at least three spreading depolarizations within three or fewer consecutive recording hours (current working definition)
peptide produced by vascular endothelial cells; potent vasoconstrictor, induces focal ischemia
any spikes, sharp-waves, or sharp-and-slow wave complexes that last for at least 10 seconds at either a frequency of at least 3/s or a frequency of at least 1/s with clear evolution in frequency, morphology, or recording sites of the electrode strip (visible as an increase in the AC-ECoG power and the integral of the power). May occur with or without overt clinical correlates.
severe vasoconstriction triggered by spreading depolarization that causing a steep and almost instantaneous decrease in local perfusion.
spreading depolarization that initiates no spreading depression because it occurs in tissue that is electrically inactive
a characteristic, abruptly developing negative shift of the slow potential recorded with a DC amplifier, often followed by a longer lasting positive shift. The negative DC shift identifies spreading depolarization, and the duration of the negativity is a measure of its local metabolic and excitotoxic effect on the tissue. Alternating current (AC) amplifiers with lower frequency limit of 0.01 Hz distort the negative DC shift to a multi-phasic slow potential change (SPC) that can still be used to identify spreading depolarization.
long-lasting, shallow negativity of the DC potential with superimposed spreading depolarizations. Experiments have shown the NUP associated with incomplete recovery of the typical ion changes after spreading depolarizations and hence with developing neuronal injury. NUP may indicate that only a fraction of neurons in the tissue has repolarized at the recording site and that the remaining fraction is persistently depolarized.
a bioradical shown to be not only a potent vasodilator, but also an important modulator of cerebrovascular reactivity and regulator of smooth muscle cell function of cerebral vessels.
simultaneous arrest of spontaneous activity in neighboring electrodes under severe energy compromise before the occurrence of spreading depolarization. At least one of the following additional criteria have to be fulfilled: (i) invasive measurements of arterial pressure to prove global arrest of the circulation and/or (ii) local partial pressure of tissue oxygen (ptiO2) has fallen to a critical level before non-spreading depression develops. If tissue is reperfused in time, there is no spreading depolarization following non-spreading depression.
pronounced hyperemia in response to spreading depolarization, variably followed by a mild, long-lasting oligemia.
the state of persistently depressed AC-band or high-frequency electrical activity induced and maintained by one spreading depolarization or a cluster of spreading depolarizations.
spreading depolarization with epileptic field potentials rising on the tailing end of the DC shift
the abrupt, sustained near-complete breakdown of the neuronal trans-membrane ion gradients and mass depolarization that propagates as a wave at approximately 1.5 – 9.5 mm/min in grey matter of the brain
spreading depolarization-induced reduction or suppression of spontaneous brain electrical activity, observed in recordings as amplitude reduction that run between adjacent electrodes
increase of regional cerebral blood flow in response to spreading depolarization, first phase of the normal, biphasic hemodynamic response
severe inverse hemodynamic response to spreading depolarization that leads to prolongation of the negative DC shift. Spreading ischemia occurs when, in a vicious circle, the perfusion deficit caused by inverse neurovascular coupling prevents neuronal repolarization and prolongs the release of vasoconstrictors. Importantly, hemodynamic responses to spreading depolarization are not binary, but exist on a continuum between normal and inverse.
mild decrease of regional cerebral blood flow after recovery from the tissue depolarization, second phase of the normal hemodynamic response