When Top-Down Meets Bottom-Up: Auditory Training Enhances Verbal Memory in Schizophrenia

Duke University Department of Psychiatry and Center for Cognitive Neuroscience, University of California, San Francisco, CA, USA.
Schizophrenia Bulletin (Impact Factor: 8.45). 10/2009; 35(6):1132-41. DOI: 10.1093/schbul/sbp068
Source: PubMed


A critical research priority for our field is to develop treatments that enhance cognitive functioning in schizophrenia and thereby attenuate the functional losses associated with the illness. In this article, we describe such a treatment method that is grounded in emerging research on the widespread sensory processing impairments of schizophrenia, as described elsewhere in this special issue. We first present the rationale for this treatment approach, which consists of cognitive training exercises that make use of principles derived from the past 2 decades of basic science research in learning-induced neuroplasticity; these exercises explicitly target not only the higher order or "top-down" processes of cognition but also the content building blocks of accurate and efficient sensory representations to simultaneously achieve "bottom-up" remediation. We then summarize our experience to date and briefly review our behavioral and serum biomarker findings from a randomized controlled trial of this method in outpatients with long-term symptoms of schizophrenia. Finally, we present promising early psychophysiological evidence that supports the hypothesis that this cognitive training method induces changes in aspects of impaired bottom-up sensory processing in schizophrenia. We conclude with the observation that neuroplasticity-based cognitive training brings patients closer to physiological patterns seen in healthy participants, suggesting that it changes the brain in an adaptive manner in schizophrenia.

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Available from: Corby L Dale
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    • "Adcock et al. (55) performed the very first study of MEG and CRT, which compared participants receiving auditory training for 50 h with healthy controls. They investigated the M1 response to two presented syllables, which relates to signal attenuation between the first and second presented syllables (Dale, 2010). "
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    ABSTRACT: Cognitive impairment is an important aspect of schizophrenia, where cognitive remediation therapy (CRT) is a promising treatment for improving cognitive functioning. While neurobiological dysfunction in schizophrenia has been the target of much research, the neural substrate of cognitive remediation and recovery has not been thoroughly examined. The aim of the present article is to systematically review the evidence for neural changes after CRT for schizophrenia. The reviewed studies indicate that CRT affects several brain regions and circuits, including prefrontal, parietal, and limbic areas, both in terms of activity and structure. Changes in prefrontal areas are the most reported finding, fitting to previous evidence of dysfunction in this region. Two limitations of the current research are the few studies and the lack of knowledge on the mechanisms underlying neural and cognitive changes after treatment. Despite these limitations, the current evidence suggests that CRT is associated with both neurobiological and cognitive improvement. The evidence from these findings may shed light on both the neural substrate of cognitive impairment in schizophrenia, and how better treatment can be developed and applied.
    Full-text · Article · Aug 2014 · Frontiers in Psychiatry
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    • "For example, following 50 h of plasticity-based auditory training , chronic schizophrenia patients made significant gains in global cognition, processing speed, verbal working memory, and learning and memory metrics (e.g., Fisher et al., 2009a,b). In parallel, brains of trained subjects compared with controls recovered more normal M100 responses to successive signals consistent with recovery of more normal perceptual abilities resulting from training (Adcock et al., 2009; Dale et al., 2010); recovered more strongly correlated (recovered) gamma frequency responses in the lower gamma frequency (Popov et al., 2012); recovered stronger responses to rapidly successive stimuli in the gamma high-frequency domain (Dale et al., under review); more strongly synchronized alpha frequency responses for target stimuli, and more strongly de-synchronized non-target domain alpha-band responses in an attention-controlled task (Popov et al., 2012; Dale et al., under review); recovered more normal sensory gating (Popov et al., 2011); recovered more normal dorsolateral frontal responses in a working memory task (Dale et al., under review); restored more normal patterns of response in an attributionof-source task (Subramaniam et al., 2012; see Figure 1); recovered more normal amygdala and ventral-lateral-frontal cortical responses in an emotion recognition task (Hooker et al., 2012, 2013); recovered more normal BDNF expression (Vinogradov et al., 2009); among other physical and functional neurological measures of plastic training-driven recovery. While these studies are still a work in progress, taken together, they indicate that this form of computerized, neuroplasticitybased training is effective for broadly driving behavioral "
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    ABSTRACT: The primary objective of this review article is to summarize how the neuroscience of brain plasticity, exploiting new findings in fundamental, integrative and cognitive neuroscience, is changing the therapeutic landscape for professional communities addressing brain-based disorders and disease. After considering the neurological bases of training-driven neuroplasticity, we shall describe how this neuroscience-guided perspective distinguishes this new approach from (a) the more-behavioral, traditional clinical strategies of professional therapy practitioners, and (b) an even more widely applied pharmaceutical treatment model for neurological and psychiatric treatment domains. With that background, we shall argue that neuroplasticity-based treatments will be an important part of future best-treatment practices in neurological and psychiatric medicine.
    Full-text · Article · May 2014 · Frontiers in Human Neuroscience
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    • "One of the reasons that bottom-up influences are still underrepresented in scientific literature may be the implicit nature of sensory integration disturbances. The interplay between top-down and bottom-up processes is however evident (Adcock et al., 2009; Silverstein et al., 2012). Many mechanisms investigated from various perspectives, support our hypothesis: disturbances of neural synchrony and reduced NMDA neurotransmission (Uhlhaas et al., 2008; Woo et al., 2010), dysconnectivity and plasticity (Stephan et al., 2009), changes in brain architecture involved in self-processes (Wylie and Tregellas, 2010; Guo et al., 2012), cognitive dissonance theory (Festinger, 1957; van Veen et al., 2009), aberrant salience (Kapur, 2003), social defeat hypothesis (Selten and Cantor-Grae, 2005), and psychodynamic theories in which is surmised that psychosis can be explained as an attempt to restore the defective 'self' (Kohut and Wolfe, 1978; Schore, 2009). "
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    ABSTRACT: The aim of this review is to describe the potential relationship between multisensory disintegration and self-disorders in schizophrenia spectrum disorders. Sensory processing impairments affecting multisensory integration have been demonstrated in schizophrenia. From a developmental perspective multisensory integration is considered to be crucial for normal self-experience. An impairment of multisensory integration is called 'perceptual incoherence'. We theorize that perceptual incoherence may evoke incoherent self-experiences including depersonalization, ambivalence, diminished sense of agency, and 'loosening of associations' between thoughts, feelings and actions that lie within the framework of 'self-disorders' as described by Sass and Parnas (2003). We postulate that subconscious attempts to restore perceptual coherence may induce hallucinations and delusions. Increased insight into mechanisms underlying 'self-disorders' may enhance our understanding of schizophrenia, improve recognition of early psychosis, and extend the range of therapeutic possibilities.
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