Gray matter abnormalities in subjects at ultra-high risk for schizophrenia and first-episode schizophrenic patients compared to healthy controls

White matter alterations related to P300 abnormalities in individuals at high risk for psychosis: an MRI–EEG study

“…The only available VBM study of white matter volume comparing high-risk patients and controls found white matter reductions in the temporal lobe of the patient group. 18 Our results further confirm that the temporal lobe plays a crucial role in the prodromal phases of psychosis. In addition, to our knowledge, we showed for the first time concurrent temporal and prefrontal white matter reductions on the left side.…”

“…In particular, the first study exploring white matter in the prepsychotic phases found reduced temporal lobe volume in patients at increased clinical risk for psychosis. 18 Another study found that the ARMS patients who later became psychotic had larger volumes of white matter in the frontal lobe. 19 These alterations resemble those observed during the established phases of the illness but are less marked.…”

“…[13][14][15] P300 can index a neuro biologic vulnerability to schizophrenia, in line with other studies showing P300 abnormalities in relatives of individuals with psychosis. 16,17 On the other hand, neuroimaging studies have indicated that patients at high risk for psychosis show alterations in white matter 18,19 volume in fronto-temporal regions. In particular, the first study exploring white matter in the prepsychotic phases found reduced temporal lobe volume in patients at increased clinical risk for psychosis.…”

Cortical thinning and caudate abnormalities in first episode psychosis and their association with clinical outcome

“…Others identified right (Witthaus et al, 2009) and bilateral (Takahashi et al, 2010) STG reduction in individuals at ultra-high risk of psychosis (UHR), and a recent meta-analysis associated STG volume reduction with transition from UHR to psychosis (Fusar-Poli et al, 2011a). Our study also supports STG volume loss as an early morphometric marker in psychosis.…”

The human brain representation of odor identification

“…Indeed, the early and specific OI deficit in AD correlates with the number of tangles in entorhinal cortex and the hippocampus (Wilson et al 2007), and left hippocampal atrophy (Murphy et al 2003). Structural changes in the entorhinal cortex and hippocampus are also present in patients with schizophrenia (Baiano et al 2008;Bogerts et al 1985;Ebdrup et al 2010;Schultz et al 2009;Witthaus et al 2009), another group of patients with a specific OI deficit (Atanasova et al 2008;Moberg et al 1997Moberg et al , 2006Rupp 2010). The utility of OI tests as a clinical tool depends on a better understanding of the neuronal processes underlying OI, and how OI differs from passive smelling (PS).…”