Palate Width as Developmental Marker of Deficit vs Nondeficit Schizophrenia

People with deficit schizophrenia, those with primary negative symptoms, were found to have significantly wider palates than individuals with nondeficit schizophrenia, which likely reflects developmental differences occurring by the early second trimester, according to a study published in Schizophrenia Bulletin. These findings also support the hypothesis that deficit schizophrenia is a separate disease within the schizophrenia syndrome.

Previous studies have found that people with schizophrenia have wider palates than control participants. The current study was designed to assess whether there are palate width differences between participants with deficit compared with nondeficit schizophrenia. Deficit and nondeficit participants were classified using the proxy for the deficit syndrome, which quantifies the combination of low emotionality and high negative symptoms characteristic of deficit schizophrenia. Blinded measurements of palate width, length, and depth were made by a dentist who was blinded for 21 patients with deficit schizophrenia, 25 patients with nondeficit schizophrenia, and 127 control participants, all similar in age and sex.

The participants with deficit schizophrenia had significantly wider palates compared with both participants who were nondeficit and control participants, but no significant difference was found in palate length or depth (respective mean widths [standard deviation] 37.5 [3.9] deficit, 33.7 [3.1] nondeficit, and 34.0 [2.9] control; P < .001). Effect sizes were 1.08 and 1.01 (Cohen’s d) for the difference in width for deficit/nondeficit and deficit/control, respectively. The power to detect a nondeficit/control difference in width equal to that of the deficit/control difference (3.5 mm) was 0.99 vs 0.92 to detect the nondeficit/control difference of 2.0 mm.

Study investigators concluded, “If replicated, the association of a wider palate would represent a marker of a different developmental history for deficit compared to nondeficit schizophrenia and would support the concept that deficit schizophrenia is a separate disease within the syndrome of schizophrenia. This association also raises the possibility that a gene-environment interaction involving [cytomegalovirus] may constitute a [causal] pathway to the development of deficit schizophrenia.”

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

Reference

Kirkpatrick B, Gürbüz Oflezer Ö, Delice Arslan M, Hack G, Fernandez-Egea E. An early developmental marker of deficit versus nondeficit schizophrenia [published online August 19, 2019]. Schizophr Bull. doi: 10.1093/schbul/sbz024