in the next section). But likely due to its evolutionary novelty, the network’s
balance is fragile, with even subtle structural anomalies giving rise to cortico-
thalamic misconnection (Agarwal et al. 2008, Blatt 2012, Sun et al. 2013). For
instance, Par naudeau et al. (2013) found that a subtle decrease in the activit y
of the mediodorsal thalamus is sufficient to trigger selective impairments in
prefrontal-dependent cognitive tasks. In a similar vein, Zikopoulos and Barbas
(2007) talk of an “imbalance in the communicat ion between the thalamus and
cortex at the core of a host of psychiatric and neurological conditions.” (Numer-
ous authors cited above talk of hypo- or hyper-connectivity syndromes.)
The idea of disrupted balance emerged in the context of the role of the
thalamus in consciousness (see Llinás and Steriade 2006, Steriade 2004, Con-
treras et al. 1996, Ster iade et al. 1993), but it has since then been extended
to other cognitive impairments. “Aberrant rhythmic activity” giving rise to
“excitation leaks” (Frantseva et al. 2014), or “abnormal thalamic modulation”
of cortica l or subcortical structures (Normand et al. 2013), now regularly
feature as causal explanations f or endophenotypes. As Normand et al. (2013)
observe, the relevance of the thalamus lies in the fact that this is a brain
structure that “feature complex feedback loops and widespread reciprocal
connectivity that could amplify and spread the effects of a slight functional
imbalance”, an effect that we saw may be even reflected in minor physical
anomalies, cf. Cheung et al. 2011.
As Kircher and Glendenning (2002) point out, an expanded brain that is out
of control is not helpful. There must be modulation of this enhanced cortex.
Kircher and Glendenning show that a primary source of this modulation comes
from the enhanced inhibitory capabilities of the thalamus, and the increased number
of neurons sensitive to the most common inhibitory neurotransmitter found
(GABA). By its influence on our neocortex, the thalamus provides greater control
of neural processing. Kircher and Glendenning propose that it may be our ability
to inhibit our cortex that has resulted in our increased ‘intelligence’, or, to put it
in terms that we prefer, our specific, linguistic mode of cognition. In this context,
it is worth recalling that many studies reporting volume abnormalities in the thala-
mus are talking of the size of the whole thalamus relative to total brain size. Thus,
Tsatsanis et al. (2003) report for autistics that the size of the whol e thalamus was
less strongly correlated to total brain size, and the sizes of the right and left thala-
mus were less strongly correlated in autistic versus control subjects. In addition,
within the subgroup with larger brain sizes, thalamic volume was significantly
reduced in individuals with autism compared with normal controls.
Due to its strategically central position, both in the course of brain develop-
ment, and in the sapiens-specific, globular brain, the thalamus impacts the
organization of neural pathways and functional connectivity in the developing
brain (see Courchesne and Pierce (2005) and Tsatsanis et al. (2003) for clear
art iculations of this idea in the co ntext of autism). Damage to the thalamus is
bound to result in compromised functional integration between brain regions,
reducing the efficiency of the whole network (“network fragmentation” as the
phenomenon is called in the literature on the default-mode network cited above).
240 Constantina Theofanopoulou and Cedric Boeckx