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ABSTRACTS

Functional plasticity after subcortical stroke studied with


Stroop-like cognitive activation and P E T
U. Miiller 1'2, R. Wenzel 3'4, U. Arnold 2, K. Villringer 3, S. Ziegler 3, S. Minoshima 5,
P. Bartenstein 3, M. Schwaiger 3, A. Villringer 4
1Department of Neurology, Max-Planck-lnstitute of Cognitive Neuroscience, lnselstr. 22-26, D-04103 Leipzig,
Germany; Department of Neuropsychology, Czty-Hospttal Muntch-Bogenhausen, Germany," Department of Nuclear
2 9 9 9 3

Medicine, Technical University Munich, Germany," 4Department of Neurology, Charit(, Humboldt-University Berlin,
Germany," 5Department of Nuclear Medicine, University of Michigan, Ann Arbor, USA

Introduction: Subcortical strokes provide an unique clinical model to study brain plasticity and
recovery of function (1). Previous PET studies focused on motor deficits in these patients and found
compensatory activations in ipsilateral as well as contralateral brain areas during complex motor tasks
(2,3). Attentional tasks based on the Stroop colour-word interference increase rCBF mainly in the
anterior cingulate cortex and frontal areas (3,4) but have so far not been studied in neuropsychological
patients with attentional deficits.

Subjects and Methods:


Subjects: Four patients met the inclusion criteria (first stroke, right subcortical lesion as demonstrated by MRI, attentional
deficit on admission to cognitive rehabilitation, written informed consent) and were investigated in a chronic stage, 1.7 (1.2-
2.5) years after stroke onset. They were compared to a group of six previously investigated normal volunteers (6).
Activation paradigm: In the Stroop condition the subjects had to name the colour of inconcruent and concruent colour
words randomly presented on a PC monitor with a frequency of 1/sec. In the rest condition they looked at a screen
protection picture (New York City by Night). The paradigm was designed for maximal cognitive rest-activation differences.
Neuroimaging: PET scanning with the H2150-bolus technique, image analysis and single subject to group comparisons
were performed as previously described (7).

Results: All subjects performed the task with less than 3% of errors. As compared to normal controls
the patients show fronto-parietal cortical deactivations of the right hemisphere under rest conditions
and individual patterns of areas with significant hyperactivation in the Stroop condition (table 1):
Table 1 : Lesion extension and brain areas with significant hyperactivation durin~l Stroop-like activation in four stroke patients
~atient MRI lesion sites coordinates and neuro- anatomical names of hyperactivation areas
a~le/sex x y z
1 putamen/claustrum right, internal capsule (crus ant.) 1 -19 7 medial thalamus left
59/m right, supralenticular white matter right; 30 -42 27 suprainsular (parietal) white matter left
head of caudate nucleus left -15 -13 9 lateral thalamus right
2 putamen/claustrum right, internal capsule right, -37 -10 4 insula / claustrum left
44/m supralenticular white matter right -51 -51 34 supramarginal gyms r i g h t
3 lenticular nucleus right, head of caudate nucleus right, 30 -42 27 suprainsular (parietal) white matter left
22/f external and internal capsule (crus ant.) right, -28 28 43 medial frontal gyrus right (BA 8)
posterior insular cortex right -51 28 22 medial frontal gyrus right (BA 46)
lenticular nucleus right, lateral thalamus right, head of 44 1 20 preinsular (frontal) white matter left
caudate nucleus right, internal capsule (crus ant.) right, -19 57 27 superior frontal gyrus right (BA 9)
supralenticular white matter right 1 -22 7 medial thalamus left

Conclusions: This is the first PET study that investigates the recovery of attentional functions in
patients with subcortical stroke. There are individual patterns of functional plasticity involving ipsa-
and contralateral brain areas relevant to aspects of speech and attentional processing.
References: (1) Seitz RJ, et al. Hum. Brain Map 1994, 1: 81-100. (2)Weiller C, et al. Ann. Neurol. 1992, 33: 181-189. (3)
Weder B, et al. Brain 1994, 117: 593-605. (4) Pardo JV, et al. Proc. Natl. Acad. Sci. USA 1990, 87: 256-259. (5) Bench CJ,
et al. Neuropsychologia 1993, 31: 907-922. (6) Villringer K, et al. Hum. Brain Map. 1995, Suppl. 1: 146. (7) Wenzel R, et
al. Brain 1996 (in press).

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