Modeling Deficits From Early Auditory Information Processing to Psychosocial Functioning in Schizophrenia

Michael, Thomas; Green, Michael F.; Hellemann, Gerhard; Sugar, Catherine A.; Tarasenko, Melissa; Calkins, Monica E.; Greenwood, Tiffany A.; Gur, Raquel E.; Gur, Ruben C.; Lazzeroni, Laura C.; Nuechterlein, Keith H.; Radant, Allen D.; Seidman, Larry J.; Shiluk, Alexandra; Siever, Larry J.; Silverman, Jeremy M.; Sprock, Joyce; Stone, William S.; Swerdlow, Neal R.; Tsuang, Debby W.; Tsuang, Ming T.; Turetsky, Bruce I.; Braff, David L.; Light, Gregory A.

doi:10.1001/jamapsychiatry.2016.2980

Cited by 168 publications

(151 citation statements)

References 83 publications

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“…Similar patterns are observed in the auditory P50 measure of sensory-motor gating (Freedman et al, 1987) and in auditory mismatch negativity. Some data support a model in which early auditory processing deficits lead to poor functional outcome via impaired cognition and greater negative symptoms (Thomas et al, 2017).…”

Section: Erpsmentioning

confidence: 84%

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Seidman

Mirsky

2017

J Int Neuropsychol Soc

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We review the changing conceptions of schizophrenia over the past 50 years as it became understood as a disorder of brain function and structure in which neurocognitive dysfunction was identified at different illness phases. The centrality of neurocognition has been recognized, especially because neurocognitive deficits are strongly related to social and role functioning in the illness, and as a result neurocognitive measures are used routinely in clinical assessment of individuals with schizophrenia. From the original definitions of the syndrome of schizophrenia in the early 20th century, impaired cognition, especially attention, was considered to be important. Neurocognitive impairments are found in the vast majority of individuals with schizophrenia, and they vary from mild, relatively restricted deficits, to dementia-like syndromes, as early as the first psychotic episode. Neurocognitive deficits are found in the premorbid phase in a substantial minority of pre-teenage youth who later develop schizophrenia, and they apparently worsen by the prodromal, high-risk phase in a majority of those who develop the illness. While there is limited evidence for reversibility of impairments from pharmacological interventions in schizophrenia, promising results have emerged from cognitive remediation studies. Thus, we expect cognitive interventions to play a larger role in schizophrenia in the coming years. Moreover, because youth at risk for schizophrenia can be identified by an emergent high-risk syndrome, earlier interventions might be applied in a preemptive way to reduce disability and improve adaptation. The notion of schizophrenia as a developmental neurocognitive disorder with stages opens up a window of possibilities for earlier interventions. (JINS, 2017, 23, 881-892)

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Section: Erpsmentioning

confidence: 84%

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Seidman

Mirsky

2017

J Int Neuropsychol Soc

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“…MMN deficits are tied to poor functional outcome [136, 137], as recently confirmed in a study of 1,415 subjects with schizophrenia. In this study, early auditory processing event-related potential (MMN, P300, and reorienting negativity) predicted cognition (β = 0.37, p < 0.001), while cognition itself directly predicted negative symptoms (β = −0.16, p < 0.001) and indirectly predicted functional outcome [138]. Furthermore, MMN is highly predictive of response to auditory cognitive remediation [139].…”

Section: Mismatch Negativitymentioning

confidence: 99%

Potential Role of Antipsychotic-Galantamine-Memantine Combination in the Treatment of Positive, Cognitive, and Negative Symptoms of Schizophrenia

Koola¹

2018

Complex Psychiatry

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Schizophrenia is, in part, a cognitive illness. There are no approved medications for cognitive impairments associated with schizophrenia (CIAS) and primary negative symptoms. Cholinergic and glutamatergic systems, alpha-7 nicotinic acetylcholine (α-7nACh) and N-methyl-D-aspartate (NMDA) receptors, kynurenic acid (KYNA), and mismatch negativity have been implicated in the pathophysiology of CIAS and negative symptoms. Galantamine is an acetylcholinesterase inhibitor that is also a positive allosteric modulator at the α4β2 and α7nACh receptors. Memantine is a noncompetitive NMDA receptor antagonist. Galantamine and memantine alone and in combination were effective for cognition in animals and people with Alzheimer’s disease. The objective of this article is to critically dissect the published randomized controlled trials with galantamine and memantine for CIAS to highlight the efficacy signal. These studies may have failed to detect a clinically meaningful efficacy signal due to limitations, methodological issues, and possible medication nonadherence. There is evidence from a small open-label study that the galantamine-memantine combination may be effective for CIAS with kynurenine pathway metabolites as biomarkers to detect the severity of cognitive impairments. Given that there are no available treatments for cognitive impairments and primary negative symptoms in schizophrenia, testing of this “five-pronged strategy” (quintuple hypotheses: dopamine, nicotinic-cholinergic, glutamatergic/NMDA, GABA, and KYNA) is a “low-risk high-gain” approach that could be a major breakthrough in the field. The galantamine-memantine combination has the potential to treat positive, cognitive, and negative symptoms, and targeting the quintuple hypotheses concurrently may lead to a major scientific advancement – from antipsychotic treatment to antischizophrenia treatment.

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“…To avoid inefficient energy consumption in dealing with all the input sounds, our brains show strong response to important auditory information but weak response to unimportant auditory information based on the context of auditory stimuli even when we do not attend to the auditory stimuli. This “auditory contextual processing” is one of the neurocognitive bases of language‐based social communication (Hickok & Poeppel, ), deficits in which play a key role in the pathophysiology of psychiatric disorders relevant to the impairment of such social functions (Thomas et al, ). Mismatch negativity (MMN) has been intensively studied, as this is a feasible and reliable index of auditory contextual processing.…”

Section: Introductionmentioning

confidence: 99%

“…Mismatch negativity (MMN) has been intensively studied, as this is a feasible and reliable index of auditory contextual processing. In addition to the historical contribution to the understanding of auditory contextual processing (Näätänen, Gaillard, & Mantysalo, ), MMN has also been revealed to be reduced in patients with psychiatric disorders such as schizophrenia, reflecting impairment in pre‐attentive cognitive processing (Thomas et al, ) and mechanisms of illness onset (Bodatsch et al, ; Nagai et al, ; Perez et al, ). Reduced MMN is the most robust finding regarding brain changes in schizophrenia (Erickson, Ruffle, & Gold, ; Shelley et al, ; Umbricht & Krljes, ), and therefore could represent an important electrophysiological clue to elucidating the pathophysiology of schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Deviance detection is the dominant component of auditory contextual processing in the lateral superior temporal gyrus: A human ECoG study

Ishishita

Kunii

Shimada

et al. 2018

Human Brain Mapping

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Auditory contextual processing has been assumed to be based on a hierarchical structure consisting of the primary auditory cortex, superior temporal gyrus (STG), and frontal lobe. Recent invasive studies on mismatch negativity (MMN) have revealed functional segregation for auditory contextual processing such as neural adaptation in the primary auditory cortex and prediction in the frontal lobe. However, the role of the STG remains unclear. We obtained induced activity in the high gamma band as mismatch response (MMR), an electrocorticographic (ECoG) counterpart to scalp MMN, and the components of MMR by analyzing ECoG data from patients with refractory epilepsy in an auditory oddball task paradigm. We found that MMR localized mainly in the bilateral posterior STGs, and that deviance detection largely accounted for MMR. Furthermore, adaptation was identified in a limited number of electrodes on the superior temporal plane. Our findings reveal a mixed contribution of deviance detection and adaptation depending on location in the STG. Such spatial considerations could lead to further understanding of the pathophysiology of relevant psychiatric disorders.

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Modeling Deficits From Early Auditory Information Processing to Psychosocial Functioning in Schizophrenia

Cited by 168 publications

References 83 publications

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Potential Role of Antipsychotic-Galantamine-Memantine Combination in the Treatment of Positive, Cognitive, and Negative Symptoms of Schizophrenia

Deviance detection is the dominant component of auditory contextual processing in the lateral superior temporal gyrus: A human ECoG study

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