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Conceptualization of psychotic disorders changed throughout the 20th century, with previously postulated etiologies including biological disease (1), faulty socialization from double-blind communication (2), and primitive defense mechanisms resulting in primary process thinking (3). Current evidence strongly indicates that schizophrenia and other psychosis are brain disorders (4). The DSM-IV nomenclature distinguishes between primary psychosis and secondary psychosis (5). While there have been several definitions of psychosis, symptoms such as delusions and (or) prominent hallucinations are considered to be the defining features for this diagnosis. The most common primary psychotic disorders are the schizophrenia spectrum disorders. In schizophrenia spectrum disorders, diagnosis is based on the presence of positive and (or) negative symptoms that rule out other etiologies such as mood disorders, medical conditions, pervasive developmental disorder, or schizoaffective disorder. The specific type of schizophrenia spectrum disorder is primarily defined by severity, duration, progression, presence of stressors, recovery of function, and nature of psychotic symptoms. For example, in brief psychotic reaction, the duration is less than 1 month with full recovery of functioning, whereas in schizophreniform disorder, the duration of the episode lasts between 1 and 6 months. In contrast to the criteria for schizophrenia, a significant decline in premorbid abilities is not required. For patients meeting the criteria for schizophrenia, subtypes are then delineated by the presence of such major clinical features as paranoia, disorganization, and catatonia. By contrast, secondary psychotic disorders are those believed to have etiologies from a medical condition and (or) substance abuse. Diagnosis for these conditions is based on the presence of psychotic symptoms that are attributed to an identified medical condition or substance abuse. It is argued that the separate categories for primary and secondary psychoses may be an unnecessary distinction, because psychosis in schizophrenia could be considered secondary to intrauterine (6,7), viral (8), or genetic factors (9). Indeed, schizophrenia may be a group of psychoses with different presentations related to different etiologies (10). This alternative conceptualization of schizophrenia and psychotic disorders illustrates many of the major criticisms of the DSM-IV nomenclature, including the following:
On a practical level, the symptom-based nosology of the DSM-IV results in both diagnostic and treatment problems for clinicians. Diagnostic problems arise because symptoms are not pathonomonic of disorders (16). Thus many diagnostic dilemmas occur because of an overlap in criteria, for example, in the case of methamphetamine-induced psychosis. This disorder often presents with auditory hallucinations and paranoid delusions that are very similar to the presentation of persons with schizophrenia (18). The diagnostic problem occurs when the psychosis persists more than a month after withdrawal. According to long-term studies in Japan, this is not uncommon: 18% to 26% of those suffering from methamphetamine psychosis continued to experience symptoms more than a month after drug discontinuation (18,19). In such cases of treatment-refractory methamphetamine psychosis, where there is a suspected etiology and temporal association between risk factor and onset of symptoms, the DSM-IV criteria indicate that schizophrenia should still be considered as the primary diagnosis. Similar problems of comorbidity exist because many patients diagnosed with schizophrenia also have medical problems such as traumatic brain injury (20,21) and substance abuse conditions (22), which may contribute to the psychosis. Other problems involve conceptualization and treatment. Once a diagnosis is made, many clinicians discontinue searching for other possible causes, which can result in a false sense of having more understanding of the disorder than they actually do (14), possibly leading to improper or inadequate treatment. Given the symptom-based criteria of the DSM-IV, the etiology of many disorders is still unknown after a diagnosis is made (12). For example, the diagnosis of schizophrenia has limited prognostic value, owing to the heterogeneity of the disorder. In a study of long-term outcome in schizophrenia, Bleuler identified 9 different courses of illness (23). In addition, cluster analytic studies of neuropsychological functioning consistently report 4 to 5 cluster solutions that are associated with functional outcome (24). A better understanding of psychotic illness, one involving knowledge of the biological mechanisms and etiology, is especially important for further refinement of treatment, particularly psycho- pharmacologic treatment. Because different atypical antipsychotics selectively target different neurotransmitter systems (25), treatment can potentially be individualized with a better conceptualization of underlying mechanisms of psychosis across all diagnostic categories. Similarly, in conditions where other mechanisms may be involved in the development of psychotic symptoms, such as abnormal temporolimbic activation in temporal lobe epilepsy (TLE) or cholinergic mechanisms in Alzheimer’s dementia, other agents, such as anticonvulsants or even cholinesterase inhibitors, may be used along with antipsychotics (26,27). Given that schizophrenia and other psychotic disorders are disturbances in brain function and that there are weaknesses in DSM-IV nomenclature, this paper argues for conceptualizing psychotic disorders as a neurobiological syndrome with different etiologies. This syndrome consists of a constellation of symptoms, such as hallucinations and delusions, that are similar in nature to other symptoms with a neurobiological basis, such as aphasia, acalculia, or apraxia. The psychotic syndrome would indicate an underlying neural network dysfunction similar to those seen in syndromes such as dementia (with its subtypes of cortical and frontal-subcortical dementia), Kluver Bucy syndrome, and Gerstmann’s syndrome. We argue that a neurobiological conceptualization of psychotic disorders provides a more accurate understanding of the disorder than the diagnostic criteria of the DSM-IV, which are both symptom-based and arbitrary duration cut-off based. Such a conceptualization would therefore be more useful clinically and would facilitate integration of research in psychosis. We organized this paper into 4 parts. In Part 1, we describe the criteria for a neurobiological syndrome; in Part 2, we present the empirical evidence for conceptualizing psychosis as a neurobiological disorder; in Part 3, we present clinical and research implications of our proposed conceptualization; and finally, in Part 4, we discuss the limitations of current literature supporting psychosis as a neurobiological syndrome. Criteria for a Neurobiological SyndromeWe propose 5 criteria for a neurobiological syndrome, presented below and summarized in Table 1. First, a neurobiological syndrome is a constellation of symptoms that are reliably associated with disturbance that is functional, structural, neurochemical, or neuropathological in a circumscribed structural location or neural circuit. For example, in aphasia, there is impairment of specific brain function (such as language comprehension) associated with Wernicke’s area in the posterior left auditory association cortex and impairment of language production associated with Broca’s area in the inferior left frontal gyrus. Dysfunction of both Wernicke’s and Broca’s areas, as well as of the arcuate fasciculus, which connects them, leads to problems in the repetition of language. There is also evidence indicating that dysfunction in subcortical areas such as white matter connections and the thalamus can lead to problems in language production and comprehension (28). Problems in prosody are associated with dysfunction of the right hemispheric counterparts of Wernicke’s and Broca’s areas (29).
Second, similar neurobiological disturbances (that is, in the location or in the neural circuit) that are secondary to different etiologies would result in similar cognitive or behavioural symptoms. For example, there are many different neuropathological processes that can result in aphasic symptoms. Aphasia can be secondary to traumatic brain injury (TBI), cerebral vascular accidents, dementia of the Alzheimer’s type (DAT), or neoplasms (that is, if Broca’s or Wernicke’s areas, connections, or related circuits are affected by these disease processes; 28). Third, smaller amounts of similar neurobiologic disturbances are associated with milder symptoms. The severity of aphasia of different etiologies is generally mediated by the amount of damage, with larger amounts of damage associated with more severe symptoms. In addition, damage to connecting areas of the circuit, such as the thalamus, cerebellum, or subcortical white matter or areas adjacent to Broca’s and Wernicke’s can result in similar but generally milder aphasic symptoms (28). Fourth, additional symptoms such as cognitive, mood, psychiatric, or other associated neurological symptoms are related to other networks being simultaneously affected by underlying neurochemical or neuropathologic processes. Aphasia owing to anterior lesions has been associated with depression, while posterior lesions have been associated with unawareness, unconcern, or paranoia (28). Other associated neurological disorders include ideomotor apraxia, mild hemisensory loss, and Gerstmann’s syndrome (28). Fifth, aside from treating the underlying disease process, treatment for the associated symptoms of a neurobiological disorder of different etiologies is similar. Treatment of aphasic symptoms generally involves speech therapy and is the same for all types of aphasias, independent of etiology (28). Evidence for Schizophrenia-Like Psychosis as a Neurobiological SyndromePsychotic disorder has been conceptualized as an impairment of consciousness affecting the individual’s ability to determine boundaries between the self and the environment and to formulate effective behaviours and decisions for everyday life (4). Andreasen coined the term “cognitive dysmetria” to describe the fundamental cognitive problem in schizophrenia. She described this as poor coordination or synchronization of thought and action (30). Frith describes schizophrenia-like psychosis as a breakdown in the self-monitoring of thoughts, internal language, or initiation, similar to the phenomenon of corollary discharge in vision (31). The neuropathology of schizophrenia-like psychosis is purported to result from dysfunction in a widespread neural circuit, resulting in both structural and neurochemical abnormalities (4,32). Accumulating evidence from structural and functional brain-imaging studies suggests that psychosis is associated with neuropathology in the frontal and temporal systems at both the gross anatomical and neuronal levels (33,34). Similarly, several neurotransmitter systems underlying these brain regions, such as the dopaminergic and serotonergic projections, glutamatergic pyramidal neurons, N-methyl-D-aspartate (NMDA) receptors, and GABA interneurons and receptors, also appear to be involved in the symptomatology of psychotic disorders such as schizophrenia (35). These abnormalities are believed to result in a breakdown of the normal relation between the temporolimbic areas and the frontal subcortical structures (36,37). More specifically, there seems to be a relative overactivity of the temporolimbic system in relation to the monitoring activity by the frontal-thalamic-cerebellar executive system (30,38,39). There is converging evidence indicating that psychotic disorders of different etiologies are associated with abnormalities to frontal and temporal areas. Frontal and temporal disorders have been associated with psychosis secondary to cerebral vascular accidents (40), brain tumors (41), TBI (42), and affective psychosis (43). Impairment in these regions has also been implicated in delusional disorders such as erotomania (44), Capgras syndrome (45), and Cotard’s delusion (46). In addition, neurologic disorders most commonly associated with secondary psychosis, such as DAT, TLE, and velocardiofacial syndrome, are associated with pathology in the temporal areas (47–49). Evidence suggests that individuals with DAT and TLE who develop psychosis also demonstrate frontal abnormalities or a more generalized cerebral disturbance (50–52). Other disorders presenting with psychotic symptoms include systemic lupus erythrematous (53) and multiple sclerosis (54). Neurochemically, psychosis is most commonly associated with drugs that increase dopamine, such as cocaine and methamphetamine, or that affect the NMDA receptor, such as phencyclidine and ketamine (18,19,55,56). Evidence for the next proposed criterion (that is, that smaller amounts of similar neurobiological disturbances are associated with milder symptoms) comes from studies on schizotypal personality disorder (SPD). Neuroimaging studies indicate that persons with SPD demonstrate structural abnormalities similar to those found in persons with schizophrenia; however, SPD patients have smaller volumetric decreases either in the frontal cortex and mediodorsal nucleus of the thalamus (57) or in the medial temporal lobes and lateral ventricles (58). Torgerson and others reported that persons with SPD without a first relative with schizophrenia demonstrated milder positive and general psychiatric symptoms than did those with a first relative (59). Additional support for a dosage-related pathology comes from studies of persons with late-onset schizophrenia. In their review of the late-onset schizophrenia literature, Palmer and others reported that persons with middle-age and late-onset schizophrenia demonstrated less severe negative symptoms and larger thalamic volumes and responded to lower dosages of neuroleptic medication (60). There is evidence that other common comorbid symptoms of schizophrenia-like psychosis share similar pathologies. For example, depression has been associated with pathology to the subgenual cingulate and its connection to medial temporal lobe structures, such as the amygdala (61), while lack of initiation or avolition has been associated with mesial-frontal and dorsolateral prefrontal pathology (62). Common cognitive deficits of executive dysfunction and memory are not only associated with abnormalities to frontal and temporal areas but have also been found in persons with psychosis secondary to epilepsy (63), TBI (63,64), and psychotic depression (43,65). Evidence for psychosis as a neurobiological syndrome is also supported by the treatment approach used in psychosis. Antipsychotics, including the atypical neuroleptics, reduce psychotic symptoms, regardless of diagnosis or etiology. They seem to work by similar mechanisms of action, involving dopaminergic or serotonergic mechanisms, particularly in the mesolimbic and mesocortical systems (66–68). Other treatments may be necessary to address other etiologic mechanisms, such as antiepileptics for psychosis in epilepsy or other associated functional deficits (11). Also, if the antipsychotic agents are not effective, the issue may be whether other confounding pharmacologic properties, such as anticholinergic effects, worsen the psychosis. Clinical and Research ImplicationsWe believe that the conceptualization of psychosis as a neurobiological syndrome will have implications for both clinicians and researchers. Currently, when diagnosing psychotic disorders without an obvious organic or drug-induced etiology, the general practice is to match the symptoms with criteria for schizophrenia spectrum disorder. As previously mentioned, this practice often results in a false sense of explanation, because etiologic processes and pathogenesis of symptoms are still unknown. In contrast, if psychosis is conceptualized as a neurobiological syndrome that can result from different etiologic factors affecting a distinct neural network and neurochemical circuit, the clinician is forced to search for potential etiologic factors and relate these factors to the patient’s presentation. We argue that using such a neurobiological syndromal approach would be more clinically useful and more accurate in describing individual presentations than would current DSM-IV nomenclature. The former approach has the following advantages: First, this manner of conceptualization ties presentation with neuropathology and etiology. Second, clinical conceptualization would be more individualized, with an emphasis on clinically useful information not available in a broad diagnostic category. Third, diagnostic dilemmas would be avoided because clinicians would search and determine pertinent etiologic factors affecting the neurobiological network, rather than expending time and energy placing a patient into a classification scheme of primary and secondary psychotic disorders with little bearing on actual treatment. Fourth, the heterogeneity issue is addressed by associating psychosis with etiology and neuropathology. Fifth, this manner of conceptualization, based on patient-specific descriptors, facilitates individualized treatment, which is particularly important with the development of atypical antipsychotics that selectively target different neurotransmitter systems. In addition to its clinical utility, conceptualizing psychosis as a neurobiological syndrome could profoundly influence research. The current tendency in research is to compartmentalize psychotic disorders of different etiologies and diagnostic categories. Although this practice is methodologically important, it can result in artificial and disparate knowledge bases with little integration of information. Unfortunately, current practice prevents a broader understanding of psychosis by comparing psychotic disorders with different etiologies. It is argued that a broad spectrum of psychosis can not only expedite our understanding of brain mechanisms underlying the disorder but can also provide clues to the heterogeneity of presentation. Similar approaches are being considered for disorders such as depression (59,69). LimitationsAlthough a neurobiological approach to conceptualizing psychotic disorders holds promise for improving patient diagnosis and treatment, there are currently several limitations. First, neurobiological circuits in psychosis are not well understood in terms of general functioning, such as the interaction between the brain structure and neurotransmitters, the interaction between neurotransmitter systems, and how these interactions change over time. Second, the localization literature on psychosis is inconsistent, and there are many contradictions. Third, the current research on psychotic symptoms other than schizophrenia is sparse, with little data on prognosis. Still, it is argued that there is enough consistency in the accumulating data to consider such a framework, and indeed, other neurobiological models have already been proposed (30,32,70). It is also likely that current studies are based on relatively crude neuroimaging technology and will improve with research employing more sophisticated technology with higher resolution, such as functional neuroimaging (fMRI) and magnetic resonance (that is, MR spectroscopy and positron emission tomography scanning). 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Does fast dissociation from the dopamine D2 receptor explain the action of atypical antipsychotics? A new hypothesis. Am J Psychiatry 2001;158:360–9. 69. Mayberg HS. Limbic-cortical dysregulation: a proposed model of depression. J Neuropsychiatry Clin Neurosci 1997;9:471–81. 70. Tsuang M, Stone W, Faraone S. Toward reformulating the diagnosis of schizophrenia. Arch Gen Psychiatry 2000:157:1041–50. 71. Heilman KM, Gonzalez Rothi LJ. Apraxia. In: Heilman KM, Valenstein E, editors. Clinical neuropsychology. 4th ed. New York: Oxford University Press; 2003. p 215–35. Author(s)Manuscript received July 2003, revised, and accepted August 2004. 1. Clinical Neuropsychologist, Department of Psychology, Department of Psychiatry, Hawaii State Hospital, Kaneohe, Hawaii. 2. Professor of Psychiatry, John A Burns School of Medicine, University of Hawaii, Manoa, Hawaii. Address for correspondence: Dr D Fujii, Department of Psychiatry, 1356 Lusitana St, 4th Floor, Honolulu, HI 96813 e-mail: defujii@hsh.health.state.hi.us
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