ERP abnormalities in schizophrenia prior to neuroleptic treatment

Hirayasu, Yoshio; Asato, Naohiko; Ohta, Hirokazu; Hokama, Hiroto; Arakaki, Hajime; Ogura, Chikara

doi:10.1016/0006-3223(96)84459-3

Cited by 1 publication

(2 citation statements)

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“…Because of the low resolution of PET, a reduction of grey matter would appear as reduced CBF and metabolism due to partial volume averaging effects. 83 These MRI-based findings were replicated and extended by Hirayasu et al, 86 who confirmed this left lateralized abnormality in familial but not non-familial BD samples, and Botteron et al, 87 who showed this abnormality is present in both affected and unaffected co-twins from monozygotic twin pairs (ages 18 to 24) discordant for MDD.…”

Section: The Subgenual Prefrontal Cortexmentioning

confidence: 80%

“…103 Sullivan and Grattan 103 hypothesized that left ventromedial PFC lesions disinhibit the right ventromedial PFC, yielding heightened sympathetic and HPA-axis arousal. Given the left-lateralization of neuroimaging abnormalities in the subgenual PFC 84,86,87 it might be hypothesized that left subgenual PFC dysfunction contributes to the heightened neuroendocrine and sympathetic autonomic arousal seen in depression. 58,60,104 Prelimbic and infralimbic cortex lesions reduce HR variability at rest and during exposure to fear-conditioned stimuli.…”

Section: Clinical Implications Of Subgenual Pfc Dysfunctionmentioning

confidence: 99%

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Prefrontal Cortical‐Amygdalar Metabolism in Major Depression

Drevets

1999

Annals of the New York Academy of Sciences

515

298

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Functional neuroimaging studies of the anatomical correlates of familial major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of resting blood flow (BF) and glucose metabolism in depression in the amygdala and the orbital and medial prefrontal cortical (PFC) areas that are extensively connected with the amygdala. The amygdala metabolism in MDD and BD is positively correlated with both depression severity and "stressed" plasma cortisol concentrations measured during scanning. During antidepressant drug treatment, the mean amygdala metabolism decreases in treatment responders, and the persistence of elevated amygdala metabolism during remission is associated with a high risk for the development of depressive relapse. The orbital C metabolism is also abnormally elevated during depression, but is negatively correlated with both depression severity and amygdala metabolism, suggesting that this structure may be activated as a compensatory mechanism to modulate amygdala activity or amygdala-driven emotional responses. The posterior orbital C and anterior cingulate C ventral to the genu of the corpus callosum (subgenual PFC) have more recently been shown in morphometric MRI and/or post mortem histopathological studies to have reduced grey matter volume and reduced glial cell numbers (with no equivalent loss of neurons) in familial MDD and BD. These data suggest a neural model in which dysfunction of limbic PFC structures impairs the modulation of the amygdala, leading to abnormal processing of emotional stimuli. Antidepressant drugs may compensate for this dysfunction by inhibiting pathological limbic activity.

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Section: The Subgenual Prefrontal Cortexmentioning

confidence: 80%