The Relationship Between Acoustic Startle Response Measures and Cognitive Functions in Japanese Patients with Schizophrenia

Abstract

Recently, schizophrenia endophenotypes have been actively investigated to better understand the pathophysiology of schizophrenia. Past studies have shown that cognitive functions, including working memory and executive function, correlate with acoustic startle responses, such as prepulse inhibition (PPI), in patients with schizophrenia. The aim of this study was to investigate the relationship between cognitive functions and acoustic startle response in Japanese patients with schizophrenia. In 100 patients with schizophrenia, we evaluated cognitive function, using the Brief Assessment of Cognition in Schizophrenia, Japanese-language version (BACS-J), and acoustic startle responses, including acoustic startle reflex, habituation, and PPI (three different intensities: 82, 86, and 90 dB SPL, equivalent to signal-to-noise ratios of +12, +16, and +20 dB, respectively). Using multiple regression analysis, we examined the relationship between acoustic startle responses and BACS-J primary measures or composite score. Level of attention was associated with magnitude of habituation in schizophrenia (P = 0.0009, β = -0.357). None of the other domains of cognitive function were significantly associated with any measure of acoustic startle response. This included attention regarding ASR (P = 0.513), PPI (P = 0.521-0.842), verbal memory (P = 0.423-0.981), working memory (P = 0.312-0.966), motor speed (P = 0.323-0.955), verbal fluency (P = 0.125-0.920), executive function (P = 0.118-0.470), and the BACS-J composite score (P = 0.230-0.912). In this first investigation of the relationship between cognitive functions and acoustic startle responses in Japanese patients with schizophrenia, attentional deficits correlated highly with the level of habituation. However, a replication study using other population samples is required to further investigate this relationship.

Deficient prepulse inhibition in schizophrenia detected by the multi-site COGS

“…due to site-specific idiosyncrasies in testing) or other confounding effects that prevented detection of the endophenotype, this might greatly diminish the scientific value of such an undertaking. The present findings support the utility and fidelity of the COGS-2 multi-site platform, because the general pattern of results with PPI and its moderating factors have been detected in single-site studies by a number of different investigative groups (Aggernaes et al, 2010; Braff et al, 1978, 1999, 2001; Csomor et al, 2009; Hammer et al, 2011, 2013; Hong et al, 2007; Kishi et al, 2012; Kumari et al, 1999, 2007; Kunugi et al, 2007; Light et al, 2012; Ludewig et al, 2003; Mackeprang et al, 2002; Martinez-Gras et al, 2009; Meincke et al, 2004; Molina et al, 2011; Moriwaki et al, 2009; Oranje and Glenthoj, 2013; Preuss et al, 2011; Quednow et al, 2006; Rabin et al, 2009; Takahashi et al, 2008; Wang et al, 2013; Weike et al, 2000; Xue et al, 2012), one of which (UCSD) is represented in this study (see reference data from UCSD, Figure 5). …”

“…Less consistent findings across recent single-site studies, as well as the present multi-site study, include the relationship between smoking and the magnitude of PPI deficits among SZ patients (Hong et al, 2008; Moriwaki et al, 2009), and the associations between PPI and either clinical symptoms (Braff et al, 1999; Duncan et al, 2006; Light et al, 2012; Martinez-Gras et al, 2009; Meincke et al, 2004; Quednow et al, 2010; Swerdlow et al, 2006a; Wang et al, 2013; Xue et al, 2012) or neurocognitive measures (Bitsios and Giakoumaki, 2005; Kishi et al, 2012) in SZ patients. Perhaps such variability should not be surprising: studies vary widely in the precision with which nicotine use and levels are documented, and many studies – including our own – use very blunt self-report measures of current and lifetime smoking history.…”

Prepulse Inhibition in HIV-Associated Neurocognitive Disorders

“…In individuals with schizophrenia however, where PPI has been proposed as an endophenotype of the disease, some studies show relationships between sensorimotor inhibition deficits and impaired cognition (Butler, Jenkins, Sprock, & Braff, 1992; Rabin, Sacco, & George, 2009), while others do not (Hasenkamp et al, 2011; Kishi et al, 2012; Molina et al, in press; N. R. Swerdlow et al, 2006).…”

Lower prepulse inhibition in clinical high‐risk groups but not in familial risk groups for psychosis compared with healthy controls

“…Additionally, Rabin et al () reported a relationship between PPI and executive functions only in smokers with schizophrenia. On the other hand, some other studies (Bitsios & Giakoumaki, ; Kishi et al, ; Swerdlow et al, ) found no relationship between PPI and cognition. To our knowledge, the relationship between PPI and cognition in individuals with UHR has not yet been studied.…”