Background and Purpose-Loss of psychic self-activation has been described a
fter bilateral lesions to the globus pallidus, striatum, and white matter o
f the frontal lobes, but it is a very rare sign of bithalamic lesions. The
exact functional-anatomic mechanism underlying loss of psychic self-activat
ion following bithalamic lesions remains to be elucidated.
Case Description-We present clinical, neuropsychological, structural, and f
unctional neuroimaging data of an Is-month follow-up period of a man with p
rominent loss of psychic self-activation after coronary arteriography. Exce
pt for memory decline, accompanying symptoms remained restricted to the acu
te phase. The neurobehavioral syndrome consisted mainly of apathy, indiffer
ence, poor motivation, and flattened affect, and this remained unchanged du
ring the entire follow-up period. MRI showed a bithalamic infarction involv
ing the nucleus medialis thalami bilaterally. Single-photon emission CT rev
ealed a severe relative hypoperfusion of both thalami, a relative hypoperfu
sion of both nuclei caudati, and a relative hypoperfusion mesiofrontally.
Conclusions-Single-photon emission CT data support the hypothesis that the
neurobehavioral manifestations after bithalamic paramedian infarction are c
aused by disruption of the striatal-ventral pallidal-thalamic-frontomesial
limbic loop. Probably, bilateral disruption at different levels of the stri
atal-ventral pallidal-thalamic-frontomesial loop may lead to a similar clin
ical picture consisting of loss of psychic self-activation.