A study recently published online in Schizophrenia Bulletin found that people with schizophrenia with primary negative symptoms, known as deficit schizophrenia, had significantly wider oral palates compared with patients with nondeficit schizophrenia as well as control subjects.
Here, lead author Brian Kirkpatrick, MD, chair of the department of psychiatry and behavioral sciences, University of Nevada, Reno School of Medicine, and coauthor Gary Hack, DDS, associate professor, University of Maryland School of Dentistry, Baltimore, discuss the findings, its real-world implications, and possible future research.
Q: What existing data led you and your co-investigators to conduct this research?
A: Minor physical anomalies of the face and oral cavity have previously been observed in patients suffering from schizophrenia and may be associated with aberrant brain development. It has been suggested that craniofacial morphology and palatal abnormalities may be informative in elucidating the specific pathophysiology of schizophrenia, as there is a well-described interdependence between the developing brain and the developing face. The palate is part of the bony structure that includes bones at which the base of the temporal lobe of the brain sits. While most previous studies, over the past century, have indicated narrow palates in patients suffering from schizophrenia, those studies were carried out with subjective assessment without quantitative measurements and were performed by examiners who were not blinded to the patients’ diagnosis. Our 2007 study used quantitative measures of the palate, and those doing the measurements did not know which participants had schizophrenia and which did not. In 2016, Delice et al. (a group of Turkish investigators) also used quantitative assessment of palatal dimensions in a blinded manner, and confirmed people with schizophrenia have wider palates. As a result of those two studies we tested the hypothesis that individuals with deficit vs nondeficit schizophrenia would differ on palate width.
Q: Please briefly describe your study and its findings. Were any of the outcomes particularly surprising?
A: The study, which involved an international, interprofessional collaboration on palatal dimensions, compared two groups of people with schizophrenia, those with and those without deficit features, and a group of people without schizophrenia. Individuals with schizophrenia and primary negative symptoms (deficit schizophrenia) differ from those without such symptoms (nondeficit schizophrenia) on risk factors, course of illness, other signs and symptoms, treatment response, and biological correlates. We found that the deficit group had significantly wider palates than both the nondeficit patients and the comparison control group.
Q: What are the possible real-world applications of these findings in clinical practice?
A: Our finding is consistent with the existence of a divergence in development between people with deficit vs nondeficit schizophrenia that occurs no later than the early second trimester of pregnancy, as a recognizable palate forms between weeks 6 and 17. This finding therefore gives a timeline for when the deficit patients diverge in terms of their development from other people with schizophrenia as well as from individuals without psychosis. If replicated, our findings would support the concept that deficit schizophrenia is a separate disease within the syndrome of schizophrenia. This has implications for the design of many future studies of schizophrenia.
Q: Do you and your co-investigators intend to expand upon this research?
A: Patients with deficit schizophrenia have also been shown to have a greater prevalence of seropositivity for cytomegalovirus (CMV), but not other human herpes viruses, compared to those with nondeficit schizophrenia. CMV appears to increase the risk of cleft palate and cognitive impairment. Those studies suggest that CMV may be a risk factor for deficit but not for nondeficit schizophrenia. There is also evidence that a gene-environment interaction between certain genes and CMV exposure increases the risk of schizophrenia. Our hypothesis is that a gene x environment interaction may provide the causal pathway in the development of deficit but not nondeficit schizophrenia. We propose to conduct a pilot study to gather pilot data on deficit/nondeficit differences in palate width and CMV seropositivity.
Q: Is there anything else pertaining to your research and findings that you would like to add?
A: Our research findings will broaden the thinking about the many complex factors that come into play as the human brain and face develop. We hope that our interdisciplinary research, involving both psychiatrists and dentists, may lead to further collaborations to improve the dental experience for this population, which already faces numerous social and financial barriers as well as many oral health issues.
Kirkpatrick B, Gürbüz Oflezer Ö, Delice Arslan M, Hack G, Fernandez-Egea E. An early developmental marker of deficit versus nondeficit schizophrenia [published online ahead of print August 19, 2019]. Schizophrenia Bulletin. 2019 August 19;[Epub ahead of print].