Effect of ketamine on the neuromagnetic mismatch field in healthy humans

Kreitschmann-Andermahr, Ilonka; Rosburg, Timm; Demme, U.; Gaser, Elke; Nowak, H.; Sauer, Heinrich

doi:10.1016/s0926-6410(01)00043-x

Cited by 124 publications

(81 citation statements)

References 25 publications

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“…26 Deficits similar to those observed in schizophrenia are induced by administration of PCP, ketamine, or other NMDA antagonists in both monkeys 27 and normal human volunteers. [28][29][30] Similar deficits have recently been demonstrating in rodents 31,32 as well, supporting the use of rodent models of sensory processing dysfunction in schizophrenia. 33 The latest in the series of informative auditory paradigms is the auditory 40 Hz response.…”

Section: Auditory Dysfunction In Schizophreniasupporting

confidence: 67%

Sensory Processing in Schizophrenia: Neither Simple nor Intact

Javitt

2009

Schizophrenia Bulletin

274

186

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This special issue focuses on the theme of sensory processing dysfunction in schizophrenia. For more than 50 years, from approximately the time of Bleuler until the early 1960s, sensory function was considered one of the few preserved functions in schizophrenia (Javitt 1 ). Fortunately, the last several decades have brought a renewed and accelerating interest in this topic. The articles included in the issue range from those addressing fundamental bases of sensory dysfunction (Brenner, Yoon, and Turetsky) to those that examine how elementary deficits in sensory processing affect the sensory experience of individuals with schizophrenia (Butler, Kantrowitz, and Coleman) to the question of how sensory-based treatments may lead to improvement in remediation strategies (Adcock). Although addressing only a small portion of the current complex and burgeoning literature on sensory impairments across modalities, the present articles provide a cross-section of the issues currently under investigation. These studies also underscore the severe challenges that individuals with schizophrenia face when trying to decode the complex world around them.

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Section: Auditory Dysfunction In Schizophreniasupporting

confidence: 67%

Sensory Processing in Schizophrenia: Neither Simple nor Intact

Javitt

2009

Schizophrenia Bulletin

274

186

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“…Likewise, we recently demonstrated that the NMDAR antagonist ketamine induces a significant reduction of MMN, but not of N1, in healthy volunteers (Umbricht et al, 2000). Similarly, ketamine and other NMDAR antagonists significantly reduced MMNm (the magnetic counterpart of MMN) and MMN, respectively, in healthy volunteers (Jääskeläinen et al, 1995a(Jääskeläinen et al, , b, 1996Kreitschmann-Andermahr et al, 2001;Pang and Fowler, 1999). In addition, subanesthetic doses of ketamine induce a pattern of deficits in AX-CPT performance in healthy volunteers that is characterized by a specific increase of context-dependent (BX) errors and closely resembles the deficits observed in schizophrenia (Umbricht et al, 2000).…”

Section: Introductionmentioning

confidence: 79%

Effects of the 5-HT2A Agonist Psilocybin on Mismatch Negativity Generation and AX-Continuous Performance Task: Implications for the Neuropharmacology of Cognitive Deficits in Schizophrenia

Umbricht

Vollenweider

Schmid

et al. 2003

Neuropsychopharmacol

161

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Previously the NMDA (N-methyl-D-aspartate) receptor (NMDAR) antagonist ketamine was shown to disrupt generation of the auditory event-related potential (ERP) mismatch negativity (MMN) and the performance of an 'AX'-type continuous performance test (AX-CPT)Fmeasures of auditory and visual context-dependent information processingFin a similar manner as observed in schizophrenia. This placebo-controlled study investigated effects of the 5-HT 2A receptor agonist psilocybin on the same measures in 18 healthy volunteers. Psilocybin administration induced significant performance deficits in the AX-CPT, but failed to reduce MMN generation significantly. These results indirectly support evidence that deficient MMN generation in schizophrenia may be a relatively distinct manifestation of deficient NMDAR functioning. In contrast, secondary pharmacological effects shared by NMDAR antagonists and the 5-HT 2A agonist (ie disruption of glutamatergic neurotransmission) may be the mechanism underlying impairments in AX-CPT performance observed during both psilocybin and ketamine administration. Comparable deficits in schizophrenia may result from independent dysfunctions of 5-HT 2A and NMDAR-related neurotransmission.

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“…This has already been reported in subhuman primates 16 and has been proven by several ketamine studies with different doses. 59,60 One study using a low ketamine dose even reported no deficits of MMN due to drug intervention. 61 As opposed to the present study, Umbricht and colleagues 27 used a higher dose of ketamine (0.24 mg/kg over 5 minutes followed by 0.9 mg/kg/h).…”

Section: Discussionmentioning

confidence: 99%