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Brain metabolite alterations in subjects at ultra-high risk for psychosis: magnetic resonance spectroscopy study

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Byun, M.; Choi, J.; Yoo, S.; Kang, D.; Jang, D.; Lee, J.; Kwon, J.; Jung, W.; Choi, C.

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Recent neuroirnaging studies have suggested that brain changes
occur in subjects at ultra-high risk (UHR) for psychosis while
experiencing prodromal symptoms, among which depression may
increase the risk of developing a psychotic disorder. We used
proton magnetic resonance spectroscopy to examine brain metabolite
levels in the anterior cingulate cortex, the left dorsolateral
prefrontal cortex and the left thalamus in subjects at UHR for
psychosis. In addition, we compared brain metabolites between the
UHR subjects with comorbid major depressive disorder (MDD)
and healthy controls.
Twenty UHR subjects and 20 age- and IQ-matched healthy
controls were included in this study. UHR was determined based
on the Comprehensive Assessment of At-Risk Mental States
(CAARMS) criteria [1]. At intake, all potential subjects participated
in an intensive clinical interview with two experienced
psychiatrists who used the Structured Clinical Interview for DSM-IV Axis I section (SCID) to identify past and current
psychiatric illnesses. Eleven subjects in the UHR group (55%)
were diagnosed with comorbid MDD, eight with anxiety disorder,
and one with bipolar disorder. A modified 24-item version of
the Brief Psychiatric Rating Scale (BPRS) and the Positive and
Negative Syndrome Scale (PANSS), the Hamilton Rating Scale for
Depression (HAM-D), and the Hamilton Rating Scale for Anxiety
(HAM-A), the Korean version of the Wechsler Adult Intelligence
Scale (K-WAIS) were also used to assess the participants. Subjects
were longitudinally monitored for progression to psychosis. The
UHR group was subsequently divided into two subgroups: UHRpsychotic
(n = 2) and UHR-nonpsychotic (n = 17). Nine subjects
were receiving psychotropic drugs at baseline (low-dose atypical
antipsychotics, n = 8; antidepressant, n = 1).
No significant differences were observed between the UHR and
healthy control groups in terms of age, sex ratio, or IQ. Compared
to the UHR subjects without MDD (n = 9), UHR subjects
with MDD (n = 11) scored significantly higher on the PANSS
total (60.00±5.98, p=0.012), BPRS (46.55±3.67, p=0.014), and
HAM-D (17.18±4.24, p=0.046). There were no significant differences
in any other metabolite level in any brain region among
UHR subjects with MDD, UHR subjects without MDD, or healthy
controls. However, UHR subjects with MDD showed significantly
higher myo-inositol (Ins) levels in the left thalamus, compared to
the healthy control (Ins: 3.33±0.63mM versus 2.58±0.71 mM,
F=3.825, p=0.031). Additional analysis in drug-naive UHR
subjects (n = 11) to control the effect of medication revealed
significantly increased Ins concentrations in the left thalamus
of drug-naive UHR subjects compared to healthy controls (Ins:
F=5.032, p=0.033). However, a significant comorbidity effect
was observed for Ins concentrations in the left thalamus among
drug-naive UHR subjects with MDD, those without MDD, and
healthy controls (Ins: F = 3.656, p = 0.039), although the sample
size was small. There was no significant difference in any metabolites
concentrations between UHR subjects who progressed to
psychosis and subjects who did not.
Our results demonstrate that increased thalamic Ins level is
associated with prodromal depressive symptoms. Further longitudinal
follow-up studies with larger UHR sample sizes are required
to investigate the function of Ins concentrations as a biomarker of
vulnerability to psychosis.
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