Dysfunctional encoding of auditory information in schizophrenia

Strous, Rael D.; Grochowski, Sandra; Cowan, Naomi; Javitt, D.C.

doi:10.1016/0920-9964(95)95420-e

Cited by 4 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Over recent years, we (16, 17) and others (18, 19) have documented deficits in basic pitch perception (i.e. tone matching) in schizophrenia related to structural (20) and functional (21, 22) impairments at the level of primary auditory cortex.…”

Section: Introductionmentioning

confidence: 99%

Auditory Emotion Recognition Impairments in Schizophrenia: Relationship to Acoustic Features and Cognition

Gold

Butler²,

Revheim³

et al. 2012

AJP

106

View full text Add to dashboard Cite

Objective Schizophrenia is associated with deficits in ability to perceive emotion based upon tone of voice. The basis for this deficit, however, remains unclear and assessment batteries remain limited. We evaluated performance in schizophrenia on a novel voice emotion recognition battery with well characterized physical features, relative to impairments in more general emotional and cognitive function. Methods We studied in a primary sample of 92 patients relative to 73 controls. Stimuli were characterized according to both intended emotion and physical features (e.g., pitch, intensity) that contributed to the emotional percept. Parallel measures of visual emotion recognition, pitch perception, general cognition, and overall outcome were obtained. More limited measures were obtained in an independent replication sample of 36 patients, 31 age-matched controls, and 188 general comparison subjects. Results Patients showed significant, large effect size deficits in voice emotion recognition (F=25.4, p<.00001, d=1.1), and were preferentially impaired in recognition of emotion based upon pitch-, but not intensity-features (group X feature interaction: F=7.79, p=.006). Emotion recognition deficits were significantly correlated with pitch perception impairments both across (r=56, p<.0001) and within (r=.47, p<.0001) group. Path analysis showed both sensory-specific and general cognitive contributions to auditory emotion recognition deficits in schizophrenia. Similar patterns of results were observed in the replication sample. Conclusions The present study demonstrates impairments in auditory emotion recognition in schizophrenia relative to acoustic features of underlying stimuli. Furthermore, it provides tools and highlights the need for greater attention to physical features of stimuli used for study of social cognition in neuropsychiatric disorders.

show abstract

Section: Introductionmentioning

confidence: 99%

Auditory Emotion Recognition Impairments in Schizophrenia: Relationship to Acoustic Features and Cognition

Gold

Butler²,

Revheim³

et al. 2012

AJP

106

View full text Add to dashboard Cite

show abstract

“…Although AHs were not formally assessed during the testing sessions, it is possible that NMDAR antagonism induced an abnormality in auditory signaling and increased hallucinating activity, which may have impacted MMN generation. In support of this argument, patients in general exhibit reduced sensory-level processing of auditory input (e.g., diminished auditory acuity, elevated thresholds for tone discrimination; Mathew et al, 1993 ; Holcomb et al, 1995 ; Strous et al, 1995 ; Wexler et al, 1998 ; Rabinowicz et al, 2000 ); patients with (vs. without) AHs have greater difficulty in sound (speech) discrimination (Hugdahl et al, 2008 ), and the temporal cortex evidences both high glutamate levels in patients (Marsman et al, 2011 ) and hypofunctional activation in controls during ketamine infusion (Hugdahl et al, 2008 ). However, impaired auditory MMN generation during ketamine infusion is unlikely to be related to competing influences resulting from increasing auditory verbal hallucinations as organized AH (i.e., identifiable as speech) as seen in established schizophrenia are rarely observed during a ketamine challenge (Kantrowitz and Javitt, 2010 ).…”

Section: Discussionmentioning

confidence: 98%

Nicotine, Auditory Sensory Memory, and sustained Attention in a Human Ketamine Model of Schizophrenia: Moderating Influence of a Hallucinatory Trait

et al. 2012

View full text Add to dashboard Cite

Background: The procognitive actions of the nicotinic acetylcholine receptor (nAChR) agonist nicotine are believed, in part, to motivate the excessive cigarette smoking in schizophrenia, a disorder associated with deficits in multiple cognitive domains, including low-level auditory sensory processes and higher-order attention-dependent operations. Objectives: As N-methyl-d-aspartate receptor (NMDAR) hypofunction has been shown to contribute to these cognitive impairments, the primary aims of this healthy volunteer study were to: (a) to shed light on the separate and interactive roles of nAChR and NMDAR systems in the modulation of auditory sensory memory (and sustained attention), as indexed by the auditory event-related brain potential – mismatch negativity (MMN), and (b) to examine how these effects are moderated by a predisposition to auditory hallucinations/delusions (HD). Methods: In a randomized, double-blind, placebo-controlled design involving a low intravenous dose of ketamine (0.04 mg/kg) and a 4 mg dose of nicotine gum, MMN, and performance on a rapid visual information processing (RVIP) task of sustained attention were examined in 24 healthy controls psychometrically stratified as being lower (L-HD, n = 12) or higher (H-HD) for HD propensity. Results: Ketamine significantly slowed MMN, and reduced MMN in H-HD, with amplitude attenuation being blocked by the co-administration of nicotine. Nicotine significantly enhanced response speed [reaction time (RT)] and accuracy (increased % hits and d′ and reduced false alarms) on the RVIP, with improved performance accuracy being prevented when nicotine was administered with ketamine. Both % hits and d′, as well as RT were poorer in H-HD (vs. L-HD) and while hit rate and d′ was increased by nicotine in H-HD, RT was slowed by ketamine in L-HD. Conclusions: Nicotine alleviated ketamine-induced sensory memory impairment and improved attention, particularly in individuals prone to HD.

show abstract

“…Impaired intracortical MMN generation induced by NMDA antagonists may be relevant to the pathophysiology of disorders associated with working memory impairments, such as schizophrenia (23). Schizophrenic subjects show significant deficits in MMN generation (24)(25)(26)(27), along with impaired performance of auditory sensory memory tasks (28). It has been suggested that impairments in NMDA receptor activity (29) may contribute significantly to the pathophysiology of schizophrenia.…”

Section: Methodsmentioning

confidence: 99%

Role of cortical N-methyl-D-aspartate receptors in auditory sensory memory and mismatch negativity generation: implications for schizophrenia.

Javitt

Steinschneider

Schroeder

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

609

442

View full text Add to dashboard Cite

Working memory refers to the ability of the brain to store and manipulate information over brief time periods, ranging from seconds to minutes. As opposed to long-term memory, which is critically dependent upon hippocampal processing, critical substrates for working memory are distributed in a modality-specific fashion throughout cortex. N-methyl-D-aspartate (NMDA) receptors play a crucial role in the initiation of long-term memory. Neurochemical mechanisms underlying the transient memory storage required for working memory, however, remain obscure. Auditory sensory memory, which refers to the ability of the brain to retain transient representations of the physical features (e.g., pitch) of simple auditory stimuli for periods of up to approximately 30 sec, represents one of the simplest components of the brain working memory system. Functioning of the auditory sensory memory system is indexed by the generation of a well-defined event-related potential, termed mismatch negativity (MMN). MMN can thus be used as an objective index of auditory sensory memory functioning and a probe for investigating underlying neurochemical mechanisms. Monkeys generate cortical activity in response to deviant stimuli that closely resembles human MMN. This study uses a combination of intracortical recording and pharmacological micromanipulations in awake monkeys to demonstrate that both competitive and noncompetitive NMDA antagonists block the generation of MMN without affecting prior obligatory activity in primary auditory cortex. These findings suggest that, on a neurophysiological level, MMN represents selective current flow through open, unblocked NMDA channels. Furthermore, they suggest a crucial role of cortical NMDA receptors in the assessment of stimulus familiarity/unfamiliarity, which is a key process underlying working memory performance.Working memory refers to the ability of the brain to store and manipulate information over brief time periods, ranging from seconds to minutes. As compared with long-term memory, which is critically dependent upon hippocampal long-term potentiation, critical substrates for working memory are distributed in a modality specific fashion throughout cortex (1, 2). On a neurophysiological level, working memory has been linked to transient, task-related alterations in the firing rates of neurons in modality-specific brain regions, permitting the use of intracortical recordings to investigate neurochemical mechanisms underlying functioning of the brain working memory system (3-5).Cortical information processing is critically dependent upon the interplay between glutamatergic and y-aminobutyric acid (GABA)ergic neurotransmission. Glutamate is the primary excitatory amino transmitter in mammalian cortex, being present in approximately 60% of cortical neurons and 100% of cortical pyramidal neurons. Glutamatergic fibers mediate all thalamocortical and corticortical projections within cortex, as well as corticofugal projections from cortex to subcortical structures. Within cortex, the interplay...

show abstract

Dysfunctional encoding of auditory information in schizophrenia

Cited by 4 publications

References 0 publications

Auditory Emotion Recognition Impairments in Schizophrenia: Relationship to Acoustic Features and Cognition

Auditory Emotion Recognition Impairments in Schizophrenia: Relationship to Acoustic Features and Cognition

Nicotine, Auditory Sensory Memory, and sustained Attention in a Human Ketamine Model of Schizophrenia: Moderating Influence of a Hallucinatory Trait

Role of cortical N-methyl-D-aspartate receptors in auditory sensory memory and mismatch negativity generation: implications for schizophrenia.

Contact Info

Product

Resources

About