Contribution of Impaired Early-Stage Visual Processing to Working Memory Dysfunction in Adolescents With Schizophrenia

Haenschel, Corinna; Bittner, Robert A.; Haertling, Fabian; Rotarska-Jagiela, Anna; Maurer, K.; Singer, Wolf; Linden, David Edmund Johannes

doi:10.1001/archpsyc.64.11.1229

Cited by 203 publications

(166 citation statements)

References 79 publications

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“…P100 amplitude was greater under ketamine than under placebo, which went against our prediction that the pattern observed in schizophrenia (8,(10)(11)(12)59,63) would be replicated. There are several potential ways to interpret our unexpected finding .…”

Section: P100 Effectcontrasting

confidence: 61%

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Koychev

Deakin

El‐Deredy

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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This is the accepted version of the paper.This version of the publication may differ from the final published version. ABSTRACT BACKGROUND: Working memory (WM) deficits are a core feature of schizophrenia. Electrophysiological studies suggest that impaired early visual processing may contribute to impaired WM in the visual domain. Abnormal N-methyl-D-aspartate (NMDA) receptor function has been implicated both in WM and in early visual processing deficits in schizophrenia. We investigated whether ketamine, a noncompetitive NMDA antagonist, would replicate in healthy volunteers the WM performance and early visual processing abnormalities we and others have reported in patients with schizophrenia. METHODS: Forty-four healthy volunteers were randomly assigned to receive intravenous ketamine or placebo. During infusion, the effects of ketamine were recorded using standardized psychiatric scales. Visual evoked potentials (P100 and P300 components) were recorded during performance of a delayed matching to sample task. RESULTS: Ketamine induced mild psychosis-like symptoms and impaired WM performance. It also significantly increased the P100 amplitude, while P300 amplitude decreased in a load-dependent manner. Amplitudes of P100 during retrieval correlated with cognitive performance only in the placebo group. CONCLUSIONS: We confirmed previous studies showing that ketamine reproduces the impairment of WM performance and smaller P300 amplitudes observed in schizophrenia. However, ketamine increased visual P100 amplitude in contrast to our observation of reduced P100 amplitudes in established schizophrenia. The effects of ketamine on WM and P300 are likely to involve impaired NMDA function, as these receptors are implicated in changes of synaptic strength underlying associative learning and memory. Increased P100 amplitude may reflect the secondary disinhibition of cortical glutamate release that occurs after NMDA blockade. Permanent repository link

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Section: P100 Effectcontrasting

confidence: 61%

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Koychev

Deakin

El‐Deredy

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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“…A large majority of these studies have also shown P1 deficits although eight of the twenty-six did not. The finding of the P1 deficit has been most consistent in our group of studies in chronic patients in New York [7-9, 21, 23, 26, 56] although more recently, a number of other groups have shown similar deficits [16,28,59]. However, only a few of these studies have examined the relationship between these early processing deficits and disease state.…”

Section: Introductionsupporting

confidence: 61%

“…Although these eight studies did not find P1 deficits, as above, the large majority of studies where P1 was measured have. In many of these studies [28] the effect size was very large. All in all, the weight of evidence appears to overwhelmingly favour a robust P1 deficit in patients with schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Visual sensory processing deficits in Schizophrenia and their relationship to disease state

Yeap

Kelly

Sehatpour

et al. 2008

Eur Arch Psychiatry Clin Neurosc

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Context Visual Evoked Potential (VEP) abnormalities have been a fairly consistent finding in patients with schizophrenia, and it has been suggested that electrophysiological markers of early sensory processing may be useful as trait markers for the illness, and for development as potential diagnostic measures. Objective Clear amplitude reductions in the occipital P1 component of the VEP (~100 ms), have been repeatedly demonstrated in patients with schizophrenia. Here, we investigated whether the extent of this deficit was related to age, clinical symptoms, medication status and length of illness, in a large cohort of ethnically homogenous patients. Design, setting and participants VEP responses to simple isolated-check stimuli were examined in 52 DSM-IV diagnosed patients with schizophrenia, and compared with responses from 26 healthy age-matched control subjects. Using high-density electrical scalp recordings, we assessed the integrity of the visual P1 component across the two groups. This study was conducted at St.Vincent's Psychiatric Hospital in Fairview, Dublin, Ireland. Results Substantially reduced P1 amplitude was demonstrated in the patient group compared to controls. The deficit was not linked to age, length of illness or medication status. A small positive correlation, accounting for about 11% of the variance, was found between P1 amplitude and clinical symptoms scales (BPRS and SANS). In addition, we found that a slightly later (~110 ms) fronto-central component was relatively increased in the patient group, and was inversely correlated with the occipital P1 amplitude in the patients, but not in the healthy control subjects.Conclusions Our findings clearly demonstrate a deficit in early visual processing in patients with schizophrenia (with a large effect size; Cohen's d = 0.7) that is unrelated to chronicity. The results are consistent with recent findings showing that the P1 deficit is endophenotypic of the disorder and related to genetic risk factors rather than the disease process itself.j Key words visual-evoked potential AE VEP AE ERP AE P1 deficit AE schizophrenia AE Ireland AE hyperfrontality

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“…Several behavioral studies have shown impaired performance in patients with schizophrenia linked to dysfunctional WM encoding (Javitt et al, 1997;Lencz et al, 2003;Lee and Park, 2005). Furthermore, we provided evidence that the event-related potential (ERP) component P100 is of relevance for successful WM encoding in controls and is reduced in adolescent patients with schizophrenia (Haenschel et al, 2007b). WM maintenance deficits in schizophrenia have also been observed both behaviorally (Tek et al, 2002;Badcock et al, 2008) and using functional magnetic resonance imaging (fMRI), especially in the dorsolateral prefrontal cortex (DLPFC) (Cannon et al, 2005;Lee et al, 2008) using spatial delayed response tasks.…”

Section: Introductionmentioning

confidence: 73%

“…Trials with different WM load levels were randomly distributed across sessions with a total of 50 trials obtained per WM load level. The ERP data have been reported previously (Haenschel et al, 2007b).…”

Section: Stimuli and Taskmentioning

confidence: 90%

Cortical Oscillatory Activity Is Critical for Working Memory as Revealed by Deficits in Early-Onset Schizophrenia

Haenschel¹,

Bittner²,

Waltz³

et al. 2009

J. Neurosci.

266

187

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Impairments in working memory (WM) are a core cognitive deficit in schizophrenia. Neurophysiological models suggest that deficits during WM maintenance in schizophrenia may be explained by abnormalities in the GABAergic system, which will lead to deficits in high-frequency oscillations. However, it is not yet clear which of the three WM phases (encoding, maintenance, retrieval) are affected by dysfunctional oscillatory activity. We investigated the relationship between impairments in oscillatory activity in a broad frequency range (3-100 Hz) and WM load in the different phases of WM in 14 patients with early-onset schizophrenia and 14 matched control participants using a delayed matching to sample paradigm.During encoding, successful memorization was predicted by evoked theta, alpha, and beta oscillatory activity in controls. Patients showed severe reductions in the evoked activity in these frequency bands. During early WM maintenance, patients showed a comparable WM load-dependent increase in induced alpha and gamma activity to controls. In contrast, during the later maintenance phase, patients showed a shift in the peak of induced gamma activity to the lower WM load conditions. Finally, induced theta and gamma activity were reduced in patients during retrieval.Our findings suggest that the WM deficit in schizophrenia is associated with impaired oscillatory activity during all phases of the task and that the cortical storage system reaches its capacity limit at lower loads. Inability to maintain oscillatory activity in specific frequency bands could thus result in the information overload that may underlie both cognitive deficits and psychopathological symptoms of schizophrenia.

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Contribution of Impaired Early-Stage Visual Processing to Working Memory Dysfunction in Adolescents With Schizophrenia

Cited by 203 publications

References 79 publications

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Visual sensory processing deficits in Schizophrenia and their relationship to disease state

Cortical Oscillatory Activity Is Critical for Working Memory as Revealed by Deficits in Early-Onset Schizophrenia

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