
Daniel DG, Weinberger DR, Jones DW, et al: The effect of amphetamine on regional cerebral blood flow during cognitive activation in schizophrenia. Journal of Neuroscience 11:1907-1917,  1991
[PubMed]
 
Goldstein G: Neuropsychological heterogeneity in schizophrenia: a consideration of abstraction and problem-solving abilities. Archives of Clinical Neuropsychology 5:251-264,  1990
[PubMed]
 
Weinberger D: Implications of normal brain development for the pathogenesis of schizophrenia. Archives of General Psychiatry 44:660-669,  1987
[PubMed]
 
Berman KF, Ostrem JL, Randolph C, et al: Physiological activation of a cortical network during performance of the Wisconsin Card Sorting Test: a positron emission tomography study. Neuropsychologia 33:1027-1046,  1995
[PubMed]
[CrossRef]
 
Berman KF, Torrey EF, Daniel DG, et al: Regional cerebral blood flow in monozygotic twins discordant and concordant for schizophrenia. Archives of General Psychiatry 49:927-934,  1992
[PubMed]
 
Carter CS, Perlstein W, Ganguli R, et al: Functional hypofrontality and working memory dysfunction in schizophrenia. American Journal of Psychiatry 155:1285-1287,  1998
[PubMed]
 
Parellada E, Catafau AM, Bernardo M, et al: The resting and activation issue of hypofrontality: a single-photon emission computed tomography study in neuroleptic-naïve and neuroleptic-free schizophrenic female patients. Biological Psychiatry 44:787-790,  1998
[PubMed]
[CrossRef]
 
Rubin P, Holm S, Friberg L, et al: Altered modulation of prefrontal and subcortical brain activity in newly diagnosed schizophrenia and schizophreniform disorder. Archives of General Psychiatry 48:987-995,  1991
[PubMed]
 
Ebmeier KP, Blackwood DHR, Murray C, et al: Single-photon emission computed tomography with 99mTc-exametazime in unmedicated schizophrenic patients. Biological Psychiatry 33:487-495,  1993
[PubMed]
[CrossRef]
 
Liddle PF, Friston KJ, Frith CD, et al: Patterns of cerebral blood flow in schizophrenia. British Journal of Psychiatry 160:179-186,  1992
[PubMed]
[CrossRef]
 
Wolkin A, Sanfilipo M, Wolf AP, et al: Negative symptoms and hypofrontality in chronic schizophrenia. Archives of General Psychiatry 49:959-965,  1992
[PubMed]
 
Cleghorn JM, Franco S, Szechtman B, et al: Toward a brain map of auditory hallucinations. American Journal of Psychiatry 149:1062-1069,  1992
[PubMed]
 
Cleghorn JM, Garnett ES, Nahmias C, et al: Increased frontal and reduced parietal glucose metabolism in acute untreated schizophrenia. Psychiatry Research 28:119-133,  1989
[PubMed]
[CrossRef]
 
Kishimoto H, Yamada K, Iseki E, et al: Brain imaging of affective disorders and schizophrenia. Psychiatry and Clinical Neurosciences 52(suppl):S212-S214, 1998
 
Silbersweig DA, Stern E, Frith C, et al: A functional neuroanatomy of hallucinations in schizophrenia. Nature 378:176-179,  1995
[PubMed]
[CrossRef]
 
Pettegrew JW, Keshavan MS, Panchalingam K, et al: Alterations in brain high-energy phosphate and membrane phospholipid metabolism in first-episode, drug-naïve schizophrenics: a pilot study of the dorsoprefrontal cortex by in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Archives of General Psychiatry 48:563-568,  1991
[PubMed]
 
Stanley JA, Williamson PC, Drost DJ, et al: An in vivo study of the prefrontal cortex of schizophrenic patients at different stages of illness via phosphorus magnetic resonance spectroscopy. Archives of General Psychiatry 52:399-406,  1995
[PubMed]
 
Bertolino A, Callicott JH, Elman I, et al: Regionally specific neuronal pathology in untreated patients with schizophrenia: a proton magnetic resonance spectroscopic imaging study. Biological Psychiatry 43:641-648,  1998
[PubMed]
[CrossRef]
 
Bertolino A, Callicott JH, Nawroz S, et al: Reproducibility of proton magnetic resonance spectroscopic imaging in patients with schizophrenia. Neuropsychopharmacology 18:1-9,  1998
[PubMed]
[CrossRef]
 
Bertolino A, Nawroz S, Mattay VS, et al: Regionally specific pattern of neurochemical pathology in schizophrenia as assessed by multislice proton magnetic resonance spectroscopic imaging. American Journal of Psychiatry 153:1554-1563,  1996
[PubMed]
 
Deicken RF, Zhou L, Schuff N, et al: Hippocampal neuronal dysfunction in schizophrenia as measured by proton magnetic resonance spectroscopy. Biological Psychiatry 43:483-488,  1998
[PubMed]
[CrossRef]
 
Goldman R, Axelrod B, Tompkins L: Effect of instructional cues on schizophrenic patients' performance on the Wisconsin Card Sorting Test. American Journal of Psychiatry 149:1718-1722,  1992
[PubMed]
 
Savard R, Rey A, Post R: Halstead-Reitan Category Test in bipolar and unipolar affective disorders. Journal of Nervous and Mental Disease 168:297-304,  1980
[PubMed]
[CrossRef]
 
Sackeim HA, Freeman J, McElhiney M, et al: Effects of major depression on estimates of intelligence. Journal of Clinical and Experimental Neuropsychology 14:268-288,  1992
[PubMed]
[CrossRef]
 
Ebmeier KP, Prentice N, Ryman A, et al: Temporal lobe abnormalities in dementia and depression: a study using high resolution single photon emission tomography and magnetic resonance imaging. Journal of Neurology, Neurosurgery, and Psychiatry 63:597-604,  1997
[PubMed]
[CrossRef]
 
Galynker II, Cai J, Ongseng F, et al: Hypofrontality and negative symptoms in major depressive disorder. Journal of Nuclear Medicine 39:608-612,  1998
[PubMed]
 
Ito H, Kawashima R, Awata S, et al: Hypoperfusion in the limbic system and prefrontal cortex in depression: SPECT with anatomic standardization technique. Journal of Nuclear Medicine 37:410-414,  1996
[PubMed]
 
Mayberg HS, Liotti M, Brannan SK, et al: Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness. American Journal of Psychiatry 156:675-682,  1999
[PubMed]
 
Ogura A, Morinobu S, Kawakatsu S, et al: Changes in regional brain activity in major depression after successful treatment with antidepressant drugs. Acta Psychiatrica Scandinavica 98:54-59,  1998
[PubMed]
[CrossRef]
 
Goodwin GM, Cavanagh JT, Glabus MF, et al: Uptake of 99mTc-exametazime shown by single photon emission computed tomography before and after lithium withdrawal in bipolar patients: associations with mania. British Journal of Psychiatry 170:426-430,  1997
[PubMed]
[CrossRef]
 
O'Connell RA, Vantleertum RL, Luck D, et al: Single-photon emission computed tomography of the brain in acute mania and schizophrenia. Journal of Neuroimaging 5:101-104,  1995
[PubMed]
 
Behar D, Rapoport JL, Berg CJ, et al: Computerized tomograph and neuropsychological test measures in adolescents with obsessive-compulsive disorder. American Journal of Psychiatry 145:363-369,  1984
[CrossRef]
 
Head D, Bolton D, Hymas N: Deficit in cognitive shifting ability in patients with obsessive-compulsive disorder. Biological Psychiatry 25:929-937,  1989
[PubMed]
[CrossRef]
 
King G, Hannay J, Masek B, et al: Effects of anxiety and sex on neuropsychological tests. Journal of Consulting and Clinical Psychology 46:375-376,  1978
[PubMed]
[CrossRef]
 
Martin N, Franzen M: The effect of anxiety on neuropsychological function. International Journal of Clinical Neuropsychology 11:1-8,  1989
[CrossRef]
 
Tyler S, Tucker D: Anxiety and perceptual structure: individual differences in neuropsychological function. Journal of Abnormal Psychology 91:210-220,  1982
[PubMed]
[CrossRef]
 
Charney DS, Nagy LM, Bremer JD, et al: Neurobiological mechanisms of human anxiety, in Neuropsychiatry. Edited by Fogel BS, Schiffer RB, Rao SM. Baltimore, Williams & Wilkins, 1996
 
Gur RC: Measurement and imaging of regional brain function: implications for neuropsychiatry, in Laterality in Psychopathology. Edited by Flor-Henry P, Gruzelier J. Amsterdam, Elsevier, 1983
 
Johanson AM, Risberg J, Silfverskiold P, et al: Regional changes of cerebral blood flow during increased anxiety in patients with anxiety neurosis, in The Roots of Perception. Edited by Hentsche U, Smith G, Draguns JG. Amsterdam, Elsevier, 1986
 
Wu JC, Buchsbaum MS, Hershey TG, et al: PET in generalized anxiety disorder. Biological Psychiatry 29:1181-1199,  1991
[PubMed]
[CrossRef]
 
Baxter LR, Schwartz JM, Phelps ME, et al: Cerebral glucose metabolic rates in nondepressed patients with obsessive-compulsive disorder. American Journal of Psychiatry 145:1560-1563,  1988
[PubMed]
 
Baxter LR, Phelps ME, Mazziotta JC, et al: Local cerebral glucose metabolic rates in obsessive-compulsive disorder: a comparison with rates in unipolar depression and in normal controls. Archives of General Psychiatry 44:211-218,  1987
[PubMed]
 
Insel T: Toward a neuroanatomy of obsessive-compulsive disorder. Archives of General Psychiatry 49:739-744,  1992
[PubMed]
 
Swedo SE, Schapiro MB, Grady CL, et al: Cerebral glucose metabolism in childhood-onset obsessive-compulsive disorder. Archives of General Psychiatry 46:518-523,  1989
[PubMed]
 
Benkelfat C, Nordahal TE, Semple WE, et al: Local cerebral glucose metabolic rates in obsessive-compulsive disorder: patients treated with clomipramine. Archives of General Psychiatry 47:840-848,  1990
[PubMed]
 
Nemeroff CB, Kilts CD, Berns GS: Functional brain imaging: twenty-first-century phrenology or psychobiological advance for the millennium? American Journal of Psychiatry 156:671-673,  1999
 
Moore RF: A guide to the assessment and care of the patient whose medical decision-making capacity is in question. Medscape General Medicine [online serial], Nov 10, 1999. Available at http://psychiatry.medscape.com/medscape/generalmedicine/journal/1999/v01.n11/mgm1110.moor/mgm1110.moor-01.html
 
American Psychiatric Association resource document on the principles of informed consent in psychiatry. Journal of the American Academy of Psychiatry and Law 25:121-125,  1997
 
Royall DR, Mahurin RK, Gray KF: Bedside assessment of executive cognitive impairment: the Executive Interview. Journal of the American Geriatrics Society 40:1221-1226,  1992
[PubMed]
 
Scully PJ, Coakley G, Kinsella A, et al: Psychopathology, executive (frontal), and general cognitive impairment in relation to duration of initially treated versus subsequently treated psychosis in chronic schizophrenia. Psychological Medicine 27:1303-1310,  1997
[PubMed]
[CrossRef]
 
+
+

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