major/treatment-resistan t depression (Greicius et al. 2007), Cerebral Autoso-
mal-Domi nant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
(O’Sullivan et al. 2004), and Alzheimer’s disea se (Binnewijzend et al. 2012,
Zhou et al. 2013). In the context of Alzheimer’s disease, it is worth mention-
ing that thalamic volume was found to be predictive of performance on tests
of cognitive speed and decreases in healthy aging (Van Der Werf et al. 2001):
“A significant decreas e in volume of the thalamus with increasing age was
found, relatively stronger than and independent of the decrease of total brain
volume”.
So frequent is the association between thalamic shape and cognitive disorders
that Vila-Rodriguez et al. (2008) talks of thalamic sh ape as a potential
“endophenotype”.
Thalamic reductions have also been found to correlate with verbal fluency
impairment in those born prematurely (Giménez et al. 2006). Interestingly, in
this case , the aspects of verbal fluency most affected are not phonological, but
syntactico-semantic, which is reminiscent of Wahl et al. (2008), where syntacto-
semantic viola tions were shown to activate the thalamus of normal adults more
than phonological violations.
Perhaps the most frequently reported involvement of the thalamus in pathologi-
cal contexts has to do with impaired consciousness (see, e.g., Crone et al. (2014),
Fernández-Espejo et al. (20 10), Maxwell et al. ( 2006), Zhou et al. (2011)), which
is relevant in the con text of this paper, given the way consciousness is understood
by Dehaene et al. (2014), as discussed in the previo us section.
Finally, given the strategic position occupied by the thalamus, one expects to
find aberrant thalamic circuitry in impairments that are regularly associated with
the basal ganglia, such as Parkinson’s or Huntington’s diseases (on thalamic
damage in such cases, see McKeown et al. 2008, Henderson et al. 2000, Aron
et al. 2003). Likewise, given the anatomical i nterface of the thalamus and the
characterization of dyslexia as a disconnection syndrome (Boets et al. 2013),
we should expect thalamic damag e there too (Galaburda and Eidelberg 1982,
Díaz et al. 2012). Re ports of thalamic damage givin g rise to certain types of
acalculia (Jensen 2010, Mendez et al. 2003) should also be exp ected, if ind eed
at least some kinds of mathematical computations are offshoots of our language
faculty, as is often suggested (Chomsky 1988, 2008).
To conclude this brief sur vey on the thalamu s and mental health, we would
like to mention that minor physical anomalies (MPAs) occur more frequently
in neurodevelopmental disorders such as autism (Cheung et al. 2011). As Cheung
et al. write, MPAs a re neurodevelopmental markers which manifest as unusual
morphological features of the face or physique. They occur in more than 14 per
cent of healthy newborn but significantly more often (as often as 60 per cent
of the cases) in neurodevelopmental disorders such as schizophrenia, autism,
hyperactivity, epilepsy, or mental retardation. We mention this in the context
of the present paper because, as Boeckx and Benítez-Burraco (2014) discuss
extensive ly, the thalamus plays a crucial rule in proper brain development, so
much so that MPAs could ‘mirror’ (even subtle) aberrant neurodevelopment
238 Constantina Theofanopoulou and Cedric Boeckx