Being Brains: Making the Cerebral Subject by Fernando Vidal & Francisco Ortega

Author:Fernando Vidal & Francisco Ortega [Vidal, Fernando & Ortega, Francisco]
Language: eng
Format: epub
Tags: Philosophy, Movements, Humanism, Science, Life Sciences, Neuroscience, Social Science, Anthropology, Cultural & Social
ISBN: 9780823276073
Google: Ct8LMQAACAAJ
Publisher: Fordham UP
Published: 2017-09-15T20:51:42+00:00

Again “Just Like Diabetes”

Awareness of these limitations has reinforced the view that abnormalities in neural networks rather than in discrete brain structures underlie psychiatric disorders. It has also contributed to move psychiatric neuroimaging research toward resting-state models (Broyd et al. 2009) and to come in line with emerging approaches to brain connectivity (Price and Drevets 2010) and the concurrent transformation of fMRI research (and brain science in general) into a big-data worldwide endeavor (Lohmann et al. 2013, Thompson et al. 2014). Launched by Marcus Raichle in 2001 (Raichle et al. 2001, Raichle and Snyder 2007), the notion of a “default mode” of brain function has come to describe a “resting state” characterized by very slow neural oscillation (see Callard and Margulies 2011 for a history and larger significance of these notions). The resting state is the “state” of large-scale networks that are active when the subject is awake but not focused on the external environment; their activity is therefore driven neither by tasks nor by external stimuli. Neuroimaging studies of the relationship between the default mode network and mental disorder began in the early 2000s and have shown, for example, that the network is functionally overactive in schizophrenia and hypoactive in Alzheimer’s disease (Buckner et al. 2008).

Resting-state research has also gained momentum in the field of depression neuroimaging. A 2012 review of sixteen resting-state fMRI studies published between 2005 and 2011 described various default mode network “abnormalities” in major depression (Wang et al. 2012; see also Veer et al. 2010, not included in the review, as well as the meta-analysis by Alcaro et al. 2010). What is supposed to be their role? The most ambitious resting-state model of major depressive disorder (Northoff et al. 2011) does not aim at “denosologizing” the category. Rather, it preserves major depressive disorder (MDD) in all its heterogeneity—at the level of its symptoms, the affects it encompasses (anxiety, sadness, grief, panic, pain), the bodily systems it involves (from the vegetative and endocrine to the cognitive), the neuroanatomical regions observed to be “abnormal” in the condition, and the biochemistry pertaining to each of those systems and regions. It then seeks to correlate those different levels, mustering a vast amount of neuroanatomical, psychopathological, and biochemical information to turn major depression into a specific brain system–network disorder.

MDD turns out in this model to be characterized by a subcortical-cortical imbalance, with resting-state hyperactivity in some regions and hypoactivity in others. Certain subcortical and cortical regions are hyperactive in the resting state, while others (especially cortical) show hypoactivity. Such abnormal resting-state patterns “may strongly impact the neural processing of external stimuli” in the regions concerned, and that “may enable and predispose the occurrence” of major depression symptoms (7). Higher affective and cognitive functions are “highjacked [sic]” by subcortical primary-process emotional systems (1, 11). For example, depressive hopelessness arises by way of a “psychopathologically specific” relationship with resting-state activity in the ventromedial prefrontal cortex (VMPFC). On the one hand, in depressed individuals, elevated resting-state activity in the perigenual anterior cingulate cortex

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