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Scientists Mark Olfactory Identification Impairment as A Trait for Schizophrenia Spectrum Disorders

Apr 17, 2018

Olfactory identification impairment has robustly been demonstrated in patients with established schizophrenia. However, it is still a number of unresolved issues concerning whether olfactory identification impairment may be a trait marker for schizophrenia spectrum disorders.  

Most of the previous studies were limited to patients with established schizophrenia for a long time. Their olfactory identification performance may be confounded by the chronicity of the disorders and medications.

Besides, there are very few studies examining olfactory identification in individuals with schizotypal traits. It is also not clear whether olfactory identification impairment may correlate with anhedonia, one of the core negative symptoms of schizophrenia spectrum disorders. More importantly, it is not fully unknown the underlying neural mechanism of olfactory hedonic processing in human beings. 

Dr. Raymond CHAN's team from the Neuropsychology and Applied Cognitive Neuroscience (NACN) Laboratory, CAS Key Laboratory of Mental Health, Chinese Academy of Sciences has conducted two studies to address these above issues.  

In the first study, they specifically compared olfactory identification performances in 35 first-episode schizophrenia patients, 40 individuals with schizotypy and 40 demographically matched healthy controls.  

They administered the University of Pennsylvania Smell Identification Test to assess olfactory identification in these participants. Moreover, the Temporal Experience Pleasure Scale (TEPS) was also administered to them to assess their self-reported anticipatory and consummatory pleasure.  

Their results showed that both patients with first-episode schizophrenia and individuals with schizotypy exhibited statistically poorer olfactory identification ability than healthy controls, and schizophrenia patients were also found to perform statistically poorer than individuals with schizotypy.  

Moreover, although they also found that both first-episode schizophrenia patients and individuals with schizotypy also reported less pleasurable experience than healthy controls, there was no difference being reported between schizophrenia patients and schizotypal individuals.  

They also found that such olfactory identification impairment was significantly correlated with reduced pleasure experiences in patients and schizotypy individuals. However, there was no such relationship found in healthy controls.  

In the second study, they have developed an Olfactory Incentive Delay (OLID) imaging task investigating the neural responses during anticipation and receipt of olfactory rewards and punishments.  

They showed 25 healthy volunteers two odours or two markers that indicated the two odours, i.e., Pentyl acetate (an odour likes banana) and Trimethylamine (an odour likes rotten fish) during fMRI scanning. The volunteers also completed the Temporal Experience of Pleasure Scale, a self-reported questionnaire, to assess their ability to experience pleasure. 

Their findings showed that pallidum was activated during the anticipation of both pleasant and unpleasant odours. The bilateral insula was activated independently from the odours' hedonic valence during the receipt phase.  

They also found that right caudate activation during the anticipation of unpleasant odours was correlated with self-reported anticipatory hedonic capacity, whereas bilateral insular activation during the receipt of pleasant odours was correlated with self-reported consummatory hedonic capacity. 

Taken together, these findings demonstrated that both patients with first-episode schizophrenia and individuals with schizotypy have already exhibited reduced ability to identify olfactory stimuli.  

The neuroimaging findings in healthy volunteers also highlight a useful and valid paradigm for us to investigate the neural circuitry underlying reward processing in patients with anhedonia, such as schizophrenia spectrum disorders and major depressive disorder.  

These two studies were supported by the National Key Research and Development Programme, theNational Natural Science Fund, China), the Beijing Municipal Science& Technology Commission Grant, the Beijing Training Project for the Leading Talents in Science and Technology, and the Natural Science Foundation of Guangdong Province. 

These studies are now available in Progress in Neuro-Psychopharmacology & Biological Psychiatry and Neuropsychologia.

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