Do changes in oxygen metabolism in the unaffected cerebral hemisphere underlie early neurological recovery after stroke? A positron emission tomography study

被引:57
作者
Iglesias, S
Marchal, G
Rioux, P
Beaudouin, V
Hauttement, JL
delaSayette, V
LeDoze, F
Derlon, JM
Viader, F
Baron, JC
机构
[1] INSERM U320, CTR CYCERON, F-14074 CAEN, FRANCE
[2] DSV, DRM, GRP RECH METHODOLOG TOMOG EMISS POSIT, COMMISSARIAT ENERGIE ATOM, CAEN, FRANCE
[3] CHR UNIV CAEN, CAEN, FRANCE
[4] UNIV CAEN, F-14032 CAEN, FRANCE
关键词
diaschisis; neuronal damage; oxygen; positron emission tomography;
D O I
10.1161/01.STR.27.7.1192
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose Whether an initial depression of function in the unaffected hemisphere (''transcallosal diaschisis'') plays a role in early neurological recovery after acute stroke remains controversial. Previous studies were con founded by lack of acute-stage assessment with follow-up and by the problem of defining a suitable control group, since preexisting stroke risk factors may influence prestroke cerebral metabolism. We evaluated with positron emission tomography (PET) the relationships between unaffected-hemisphere tie, contralateral) oxygen consumption (cCMRO(2)) and quantitative neurological assessments (and their respective evolution over time) after ischemic stroke. Methods Among 30 consecutive patients with first-ever middle cerebral artery ischemic stroke studied with the O-15 equilibrium method, we selected all survivors (n=19; mean age, 74.6 years) who were investigated both within the first 18 hours after stroke onset (PET,; mean, 11+/-4 hours) and 15 to 30 days later (PET(1); mean, 24+/-10 days), with each patient serving as his/her own control. Neurological deficits were quantified using Orgogozo's middle cerebral artery scale (N score) at each PET session. Neurological changes were calculated as changes in the N score. A late CT scan coregistered with PET provided infarct topography and Volume index. Results At PET(2), we observed the overall expected neurological recovery. There was a nearly significant trend for a decrease in cCMRO(2) from PET(1) to PET(2), especially for the neocortex (P=.08, F test); in a subgroup of eight patients with large infarcts, this CMRO(2) decline was significant (P<.05) in the mirror region to the infarct. There was no significant correlation (Spearman's tests) between acute-stage cCMRO(2) and same-day N scores or between changes in cCMRO(2) versus changes in N score from PET(1) to PET(2) (any region). There was a nearly significant trend for lower PET(2) cCMRO(2) in the subgroup of eight patients with large compared with Small infarcts (P=.06). Conclusions We found no evidence for an influence of cCMRO(2) on acute-stage neurological deficit or for a role of the unaffected hemisphere in early recovery after acute MCA ischemic stroke. The decline in unaffected-hemisphere metabolism from the acute to the subacute stage in the face of overall clinical recovery appears clinically irrelevant. The fact that the neocortical cCMRO(2) at PET(2) tended to be lower, and declined significantly from PET(1) to PET(2) in the mirror region in the subgroup of patients with large Infarcts, suggests that this delayed effect represents transcallosal fiber degenetration.
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收藏
页码:1192 / 1199
页数:8
相关论文
共 59 条
[1]   TRANSHEMISPHERIC DIASCHISIS - A REVIEW AND COMMENT [J].
ANDREWS, RJ .
STROKE, 1991, 22 (07) :943-949
[2]   CORPUS CALLOSOTOMY EFFECTS ON CEREBRAL BLOOD-FLOW AND EVOKED-POTENTIALS (TRANSCALLOSAL DIASCHISIS) [J].
ANDREWS, RJ ;
BRINGAS, JR ;
ALONZO, G ;
SALAMAT, MS ;
KHOSHYOMN, S ;
GLUCK, DS .
NEUROSCIENCE LETTERS, 1993, 154 (1-2) :9-12
[3]  
[Anonymous], 1969, BRAIN BEHAV
[4]  
Baron J C, 1981, Trans Am Neurol Assoc, V105, P459
[5]   EFFECTS OF THALAMIC STROKE ON ENERGY-METABOLISM OF THE CEREBRAL-CORTEX - A POSITRON TOMOGRAPHY STUDY IN MAN [J].
BARON, JC ;
DANTONA, R ;
PANTANO, P ;
SERDARU, M ;
SAMSON, Y ;
BOUSSER, MG .
BRAIN, 1986, 109 :1243-1259
[6]   THALAMOCORTICAL DIASCHISIS - POSITRON EMISSION TOMOGRAPHY IN HUMANS [J].
BARON, JC ;
LEVASSEUR, M ;
MAZOYER, B ;
LEGAULTDEMARE, F ;
MAUGUIERE, F ;
PAPPATA, S ;
JEDYNAK, P ;
DEROME, P ;
CAMBIER, J ;
TRANDINH, S ;
CAMBON, H .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1992, 55 (10) :935-942
[7]  
BIERSACK HJ, 1987, J NUCL MED, V28, P1763
[8]   CONTRIBUTION OF DIASCHISIS TO THE CLINICAL DEFICIT IN HUMAN CEREBRAL INFARCTION [J].
BOWLER, JV ;
WADE, JPH ;
JONES, BE ;
NIJRAN, K ;
JEWKES, RF ;
CUMING, R ;
STEINER, TJ .
STROKE, 1995, 26 (06) :1000-1006
[9]  
BRODAL A, 1981, NEUROLOGICAL ANATOMY, P804
[10]   MEASUREMENTS OF ACUTE CEREBRAL INFARCTION - A CLINICAL EXAMINATION SCALE [J].
BROTT, T ;
ADAMS, HP ;
OLINGER, CP ;
MARLER, JR ;
BARSAN, WG ;
BILLER, J ;
SPILKER, J ;
HOLLERAN, R ;
EBERLE, R ;
HERTZBERG, V ;
RORICK, M ;
MOOMAW, CJ ;
WALKER, M .
STROKE, 1989, 20 (07) :864-870