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Stroke. 1996;27:1192-1199

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(Stroke. 1996;27:1192-1199.)
© 1996 American Heart Association, Inc.

Articles

Do Changes in Oxygen Metabolism in the Unaffected Cerebral Hemisphere Underlie Early Neurological Recovery After Stroke?

A Positron Emission Tomography Study

S. Iglesias, MD; G. Marchal, MD; P. Rioux, MD, PhD; V. Beaudouin, AI; J.L. Hauttement, MD; V. de la Sayette, MD; F. Le Doze, MD; J.M. Derlon, MD; F. Viader, MD J.C. Baron, MD

INSERM U320 (S.I., G.M., P.R., V. de la S., F. Le D., J.M.D., F.V., J.C.B.), the Centre Cyceron (S.I., G.M., V.B., J.M.D., J.C.B.), Commissariat a l'Energie Atomique, Group de Recherche Methodologique en Tomographie d'Emission de Positons, DSV/DRM (V.B.), and CHRU Cote de Nacre (S.I., J.L.H., V. de la S., F. Le D., J.M.D., F.V.), University of Caen (France).

Correspondence to Dr Jean-Claude Baron, INSERM U320, Centre Cyceron, Blvd H. Becquerel, BP 5229, 14074 Caen Cedex, France. E-mail inserm-U320@cyceron.fr.


*    Abstract
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 *Abstract
down arrowIntroduction
 down arrowSubjects and Methods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
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 confounded 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 (ie, contralateral) oxygen consumption (cCMRO2) 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 15O 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 (PET1; mean, 11±4 hours) and 15 to 30 days later (PET2; 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 PET2, we observed the overall expected neurological recovery. There was a nearly significant trend for a decrease in cCMRO2 from PET1 to PET2, especially for the neocortex (P=.08, F test); in a subgroup of eight patients with large infarcts, this CMRO2 decline was significant (P<.05) in the mirror region to the infarct. There was no significant correlation (Spearman's tests) between acute-stage cCMRO2 and same-day N scores or between changes in cCMRO2 versus changes in N score from PET1 to PET2 (any region). There was a nearly significant trend for lower PET2 cCMRO2 in the subgroup of eight patients with large compared with small infarcts (P=.06).

Conclusions We found no evidence for an influence of cCMRO2 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 cCMRO2 at PET2 tended to be lower, and declined significantly from PET1 to PET2 in the mirror region in the subgroup of patients with large infarcts, suggests that this delayed effect represents transcallosal fiber degeneration.


Key Words: diaschisis • neuronal damage • oxygen • positron emission tomography


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowSubjects and Methods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
It has long been postulated that alleviation of an acute depression of function ("diaschisis") in the cerebral hemisphere contralateral to an ischemic insult may contribute to early neurological recovery after stroke.1 2 3 4 According to this hypothesis, acute neuronal failure in the ischemic area would induce remote depression of function in the contralateral hemisphere via transcallosal connecting fibers (mainly excitatory),5 thus exacerbating neurological deficit. One widely used method of studying such effects is to assess resting cerebral oxygen or glucose consumption or, if unavailable, CBF.

Examples of metabolic depression remote from the area of acute neuronal dysfunction have been extensively documented by means of PET and SPECT.6 7 8 9 10 11 For instance, the well-known phenomenon of contralateral cerebellar hypometabolism occurs in the acute stage (ie, <24 hours) of MCA territory stroke in over 50% of cases,12 and SPECT studies performed during Wada testing13 or balloon occlusion of the internal carotid artery14 have documented its functional and potentially reversible nature. Of the numerous investigations2 4 9 10 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 that have dealt with the corresponding phenomenon in the unaffected cerebral hemisphere, only one concerned the acute stage,22 but this study found no evidence and did not search for clinical correlates of this phenomenon. With respect to the subacute stage, however, a decline in contralateral CBF and/or metabolism has been more convincingly documented.8 26 In an extensive review of the literature on animals and humans, Andrews30 concluded that this effect, if anything, was delayed by several days after stroke onset, which is consistent with other related studies.31 Reduced contralateral-hemisphere metabolism has also been reported late after thalamic stroke.8 Nevertheless, currently no study has tested the hypothesis that acute-stage neurological deficit is exacerbated by metabolic depression in the unaffected hemisphere and that subsequent recovery is related to alleviation of this effect.

Two major methodological problems have seriously hampered this kind of investigation. First, the well-documented sensitivity of CBF to several potentially confounding physiological variables, such as PaCO2, hematocrit, and the like, is an especially serious problem in the acute stage of hemispheric stroke22 ; therefore, a direct measurement of cerebral metabolism is preferable, although this is logistically more cumbersome. The second major problem relates to defining a suitable control group, since preexisting stroke risk factors may influence cerebral metabolism,22 26 32 but to have access to premorbid measurements would be highly unlikely in humans. This explains why substantial uncertainty remains on whether, and to what extent, metabolism is reduced in the unaffected hemisphere in acute MCA stroke.22 Importantly, however, a longitudinal design without a control group is adequate if one addresses the clinical question of whether unaffected-hemisphere metabolism is linked to acute neurological impairment and subsequent recovery.

In a prospective series of consecutive patients, we therefore concomitantly obtained PET measurements of oxygen consumption in the unaffected hemisphere as well as neurological scores in both the acute and subacute stages of MCA-territory stroke. Our main aim was to look for a proportional relationship between the extent of neurological recovery and changes in cCMRO2 (ie, contralateral to the insult). Secondary aims were to assess (1) whether cCMRO2 significantly influences acute-stage neurological status and (2) whether acute-stage cCMRO2 and its time course are influenced by infarct size.


*    Subjects and Methods
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 *Subjects and Methods
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Inclusion Criteria
Patients above 18 years of age with first-ever acute MCA-territory ischemia/infarction, diagnosed on clinical and CT observations less than 18 hours from onset, were prospectively selected among all stroke patients admitted to the Medical Emergency Department of the Caen University Hospital. All patients underwent a full neurological assessment by the same neurologist (G.M.) at admission. Patients who were symptom free at the time of PET study, showed hemorrhage on admission CT scan, or had marked obtundation of consciousness, typical lacunar syndrome, recent myocardial infarction, or other organ failure were excluded from the study. After informed consent was obtained from patients or nearest relatives, enrolled patients received the best medical treatment but no specific cerebrovascular drug; arterial hypertension was treated only if systolic blood pressure exceeded 220 mm Hg. A standard rehabilitation regimen, when necessary, was started within 1 week after admission. Cervical and transcranial Doppler ultrasound studies were performed after PET and within the first 48 hours after onset.

Neurological Scores
Global neurological deficits were quantified using Orgogozo's MCA scale33 (N score) at the time of PET; this validated scale ranges from 0 to 100, with a score of 100 being normal neurological status.

Neurological evolution was expressed both as change in N score from acute-stroke PET (PET1) to the second PET (PET2) and with the Martinez-Vila34 percentage recovery index (RI) or deterioration index (DI) according to the formulas RI=(PET2-PET1)x100/(100-PET1) and DI=(PET2-PET1)x100/PET1.

PET Scanning Procedure
A PET study was performed in the acute stage and repeated in survivors about 1 month later (see Marchal et al35 for details). Patients were scanned on a LETI TTV03 PET device, which has a high intrinsic physical resolution (5.5x5.5x9 mm, x, y, z) and allows seven brain transaxial slices. We used the classic 15O steady-state inhalation technique with C15O2, C15O, and 15O2 to measure CBF, cerebral blood volume, oxygen extraction fraction, and CMRO2. After noise filtering, the lateral (x, y) resolution in the reconstructed images was approximately 11 mm. Measured oxygen extraction fraction was corrected for the unextracted label remaining in the vascular space, according to a published procedure.36 We used the Fox method37 for head positioning (and repositioning) at both PET studies; this stereotaxic approach, based on the glabella-inion line seen on a lateral skull x-ray, was also used for late coregistered CT scanning procedures. The seven transverse slices cut the brain parallel to the glabella-inion line at levels of -4, +8, +20, +32, +44, +56, and +68 mm from this line. A transmission scan with an external source of 68Ge was performed before each study for attenuation correction. Levels of arterial whole blood and plasma 15O activity, blood gases, hemoglobin, and pH were measured, with six arterial blood samples (1 mL each) for each acquisition period. Heart rate and blood pressure were monitored continuously. Studies were performed in patients at rest with eyes closed, ears partially blocked, and in a quiet environment with dimmed light. C15O2, 15O2, and C15O matrices were transformed pixel by pixel into CBF, oxygen extraction fraction, CMRO2, and cerebral blood volume images by means of well-validated equations.36 38 This PET procedure has been approved by the ethics committee of Caen.

Brain CT Scan
We used a CGR CE 12-000 model scanner (Compagnie Generale de Radiologie; resolution, 1.5x1.5x5.0 mm, x, y, z). A CT scan was performed in each subject twice (both unenhanced), first at admission to exclude hemorrhage or other nonischemic brain disease and 30 to 60 days later in survivors to evaluate tissue outcome and obtain an index of infarct volume (summed surfaces in square millimeters of the hypodensities across the relevant planes), if present. At this chronic-stage CT study, we used the same stereotaxic positioning procedure as for both PET scanning sessions (see above); this allowed us to obtain seven CT cuts with midplanes strictly coregistered with the seven PET planes.39

Patient Eligibility
Eligibility criteria for this study were (1) survival until PET2 and chronic-stage CT scan, (2) acceptance of both follow-up investigations, and (3) lack of a significant interfering medical event after PET1.

ROI Methodology
In this study, we elected to assess cCMRO2 in the contralateral cerebral hemisphere, represented as (1) the whole hemisphere, including the neocortex, white matter, and deep grey nuclei but excluding the ventricles; (2) the four main lobes and the precentral gyrus sampled with discrete neocortical circular ROIs as well as the average neocortex; and (3) the thalamus and basal ganglia.

Coregistered PET (both PET studies) and CT matrices were first realigned according to an interactive routine, and the whole contralateral hemisphere was outlined on the CT matrix plane by plane (over the six upper planes) but excluding the ventricles. This allowed us to compute a cCMRO2 value for the whole hemisphere as the average of all pixels included in the ROIs. Likewise, to assess the neocortex, thalamus, and basal ganglia, we used the standardized method described by Marchal et al.35 This method is based on circular ROI templates, with each ROI having a diameter of 14 mm; this size was considered a reasonable trade-off between the effective spatial resolution in the PET images and the size of the anatomic structures. Whole neocortex, lobar, and precentral gyrus values were computed as the average of all pixels included in the corresponding ROIs; likewise, the basal ganglia value was an average of putaminal and head-of-caudate ROIs. This procedure allowed us to obtain cCMRO2 values for PET1 and PET2.

Statistical Analysis
The PET data at PET1 and PET2 were compared using ANOVAs with repeated measures (F test). The relationships between PET data and clinical data at each time point and with respect to their time course were assessed by means of Spearman's nonparametric rank test. The same test was used to assess the relationships between the PET data and the infarct volume indices. In addition to analyzing the absolute cCMRO2 values, we also performed the same statistical procedure on the relative metabolic values normalized to the whole-hemisphere ROI (ie, region/whole-hemisphere ratios).


*    Results
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 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 *Results
down arrowDiscussion
 down arrowReferences
 
Patients
Among 30 consecutive patients prospectively enrolled according to the criteria given in "Methods," 19 were declared eligible for this study according to the criteria stated above. All had persistent neurological symptoms for more than 24 hours after onset. Their mean±SD age was 74.6±8.5 years.

Causes of noneligibility were early death (n=6, 5 from large infarcts), missing second PET study (n=3, secondary medical complications in 2 or refusal in 1), lack of coregistered chronic CT (n=1, patient moved to a different city), and loss of PET2 data set (n=1).

Clinical and CT Data
At PET2, 12 patients had made a mild to excellent recovery (increase in N score, 10 to 70), 4 had remained essentially stable (changes in N score, 0 to 5), and 3 had deteriorated (decrease in N score, >10). Overall, however, there was the expected average neurological recovery (Table 1).Down In only 1 patient did ultrasound workup reveal hemodynamically significant carotid artery disease on the side contralateral to the affected hemisphere; transcranial Doppler studies did not reveal MCA occlusion on this side in any patient.


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  		Table 1. Clinical and CT Scan Data

PET Data
The acute-stroke PET (PET1) was performed 5 to 18 hours after stroke onset (mean, 11±4) and the second (PET2) 15 to 30 days later (mean, 24±10 days) (Table 2Down). There was no significant change in the cCMRO2 values from PET1 to PET2 for any brain region, only a generalized trend for decrease that fell short of statistical significance for the whole neocortex, occipital cortex, and whole hemisphere (Fig 1Down).


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  		Table 2. Contralateral CMRO2 Values and Differences in These Values From PET1 to PET2



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  		Figure 1. Contralateral whole-neocortex CMRO2 at PET1 and PET2 for the 19 patients (each patient is represented by a square joined by a straight line). There is a trend for decrease from PET1 to PET2 (P=.08, F test).

PET Clinical Correlations
There was no significant correlation (Spearman's nonparametric rank-correlation test) between changes in cCMRO2 values from PET1 to PET2 (any region) and changes in corresponding N scores (see Fig 2Down for illustration) or evolution indices. Likewise, there was no significant correlation (Spearman's test) between cCMRO2 at PET1 (any region) and same-day N scores.



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  		Figure 2. Clinical correlations of PET. Changes in neurological score (N score) from PET1 to PET2 versus corresponding changes in contralateral whole-neocortex CMRO2 (n=19; each patient is represented by a square). There was no statistically significant correlation.

Correlations Between cCMRO2 and Infarct Size
There was no significant relationship between cCMRO2 values at PET1 or PET2 (any region) and infarct volume indices. Nevertheless, a nonsignificant trend for lower cCMRO2 values at PET2 in large (>1500 mm2, n=8) compared with small (<1500 mm2, n=11) infarcts was apparent, which was close to statistical significance (P=.06) for whole-hemisphere cCMRO2 (Fig 3Down). Finally, there were nonsignificant trends for greater declines in cCMRO2 from PET1 to PET2 with larger infarcts (see Fig 4Down for whole-hemisphere values).



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  		Figure 3. Relationships between contralateral whole-hemisphere CMRO2 at PET2 and infarct volume index for the 19 patients. There is a trend for lower CMRO2 with larger infarcts. When comparing the subgroup of 8 patients with large infarcts ({blacksquare}; infarct volume index >1500 mm2) with the 11 with small infarcts ({square}), this trend is close to statistical significance (P=.06, F test).



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  		Figure 4. Relationships between changes in contralateral whole-hemisphere CMRO2 and infarct volume index (n=19; each patient is represented by a square). No statistically significant correlation was found. This result also applied to all other brain regions analyzed.

Normalized Metabolic Values
There were no statistically significant results in any of the above analyses.


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 *Discussion
down arrowReferences
 
On the basis of measurements of resting CMRO2 (either absolute or relative values), we found no evidence for a link between oxygen metabolism in the unaffected cerebral hemisphere and early neurological recovery after MCA-territory stroke. Furthermore, there was no significant relationship between acute-stage cCMRO2 and same-day neurological status, providing no clear evidence in this sample for an accentuation of initial neurological deficit from unaffected-hemisphere dysfunction. These negative findings do not exclude the possibility that other mechanisms operating in this hemisphere, such as reorganization of neocortical neural maps,40 41 42 43 may participate in neurological recovery after stroke and explain the well-known instances of secondary reaggravation of neurological deficit after a contralateral second stroke.44 45 46

This is the first study to assess quantitatively the relationships between early neurological recovery from acute MCA-territory stroke and parallel changes in cCMRO2. Wise et al22 studied neocortical cCMRO2 of MCA stroke patients in the acute stage but did not perform a sequential study or obtain neurological scores. Demeurisse et al20 and Knopman et al47 performed sequential studies of both neurological status and resting contralateral 133Xe-inhalation CBF, but the initial assessment took place weeks to months after the ictus. SPECT with 99mTc-hexamethylpropyleneamine oxime assesses brain perfusion but does so in a nonquantitative way and therefore is not well suited for the investigation of such effects.48 Overall, our results cannot be directly compared with previous studies.

Could the overall negativity of our findings be due to confounding methodological factors? First, one might wonder whether the inevitable variability in topography and size of infarcts may have adversely affected our results. Small infarcts would be expected to have correspondingly mild effects on cCMRO2, whereas variable infarct topography could have affected the distribution of contralateral effects, if any. However, because the neurological deficit was assessed with a scale specifically designed for MCA-territory stroke, variability in topography of the ischemic process should have affected the neurological scores correspondingly.49 The resulting added variance in both cCMRO2 and neurological scores should have facilitated rather than impeded the detection of a correlation between changes in unaffected-hemisphere metabolism and clinical recovery.

Second, the noneligibility of both comatose patients (for logistic and ethical reasons, primary criterion) and early deceased ones (secondary criterion) might represent a selection bias. Thus, according to the classic belief that "transhemispheric diaschisis" subtends acute consciousness alterations after supratentorial ischemic stroke,9 17 we might have excluded potentially important patients. However, since most patients who are still comatose hours after onset of MCA stroke usually deteriorate and die within days,50 a relationship between return of consciousness and improvement in cCMRO2 would be hard to prove. Furthermore, recalculation of the correlation between cCMRO2 and N scores at PET1, this time including our 6 early deceased patients (most of whom had a large hemispheric lesion and some degree of obtundation), still failed to reveal statistical significance (data not shown). Previously, Lenzi et al9 found a nearly significantly lower cCMRO2 in stroke patients with stupor/coma compared with alert patients. However, 4 of their 5 stuporous patients were studied 2 to 4 days after the ictus, and thus the lower cCMRO2 presumably merely reflected the importance of brain edema; furthermore, a follow-up assessment of cCMRO2 in their cases was not reported.

Third, because we used a neurological scale heavily weighted by motor items, recovery in other functions could have been obscured. However, Orgogozo's scale includes nonmotor items for 35% of its full range, while motor deficit is the predominant expression of MCA stroke. Nevertheless, the lack of a significant relationship between changes in N score and corresponding metabolic changes in the unaffected hemisphere also concerned the precentral gyrus.

Fourth, because of our relatively broad ROIs, we could have missed a circumscribed effect.24 Although our selection of ROIs included those most likely to be affected in a transcallosal hypothesis, an effect focusing on the neuronal layers that mainly receive the callosal afferents (ie, layers III and IV)51 52 could go undetected with the PET methodology. A related but never convincingly demonstrated hypothesis posits that any transcallosal metabolic effect should predominate in the neocortical region homologous to the infarct ("mirror effect").9 21 23 One major issue in assessing such "mirror effects" relates to which contralateral region to analyze precisely, since not all infarcts are purely cortical, and thus one should theoretically account for both direct damage to the transcallosal fibers from, and indirect remote effects of, subcortical damage.3 Previously, with use of "mirror ROIs" but uncontrolled with CT scans, Wise et al53 reported no significant change in mirror cCMRO2 from the acute to the subacute stage in 9 MCA stroke patients; Lenzi et al9 claimed reduced mirror CMRO2 in the subacute stage (neurological scores assessed in neither study). To further evaluate this controversial issue, we performed an analysis of mirror ROIs for the subgroup of 8 subjects with the largest infarcts (see "Results" for details of this subgroup), all affecting the cortical mantle; to define this ROI, the CT-defined infarct contours were copied by symmetry onto the contralateral hemisphere for each relevant PET plane. Although the CMRO2 significantly decreased from PET1 to PET2 in this mirror region (from ±2.36 to ±1.81 mL/100 mL per minute; P<.05 by paired t test; P<.02 by Wilcoxon), these changes were not significantly correlated with corresponding neurological changes (Spearman's test).

Fifth, because of the already mentioned problems related to the suitability of a control group and the unavailability of a premorbid assessment, we have no reference value with which to compare our measurements; thus, we cannot exclude the possibility that a decrease of cCMRO2 occurred after the stroke and persisted until the second PET study. If this were so, however, any such persistence of low cCMRO2 would have occurred in the face of overall neurological improvement and would be clinically irrelevant. Nevertheless and for scientific interest, we extracted a subgroup of 7 patients from our series matched in age with the 5 oldest from the series of 30 optimally healthy subjects studied in our laboratory with exactly the same methodology35 ; this procedure of matching was necessary because in the sample of normal subjects we found a significant decline in neocortical CMRO2 with age.35 The mean±SD ages of these two age-matched subgroups were 66.7±2.7 and 64.1±1.9 years, respectively. The mean±SD neocortical cCMRO2 values of the stroke subgroup were 2.75±0.37 and 2.60±0.47 mL/100 g per minute at PET1 and PET2, respectively; neither of these values is significantly different (t test) from the corresponding value in the control subjects (2.72±0.59 mL/100 g per minute). These results are at variance with those of Wise et al,22 who found a significantly reduced cCMRO2 in an acute-stroke series when compared with healthy subjects; however, the two groups of subjects were not matched for age. However, like those of Wise et al,22 the values for our stroke subgroup did not significantly differ from an age-matched group of patients with unilateral or bilateral severe carotid stenosis or occlusion but without infarction on CT (n=6; age, 67.2±9.6 years; CMRO2, 2.34±0.49/100 g per minute, asymptomatic hemisphere). Consistent with these results, PET studies in baboons found no significant change in cCMRO2 hours to days after MCA occlusion compared with premorbid measurements.27 54

Since in our study we obtained only two "snapshot" measurements separated by about 20 days, a biological phenomenon with a nonlinear time course or a very slow evolution could have been missed. For instance, an immediate but short-lasting (ie, minutes to a few hours) phenomenon is an intriguing possibility. It is known that some remote metabolic effects, such as crossed cerebellar hypometabolism, do occur instantaneously,13 14 but they are likely to persist in cases of permanent damage.9 10 11 12 There is, however, some evidence from MCA occlusion experiments in cats28 for a precipitous but transient fall (ie, lasting only about 60 minutes) in mean electroencephalographic amplitude in the unaffected hemisphere. Being so brief, such an event would have only tenuous influence, if any, on neurological recovery as we assessed it. Still, with respect to confounding effects due to "snapshot" PET assessments, recovery from initial unaffected-hemisphere hypometabolism might have been too slow to be appreciated with a 20-day interval between PET studies, while delayed hypometabolism (eg, around day 7 after stroke)28 30 followed by return to normal values would also have gone undetected. It nevertheless remains that during this interval there was no increase, and even a decline, in cCMRO2 despite concomitant overall neurological recovery.

We found that the cCMRO2 at PET2 (but not at PET1) exhibited a nearly significant trend for lower values with larger infarcts. This observation, taken together with the trend (also nearly significant) for a secondary decrease in cCMRO2 mainly observed in the neocortex (and significant for the mirror ROI of large infarcts), would be consistent with the decline in unaffected-hemisphere perfusion and metabolism already reported around the second week after MCA stroke.9 16 17 19 26 This delayed hypometabolism could be anatomically underscored by transcallosal fiber degeneration,55 as has also been postulated in patients with chronic occlusive cerebrovascular disease, callosal atrophy, and reduced CMRO2.56 However, if this "disconnection" hypothesis were correct, one would expect more marked effects in the ipsilateral hemisphere compared with that contralateral to the ischemic lesion.3 Consistent with this, in the present series of patients there was a more substantial and statistically significant CMRO2 decline from PET1 to PET2 in the affected whole-hemisphere ROI (mean, 10.6%, excluding the infarcted areas compared with 6.4% in the unaffected hemisphere [S. Iglesias, G. Marchal, F. Viader, J.M. Derlon, J.C. Baron, unpublished results, 1996]). Although this putative callosal fiber degeneration does not appear to interfere with an early recovery process, a delayed synaptic reorganization of deafferented transcallosal fields57 might be involved in both late recovery40 41 43 44 and the occasionally reported secondary partial reversal of unaffected-hemisphere hypometabolism.8 58 59


*    Selected Abbreviations and Acronyms
 
CBF = cerebral blood flow
cCMRO2 = contralateral cerebral metabolic rate of oxygen
MCA = middle cerebral artery
PET = positron emission tomography
ROI = region of interest
SPECT = single-photon emission computed tomography


*    Acknowledgments
 
This work was supported by Caisse Nationale d'Assurance-Maladie-INSERM grant 82/90 (Drs Marchal and Baron). We are grateful to the physicians of the emergency department and to the cyclotron and computer science technicians for their help in this work. We also thank Dr A. Vlassenko for providing the CMRO2 values for patients with severe carotid artery disease.

Received December 27, 1995; revision received March 21, 1996; accepted March 25, 1996.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 up arrowDiscussion
 *References
 

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