Loss of psychic self-activation after paramedian bithalamic infarction

Citation
S. Engelborghs et al., Loss of psychic self-activation after paramedian bithalamic infarction, STROKE, 31(7), 2000, pp. 1762-1765
Citations number
17
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
31
Issue
7
Year of publication
2000
Pages
1762 - 1765
Database
ISI
SICI code
0039-2499(200007)31:7<1762:LOPSAP>2.0.ZU;2-8
Abstract
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.