TY - JOUR
T1 - Multimodal functional imaging of prolonged neurological deficits in a patient suffering from familial hemiplegic migraine
AU - Gutschalk, Alexander
AU - Kollmar, Rainer
AU - Mohr, Alexander
AU - Henze, Marcus
AU - Ille, Nicole
AU - Schwaninger, Markus
AU - Hartmann, Marius
AU - Hähnel, Stefan
AU - Haberkorn, Uwe
AU - Rupp, André
AU - Meyding-Lamade, Uta
PY - 2002/10/31
Y1 - 2002/10/31
N2 - The case of a patient with familial hemiplegic migraine (FHM) suffering from prolonged right sided hemiparesis and aphasia that persisted for more than 10 days is reported. The symptoms were accompanied by slowing of the magnetoencephalogram over the left hemisphere, which normalized parallel to the clinical improvement. Positron emission tomography obtained on the 6th day revealed glucose-hypometabolism (hemispheric difference ≥10%) in left hemisphere's fronto-basal cortex, caudate nucleus, and thalamus. In contrast, magnetic resonance imaging including perfusion and diffusion weighted imaging was normal and did not show significant alterations of cortical perfusion or water mobility during the episode. We hypothesize that this finding provides evidence for a primary neuronal dysfunction causing the prolonged neurological deficits in FHM.
AB - The case of a patient with familial hemiplegic migraine (FHM) suffering from prolonged right sided hemiparesis and aphasia that persisted for more than 10 days is reported. The symptoms were accompanied by slowing of the magnetoencephalogram over the left hemisphere, which normalized parallel to the clinical improvement. Positron emission tomography obtained on the 6th day revealed glucose-hypometabolism (hemispheric difference ≥10%) in left hemisphere's fronto-basal cortex, caudate nucleus, and thalamus. In contrast, magnetic resonance imaging including perfusion and diffusion weighted imaging was normal and did not show significant alterations of cortical perfusion or water mobility during the episode. We hypothesize that this finding provides evidence for a primary neuronal dysfunction causing the prolonged neurological deficits in FHM.
UR - http://www.scopus.com/inward/record.url?scp=0037206675&partnerID=8YFLogxK
U2 - 10.1016/S0304-3940(02)00940-0
DO - 10.1016/S0304-3940(02)00940-0
M3 - Journal articles
C2 - 12384224
AN - SCOPUS:0037206675
SN - 0304-3940
VL - 332
SP - 115
EP - 118
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 2
ER -