scholarly journals Parenchymal Spin-Lock fMRI Signals Associated with Cortical Spreading Depression

2014 ◽  
Vol 34 (5) ◽  
pp. 768-775 ◽  
Author(s):  
Joonas A Autio ◽  
Artem Shatillo ◽  
Rashid Giniatullin ◽  
Olli H Gröhn
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
High Energy ◽  
Blood Oxygenation ◽  
Acute Ischemia ◽  
High Energy Phosphates ◽  
Ph Change ◽  
Spin Lock ◽  
Fmri Signal

We found novel types of parenchymal functional magnetic resonance imaging (fMRI) signals in the rat brain during large increases in metabolism. Cortical spreading depression (CSD), a self-propagating wave of cellular activation, is associated with several pathologic conditions such as migraine and stroke. It was used as a paradigm to evoke transient neuronal depolarization leading to enhanced energy consumption. Activation of CSD was investigated using spin-lock (SL), diffusion, blood oxygenation level-dependent and cerebral blood volume fMRI techniques. Our results show that the SL-fMRI signal is generated by endogenous parenchymal mechanisms during CSD propagation, and these mechanisms are not associated with hemodynamic changes or cellular swelling. Protein phantoms suggest that pH change alone does not explain the observed SL-fMRI signal changes. However, increased amounts of inorganic phosphates released from high-energy phosphates combined with pH changes may produce SL- power-dependent longitudinal relaxation in the rotating frame ( R1ρ) changes in protein phantoms that are similar to those observed during CSD, as seen before in acute ischemia under our experimental conditions. This links SL-fMRI changes intimately to energy metabolism and supports the use of the SL technique as a new, promising functional approach for noninvasive imaging of metabolic transitions in the active or pathologic brain.

scholarly journals MR Detection of Cortical Spreading Depression Immediately after Focal Ischemia in the Rat

1996 ◽  
Vol 16 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Joachim Röther ◽  
Alexander J. de Crespigny ◽  
Helen D'Arceuil ◽  
Michael E. Moseley
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Tissue Perfusion ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Planar Imaging ◽  
Mr Perfusion Imaging ◽  
Before And After ◽  
Apparent Diffusion ◽  
Cortical Regions

The suture model for middle cerebral artery occlusion (MCAO) was used to induce acute ischemia in rats remotely within a magnetic resonance (MRI) scanner. Serial MR diffusion weighted imaging (DWI) was performed during remote MCAO using an echo planar imaging technique. MR perfusion imaging was performed before and after occlusion using the bolus tracking technique. Transient apparent diffusion coefficient (ADC) changes were detected in six of seven rats as early as 2.7 ± 1.5 min post MCAO. ADC values declined transiently to 70.1 ± 6.0% of control and recovered to 95.5 ± 6.8% of control within 3.3 ± 2.9 min. These ADC changes propagated bidirectionally away from the ischemic core with a speed of 3.0 ± 1.1 mm/min. Transient ADC decreases only occurred in ischemic areas characterized by moderately decreased tissue perfusion. Propagation toward cortical regions with severe tissue perfusion deficits was not detected. DWI can detect the earliest dynamic, reversible ADC changes in the ischemic tissue. The speed of propagation of the decreasing ADC wave, the waveform characteristics, and the occurrence in moderately perturbated tissue are compatible with cortical spreading depression.

scholarly journals Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

2005 ◽  
Vol 10 (1) ◽  
pp. 011004 ◽  
Author(s):  
Michael Guiou ◽  
Sameer Sheth ◽  
Masahito Nemoto ◽  
Melissa Walker ◽  
Nader Pouratian ◽  
...  
Keyword(s):  
Blood Volume ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
Neurovascular Coupling

Microfabricated Electrode Array Compatible With Optical Imaging of Intrinsic Signals During Somatosensory Stimulation and Cortical Spreading Depression

2006 ◽  
Author(s):  
Jeremy J. Theriot ◽  
Neal Prakash ◽  
Arthur W. Toga ◽  
Y. Sungtaek Ju
Keyword(s):  
Optical Imaging ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
Electrode Array ◽  
Transparent Electrode ◽  
Electrophysiological Recording ◽  
Pathological State ◽  
Somatosensory Stimulation ◽  
Intrinsic Signals

Accurate interpretation of functional brain images requires knowledge of the relationship between neurons and their supporting cells and vasculature. Our understanding of this complex and dynamic system would improve if we measure multiple aspects of brain function simultaneously. We have developed a semi-transparent electrode array which allows for concurrent multi-site electrophysiological recording and high-resolution optical imaging of intrinsic signals. The 8-channel electrode array is fabricated on a transparent glass substrate with platinum recording surfaces. We map stimulus-induced field potentials (evoked potentials) and changes in cerebral blood volume in rat somatosensory cortex. We also examine the evolution of these responses during the neuro-pathological state of cortical spreading depression. We have developed a planar multi-electrode array that is fully compatible with Optical imaging of Intrinsic Signals. It provides a sensitive and reliable tool to use in the study of neurovascular coupling in brain activation.

Abstract 1571: Hibernating Myocardium has Reduced High Energy Phosphate Levels and a Preconditioning-Like Effect with Slower ATP Depletion in Response to Acute Ischemia

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Qingsong Hu ◽  
Gen Suzuk ◽  
John M Canty ◽  
James A Fallavollita
Keyword(s):  
High Energy ◽  
Atp Depletion ◽  
Energy Utilization ◽  
Hibernating Myocardium ◽  
Wall Thickening ◽  
Acute Ischemia ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Chronic Coronary Artery Disease ◽  
Atp Levels

Background. Pigs with a chronic LAD stenosis develop hibernating myocardium with contractile dysfunction and reduced resting flow. We hypothesized that this reduced energy utilization preserves ATP and protects the heart from irreversible injury during acute ischemia. Methods. Pigs with hibernating myocardium were studied 3-months after instrumentation with a 1.5 mm proximal LAD stenosis (n=7). Hibernating myocardium was confirmed by reduced LAD wall thickening (2.4±0.2 vs.6.1±0.6 mm in remote, p<0.05) and reduced resting flow (0.95±0.15 vs. 1.66±0.29 ml/min/g in remote, p<0.05) without infarction. Subendocardial samples were rapidly excised from propofol anesthetized pigs and serial depletion of high energy phosphates quantified by HPLC (in μmol/g dry weight) during simulated total ischemia in vitro (37°C). Results. At Baseline, ATP and ADP were significantly reduced in the hibernating LAD region in comparison to controls (n=8, Table ), with preserved CP/ATP and ATP/ADP ratios. During simulated ischemia, hibernating myocardium displayed a markedly reduced rate of ATP depletion (ΔATP), with ATP levels at 20 min significantly higher than control (Table ). Higher ATP levels were maintained throughout 80 min of ischemia. Interestingly, identical preservation of high energy phosphates occurred in the remote normally perfused region of hearts with hibernating myocardium (Table ). Conclusion. These data indicate that there is a balanced reduction in high energy phosphate levels in hibernating myocardium with chronic protection from ischemia manifested by a slower rate of ATP depletion during acute ischemia. This preconditioning-like effect is global suggesting that it arises from stimuli that are not directly related to ischemia. This raises the possibility that stretch from cyclical elevations in LV filling pressure or a circulating factor released from the heart in response to ischemia can protect the heart in chronic coronary artery disease.

scholarly journals Initial Oligemia with Capillary Flow Stop Followed by Hyperemia during K+-Induced Cortical Spreading Depression in Rats

2005 ◽  
Vol 25 (6) ◽  
pp. 742-747 ◽  
Author(s):  
Minoru Tomita ◽  
Istvan Schiszler ◽  
Yutaka Tomita ◽  
Norio Tanahashi ◽  
Hidetaka Takeda ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
Capillary Flow ◽  
Region Of Interest ◽  
Cell Swelling ◽  
Astroglial Cell ◽  
Initial Flow ◽  
Cyclic Changes

Local cerebral blood volume (CBV) and capillary flow changes in regions of depolarizing neurons during K+-induced cortical spreading depression (CSD) in the cerebral cortex of α-chloralose-urethane-anesthetized rats were examined employing a transillumination (550 nm) video system. Capillary flow was calculated as the reciprocal of mean transit times of blood in pixels of 40 μm × 40 μm, each of which contains a few capillaries. Potassium microinjection into the cortex evoked repetitive wave-ring spreads of oligemia at a speed of ca. 2.33±0.48 mm/min. During the spread of CSD, tracer (either saline or carbon black) was injected into the internal carotid artery. Colocated with the oligemic wave, we detected capillary flow stop as evidenced by disappearance of the hemodilution curves. At any location in the region of interest within the cerebral cortex, we observed cyclic changes of capillary flow stop/hyperperfusion in synchrony with oligemia/hyperemia fluctuations. The initial flow stop and oligemia were ascribed to capillary compression by astroglial cell swelling, presumably at the pericapillary endfeet, since the oligemia occurred before larger vessel changes. We conclude that local depolarizing neurons can decrease adjacent capillary flow directly and immediately, most likely via astroglial cell swelling, and that the flow stop triggers upstream arteriolar dilatation for capillary hyperperfusion.

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