Olfactory Dysfunction in Schizophrenia: A Review of Neuroanatomy and Psychophysiological Measurements

Abstract

Olfactory processing is thought to be mediated via the frontal and temporolimbic brain regions, both of which, as well as olfactory dysfunction, are implicated in schizophrenia. Likewise, several empirical studies of olfactory dysfunction--in particular, olfactory deficits in identification, odor detection threshold sensitivity, and odor memory, along with associated brain structural changes--have been conducted to illuminate the pathophysiology of schizophrenia. These anomalies have been investigated, more recently, as possible biological markers of that disabling illness. This article summarizes recent research on neuroimaging changes associated with olfactory impairments in schizophrenia patients and on related functional changes in psychophysiological measurements (e.g., odor identification, odor discrimination, odor detection threshold, and odor memory). The possible role of these changes as biological markers of the disorder will be discussed, as will potentially productive directions for future research.

Adult Neurogenesis and Mental Illness

“…Although the olfactory bulb may not come to mind as a key region for mental illness, the depressive-like state produced in rodents by removal of the olfactory bulbs and the olfactory changes in depressed human patients suggests a potential association between olfaction and depression (Schablitzky and Pause, 2014;Yuan and Slotnick, 2014). Olfactory deficits are observed in schizophrenia as well (Nguyen et al, 2010;Rupp, 2010). The effects of antipsychotic and anxiolytic medications on cell proliferation in the subventricular zone (SVZ), the source of olfactory bulb neurons, have been examined in a handful of studies, but with mixed results (Green et al, 2006;Kippin et al, 2005;Kodama et al, 2004;Wakade et al, 2002;Yamaguchi and Mori, 2005).…”

Olfactory sulcal depth and olfactory bulb volume in patients with schizophrenia: an MRI study

“…Moreover, the olfactory system holds special potential for understanding neurodevelopmental processes in the context of schizophrenia, given that it retains plasticity throughout the lifespan. Due to evidence that suggests deficits in olfaction may be associated with morphological changes in the brain and clinical symptoms, (Crespo-Facorro et al 2001;Moberg et al 1999;Nguyen et al 2010;Rupp 2003;Turetsky et al 2003a;b;2009a;Wu et al 1993) there has been a growing interest in studying the olfactory system in the context of schizophrenia. Abnormalities in the olfactory cortex have been linked to olfactory deficits as well as to schizophrenia (Skosnik et al 2001;Seidman et al 1992; Kopala and Clark 1990).…”

N-acetyl Cysteine Treatment Rescues Cognitive Deficits Induced by Mitochondrial Dysfunction in G72/G30 Transgenic Mice

“…Behavioral analyses of these mice showed several phenotypes, such as a PPI deficit that is reversible by haloperidol treatment, increased compulsive behaviors, impaired locomotor coordination, increased sensitivity to phencyclidine, and impaired odorant discrimination. These behavioral phenotypes are regarded as rodent correlates to symptoms of schizophrenia (Bottas et al, 2005;Braff and Geyer, 1990;Murray, 2002;Nguyen et al, 2010). However, many clinical features of schizophrenia can also be observed in other psychiatric disorders like bipolar disorder (Taylor et al, 1993;Tsuang et al, 1980;Valles et al, 2000) and genetic risk factors contributing to psychiatric disorders, including G72/G30 that are typically associated with more than one disorder.…”