84 Olfaction and Autism
In recent years, research has focused increasingly on olfactory perfor-
mance as an indicator of neurodegeneration. Viewed as a biomarker, such
capacity, or lack thereof, has been linked to serious neurodegenerative
conditions such as Parkinson’s disease, Alzheimer’s disease, Huntington’s
chorea, and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease).
Olfactory dysfunction has, at times, been associated with severe psychiatric
disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease
and many other diseases of the elderly, and in autism spectrum disorder
(ASD) [4–19]. Moreover, loss of olfactory function may also be a meaningful
predictor of 5‐year survival rates (5‐year mortality) for the elderly. Impaired
olfactory ability has been observed in ASDs and other serious psychiatric
disorders in adolescents and children, especially linked to tasks of identifi-
cation [3–19]. Significantly, atypical capacity in the area of sensory process-
ing is included as a diagnostic criterion in the latest version of the Diagnostic
and Statistical Manual of Mental Disorders, DSM‐5. Atypical ability to
process sensory information has been attributed to between 69% and 100%
of ASD individuals in multiple studies. These sensory difficulties add to the
observed symptoms in cognitive, social, and behavioral deficits identified
with ASDs [3–19].
In anatomical terms, dysfunctions stemming from the brain’s orbitofrontal
and medial temporal regions, which may be causative agents in olfactory
deficits, are commonly associated with ASD symptoms. Although more
difficult to examine through neuroimaging technology than areas of the brain
that process auditory or visual responses, due to nearness of bony structures or
cavities filled with air, progress has been made in the past decade in examining
olfactory function. Particularly useful has been functional magnetic resonance
imaging (fMRI), which has been utilized to assess the human brain’s olfactory
function. The areas of the brain that process olfactory data have been more
precisely identified, including the primary olfactory cortex, thalamus, hip-
pocampus and parahippocampal cortex, entorhinal cortex, amygdala, insular
cortex, hypothalamus, inferior lateral frontal region, and orbitofrontal cortex
(Figure 3.1).
Age is one of the primary influences on olfactory function with regard to
ASD. Identification is more complex than mere detection. Odor detection
capacity begins early in childhood (and according to some scientists in utero,
in mid‐gestational period week 20). Odor detection ability occurs during
adolescence but does so with less predictability for those with ASD than for
normal (neurotypicals) genetic conditions not part of ASD but which com-
monly co‐present; this may shed light on olfactory realities but causation must
be considered with caution [21,22].
More effective assessment of olfactory capacity has a number of possible
clinical implications for ASD diagnosis and treatment. It could improve
the accuracy and depth of ASD diagnosis. Standardized tools are still needed