A decrease in regional cerebral blood volume and hematocrit in crossed cerebellar diaschisis.

BACKGROUND AND PURPOSE: The pathophysiology of crossed cerebellar diaschisis (CCD) remains to be elucidated. In CCD, the metabolic suppression resulting from deafferentation may cause vasoconstriction, which may result in a decrease in cerebral blood volume (CBV) and may differentially affect the flows of red blood cells and of plasma. The purpose of this study was to investigate whether CCD decreases the total CBV (cerebral red blood cell volume [CRCV] plus cerebral plasma volume [CPV]) and, if so, whether CCD differentially affects the CRCV and CPV, resulting in a change in hematocrit. METHODS: We used positron emission tomography to study 7 patients with a unilateral supratentorial infarct and CCD. The distributions of CRCV and CPV were assessed by using 15O-labeled carbon monoxide and 62Cu-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The CRCV, CPV, and calculated hematocrit values were compared between the cerebellar hemispheres. RESULTS: In the cerebellar cortex contralateral to the supratentorial infarct, the values of CRCV, CPV, and total CBV were significantly decreased compared with those in the ipsilateral cerebellar cortex. The CRCV was decreased to a greater degree than the CPV, and the value of the hematocrit was decreased in the contralateral cerebellar cortex. CONCLUSIONS: CCD may decrease the total CBV, which may reflect vasoconstriction caused by decreased metabolism due to deafferentation. In addition, the more pronounced decrease in CRCV than in CPV may result in a decrease in hematocrit in CCD.     

Cerebellar reorganization following cortical injury in humans: effects of lesion size and age

OBJECTIVE: The authors investigated chronic cerebellar reorganization following unilateral cortical lesions in children and adults using PET to measure benzodiazepine receptor (BZR) binding with [11C]flumazenil (FMZ) and glucose metabolism with 2-deoxy-2[18F]fluoro-D-glucose (FDG). BACKGROUND: Crossed cerebellar diaschisis (CCD) is defined as decreased metabolism or blood flow in the cerebellum contralateral to a cortical insult measured by functional neuroimaging, and is typically seen in adults with large frontal or parietal lesions. The authors previously reported that CCD of glucose metabolism was not as prominent in children as in adults, and that some children showed a paradoxical pattern of increased glucose utilization in cerebellar cortex contralateral to the cortical lesion. The current study investigated whether CCD is associated with alterations in the gamma-aminobutyric acid (GABA(A))/BZR complex. METHODS: Patients with frontal lesions alone or with parietal lesions were compared with patients with temporal lesions, which are typically not associated with CCD. RESULTS: Children with lesion onset before 1 year of age showed significantly higher glucose utilization in contralateral posterior quadrangular and superior semilunar lobules of cerebellar cortex than did adults. Two patterns of change in cerebellar BZR binding were seen in children: 1) Five of 10 children showed increased BZR binding in the dentate nucleus contralateral to the lesion, and 2) the remaining five children showed no increase in dentate nucleus BZR binding but showed increased binding in the lateral lobules of the cerebellar cortex contralateral to the lesion. Adults showed increased binding only in contralateral dentate nucleus and not in cerebellar cortex. The size and severity of the supratentorial lesion, as well as age at the time of injury, were important factors in these findings. CONCLUSIONS: Reorganization of GABA-mediated mechanisms and glucose metabolism in cerebellum following cortical injury differs with size of lesion and age at the time of injury.     

Hemodynamic and metabolic changes in crossed cerebellar hypoperfusion.

BACKGROUND AND PURPOSE: The pathophysiology of crossed cerebellar diaschisis remains to be elucidated. The mechanism responsible appears to be deafferentation through the corticopontocerebellar tract, which terminates in the cerebellar gray matter. However, few studies have demonstrated the hemodynamic and metabolic changes in the cerebellar gray matter and pons in crossed cerebellar diaschisis. METHODS: Using positron emission tomography in 24 patients with unilateral supratentorial stroke, we evaluated regional blood flow, metabolic rate of oxygen, oxygen extraction fraction, and blood volume in the cerebellar cortex and pons. Sixteen patients with significant cerebellar blood flow asymmetry, defined as a percentage difference in blood flow beyond the upper 95% confidence limit defined in eight normal subjects, were selected as the group with crossed cerebellar hypoperfusion. RESULTS: In patients with crossed cerebellar hypoperfusion, the metabolic rate of oxygen was significantly decreased in the cerebellar cortex contralateral to the supratentorial stroke, compared with that in the ipsilateral cerebellar cortex; this decrease was less than the decrease in cerebellar blood flow. The degrees of cerebellar asymmetry in these two parameters were negatively correlated with the metabolic rate of oxygen in the pons. The oxygen extraction fraction was slightly, but significantly, increased. In contrast to the ischemic state, however, the cerebellar blood volume was decreased, with no difference in the ratio of cerebellar blood flow to blood volume. CONCLUSIONS: These findings support interruption of the corticopontocerebellar tract as the mechanism of crossed cerebellar hypoperfusion. Our results also suggest a mild elevation in the oxygen extraction fraction in this state, with a mechanism distinct from ischemia.     

Crossed cerebellar diaschisis accompanied by hemiataxia: a PET study.

To study crossed cerebellar diaschisis (CCD), cerebellar blood flow and oxygen metabolism were measured with positron emission tomography (PET) in 12 patients who showed a minimal degree of hemiparesis due to single unilateral supratentorial lesion. Six patients presenting with mild to moderate cerebellar type hemiataxia showed CCD, that is, decreased blood flow and oxygen metabolism in the cerebellar hemisphere contralateral to the side of supratentorial lesion. Hemiataxia and reduced cerebellar blood flow and metabolism occurred in the ipsilateral side. Lesions were located in the thalamus in four patients and the parietal lobe and internal capsule in one each. The other six patients did not exhibit ataxia, and oxygen metabolism was not reduced in the contralateral cerebellar hemisphere. In two of these cases, however, reduced cerebellar perfusion was observed in the contralateral cerebellar hemisphere. These findings indicate that CCD occurs with hemiataxia and suggest that it results not only from disruption of the corticopontocerebellar pathway but also of the dentatorubrothalamic pathway. CCD associated with hemiataxia, demonstrated in patients with thalamic lesions, was presumed to result from retrograde deactivation of the cerebellar hemisphere via the dentatorubrothalamic pathway.     

Hemodynamic and metabolic changes in crossed cerebellar hypoperfusion--similarity to the early stage of olivo-ponto-cerebellar atrophy]

Using positron emission tomography in twenty-four unilateral supratentorial stroke patients, we evaluated regional blood flow, metabolic rate of oxygen, oxygen extraction fraction, and blood volume in the cerebellar cortex and pons. Sixteen patients with a significant cerebellar blood flow asymmetry, which lay beyond the upper ninety-five percent confidence limits defined in eight normal subjects, were selected as the group with crossed cerebellar hypoperfusion. In these patients, cerebellar metabolic rate of oxygen was also significantly decreased in the cerebellar cortex contralateral to the supratentorial stroke, compared with the ipsilateral cerebellar cortex, although to a lesser degree than the cerebellar blood flow. The degrees of cerebellar asymmetry in these two parameters were negatively correlated with the metabolic rate of oxygen in the pons. Oxygen extraction fraction was slightly, but significantly, increased in the cerebellar cortex contralateral to the stroke. In contrast to the ischemic state, cerebellar blood volume was decreased, with no difference in the ratio of cerebellar blood flow to blood volume. These findings suggest 1) interruption of the cortico-ponto-cerebellar tract as the mechanism of crossed cerebellar hypoperfusion and 2) mild elevation in the oxygen extraction fraction in this state, with a mechanism distinct from primary hypoperfusion. We also studied six patients with sporadic olivo-ponto-cerebellar atrophy who were in the incipient stage of the disease with slight cerebellar atrophy on magnetic resonance images. The cerebellar cortex in these patients showed the same hemodynamic and metabolic changes as in crossed cerebellar hypoperfusion, suggesting the cerebellar metabolic depression by transneuronal mechanism in the early stage of olivo-ponto-cerebellar atrophy.     

Cerebellar diaschisis revisited: pontine hypometabolism and dentate sparing.

A unilateral supratentorial lesion may cause hypometabolism in the contralateral cerebellar hemisphere (crossed cerebellar diaschisis). We analyzed glucose metabolism, measured by PET-FDG, in the posterior fossa in 67 patients (78 PET studies) with primary unilateral supratentorial brain tumors selected for visually obvious metabolic asymmetry in the cerebellar hemispheres. We found that glucose utilization was 17% lower in the contralateral cerebellar cortex (compared with the ipsilateral one), consistent with the selection criterion, and 19% lower in the ipsilateral pons, wherein lie the first order synapses of the corticopontocerebellar pathway. This finding helps to validate the prevalent view that cerebellar diaschisis is due to interruption of afferent input from the corticopontocerebellar pathway. However, glucose metabolism in the contralateral dentate nucleus was relatively preserved--only 2% less than the ipsilateral dentate. This "dentate sparing" suggests preservation of afferent input to the largest of the deep cerebellar nuclei from the Purkinje cells in the cortex, despite interruption of the major excitatory input to the Purkinje cells.     

In vivo disturbance of the oxidative metabolism of glucose in human cerebral gliomas

Abnormalities in the oxidative metabolism of glucose in human cerebral gliomas have been studied in seven patients using positron emission tomography. Measurements of regional cerebral blood flow and oxygen consumption were obtained using the oxygen-15 steady-state inhalation technique. Values of regional cerebral glucose consumption were obtained using fluorine 18-labeled 2-fluoro-2-deoxy-D-glucose and a simplification of the method of Sokoloff. Functional values were obtained for regions of tumor and brain tissue in the middle cerebral artery territory of the contralateral cortex. Values of regional glucose consumption were calculated for both regions using a value of the lumped constant quoted for normal brain tissue (0.42). Tumor regional cerebral blood flow was comparable to that in the contralateral cortex, whereas regional cerebral oxygen consumption was depressed. This depression resulted in low tumor values of the fractional oxygen extraction ratio (0.21 +/- 0.07), indicating that oxygen supply exceeded the metabolic demand. In contrast, tumor regional cerebral glucose consumption was not depressed and regional glucose extraction ratios were similar for tumor and brain tissue. The metabolic uncoupling between regional oxygen consumption and regional glucose consumption (CMRO2/CMRGlu = 0.24 +/- 0.07 ml of oxygen per milligram of glucose) is indicative of increased aerobic glycolysis.     

Clinical and etiological study of crossed cerebellar diaschisis. Report of two cases

With the great progress in the imaging technique of cerebro-cerebellar perfusion and metabolism, it has been revealed that supratentorial cerebrovascular disorders often cause some reduction of contralateral cerebellar blood flow and metabolism. The phenomenon, termed crossed cerebellar diaschisis (CCD), is interpreted to be brought about by transneuronal deactivation of cerebellum via the corticopontocerebellar pathway and usually not to accompanied by limb-incoordination. We have experienced 2 cases presenting ataxia clinically and CCD in positron emission tomography (PET) which are thought to be caused by the interruption of two distinctive neural pathways, the corticopontocerebellar and cerebellorubrothalamic pathways. Case 1 was a 34-year-old housewife with cerebral infarction which magnetic resonance imaging disclosed in the left parietal cortex and subcortical white matter. She showed mild right-sided hemiataxia featured by dysarthria, hypermetria, dysrhythmia, decomposition, dysdiadochokinesis and rebound phenomenon. Cheirooral syndrome, a hand-pronation sign and defects of combined sensation were present on the right but not accompanied by any disturbances of deep sensation. PET with 15O-labeled CO2 and O2 demonstrated the left frontoparietooccipital and contralateral cerebellar hypoperfusion and hypometabolism. Case 2 was a 69-year-old female suffering from aftereffects of old thalamic hemorrhage. Neurological examination revealed moderate degree of right-sided hemiataxia suggesting a cerebellar type of dysfunction like in case 1. Muscle power and sensory system were well-preserved. Brain CT revealed a small and restricted low density area in the left posterolateral thalamus indicating destruction of the Vim nucleus. PET study confirmed reduced blood flow and oxygen metabolism in the left thalamus and contralateral cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of cerebral angiomas on perifocal and remote tissue: a multivariate positron emission tomography study.

BACKGROUND AND PURPOSE: Using multitracer positron emission tomography, I investigated regional hemodynamic and metabolic changes in both perifocal and remote tissues of cerebral angiomas, with special reference to steal phenomena. METHODS: In 22 patients (14 with arteriovenous malformations and eight with cavernomas) cerebral blood flow, cerebral blood volume, mean vascular transit time, cerebral metabolic rate for oxygen, oxygen extraction fraction, cerebral metabolic rate for glucose, and glucose extraction fraction were measured using standard positron emission tomographic methods. Twelve patients also had their cerebral glucose metabolism assessed during psychophysical activation. Regions of interest representing the angioma, perifocal and remote tissues, contralateral mirror regions, and standard brain regions were analyzed. RESULTS: There were no significant changes in hemodynamic variables or oxygen metabolism in the ipsilateral cerebral hemisphere, but ipsilateral glucose metabolism was reduced both at rest (p less than 0.01) and during activation (p less than 0.05). Glucose (p less than 0.001) and oxygen (p less than 0.001) metabolism in regions of perifocal tissue with low blood flow were decreased, with substrate extraction fractions showing no increase to compensate for insufficient blood flow. Functional recruitment of the cortex overlying the angioma beyond its periphery and supplied by the same arterial branches was subnormal (p less than 0.05) despite relatively unchanged hemodynamics in this tissue compartment. CONCLUSIONS: These data suggest that dysfunction of the cortex supplied by arterial branches also feeding the vascular malformation is related to neuronal deafferentation, while the proportionate decrease in blood flow and metabolism of perifocal tissue may be ascribed to neuronal loss in chronically hypoperfused areas, rather than to persistent hemodynamic steal effects.     

Crossed cerebellar diaschisis after stroke: can perfusion-weighted MRI show functional inactivation?

In this study, we aimed to assess the detection of crossed cerebellar diaschisis (CCD) following stroke by perfusion-weighted magnetic resonance imaging (PW-MRI) in comparison with positron emission tomography (PET). Both PW-MRI and 15O-water-PET were performed in acute and subacute hemispheric stroke patients. The degree of CCD was defined by regions of interest placed in the cerebellar hemispheres ipsilateral (I) and contralateral (C) to the supratentorial lesion. An asymmetry index (AI=C/I) was calculated for PET-cerebral blood flow (CBF) and MRI-based maps of CBF, cerebral blood volume (CBV), mean transit time (MTT), and time to peak (TTP). The resulting AI values were compared by Bland–Altman (BA) plots and receiver operating characteristic analysis to detect the degree and presence of CCD. A total of 26 imaging procedures were performed (median age 57 years, 20/26 imaged within 48 hours after stroke). In BA plots, all four PW-MRI maps could not reliably reflect the degree of CCD. In receiver operating characteristic analysis for detection of CCD, PW-CBF performed poorly (accuracy 0.61), whereas CBV, MTT, and TTP failed (accuracy <0.60). On the basis of our findings, PW-MRI at 1.5 T is not suited to depict CCD after stroke.     

Cerebellar blood flow and metabolism in cerebral hemisphere infarction

Positron emission tomography was used to study the effect of supratentorial infarction on cerebellar metabolic rate for oxygen and cerebellar blood flow. In a control group of patients, the mean cerebellar metabolic rate for oxygen was 2.97 +/- 0.11 (standard error of the mean [SEM] ) ml-1 . min-1 . hg-1 and mean cerebellar blood flow was 41.1 +/- 1.5 ml . min-1 . hg-1. No significant right-left asymmetry in either cerebellar metabolic rate for oxygen or cerebellar blood flow was noted. Patients with frontal lobe infarction showed 16.8 +/- 1.8% (cerebellar metabolic rate for oxygen) and 19.6 +/- 2.1% (cerebellar blood flow) differences between cerebellar hemispheres, with the hemisphere contralateral to the cerebral infarction having the lower values. These differences were highly significant (p less than 0.001). In addition, cerebellar blood flow and cerebellar metabolic rate for oxygen were significantly decreased in the ipsilateral cerebellar hemisphere (metabolism: 2.13 +/- 0.19 ml . min-1 . hg-1; p less than 0.002; blood flow: 35.2 +/- 2.4 ml . min-1 . hg-1; p less than 0.05). Patients with parietooccipital infarction also showed a significant bilateral decrease in cerebellar metabolic rate for oxygen (2.43 +/- 0.11 ml . min-1 . hg-1) and cerebellar blood flow (34.6 +/- 2.5 ml . min-1 . hg-1) relative to control subjects, but no significant cerebellar asymmetry. Our findings demonstrate a general depression of cerebellar blood flow and metabolism from cerebral hemisphere infarction unrelated to the site of infarction as well as a specific depression occurring contralateral to infarction involving the frontal lobe. These are among the first quantitative data concerning regional cerebellar metabolic rates for oxygen and cerebellar blood flow in humans.     

Crossed cerebellar hypoperfusion in hyperacute ischemic stroke

OBJECTIVE: In chronic stage of cerebral hemispheric infarction, contralateral cerebellar blood flow and metabolism are depressed, which is known as crossed cerebellar diaschisis (CCD). The present study was performed to elucidate (1) whether the diaschisis occurs in hyperacute stage of ischemic stroke when computed tomography (CT) scans is not able to identify infarction, and (2) which site of lesion in the cerebrum is responsible for the depression in contralateral cerebellar blood flow. METHODS: Single photon emission computed tomography was performed in 21 patients with middle cerebral artery (MCA) embolic infarction within 6 h of the onset (3.2+/-1.1 h, mean+/-S.D.). Regions of interest (ROIs) were symmetrically located in the cerebral hemispheres including cerebral cortex and subcortex, and in the cerebellar hemispheres. RESULTS: The side-to-side ratio of cerebellar blood flow ipsilateral to that contralateral to cerebral infarct was significantly increased compared with that in normal control (P<0.001), indicating that contralateral cerebellar blood flow was significantly depressed. In hyperacute stage, the ratio of cerebellar blood flow appeared to be associated with the ratio of cerebral blood flow in whole hemispheres (r=0.44, P<0.05), in anterior frontal lobe (r=0.44, P<0.05) and in anterior temporal lobe (r=0.58, P<0.01), but not in infarct areas (r=0.26, P=0.3). Stepwise regression analysis revealed that the ratios in cerebellar hemispheres were associated with those in anterior temporal lobe (multiple regression analysis, r=0.58, P<0.01). CONCLUSIONS: Crossed cerebellar diaschisis occurs at hyperacute stage of stroke of the MCA infarction. It may be related to the hypoperfusion in the anterior frontal and anterior temporal lobes of the cerebrum where regional blood flow is decreased by ischemic infarction per se or by ipsilateral hemispheric depression from infarct area (diaschisis mechanism).     

Crossed cerebellar diaschisis in the Sturge-Weber syndrome

Crossed cerebellar diaschisis (CCD) is known as a cerebellar hemispheric hypometabolism due to contralateral supratentorial infarction or tumor. We report a case with the Sturge-Weber syndrome (SWS), whose cerebral blood flow was reduced in the anatomically affected lesion of cerebrum and in the contralateral cerebellar hemisphere. Not only acquired diaschisis, but congenital ischemic disorders such as SWS also showed CCD.     

Quantitative Ischemic Characteristics and Prognostic Analysis of Crossed Cerebellar Diaschisis in Hyperacute Ischemic Stroke

ObjectivesCrossed cerebellar diaschisis (CCD) is a secondary phenomenon caused by supratentorial brain injury, characterized by hypoperfusion and hypometabolism of the contralateral cerebellum. This study aimed to investigate the correlation between the quantitative data of initial supratentorial ischemia and CCD, and to further explore the prognosis value of CCD in the hyperacute phase.Materials and MethodsThe imaging and clinical data of 109 patients with hyperacute ischemic stroke were analyzed retrospectively, univariate analysis and multivariate logistic regression were used to observe the relationship between the volume and degree of initial supratentorial ischemia and CCD, respectively, and to further analyze the effects of CCD in the hyperacute phase on neurological function and clinical prognosis.ResultsThe degree and volume of initial supratentorial ischemia was significantly correlated with hyperacute CCD. The volume of ischemic penumbra (OR=1.021 [95% CI: 1.009–1.033], P<0.001) and the reduction rate of cerebral blood volume (CBV) (OR=1.338 [95% CI: 1.073–1.668], P=0.01) were the main influencing factors of CCD; patients with hyperacute CCD had higher admission and discharge National Institutes of Health Stroke Scale (NIHSS) (P=0.046 and P=0.01), and more hemorrhagic transformation (P=0.021), but there was no significant difference in the final infarction volume (P=0.347) and the 90-day modified Rankin Scale (mRS) (P=0.757).ConclusionPatients with CCD had larger initial supratentorial ischemic volume and more severe ischemic degree in the hyperacute ischemic stroke, more short-term neurological impairment, and worse short-term treatment effect, however, but the long-term functional prognosis was not be affected.     

A relationship between metabolism in frontal lobes and cerebellum in normal subjects studied with PET

Lesions of one cerebral hemisphere are associated with decreased glucose metabolism, oxygen metabolism, and blood flow in the contralateral cerebellar hemisphere. We used positron emission tomography to look for a functional relationship in cerebral metabolism between the cerebral cortex and the contralateral cerebellum in normal human subjects. Twenty-four normal subjects were scanned with [18F]fluoro-2-deoxy-D-glucose while in a resting state. Asymmetry in local CMRglu (LCMRglu) in the frontal cortex was strongly correlated with asymmetry in LCMRglu in the opposite direction in the cerebellar hemispheres (r = -0.60, p less than 0.001). Widespread subregions of the frontal cortex were found to contribute to this relationship. Considering these results together with previous studies demonstrating that frontal lesions are associated with decreased metabolism in the contralateral cerebellum, we conclude that the frontal cortex exerts a strong modulating influence on metabolism in the contralateral cerebellum in normal subjects, and that this influence may be asymmetrical.     

Crossed cerebellar diaschisis in patients with cerebral ischemia assessed by SPECT and 123I-HIPDM

Crossed cerebellar diaschisis (CCD) was investigated in a series of 59 patients (34 completed strokes and 25 reversible ischemic attacks, RIAs) using single photon emission computerized tomography (SPECT) with 123I-HIPDM as a cerebral blood flow (CBF) indicator. CCD was present in 17 (50%) of the patients with completed stroke and in 6 (24%) of the patients with RIAs. CCD was significantly correlated to the clinical severity (p less than 0.001) and to the extension of the supratentorial lesion (p less than 0.05). However, CCD was also recorded in 3 out of 16 patients with normal neurological examination and CT scan, suggesting that a 'functional' hemispheric disturbance may be sufficient to produce a remote effect on the contralateral cerebellar hemisphere. Time elapsed between the clinical onset and SPECT study was not critical, since CCD was recorded in the acute as well as in chronic studies. Follow-up SPECT studies showed that CCD disappeared in 5 out of 18 patients after a successful extra-intracranial bypass, while a spontaneous recovery was observed in only one of 16 nonsurgical patients.     

Correlation between crossed cerebellar diaschisis and clinical neurological scales

Szilágyi G, Vas Á, Kerényi L, Nagy Z, Csiba L, Gulyás B. Correlation between crossed cerebellar diaschisis and clinical neurological scales.
Acta Neurol Scand: 2012: 125: 373–381.
© 2011 John Wiley & Sons A/S. Background – A common consequence of unilateral stroke is crossed cerebellar diaschisis (CCD), a decrease in regional blood flow (CBF) and metabolism (CMRglu) in the cerebellar hemisphere contralateral to the affected cerebral hemisphere. Former studies indicated a post‐stroke time‐dependent relationship between the degree of CCD and the clinical status of acute and sub‐acute stroke patients, but no study has been performed in post‐stroke patients. Objectives – The objective of this investigation was to evaluate the quantitative correlation between the degree of CCD and the values of clinical stroke scales in post‐stroke patients. Materials and Methods – We measured with positron emission tomography (PET) regional CBF and CMRglu values in the affected cortical regions and the contralateral cerebellum in ten ischaemic post‐stroke patients. Based on these quantitative parameters, the degree of diaschisis (DoD) was calculated, and the DoD values were correlated with three clinical stroke scales [Barthel Index, Orgogozo Scale and Scandinavian Neurological Scale (SNS)]. Results – There were significant linear correlations between all clinical stroke scales and the CCD values (Barthel Index and Orgogozo Scale: P < 0.001, for both CBF and CMRglu; SNS: P = 0.007 and P = 0.044; CBF and CMRglu, respectively). Conclusions – The findings indicate that DoD can be used as a quantitative indicator of the functional impairments following stroke, i.e. it can serve as a potential surrogate of the severity of the damage.     

Disturbance of oxidative metabolism of glucose in recent human cerebral infarcts

Eight patients with recent cerebral hemispheric infarction were studied with positron emission tomography and the oxygen-15 steady-state inhalation and [¹⁸F]deoxyglucose techniques to obtain values of regional cerebral blood flow, oxygen consumption, and glucose metabolism. The Sokoloff equation, used to calculate glucose metabolism, was simplified to exclude the exponential terms containing the rate constants. A value of the lumped constant quoted for normal brain (0.42) was used for infarcted regions and contralateral hemisphere. Mean regional cerebral blood flow, oxygen consumption, and glucose metabolism were all significantly depressed within the infarcts compared with the mirror regions in the contralateral cerebral hemisphere. The mean fractional extraction of oxygen was low, indicating an adequate supply of oxygen for residual oxidative metabolism. Regional oxygen consumption and glucose metabolism were significantly correlated within the infarcts, but with a relationship of 2 moles of oxygen per mole of glucose—one-third that in the contralateral hemisphere and in normal brain. Although these results suggest that the metabolizing tissue of a recent cerebral infarct utilizes aerobic glycolysis, caution about the validity of this pathophysiological observation is dictated by limitations in current positron emission tomographic tracer methodology.     

Senile dementia and Alzheimer's disease. Brain blood flow and metabolism

Dementia of Alzheimer type is not form of accelerated aging. Blood flow, oxygen consumption and glucose utilization of the normally aged brain are maintained unchanged from the 3rd to the 7th decade of life. Thereafter, these parameters may decrease. Brain blood flow and oxidative metabolism is reduced in dementia of Alzheimer type and thus is different from the aged-matched mentally healthy subjects. There is evidence that the predominant impairment among these parameters may occur in cerebral glucose metabolism. This disturbance may precede changes in cerebral oxygen consumption and blood flow. Cerebral hypometabolism of glucose is accentuated in the temporo-parietal cortex. This finding may be helpful in diagnosing dementia of Alzheimer type.     

Biochemical evidence of crossed cerebellar diaschisis in terms of nitric oxide indicators and lipid peroxidation products in rats during focal cerebral ischemia

OBJECTIVES: Cerebral hypoperfusion in the contralateral cerebellar hemisphere after stroke is interpreted as a functional and metabolic depression, possibly caused by a loss of excitatory afferent inputs on the corticopontocerebellar pathway terminating in the cerebellar gray matter. This phenomenon is defined as crossed cerebellar diaschisis and can be diagnosed clinically by positron emission tomography, single-photon emission computed tomography, brain magnetic resonance imaging and electroencephalography in terms of regional cerebral blood flow or metabolic rate of oxygen measurements. MATERIALS AND METHODS: In the present study, nitric oxide indicators (nitrite and cyclic guanosine monophosphate) and lipid peroxidation products (malondialdehyde and conjugated dienes) were measured in rat cerebral cortices and cerebella after permanent right middle cerebral artery occlusion in order to assess the crossed cerebellar diaschisis. RESULTS: Nitrite values in ipsilateral cortex were significantly higher than those in contralateral cortex at 10 (P < 0.001) and 60 (P < 0.05) min of ischemia but no significant changes were observed in both cerebellum compared to the 0 min values. In both cerebral cortex and cerebellum cGMP levels at 10 and 60 min were significantly increased (P < 0.001). This increase was marked in ipsilateral cortex and contralateral cerebellum when compared with opposite cortex and cerebellum (P < 0.001). MDA values in ipsilateral cortex were significantly higher than those in contralateral cortex at 60 min of ischemia (P < 0.05). Contralateral cerebellar MDA values were found significantly higher than those in ipsilateral cerebellum at 0 (P<0.001) and 60 (P < 0.05) min of ischemia. In ipsilateral cortex, conjugated diene values at 0, 10, 60 min of ischemia were higher than those in contralateral cortex. On the other hand 0, 10, 60 min conjugated diene levels in contralateral cerebellum were significantly higher than those in ipsilateral cerebellum (P < 0.001). CONCLUSION: These findings support the interruption of the corticopontocerebellar tract as the mechanism of the crossed cerebellar diaschisis.