The slow voltage variation of cortical spreading depression of activity

Leäo, A. A. P.

doi:10.1016/0013-4694(51)90079-x

Cited by 125 publications

(55 citation statements)

References 13 publications

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“…In the normal brain spreading de pression is a fully reversible process, and the ion gradients are reestablished within 1-2 min (Hansen and Lauritzen, 1985). The waves of spreading de pression propagate preferentially in the upper cor tical layers (Leao, 1951). They are associated with increased glucose utilization that rises before the ion shifts between extra-and intracellular space (Shinohara et aI., 1979;Gjedde et aI., 1981).…”

Section: Discussionmentioning

confidence: 99%

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation

Nedergaard

Astrup

1986

J Cereb Blood Flow Metab

324

189

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Summary: Focal ischemia was produced by occlusion of the right middle cerebral artery (MCA) in normo-and hy perglycemic rats. In the cortical infarct rim, regional [14Cl2-deoxyglucose (f14C]2-DG) phosphorylation was correlated to spontaneous transient changes in extracel lular potassium recorded as direct current (DC) potential deflections. In normoglycemic rats the DC potential showed transient but recurrent deflections in the first hours following MCA occlusion. The 2-DG phosphoryla tion was elevated by 200% in the same area. In contrast, hyperglycemic rats had no, or a single, deflection of the DC potential in the rim, and the 2-DG phosphorylation remained normaL The same pattern was obtained by ap plication of 3 M KCI to the exposed cortex. In normogly cemia potassium application resulted in recurrent deflec-The present study deals with the events occur ring in the cortical rim around the infarct in rats with middle cerebral artery (MCA) occlusion. Pre vious work in this model has clearly shown in creased glucose phosphorylation in the infarct border (Shigeno et aI. , 1983; Sako et aI., 1985; Ne dergaard et aI. , 1986). This may have two causes: either enhanced anaerobic glycolysis due to hypo perfusion and reduced oxygen supply (Pasteur ef fect) or enhanced glucose utilization due to an in crease in metabolism. The latter explanation is fa vored by observations in other models of focal cerebral ischemia of repeated transient elevations of extracellular potassium in the infarct border (Branston et aI. , 1977; Harris et aI. , 1981; Strong et aI. , 1983). Elevation of extracellular potassium

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Section: Discussionmentioning

confidence: 99%

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation

Nedergaard

Astrup

1986

J Cereb Blood Flow Metab

324

189

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“…Potas sium transients are related to the phenomenon of spreading depression. Spreading depression is as sociated with increased glucose consumption (Shinohara et aI., 1979;Gjedde et aI., 1981) and spreads preferentially in the upper cortical layers (Leao, 1951). In the marginally perfused borders of focal ischemia, failure of potassium clearance may prolong the otherwise transient elevations of the extracellular potassium.…”

Section: Discussionmentioning

confidence: 99%

Focal Ischemia of the Rat Brain: Autoradiographic Determination of Cerebral Glucose Utilization, Glucose Content, and Blood Flow

Nedergaard

Gjedde

1986

J Cereb Blood Flow Metab

159

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Summary: Focal cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. By a triple tracer technique, cerebral glucose utilization, glucose content, and blood flow were simultaneously determined. Computer-assisted autoradiography revealed a core of dense ischemia in the lateral two-thirds of the striatum. A border zone of increased 2-deoxy-o-glucose (DG) uptake surrounded the ischemic insult in the acute stage. The lumped constant was increased only moderately in the border zone. Therefore, the enhanced DG uptake re flected increased glucose consumption. CBF was re duced to 20-30% in the cortical border, while minor deClinical imaging of acute stroke requires a reli able indicator of irreversible damage and poten tially viable tissue. The visualization of CBF does not faithfully reflect the severity of ischemic damage. Positron emission tomography (PET) of the acute phase of stroke reveals a wide range of CBF values that change in either direction with time, "lUXury perfusion" being one of the extremes (Lassen, 1966). Several authors have raised the question of whether the changes of CBF are sec ondary to more fundamental changes and thus no more than an epiphenomenon (Ackerman et aI., 1981).Received August 16, 1985; 414pression and in some animals hyperemia were evident in the striate border. Six hours after the insult, the border zones of increased glucose consumption had disappeared in half the animals. In no animals examined after 20 h was glucose consumption enhanced. The study indicated a stable metabolic response to a reproducible focal insult. We conclude that continued enhancement of glucose consumption in marginally perfused areas indicates neuronal damage. Key Words: Autoradiography-Cere bral blood flow-Cerebral ischemia-2-Deoxyglucose method-Lumped constant-Middle cerebral artery oc clusion.Quantitative 2-deoxY-D-glucose (DG) autoradiog raphy has been used in animal models of ischemia and 18F-labeled 2-fluoro-2-deoxY-D-glucose (FDG) in PET of stroke patients. Heterogeneous distur bances including increased, decreased, or normal accumulation of DG and FDG have been reported in the early phase of ischemia (Fieschi et aI. , 1978;Diemer and Siemkowicz, 1980; Wise et aI. , 1983). In experimental focal ischemia, several authors have found foci of greatly suppressed DG uptake surrounded by a rim of increased DG accumulation (Ginsberg et a\. , 1977; Welsh et aI. , 1980; Choki et aI. , 1983). In the method of Sokoloff et al. (1977), local DG accumulation is the basis for estimation of local glucose phosphorylation. However, only in normal tissue can the rate of DG be assumed to be a known fraction of glucose consumption. The "iso tope" correction ratio of DG accumulation to glu cose consumption, the lumped constant (LC), may change in conditions in which the relationship be tween plasma and brain glucose has changed.Therefore, in pathological tissue the magnitude of the LC must be determined separately before it is possible to calculate glucose consumption from the DG accumulatio...

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“…12,31 The perfusion changes may not be the inciting event; rather, the perfusion abnormality may be the response of the autoregulatory mechanisms to underlying neuronal depression. [5][6][7][8][9][10]12,13,29,[31][32][33] This concept is supported by case reports of persistent hyperperfusion despite resolution of headache with abortive therapy. 3,11 Although the exact cause of a migraine has yet to be completely defined, migraines are clinically classified on the basis of the presence or absence of aura phenomenon.…”

Section: 28mentioning

confidence: 99%

Migraine Associated Cerebral Hyperperfusion with Arterial Spin-Labeled MR Imaging

Pollock¹,

Deibler²,

Burdette³

et al. 2008

AJNR Am J Neuroradiol

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SUMMARY:We present a case series demonstrating abnormal regional cerebral hyperperfusion associated with migraine headache using arterial spin-labeling (ASL). In 3 of 11 patients, regional cortical hyperperfusion was demonstrated during a headache episode that corresponded to previous aura symptoms. Migraine is a common condition affecting 12% of the United States population per year.1 Migraines classically present with unilateral debilitating, painful headaches associated with photophobia, phonophobia, nausea, and vomiting. Less than 30% of migraines are preceded by auras, or focal neurologic deficits. Most commonly, the neurologic deficits are visual, but sensory and motor deficits can also occur. The pathophysiology of a migraine is complex and is not completely understood. The vascular theory proposes that the migraine aura is associated with vasoconstriction and the subsequent headache is associated with vasodilation and hyperperfusion.3,4 The second theory is that a contiguous wave of neuronal depression spreads through the cortex causing the aura symptoms.5-10 The vascular changes have been evaluated with nuclear medicine studies including single-photon emission CT and positron-emission tomography as well as blood oxygen level-dependent functional MR imaging and T2* dynamic susceptibility contrast (DSC) MR perfusion imaging. 3,8,9,[11][12][13] These methods are limited in the evaluation of the patient with migraine because of the dynamic nature of the perfusion abnormalities.Spin tag perfusion imaging is an MR imaging method that measures quantitative cerebral blood flow (CBF).14 The advantages of arterial spin-labeling (ASL) compared with conventional perfusion techniques include repeatability, absolute quantification, and the avoidance of intravenous contrast administration. 15,16 We performed a retrospective analysis of MR imaging examinations including ASL perfusion in patients with an indication of headache from the past 12 months and identified 11 clinical patients with a history of migraine headache. We present the 3 patients with migraine-associated regional cerebral hyperperfusion corresponding to the clinical presentation. Case Reports Patient 1A 55-year-old woman with a history of hemiplegic migraines presented with new-onset right frontal headache, left-sided numbness, weakness, and dysarthria. The patient took prochlorperazine (Compazine) at home without relief of her symptoms. We performed cerebral MR imaging 6 hours after onset of symptoms using our standard stroke protocol including conventional sequences and ASL perfusion. Conventional MR imaging sequences demonstrated subtle sulcal effacement and mild edema in the right frontal cortex without evidence of diffusion abnormality (Fig 1).We generated quantitative CBF maps using quantitative imaging of perfusion and a single subtraction with thin-section inversion time (TI) 1 periodic saturation with a flow-sensitive alternating inversion recovery sequence as described previously.17 This sequence generates 60 tag and control image pairs. Imag...

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The slow voltage variation of cortical spreading depression of activity

Cited by 125 publications

References 13 publications

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation

Focal Ischemia of the Rat Brain: Autoradiographic Determination of Cerebral Glucose Utilization, Glucose Content, and Blood Flow

Migraine Associated Cerebral Hyperperfusion with Arterial Spin-Labeled MR Imaging

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The slow voltage variation of cortical spreading depression of activity

Cited by 125 publications

References 13 publications

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [14C]2-Deoxyglucose Phosphorylation

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [14C]2-Deoxyglucose Phosphorylation

Focal Ischemia of the Rat Brain: Autoradiographic Determination of Cerebral Glucose Utilization, Glucose Content, and Blood Flow

Migraine Associated Cerebral Hyperperfusion with Arterial Spin-Labeled MR Imaging

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Product

Resources

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Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation

Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [¹⁴C]2-Deoxyglucose Phosphorylation