Autistic facial phenotypes as a possible cause of Frontal Sinus Inflammation

by Yuval Levental
Abstract
It has been shown that certain autistics may have a distinct facial structure which could be
indicative of autism. The hypothesis presented is that this structure may possible produce
horizontal inflammation of the frontal sinus. This is based on the idea that for the autistics with
the distinct facial features, the distance between the inner and outer canthi is longer than average,
but the distance between the inner canthi is shorter than average, causing horizontal strain in the
middle. To counteract the excess strain, the nasal bridge possibly pushes perpendicularly
inwards towards the direction of the frontal sinuses. Many autistics experience sensory overload,
and one possible cause could be inflamed frontal sinuses, caused by the tension applied by the
ASD facial morphology.
Background
In a 2011 study, Kristina Aldridge of the University of Missouri discovered significant
differences in facial morphology in studied boys with autism spectrum disorder (ASD) compared
to typically developing (TD) boys. The study also found that the facial morphology of boys with
ASD could be divided into two unique subgroups
(http://molecularautism.biomedcentral.com/articles/10.1186/2040-2392-2-15). A follow-up 2014
study found three distinct subgroups of facial morphology among ASD boys
(https://www.researchgate.net/publication/267742068_Facial_Structure_Analysis_Separates_Aut
ism_Spectrum_Disorders_into_Meaningful_Clinical_Subgroups).
The 2011 study used 17 landmarks on 3dMD images of the faces (Fig. 1). There were 136 total
linear distances compared, and 39 were statistically significantly different. Linear distances that
were significantly reduced in the ASD group included those connecting glabella and nasion to
the inner canthi and those connecting nasion with landmarks located on the nose and philtrum.
Linear distances that were significantly increased in the ASD group connected the landmarks on
the mouth with the inferior nasal region. Additionally, significantly increased linear distances
connected the inner and outer canthi and the lateral upper face with the eyes and contralateral
side of the mouth (http://molecularautism.biomedcentral.com/articles/10.1186/2040-2392-2-15).

Figure 1 - Illustration of the anthropometric landmarks collected from the 3dMD images
Most likely, the facial features associated with autism cause possible physiological effects which
in turn cause autistic symptomology. This is done through the various forces that are exerted via
the different distances between facial features.
Hypothesis
The distinct facial structure that certain autistics have produces horizontal inflammation of the
frontal sinus, due to the smaller than average nasal bridge area, distance between nasal bridge
forehead, and the opposing surface tensions from the eyes. The distance between the inner and
outer canthi is longer than average, but the distance between the inner canthi is shorter than
average, causing horizontal strain in the middle. (Fig. 2)
(http://molecularautism.biomedcentral.com/articles/10.1186/2040-2392-2-15). To counteract the
excess strain, the nasal bridge pushes perpendicularly inwards in the direction of the frontal
sinuses, causing the inflammation. Another reason is that the nasal bridge area is smaller than
average, and that pressure is inversely proportional to area, so the smaller area could cause more
pressure to be directed towards the nasal bridge.

Figure 2. Results of Euclidean Distance Matrix Analysis analyses of landmark coordinate data
collected from 3dMD images in 2011 study. White lines are statistically significantly increased in
boys with autism spectrum disorder (ASD), and black lines are statistically significantly reduced
in boys with ASD relative to typically developing (TD) boys.
Evaluation of hypothesis
There are two frontal sinuses, each one located above each eye (Fig. 3). Because the compressed
nasal bridge is close to them, it will put thermal pressure on them, causing blood vessels to
expand producing sinus inflammation (Fig. 4). Possible evidence against this hypothesis
includes that the nasal bridge will not put enough pressure on the frontal sinuses to cause
significant differences in inflammation.

Figure. 3 Diagram of Paranasal Sinuses

Figure 4 Illustrated nose nasal cavities

To test this hypothesis, subjects with the distinct groupings of facial features seen in the Aldridge
et. al studies along with a typically developing group would undergo a sinus MRI scan. The
results from the two groups would then be compared and analyzed. Another possible test would
be to assign the subjects to sit in a head-out body plethysmograph and breathe exclusively
through a single nasal cavity, while pressure and flow values are digitally measured. The airway
resistance would be measured in 2 cm segments between the nostril and the nasopharynx.
If the hypothesis were to be confirmed, this would add more physiological knowledge of autistic
symptomology. Many autistics have reported sensory overstimulation, and one possible cause
could be inflamed frontal sinuses, caused by the tension applied by the ASD facial morphology

(http://link.springer.com/article/10.1023/A:1025850431170). A treatment plan for temporarily

reducing inflammation could be developed through the usage of nasal sprays.