Prepulse inhibition of the acoustically evoked startle reflex in patients with an acute schizophrenic psychosis—A longitudinal study

Meincke, Ulrich; Mörth, Dina; Voss, Tatjana; Thelen, B.; Geyer, Mark A.; Gouzoulis-Mayfrank, Euphrosyne

doi:10.1007/s00406-004-0523-0

Cited by 86 publications

(51 citation statements)

References 46 publications

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“…In one of our studies, schizophrenia patients with lower PPI capacity also showed lower attentional performance scores on the CANTAB rapid visual information processing (RVP) task than those with higher PPI levels (Ludewig et al, 2003b). Similarly, other studies found that PPI deficits in schizophrenia are correlated with thought disorder (Meincke et al, 2004;Perry and Braff, 1994;Perry et al, 1999). Furthermore, the finding of a positive correlation between PPI capacity and attentional performance in the present study is also of relevance to the view that a serotonergic dysfunction may contribute to the pathophysiology of cognitive deficits in schizophrenia (Meltzer and Nash, 1991;Roth et al, 2004).…”

Section: Discussionsupporting

confidence: 71%

The Effects of the Preferential 5-HT2A Agonist Psilocybin on Prepulse Inhibition of Startle in Healthy Human Volunteers Depend on Interstimulus Interval

Vollenweider

Csomor

Knappe

et al. 2007

Neuropsychopharmacol

153

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Schizophrenia patients exhibit impairments in prepulse inhibition (PPI) of the startle response. Hallucinogenic 5-HT 2A receptor agonists are used for animal models of schizophrenia because they mimic some symptoms of schizophrenia in humans and induce PPI deficits in animals. Nevertheless, one report indicates that the 5-HT 2A receptor agonist psilocybin increases PPI in healthy humans. Hence, we investigated these inconsistent results by assessing the dose-dependent effects of psilocybin on PPI in healthy humans. Sixteen subjects each received placebo or 115, 215, and 315 mg/kg of psilocybin at 4-week intervals in a randomized and counterbalanced order. PPI at 30-, 60-, 120-, 240-, and 2000-ms interstimulus intervals (ISIs) was measured 90 and 165 min after drug intake, coinciding with the peak and post-peak effects of psilocybin. The effects of psilocybin on psychopathological core dimensions and sustained attention were assessed by the Altered States of Consciousness Rating Scale (5D-ASC) and the Frankfurt Attention Inventory (FAIR). Psilocybin dosedependently reduced PPI at short (30 ms), had no effect at medium (60 ms), and increased PPI at long (120-2000 ms) ISIs, without affecting startle reactivity or habituation. Psilocybin dose-dependently impaired sustained attention and increased all 5D-ASC scores with exception of Auditory Alterations. Moreover, psilocybin-induced impairments in sustained attention performance were positively correlated with reduced PPI at the 30 ms ISI and not with the concomitant increases in PPI observed at long ISIs. These results confirm the psilocybin-induced increase in PPI at long ISIs and reveal that psilocybin also produces a decrease in PPI at short ISIs that is correlated with impaired attention and consistent with deficient PPI in schizophrenia.

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Section: Discussionsupporting

confidence: 71%

The Effects of the Preferential 5-HT2A Agonist Psilocybin on Prepulse Inhibition of Startle in Healthy Human Volunteers Depend on Interstimulus Interval

Vollenweider

Csomor

Knappe

et al. 2007

Neuropsychopharmacol

153

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“…Of particular interest in this regard is a cross-sectional study indicating that clozapine treatment, relative to typical antipsychotic treatments, is associated with reduced PPI deficits in patients with schizophrenia (Kumari et al, 1999). While the evidence indicating that second-generation antipsychotics, especially clozapine, may ameliorate PPI deficits in schizophrenia is based largely on cross-sectional studies (Kumari et al, 1999;Hagan and Jones, 2005), some longitudinal studies are now suggesting that PPI deficits may be reversed in groups of schizophrenia patients treated primarily with second-generation compounds (Meincke et al, 2004). Although much more work is needed to clarify the effects of newer antipsychotics on both cognitive and PPI deficits in schizophrenia, it is clear that first-generation anti-psychotics fail to normalize either class of deficits.…”

Section: Prepulse Inhibition Models In Animals Using Prepulse Inhibitmentioning

confidence: 99%

The family of sensorimotor gating disorders: Comorbidities or diagnostic overlaps?

2006

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Prepulse inhibition (PPI) of startle is an operational measure of the pre-attentive filtering process known as sensorimotor gating. Originally identified in patients with schizophrenia, PPI deficits have been observed in multiple but not all psychiatric disorders. Thus, as with most signs and symptoms of psychiatric disorders, deficits in PPI cut across diagnostic categories. It remains unclear whether the diversity of disorders exhibiting deficient PPI bespeaks diagnostic overlaps or comorbidities. Given the recent focus on treatments for cognitive deficits of schizophrenia independently of treating psychosis, the relationship of PPI deficits to cognitive deficits becomes of interest. Although PPI cannot be considered to be a cognitive process per se, abnormalities in pre-attentive information processing may be predictive of or lead to complex cognitive deficits. Animal models of PPI deficits produced by dopamine agonists reliably predict existing antipsychotics. Nevertheless, since neither PPI nor cognitive deficits in schizophrenia are ameliorated by standard antipsychotics, current research is exploring the predictive value of non-dopaminergic PPI models in identifying treatments for gating disturbances independently of their relevance to specific disorders. Both PPI and cognitive deficits in schizophrenia patients are not reversed by first generation antipsychotics but may be attenuated by clozapine. Similarly, effects of glutamate antagonists on symptoms in patients and PPI in animals appear to be reduced by clozapine. Hence, treatment-induced reversals of deficits in PPI produced by glutamate antagonists may provide animal, and human, models to aid in the discovery of treatments of cognitive deficits in patients already treated with existing antipsychotics.

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“…On the other hand, several studies have failed to show PPI-enhancing effects of either typical or atypical medication in schizophrenia patients (Duncan et al, 2003a, b;Perry et al, 2002;Mackeprang et al, 2002), even though Duncan et al (2003b) found an improvement of clinical symptoms with atypical medication. In contrast to these negative findings, a recent study showed that an enhancement of PPI is associated with symptom reduction in patients treated for schizophrenia with either typical or atypical antipsychotic treatments (Meincke et al, 2004). Although it appears that atypical antipsychotics may be superior in normalizing PPI, the literature to date is inconclusive regarding the impact of antipsychotic medication on PPI.…”

Section: Introductionmentioning

confidence: 96%

Haloperidol Differentially Modulates Prepulse Inhibition and P50 Suppression in Healthy Humans Stratified for Low and High Gating Levels

Csomor

Stadler

Feldon

et al. 2007

Neuropsychopharmacol

102

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Schizophrenia patients exhibit deficits in sensory gating as indexed by reduced prepulse inhibition (PPI) and P50 suppression, which have been linked to psychotic symptom formation and cognitive deficits. Although recent evidence suggests that atypical antipsychotics might be superior over typical antipsychotics in reversing PPI and P50 suppression deficits not only in schizophrenia patients, but also in healthy volunteers exhibiting low levels of PPI, the impact of typical antipsychotics on these gating measures is less clear. To explore the impact of the dopamine D 2 -like receptor system on gating and cognition, the acute effects of haloperidol on PPI, P50 suppression, and cognition were assessed in 26 healthy male volunteers split into subgroups having low vs high PPI or P50 suppression levels using a placebocontrolled within-subject design. Haloperidol failed to increase PPI in subjects exhibiting low levels of PPI, but attenuated PPI in those subjects with high sensorimotor gating levels. Furthermore, haloperidol increased P50 suppression in subjects exhibiting low P50 gating and disrupted P50 suppression in individuals expressing high P50 gating levels. Independently of drug condition, high PPI levels were associated with superior strategy formation and execution times in a subset of cognitive tests. Moreover, haloperidol impaired spatial working memory performance and planning ability. These findings suggest that dopamine D 2 -like receptors are critically involved in the modulation of P50 suppression in healthy volunteers, and to a lesser extent also in PPI among subjects expressing high sensorimotor gating levels. Furthermore, the results suggest a relation between sensorimotor gating and working memory performance.

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Prepulse inhibition of the acoustically evoked startle reflex in patients with an acute schizophrenic psychosis—A longitudinal study

Cited by 86 publications

References 46 publications

The Effects of the Preferential 5-HT2A Agonist Psilocybin on Prepulse Inhibition of Startle in Healthy Human Volunteers Depend on Interstimulus Interval

The Effects of the Preferential 5-HT2A Agonist Psilocybin on Prepulse Inhibition of Startle in Healthy Human Volunteers Depend on Interstimulus Interval

The family of sensorimotor gating disorders: Comorbidities or diagnostic overlaps?

Haloperidol Differentially Modulates Prepulse Inhibition and P50 Suppression in Healthy Humans Stratified for Low and High Gating Levels

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