Morphological changes in secondary, but not primary, sensory cortex in individuals with life-long olfactory sensory deprivation
Moa G. Peter,
Gustav Mårtensson,
Elbrich M. Postma,
Love Engström Nordin,
Eric Westman,
Sanne Boesveldt,
Johan N. Lundström
Affiliations
Moa G. Peter
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Corresponding author. Dept. of Clinical Neuroscience, Karolinska Institutet, Nobels väg 9, 17177, Stockholm, Sweden.
Gustav Mårtensson
Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
Elbrich M. Postma
Division of Human Nutrition and Health, Wageningen University, Wageningen, the Netherlands; Smell and Taste Centre, Hospital Gelderse Vallei, Ede, the Netherlands
Love Engström Nordin
Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Department of Diagnostic Medical Physics, Karolinska University Hospital Solna, Stockholm, Sweden
Eric Westman
Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Department of Neuroimaging, Centre for Neuroimaging Sciences, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
Sanne Boesveldt
Division of Human Nutrition and Health, Wageningen University, Wageningen, the Netherlands
Johan N. Lundström
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Monell Chemical Senses Center, Philadelphia, PA, USA; Department of Psychology, University of Pennsylvania, Philadelphia, USA; Stockholm University Brain Imaging Centre, Stockholm University, Stockholm, Sweden; Corresponding author. Dept. of Clinical Neuroscience, Karolinska Institutet, Nobels väg 9, 17177, Stockholm, Sweden.
Individuals with congenital sensory deprivation usually demonstrate altered brain morphology in areas associated with early processing of the absent sense. Here, we aimed to establish whether this also applies to individuals born without a sense of smell (congenital anosmia) by comparing cerebral morphology between 33 individuals with isolated congenital anosmia and matched controls. We detected no morphological alterations in the primary olfactory (piriform) cortex. However, individuals with anosmia demonstrated gray matter volume atrophy in bilateral olfactory sulci, explained by decreased cortical area, curvature, and sulcus depth. They further demonstrated increased gray matter volume and cortical thickness in the medial orbital gyri; regions closely associated with olfactory processing, sensory integration, and value-coding. Our results suggest that a lifelong absence of sensory input does not necessarily lead to morphological alterations in primary sensory cortex and extend previous findings with divergent morphological alterations in bilateral orbitofrontal cortex, indicating influences of different developmental processes.
