RESUMEN
AIMS: Our article consists in both analysis and synthesis of contemporary cognitive models of auditory verbal hallucinations (AVHs) in schizophrenia. Our work is based on the analysis of the scientific literature including original articles, literature reviews as well as meta-analysis. METHODOLOGY: In order to identify the most pertinent studies in the electronic search, the three following databases were systematically searched: PubMed, PsycINFO and MEDLINE. For both the analysis and synthesis we selected original articles, literature reviews as well as meta-analysis referring to any cognitive explanation of the auditory hallucinatory experience in schizophrenia. A cognitive model of auditory hallucinations refers to any incorporation of cognitive frameworks and explanations in one's conceptualization of the hallucinatory phenomenon in schizophrenia. We also focused our work on past conceptualization of auditory hallucinations in order to explain the development and the contribution of current cognitive models in the understanding of the onset and the maintaining of AVHs. After a brief review of clinical characteristics and historical conceptualization of auditory verbal hallucinations, contemporary explanations were presented in the area of schizophrenia. These explanations referred to researches into cognitive psychopathology including metacognitive as well as neuroimaging studies. RESULTS: The examination of scientific literature highlighted the complexity of AVHs through multifactorial explanations here mostly explained by cognitive and metacognitive deficits. We synthesized former conceptualizations of AVHs, which were sustained on mechanistic or sensory explanations. Esquirol, Baillarger and Briere de Boismont were the first as conceiving AVHs as a perception disorder and introduced the idea that auditory hallucinations resulted from a failure to control one's memories/fantasies. Later, Broca and Wernicke discovered auditory areas in the human brain implicated in language comprehension and production. AVHs began to be conceptualized by the scientific world as being mechanistically brain-related. Sigmund Freud was among the first to study the meaning of AVHs, a domain still being investigated by todays cognitive sciences. More recently, neuroimaging studies allowed the validation of these sensory explanations in considering the onset of AVHs through the deficit of cortical and subcortical areas implicated in the process of languages (e.g. Broca and Wernicke areas) and emotions (e.g. limbic system, amygdala, hippocampus). At a more mechanistic level, contemporary cognitive models of AVHs explained AVHs as an intrusive verbal representation into the awareness which is non-inhibited (i.e. deficit in intentional inhibition) and also non-recognized as one's own experience (i.e. deficit in source monitoring, planning and metacognition), or even attributed to an external source (attribution bias). In terms of inhibitory control, inhibition is a basic cognitive mechanism defined as a collection of processes that allows the suppression of previously activated cognitive contents and the clearing of irrelevant actions or attention from consciousness. Intentional inhibition is effortful and occurs when an individual deliberately suppresses the activation of an item after deciding it is irrelevant. Theoretical support for the suggestion that an inhibitory failure is involved in AVHs in schizophrenia arises from studies that have shown that a failure in inhibition results in intrusive thoughts from long-term memory. Recent findings also found that individuals with AVHs in schizophrenia demonstrated an impaired source monitoring. In episodic memory research, a distinction was made between content (an event) and context (e.g. source or temporal characteristics of an event) information. The context of memories provides cues that allow an individual to differentiate one memory from other memories. AVHs are conceptualized as a failure to access the contextual cues that would allow voice-hearer to form an intact representation of events in memories. Regarding planning, AVHs refer to the intrusion of unwanted memories into the inner speech that are not recognized from one's own representation. Previous cognitive theories highlighted the important role played by metacognitive skills and belief (i.e. thinking about one's thinking) in the explanation of AVHs. Finally, the external attribution bias was extensively studied over the last three decades and refers to the tendency to attribute negative events (situational or cognitive) to an external source. In this framework, AVHs refer to intrusive thoughts externally attributed to a voice. CONCLUSION: For more than one century, scientific discoveries in (bio)medical science have allowed the validation of former sensory and mechanistic explanations of AVHs. Nevertheless, many explanatory models account for the way AVHs are maintained (source monitoring, deficit in planning, externalizing bias), while they scarcely expose how they are triggered (intrusive thoughts, deficit in inhibition). The relation between AVHs and intrusive thoughts still remain unclear, and further studies are needed for the understanding of a potential causal relationship.
Asunto(s)
Alucinaciones/etiología , Esquizofrenia/complicaciones , Psicología del Esquizofrénico , Encéfalo/diagnóstico por imagen , Encéfalo/fisiopatología , Cognición/fisiología , Alucinaciones/patología , Humanos , Metacognición/fisiología , Neuroimagen/métodos , Neuroimagen/estadística & datos numéricos , Esquizofrenia/diagnóstico , Esquizofrenia/patología , Esquizofrenia/fisiopatologíaRESUMEN
OBJECTIVES: Based on clinical, phenomenological and neurobiological observations, psychiatrists often report a deficit in time estimation in patients with schizophrenia. Cognitive models of time estimation in healthy subjects have been proposed and developed for approximately 30 years. The investigation of time perception is pertinent to the understanding of neurobiological and cognitive abnormalities in schizophrenia. Brain lesions and neuroimaging studies have shown that the critical brain structures engaged in time perception include the prefrontal and parietal lobes, thalamus, basal ganglia and cerebellum. These brain areas have been implicated in the physiopathology of schizophrenia in that there is impaired coordination of activity among these regions. Clinical and experimental date strongly suggest that patients with schizophrenia are less accurate in their ability to estimate time than healthy subjects. The specificity of these clinical and behavioral impairments is still in question. The aims of this article are to present an overview of the literature regarding time estimation and schizophrenia, to discuss specific issues related to how perceptual dysfunction in schizophrenia may lead to abnormalities in time perception, and to propose new perspectives towards an integrative approach between phenomenology and neuroscience. METHODS: We present a review of the literature describing the current theory in the field of time perception, which is supported by a connectionist model, postulating that temporal judgment is based upon a pacemaker-counter device that depends mostly upon memory and attentional resources. The pacemaker emits pulses that are accumulated in a counter, and the number of pulses determines the perceived length of an interval. Patients with schizophrenia are known to display attentional and memory dysfunctions. Moreover, dopamine regulation mechanisms are involved in both the temporal perception and schizophrenia. DISCUSSION: It is still unclear if temporal impairments in schizophrenia are related to a specific disturbance in central temporal processes or are due to certain cognitive problems, such as attentional and memory dysfunctions, or biological abnormalities. While psychopathological and phenomenological work strongly suggests that time perception disturbance may be the key or core symptom in schizophrenia, neuroscience studies have failed to do the same. The question of specificity of temporal perception impairments in schizophrenia remains contested. Neuroscience studies suggest that time symptoms in patients with schizophrenia are only secondary to thought disorders and primary cognitive impairments. This debate refers to the etiologic/organic versus psychogenesis/psychological dichotomy and may be over-taken. CONCLUSION: Clinical evidence associated with psychopathological, biological and cognitive theories strongly suggests that patients with schizophrenia have a deficit in time perception. Discrimination and reproduction of durations have been found to be constantly impaired and disorganized. There is still much work to be done to identify the exact sources of variability in temporal judgments in schizophrenia, and the study of developmental course of time perception could be an interesting route. Regardless of the role of temporal deficits in the pathogenesis of schizophrenia (as a general cognitive disorder or a core role), clinical and phenomenological data encourage us to conduct further studies, especially in the field of developmental psychology.