Abstract

Olfactory impairment after a traumatic impact to the head is associated with changes in olfactory cortex, including decreased gray matter density and decreased BOLD response to odors. Much less is known about the role of other cortical areas in olfactory impairment. We used fMRI in a sample of 63 participants, consisting of 25 with post-traumatic functional anosmia, 16 with post-traumatic hyposmia, and 22 healthy controls with normosmia to investigate whole brain response to odors. Similar neural responses were observed across the groups to odor versus odorless stimuli in the primary olfactory areas in piriform cortex, whereas response in the frontal operculum and anterior insula (fO/aI) increased with olfactory function (normosmia > hyposmia > functional anosmia). Unexpectedly, a negative association was observed between response and olfactory perceptual function in the mediodorsal thalamus (mdT), ventromedial prefrontal cortex (vmPFC) and posterior cingulate cortex (pCC). Finally, connectivity within a network consisting of vmPFC, fO, and pCC could be used to successfully classify participants as having functional anosmia or normosmia. We conclude that, at the neural level, olfactory impairment due to head trauma is best characterized by heightened responses and differential connectivity in higher-order areas beyond olfactory cortex.

Highlights

  • Olfactory impairment after a traumatic impact to the head is associated with changes in olfactory cortex, including decreased gray matter density and decreased BOLD response to odors

  • The current results suggest that the post-traumatic damage causing olfactory dysfunction is central and in other brain areas than the primary olfactory cortex, it is possible that this network reflects regions that have adapted to cope with olfactory loss

  • With increased post-traumatic olfactory function we observed greater responses to odor vs odorless stimuli in frontal operculum, but not in piriform cortex

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Summary

Introduction

Olfactory impairment after a traumatic impact to the head is associated with changes in olfactory cortex, including decreased gray matter density and decreased BOLD response to odors. Similar neural responses were observed across the groups to odor versus odorless stimuli in the primary olfactory areas in piriform cortex, whereas response in the frontal operculum and anterior insula (fO/aI) increased with olfactory function (normosmia > hyposmia > functional anosmia). The level of impairment may range from partial loss (hyposmia) to total loss (anosmia), while qualitative impairments include distortion (parosmia) or phantom smells (phantosmia) The etiology of these conditions may be peripheral, resulting from damage to the olfactory epithelium or its nerves, or central, with damage to either the olfactory bulb or primary/secondary cortices. Most studies of olfactory loss have focused on structural differences between healthy and impaired individuals Many of these studies include patients with. A lack of olfactory afferent input decreases the volume of the olfactory b­ ulb[19,20] and the adjacent olfactory sulcus, positioned between the gyrus rectus and medial orbitofrontal g­ yrus[21]

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