Affiliations: Department of Linguistics, Vrije Universiteit Brussel,
Brussels, Belgium | Department of Neurology, ZNA Middelheim Hospital,
Antwerp and Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge,
University of Antwerp, Antwerp, Belgium | Department of Health Care Sciences, University College
Antwerp, Antwerp, Belgium | Department of Nursing Sciences, Faculty of Medicine,
University of Antwerp, Antwerp, Belgium | Department of Language and Communication Sciences,
City University, London, UK
Note: [] Corresponding author: Prof Dr. P. Mariën, ZNA Middelheim
Hospital, Department of Neurology, Lindendreef 1, BE-2020 Antwerp, Belgium.
Tel.: +32 3 2803136; E-mail: peter.marien5@telenet.be
Abstract: Objective: Clinical, neuropsychological, structural and functional
neuroimaging results are reported in a patient who developed a unique
combination of symptoms after a bi-thalamic and right putaminal stroke. The
symptoms consisted of dysexecutive disturbances associated with confabulating
behavior and auto-activation deficits. Background: Basal ganglia and thalamic lesions may result in a
variety of motor, sensory, neuropsychological and behavioral syndromes.
However, the combination of a dysexecutive syndrome complicated at the
behavioral level with an auto-activation and confabulatory syndrome has never
been reported. Methods: Besides clinical and neuroradiological investigations, an
extensive set of standardized neuropsychological tests was carried out. Results: In the post-acute phase of the stroke, a dysexecutive
syndrome was found in association with confabulating behavior and
auto-activation deficits. MRI showed focal destruction of both thalami and the
right putamen. Quantified ECD SPECT revealed bilateral hypoperfusions in the
basal ganglia and thalamus but no perfusion deficits were found at the cortical
level. Conclusion: The combination of disrupted auto-activation,
dysexecutive and confabulating syndrome in a single patient following isolated
subcortical damage renders this case exceptional. Although these findings do
not reveal a functional disruption of the striato-ventral
pallidal-thalamic-frontomesial limbic circuitry, they add to the understanding
of the functional role of the basal ganglia in cognitive and behavioral
syndromes.
