Recurring episodes of spreading depression are spontaneously elicited by an intracerebral hemorrhage in the swine.

Intracranial bleeding damages the surrounding tissue in a complex fashion that involves contamination by blood-borne products and loss of ionic homeostasis. We used electrophysiological techniques to examine the functional changes in the developing intracerebral bleed and in surrounding regions using an in vivo swine model. Intracerebral hemorrhage (ICH) was induced by collagenase injection into the primary somatosensory cortex (SI). Somatic evoked potential (SEP) elicited by electrical stimulation of the contralateral snout as well as changes in DC-coupled potential were monitored in the SI from the time of collagenase injection in order to measure the effects of ICH. The SEP decreased in amplitude within minutes of the intracerebral injection. Its short-latency component was abolished within the first hour after collagenase injection without any sign of recovery for the duration of the experiment. As the SEP started decreasing in amplitude, we observed spontaneous, recurring episodes of cortical spreading depression (SD) as early as 20 min post-injection. The timing of SDs in SI is consistent with our interpretation that SDs were initially generated at multiple sites adjacent to the lesion core and propagated into the surrounding area. With time, SD became less frequent near the injection site, shifting to more distant electrodes in the surrounding area. Our results indicate that ICH leads to the reduction in SEP amplitude and induces spontaneous episodes of SD. Loss of ionic homeostasis is most likely the physiological basis for the SEP change and for the induction of SD. Recurring SD spontaneously generated in experimental ICH needs further study in humans with ICH.

Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip. I. Lissencephalic rabbit model.

Magnetic fields arising from the rabbit cortex during spreading cortical depression (SCD) were measured in order to study the currents in the neocortex during SCD. SCD was constrained to propagate in a rectangular cortical strip perpendicular to the midline. This simplified in vivo cortical preparation enabled us to correlate magnetoencephalographic (MEG) signals to their underlying currents within the cortical strip. The propagation of SCD was monitored with an array of electrodes placed along the strip. The propagation speed for SCD in the lissencephalic rabbit brain was 3. 5+/-0.3 mm/min (mean+/-S.E.M., n=14). Slow, quasi-dc, MEG signals were observed as the SCD entered into the longitudinal fissure. The currents giving rise to the MEG signals were perpendicular to the cortical surface and directed from the surface to deeper layers of the cortex. A distributed dipolar source model was used to relate the data to the underlying cortical current. The moment of the single equivalent current dipole source was 38+/-9 nA-m (n=17). This study clarified the nature of the cortical currents during SCD in a lissencephalic in vivo preparation.

Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip. II. Gyrencephalic swine model.

Currents produced during spreading cortical depression (SCD) in a gyrencephalic species (swine) were studied with magnetoencephalography (MEG) and electrocorticography (ECoG). SCD, initiated using electrical stimulation of the cortex, was constrained to propagate within a rectangular cortical strip in order to simplify the interpretation of the underlying currents. The ECoG signals monitored along the strip revealed that SCD propagated from an initiation site on the gyrus at a rate of 7.9+/-3.2 mm/min (n=23), entered the deep coronal sulcus and in most cases emerged from the other side of the sulcus, continuing to propagate across the next gyrus at a rate of 5.9+/-2.7 mm/min (n=22). The apparent propagation velocity within the sulcus was reduced to 1.7+/-0.8 mm/min (n=21). Strong MEG signals were observed as SCD entered the sulcus. The direction of magnetic field was opposite for SCD's on opposite banks of the sulcus. The currents were directed from a superficial layer to deeper layers of the cortex. The characteristics of SCD and associated MEG patterns from a gyrencephalic species may be similar to those in human patients during migraine aura.

Neuronal activities from a deep subcortical structure can be detected magnetically outside the brain in the porcine preparation.

We assessed whether subcortical structures can generate magnetic fields detectable outside the brain by first measuring the somatic evoked magnetic fields (SEFs) from a decorticated porcine preparation and then from an intact preparation. Strong SEFs were detected a few millimeters above the corpus callosum after electrical stimulations of the snout. The waveforms consisted of a large spike ( < or = 6 pT) with a peak latency of 11-18 ms depending on the age of the animal, followed by a slow wave. The waveform and latency of the SEF spike were virtually identical to those of the field potential within the brain. The SEF topography indicated that the underlying generator of the spike was in a region contralateral to the stimulation and inferior to the thalamus. The subcortical SEF was strong enough to be detectable even above the intact brain, after the cortically generated SEF was removed by ablation of the primary cortical area. The results indicate that a structure deep in the brain can produce remarkably strong magnetic fields detectable outside the brain.

[Interaction of reticular structures in the brain of the cat]. / O vzaimodeistvii retikuliarnykh struktur golovnogo mozga koshek.

In acute and chronic experiments on 35 cats an inhibitory influence was found of the caudal reticular nucleus of pons Varolii on unit activity of the sensorimotor cortex and dorsal part of the midbrain reticular formation. The influence of this structure on unit activity of the ventral part of the midbrain reticular formation was mainly of a facilitatory character. Activation of the ventral part inhibited the unit activity of the dorsal part of the same structure. Consequently, the caudal reticular nucleus of pons Varolii elicits inhibition at the level not only of the cerebral cortex but also of the midbrain reticular formation (of its dorsal part). The character of these influences coincides with that of unit activity changes of these two areas of the midbrain reticular formation during the development of the paradoxical phase of sleep. The obtained facts must underlie the stopping of convulsive activity in this phase of sleep.