Phuong Bui

11/13/17

Summary of Benneto et al. (2007)

Previous studies were inadequate in showing that sensory impairments, particularly poor

odor and taste identification, are specific to autism and not to Fragile X syndrome, heterogeneous

developmental disabilities, or typical development. On the other hand, previous neurobiological

studies have lent support to the connection between autism and atypical responses to tastes and

smells. To illustrate, facial nerve (CN VII) carries gustatory detection from the tongue, while

several cortical regions including the thalamus, orbitofrontal cortex, and amygdala are involved

with taste identification. Autism is linked with damage to the mentioned regions, thus suggesting a

causal effect to impairments in odor and taste processing.

The researchers, Benneto, Kuschner, and Hyman, set out to investigate if participants with

autism would show worse performance in odor and taste identification. Through a taste detection

test they also study whether brainstem or other cortical regions above the level of facial nerve

nucleus are involved. They also studied the link between olfaction and social impairment in autism.

Twenty-one children and adolescents with high-functioning autism and 27 healthy control

participants who met diagnostic criteria and clinician judgement were recruited for this study. Three

tests were performed to assess taste identification, taste detection, and odor identification. For the

first test, four tastants were delivered via a 2% carboxymethylcellulose solution: sucrose, salt, citric

acid monohydrate, and quinine sulfate dihydrate; while the carboxymethylcellulose solution alone

was used as a control. With a water rinse in between, the tastants were applied to the anterior two-

thirds of the tongue in one of two quasi-random orders, with quinine always presented last to avoid

an effect due to its lasting bitter aftertaste. For the second test, taste detection thresholds were

measured using an electrogustometer that introduced weak electrical stimuli to either side of the

tongue in a random order. Participants had to meet an initial criterion of 5 consecutive correct

responses; then, the stimulus intensity would be either increased after one incorrect response, or
decreased after two correct responses. Detection thresholds were measured as the average of the last

four trials. For the third test, participants took the widely used Sniffin Sticks Odor Identification

Screening Test, which assessed receptive identification of 12 common odors presented via felt-tip

pens saturated with each odor. Participants identified the odor among 4 choices shown with both

written words and pictures, in an effort to reduce verbal demands for children with autism.

Bennetto et al. (2007) found that participants with autism performed much worse than

control participants in detecting citric acid (p = .03) and quinine (p = .07), but just as well as control

participants in detecting sucrose (p = .84) and salt (p = .24). The authors also found no significant

difference in taste detection thresholds between the two groups of participants (p = .47). Meanwhile,

detection thresholds and sour taste identification were unrelated within the autism group (p = .71).

The authors also found that the autism group performed much worse in identifying odors (p = .007),

and such poor odor identification was strongly correlated to social skills impairment (p < .05).1

One major interpretation is that such chemosensory dysfunction is not due cognitive

limitations, because of matching based on language comprehension, IQ, and the nonverbal format

of the tasks. In addition, similar detection thresholds among both groups suggest that cortical rather

than brainstem regions were involved.

One major limitation is that electrical stimulation of the tongue only activates sour taste

receptors, so no conclusion can be drawn about the ability to detect other tastes. However, the fact

that detection thresholds and sour taste identification were unrelated within the autism group still

lends support to the authors hypothesis about cortical regions being responsible. Moving forward,

the authors suggested further research to specify the neurologic bases of these impairments.

Benneto et al. (2007) offered fair experimental methods and convincing statistical analyses.

The authors also pointed out how the results are supported by other studies. I agree with their

conclusions about significant differences in taste and odor processing in autism.

Benneto, L., Kuschner, S. E., & Hyman, L. S. (2007). Olfaction and Taste Processing in Autism. Biological Psychiatry
2007, 62:1015-1021.