Implications: Neural Mechanisms of Hyporeactivity versus Hyperexcitability in SSD
Our goal was to gain insight regarding conflicting characterizations of sensory percepts in SSD. On one hand, there is the subjective experience of sensory flooding (McGhie & Chapman, 1961) and the increased incidence of visual illusions reported here, both of which are associated with hyperexcitable sensory processing , and competing findings identifying hyporeactive responses. Importantly, the hyporeactivity/hyperexcitability conversation is not a straw-man argument. There is strong evidence associating hyporeactivity with SSD and disease progression (Javitt et al., 2018; Koshiyama et al., 2020). Hyporeactive neural responses in SSD are cataloged across a variety of measures, including preconscious deviance detection (mismatch negativity: MMN) in visual (Farkas et al., 2015; Urban et al., 2008) and auditory domains (Erickson et al., 2016; Haigh et al., 2016a; Joshi et al., 2018; Koshiyama et al., 2020; Umbricht & Krljes, 2005), and reduced N1 responses to visual (Antonova et al., 2021; Hoptman et al., 2018; Neuhaus et al., 2011) and auditory stimuli (Force et al., 2008; Mathalon et al., 2019; Osokina & Ivnyev, 2018; Perez et al., 2012). Hyporeactive BOLD responses in fMRI designs are observed in early visual, auditory, and somatosensory cortices (Gaebler et al., 2015; Haenschel et al., 2007; Haigh et al., 2016b; Hoptman et al., 2010; Martínez et al., 2018). Hyporeactivity is observed for complex sensory processing, including early face processing (Earls et al., 2016; Herrmann et al., 2004), behavioral face processing (Walther et al., 2009) and self-viewing (Zhou et al., 2020). In those with high schizotypy similar, weaker patterns appear (Broyd et al., 2016; Donaldson et al., 2021). Reduced amplitudes in the auditory MMN (Broyd et al., 2016), auditory and visual N1 (Favrod et al., 2017; Oestreich et al., 2015, 2016), are reported. Across SSD, including high schizotypy, a range of findings point to hyporeactive neural responses to sensory stimuli.
On the other hand, there is strong evidence forhyperexcitability . In the SSD population, there are reports of sensory flooding (Bunney et al., 1999; McGhie & Chapman, 1961) that are thought to reflect deficits in sensory gating (Freedman et al., 2020; Hetrick et al., 2012; Patterson et al., 2008; Potter et al., 2006) which have been observed in SSD (Brockhaus-Dumke et al., 2008; Cadenhead et al., 2000; Hazlett et al., 2015), including high schizotypy (Croft et al., 2001; Park et al., 2015; Wang et al., 2004), which include the current findings. The PGT is valuable as a behavioral measure of hyperexcitability.
It is important to note that neurological data would be required to make statements of hyperexcitability and how they relate to illusions seen in the PGT in high schizotypy. Although more research is needed, the current findings support that a feasible way to get a handle on SSD is to examine the neurotypical population who naturally vary on symptomatology. It may be the case that both hyperexcitability and hyporeactivity may be at play contributing to the impairments documented in SSD. Because of the challenge of accessing schizophrenia populations, the non-clinical population will continue to provide meaningful insight to clarify this question.