Abstract
PurposeThe dopamine hypothesis suggests that excessive dopamine release results in the symptoms of schizophrenia. The purpose of this study was to elucidate the dopaminergic and noradrenergic neurons using 3-T neuromelanin magnetic resonance imaging (MRI) in patients with schizophrenia and healthy control subjects.MethodsWe prospectively examined 52 patients with schizophrenia (M: F = 27∶25, mean age, 35 years) and age- and sex-matched healthy controls. Using a 3T MRI unit, we obtained oblique T1-weighted axial images perpendicular to the brainstem. We measured the signal intensity and area for the substantia nigra (SNc), midbrain tegmentum, locus ceruleus (LC), and pons. We then calculated the contrast ratios (CR) for the SNc (CRSN) and LC (CRLC), which were compared between patients and healthy controls using unpaired t-tests.ResultsThe SNc and LC were readily identified in both patients and healthy controls as areas with high signal intensities in the posterior part of the cerebral peduncle and in the upper pontine tegmentum. The CRSN values in patients were significantly higher than those in healthy controls (10.89±2.37 vs. 9.6±2.36, p<0.01). We observed no difference in the CRLC values between the patients and healthy controls (14.21±3.5 vs. 13.44±3.37, p = 0.25). Furthermore, there was no difference in area of the SNc and LC between schizophrenia patients and controls.ConclusionsNeuromelanin MRI might reveal increased signal intensity in the SNc of patients with schizophrenia. Our results indicate the presence of excessive dopamine products in the SNc of these patients.
Highlights
Dopamine dysfunction plays an important role in the pathogenesis of schizophrenia [1]
The SNc and locus ceruleus (LC) were readily identified by high signal intensity areas in the posterior part of the cerebral peduncle and at the upper pontine tegmentum in both patients and healthy controls (Figure 1)
Our quantitative analysis showed that the CRSN values and MaxSR SNc were significantly higher in patients with schizophrenia than in healthy controls (CRSN: 10.8962.37 vs. 9.662.36; p,0.01; Figure 2; MaxSR SNc: 1.3260.04 vs. 1.3060.04; p, 0.05)
Summary
Dopamine dysfunction plays an important role in the pathogenesis of schizophrenia [1]. In vivo positron emission tomography (PET) studies in patients with schizophrenia have indicated an increased baseline occupancy of D2 receptors by dopamine [2] and an increased capacity for striatal dopamine synthesis [3]. Neuromelanin is a byproduct of the synthesis of monoamine neurotransmitters, such as noradrenalin and dopamine, and is mainly distributed within neurons of the substantia nigra (SNc) or locus ceruleus (LC) [4]. Highfield magnetic resonance imaging (MRI), such as 3 T, is very sensitive to tissue T1 relaxation and are able to depict tissue containing neuromelanin in (SNc) or (LC) [5]. There are many previous reports which showed the signal decrease in Parkinson’s disease using neuromelanin MRI [4,6,7,8,9,10], but there are only two reports using this technique for schizophrenia [11,12]
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