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Cortical glutamatergic dysfunction is thought to be fundamental for psychosis development, and may lead to structural degeneration through excitotoxicity. Glutamate levels have been related to gray matter volume (GMV) alterations in people at ultra-high risk of psychosis, and we previously reported GMV changes in individuals with high schizotypy (HS), which refers to the expression of schizophrenia-like characteristics in healthy people. This study sought to examine whether GMV changes in HS subjects are related to glutamate levels.
We selected 22 healthy subjects with HS and 23 healthy subjects with low schizotypy (LS) based on their rating on a self-report questionnaire for psychotic-like experiences. Glutamate levels were measured in the bilateral anterior cingulate cortex (ACC) using proton magnetic resonance spectroscopy, and GMV was assessed using voxel-based morphometry.
Subjects with HS showed GMV decreases in the rolandic operculum/superior temporal gyrus (pFWE = 0.045). Significant increases in GMV were also detected in HS, in the precuneus (pFWE = 0.043), thereby replicating our previous finding in a separate cohort, as well as in the ACC (pFWE = 0.041). While the HS and LS groups did not differ in ACC glutamate levels, in HS subjects ACC glutamate was negatively correlated with ACC GMV (pFWE = 0.026). Such association was absent in LS.
Our study shows that GMV findings in schizotypy are related to glutamate levels, supporting the hypothesis that glutamatergic function may lead to structural changes associated with the expression of psychotic-like experiences.
Temporal lobe epilepsy is associated with a significant risk of psychosis but there are only limited studies investigating the underlying neurobiology.
To characterise neuroanatomical changes in temporal lobe epilepsy and comorbid psychosis.
The study population comprised all individuals with temporal lobe epilepsy on the epilepsy database at the National Centre for Epilepsy and Epilepsy Neurosurgery in Ireland (Beaumont Hospital) between 2002 and 2006. Ten people with temporal lobe epilepsy with psychosis were matched for age, gender, handedness, epilepsy duration, seizure laterality, severity of epilepsy and anti-epileptic medication with ten comparison participants with temporal lobe epilepsy only. Participants received a magnetic resonance imaging scan and voxel-based morphometry analyses were applied to grey and white matter anatomy.
Significant grey matter reduction was found bilaterally in those with temporal lobe epilepsy with psychosis in the temporal lobes in the inferior, middle and superior temporal gyri and fusiform gyri, and unilaterally in the left parahippocampal gyrus and hippocampus. Significant extra-temporal grey matter reduction was found bilaterally in the insula, cerebellum, caudate nuclei and in the right cingulum and left inferior parietal lobule. Significant white matter reduction in those with temporal lobe epilepsy with psychosis was found bilaterally in the hippocampus, parahippocampal/fusiform gyri, middle/inferior temporal gyri, cingulum, corpus callosum, posterior thalamic radiation, anterior limb of internal capsule and white matter fibres from the caudate nuclei, and unilaterally in the left lingual gyrus and right midbrain and superior temporal gyrus.
Significant grey and white matter deficits occur in temporal lobe epilepsy with psychosis. These encompass the medial temporal lobe structures but also extend to lateral temporal and extra-temporal regions. Some of these deficits overlap with those found in schizophrenia.
The pattern of brain morphological changes at the early stages of schizophrenia may depend on the age at onset of illness; in children and adolescents with schizophrenia, grey matter deficits are seen in the parietal lobe whereas in individuals with adult onset these are more widespread.
To examine whether white matter is similarly affected.
Diffusion tensor imaging was used to compare fractional anisotropy measures in individuals with adolescent-onset (n = 17) and adult-onset schizophrenia (n = 17) with those in age- and gender-matched controls.
Compared with their respective controls, individuals with adolescent-onset schizophrenia showed fractional anisotropy decrease in parietal regions; individuals with adult onset showed additional fractional anisotropy reductions in frontal, temporal and cerebellar regions. A differential effect of age at onset (adolescent v. adult) was noted bilaterally in medial prefrontal white matter.
White matter abnormalities in frontal regions in schizophrenia may depend on developmental stage at the time of illness onset.
Subtle abnormalities in frontal white matter have been reported in
To assess whether impaired integrity of white matter tracts is associated
with bipolar disorder and genetic liability for the disorder.
A total of 19 patients with psychotic bipolar I disorder from multiply
affected families, 21 unaffected first-degree relatives and 18 comparison
individuals (controls) underwent diffusion tensor imaging. Whole brain
voxel-based analyses compared fractional anisotropy between patients and
relatives with controls, and its relationship with a quantitative measure
of genetic liability.
Patients had decreased fractional anisotropy compared with controls in
the genu of the corpus callosum, right inferior longitudinal fasciculus
and left superior longitudinal fasciculus. Increased genetic liability
for bipolar disorder was associated with reduced fractional anisotropy
across distributed regions of white matter in patients and their
Disturbed structural integrity within key intra- and interhemispheric
tracts characterises both bipolar disorder and genetic liability for this
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