Cortical spreading depression (SD), a pathological cortical negative DC potential, is associated with various brain abnormalities. SD is a significant transient and localized relocation of ions within the neurons and spreads slowly like a wave in the brain tissue. SD results from a high extracellular K+ concentration, increasing neuronal excitability and, consequently, brain oxygen consumption. In our previous studies, we developed an electroencephalography (EEG) system capable of recording the SD from the surface scalp of epileptic patients. We demonstrated that SD is associated with seizures in patients with medically intractable epilepsy. In this paper, in addition to EEG measurements, near-infrared spectroscopy (NIRS) was used to measure local brain oxygen consumption during SD and seizures. NIRS is a non-invasive method to measure the hemodynamics of the tissue, such as oxy and deoxyhemoglobin concentrations, representing the gray matter's local neuronal metabolisms. By applying two or more wavelengths in the near-infrared window and measuring the attenuation variations of the relative change in the concentration of deoxyhemoglobin (HHb) and oxyhemoglobin (HbO2), the local oxygen consumption can be estimated. Method: We recorded SD and NIRS simultaneously during epileptiform EEG activities from twelve epileptic patients. Main result: SD occurred in the scalp of epileptic patients and preceded seizures with a varying time lag (0-30 minutes). HHb concentration increased during the SD duration. While HbO2 concentration decreased during the SD duration. Both returned to normal values after the SD event.
Spreading depression (SD) is an ultra-slow (30 to 90 seconds) brain electrical activity caused by the high concentration of extracellular potassium ions (K+) and plays an essential role in the pathophysiology of epilepsy. However, the SD signal amplitude is higher than the conventional EEG signal (10 to 300 microvolt). Due to filter effects of the skull and in the presence of other non-neuronal slow shift potentials (like electrode low-frequency shifts and motion artifact) the recording of an SD signal with the non-invasive method can be a difficult task. Near-infrared spectroscopy (NIRS) is wavelength-dependent absorption spectroscopy. Light absorption is a function of the molecular properties of substances within the light path. Hemodynamic variations accompany the propagation of the SD. Thus, using near-infrared spectroscopy besides EEG can provide an additional biomarker to distinguish SD from non-neuronal EEG slow shifts. This study used NIRS/EEG, a dual-modal NIRS and ultra-low frequency (0.01Hz to 80Hz) EEG device to record five Wistar rats (anesthetized). One NIRS source, NIRS detector, and EEG electrode were positioned above the somatosensory neocortex on the depilated skin. The EEG reference electrode was close to the rat’s nasion. The distance between source and detector was 8mm. KCL solution (3 mole/L, 10μl) was injected into the rat neocortex to generate the SD wave, and NIRS/EEG device performed the simultaneous recording. The increase of HHb (deoxyhemoglobin) accompanied by the slow shift of EEG was detected during SD. The rise of THb (Total hemoglobin) was also detected during the induced SD.
Electroencephalography (EEG) and cerebral near-infrared spectroscopy (NIRS) are both well-known monitoring methods to quantify cerebral neurophysiology and hemodynamics states of the brain. A stable regulatory system operates to guarantee sufficient spatial and temporal distribution of energy substrates for ongoing neuronal activity. Most EEG signals are associated with the neural activity of an enormous number of neurons that are interconnected and firing concurrently. The conventional EEG bandwidth is 0.16Hz to 70Hz. In this study, the EEG recording bandwidth is extended in low frequency (0.016Hz to 70Hz) by using a novel EEG amplifier. We aimed to investigate the low-frequency EEG and brain tissue deoxygenation by using novel multi-modal measurements. We used combined NIRS and EEG measurements for estimating the electrophysiological activity and hemodynamic changes in the adult human forehead during a hypoxic breathing condition. For the experiment, an altitude simulation kit was used to restrict the concentration of oxygen in the air that was inhaled by the subjects. The hypoxic breathing conditions led to variations in CO2 concentration (pCO2). Prolong (low-frequency) EEG signal shift, accompanied by an increase of deoxygenated hemoglobin during simulated hypoxic breathing were observed in this experiment.
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