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;
MartÃnez 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.