The present study was carried out to evaluate the effect of hypothermia and rewarming on the pattern of Cortical Spreading Depression(CSD) and predict the resultant vulnerability of the brain. Thirty four Sprague-Dawley rats, either sex, weighing 250-350gm, were used. They were devided into 4 groups, according to the degree of hypothermia and speed of rewarming, Profound Hypothermia & Slow Rewarming(G I), Profound Hypothermia & Rapid Rewarming(G II), Moderate Hypothermia & Slow Rewarming(G III), Moderate Hypothermia & Rapid Rewarming(G IV). CSD was elicited by local application of KC1 and identified by Direct Current Potential(DCP). We estimated the Frequency of DCP, Recovery time of negative shift of DCP, Area of negative shift of DCP according to the change of body temperature. The frequencies of DCP increased after rewarming compared with the normothermic state in all groups, statistical significance(P<0.05) was specially evident in Group II(Profound Hypothermia & Rapid Rewarming group), 5.1+/-0.3/30min.(mean+/-standard error) in normothermic state, while 9.3+/-0.8/30min in rewarming state. Recovery time(width) of DCP was delayed with hypothermia but decreased with rewarming but delayed state compared with normothermic state in all groups, i.e. 34.7+/-1.0sec at normothermic state, 59.9+/-4.3sec at 27.5 degrees C, 40+/-1.4sec at rewarming state in Group II. We can predict that the vulnerability of the brain tissue may be increased during the rewarming state following hypothermia in all groups. Such evidence is more significant in Group II(Profound Hypothermia & Rapid Rewarming) during the period of certain time(30-60min) after rewarming.
Animals ; Body Temperature ; Brain ; Cortical Spreading Depression* ; Hypothermia* ; Rats* ; Rats, Sprague-Dawley ; Rewarming*

Cortical spreading Depression(CSD) is a transient depression of neuronal activity that spreads across the cortical surface and is associated with profound changes in blood flow, extracellular ion concentration. Direct Current(DC) potentials and cell membrane potentials. One of the electrophysiological disturbance in the periinfarct surrounding is spontaneous occurrence of repeated CSD like DC shifts associated with increased energy demand. Due to restricted blood flow to the periinfarct border zone, elevated metabolic demand is potentially hazardous. So the authors designed this experiment to verify the correlation between periinfarct cortical spreading depression and ischemic volume following permanent middle cerebral artery(MCA) occlusion in rats. Sprague-Dawley rats(n=27) were anesthetized with 0.5~1% halothane, and artificially ventilated through a tracheal cannula. Arterial pressure, blood gases and body temperature were controlled. The middle cerebral artery(MCA) was occluded distally to the lenticulostriate branches. Measurements of CSD activity were made for 4 hours in each animal infarct volume was determined 6 hours later in 2,3,5-triphenyl tetrazolium chloride(TTC)- stained section. For 4 hours after MCA occlusion, the CSDs were found in all experimental animals with a range of 2~9 times. Those CSDs were of varying duration: "small"(1min) SDs and mean of total duration of SD was 10.5+/-10.3 min during 4 hours of MCA occlusion. Neuropathological evaluation of brain infarct in the rats, which had been allowed to survive for 6 hours after MCA occlusion showed a mean volume of 89.7+/-45.3 mm3. Serial observation of duration of CSD prologation of duration of CSD nor the frequency of CSD in the penumbral zone correlated with the volume of infarct.However total duration of CSD was slightly related with the infarct volume after 6 hours of the permanent MCA occlusion(r=0.414, p=0.0318) .
Animals ; Arterial Pressure ; Body Temperature ; Brain ; Catheters ; Cell Membrane ; Cortical Spreading Depression* ; Depression ; Gases ; Halothane ; Neurons ; Rats* ; Rats, Sprague-Dawley

AIMTo observe the effect of cortical spreading depression (CSD) on the spontaneous firing activities of neurons of subthalamic nucleus (STN) in normal and model rat of Parkinson's disease (PD).

METHODSExtracellular recording was used to research the neuronal electric activities in subthalamic neurons. The changes of the discharge rates of subthalamic neurons were observed in control and PD rats after intracortical microinjection of KCl solution.

RESULTSThe discharge rates of subthalamic neurons in control and PD rats were (9.78 +/- 0.71) Hz and (23.81 +/- 1.08) Hz, respectively. The discharge rate of PD rats was increased significantly when compared with those of the control rats and the percentage of neurons discharging in bursts was obviously higher than those of control rats (P < 0.01). After a long latent period secondary to intracortical injection of KCl solution, the discharge rates in both group of subthalamic neurons were decreased apparently, then recovered slowly.

CONCLUSIONThe discharge rate and bursting pattern are increased in PD rats and these abnormal activities can be improved by cortical depression. This result indicates that the changes in cortical excitability may be one of the factors increasing the activity of STN in PD.

Animals ; Cortical Spreading Depression ; physiology ; Male ; Neurons ; Parkinson Disease ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Subthalamic Nucleus ; physiology

OBJECTIVE: Decompressive craniectomy is widely used in cases of uncontrolled intracranial hypertension, including traumatic brain injury or acute stroke. Physiological monitorings, such as intracranial pressure or electroenecephalography (EEG) are critical for patients in the acute phase. We retrospectively reviewed our experience of continuous electrocorticography (ECoG) monitoring by subdural strip electrode in patients who performed decompressive craniectomy and assessed its clinical efficacy. METHODS: Patients who underwent decompressive craniectomy because of severe intracranial hypertension were included. 4 Channel strip electrodes were inserted on the frontal cortex before closure. 24-hour continuous monitoring of ECoG was done to identify abnormal electrical activity. The level of consciousness was assessed according to Glasgow Coma Scale (GCS). In patients with malignant intracranial hypertension, barbiturate coma therapy was considered. RESULTS: Fifteen patients (9 men and 6 women) were included and the mean age was 55.7 years (from 17 to 80). The initial mean GCS score was 7.9 (from 3 to 14). In six out of fifteen patients, abnormal spike activities were identified, and one of these six patients was diagnosed as nonconvulsive status epilepticus (NCSE). Cortical spreading depression (CSD) was suspected in five. Three patients underwent barbiturate coma therapy and ECoG monitoring of these patients showed typical burst suppression pattern, which was used for indicator of therapeutic level. The mean duration of strip electrode and ECoG monitoring was 3.5 days, and there was no complication. CONCLUSION: Continuous ECoG monitoring using subdural strip electrode was useful to detect abnormal brain activity in the acute period after decompressive craniectomy.
Barbiturates ; Brain ; Brain Injuries ; Coma ; Consciousness ; Cortical Spreading Depression ; Decompressive Craniectomy* ; Electrodes* ; Glasgow Coma Scale ; Humans ; Intracranial Hypertension ; Intracranial Pressure ; Male ; Retrospective Studies ; Status Epilepticus ; Stroke

It is believed that migrainous aura is correlated with cortical spreading depression and spreading benign oligemia. A 54-year-old female with migraine with aura presented with left hemianopia preceding pulsating headache. Perfusion-weighted images revealed delayed contrast arrival to the right occipital lobe and nearly normal relative cerebral blood volume images, indicating benign oligemia. Follow-up perfusion-weighted images revealed resolution of the perfusion abnormalities. We report herein a case of migraine with aura presenting with reversible delayed perfusion in the right occipital lobe on perfusion-weighted images.
Blood Volume ; Cortical Spreading Depression ; Epilepsy ; Female ; Follow-Up Studies ; Headache ; Hemianopsia ; Humans ; Middle Aged ; Migraine Disorders ; Migraine with Aura* ; Occipital Lobe ; Perfusion*

PURPOSE: Migraine is a common neurological disorder, but the mechanism has not yet been apparently discovered. Recent studies have found that migrainous headache comes from the hemodynamic changes based on the cortical spreading depression and matrix metalloproteinase(MMP)-9 has an important role in this phenomenon. The aim of this study is to investigate the significance of the serum concentration of MMP-9 in children with migraine. METHODS: Among 33 children who visited the headache clinic, from June 2004 to August 2004 we identified and analyzed the clinical findings of 17 patients, who were diagnosed as migraine or tension-type headache. Also we selected 9 children as a healthy control group. The serum concentrations of MMP-9 from all of those were obtained via ELISA kits. RESULTS: The mean duration of headache was 1.3 years in the migraine group. Also, the frequency of migraine is as follows:everyday in 4 patients and more than once during weekdays in 5 patients. The character of headache was throbbing in 8 patients out of 9 patients with migraine. There were no significant differences found in the serum concentrations of MMP-9 between the control group and the migraine group. The serum concentrations of MMP-9 were significantly high, of those who had frequent attacks of migrainous headache. CONCLUSION: The serum concentrations of MMP-9 in the migraine group were not significantly high compared with those in the control group. However, the levels were high from those who complained of migraine frequently. This study suggests that the serum concentration of MMP-9 is not high during a normal period but increases when migraine occurrs.
Child ; Cortical Spreading Depression ; Enzyme-Linked Immunosorbent Assay ; Headache ; Hemodynamics ; Humans ; Matrix Metalloproteinase 9* ; Migraine Disorders* ; Nervous System Diseases ; Tension-Type Headache

The object of this study was to investigate the influences of hypoglycemia and hypothermia on the direct current(DC) pontetial changes during cortical spreading depression(CSD) in rats. The induction of CSD was achieved by the application of KCI solution on the cortex of the frontal lobe. Hypoglycemia and hypothermia were induced respectively by insulin injection and the application of an ice pack. The DC potential changes during progressive hypoglycemia and hypothermia were measured with microelectrodes from the cortex of the parietal lobe of rats. Under contril condition, the rate of CSD was one per 5-10 min and the negative shift of DC potential was about 30 mV. The recovery time from negative shift to base line of DC potential was about 40 sec. In rats treated with insulin, the amplitude of DC potential shift was unaffected by hypoglycemia. The recovery time of DC shift was 40+/-2.26 sec at normoglycemia and it was delayed progressively as the blood glucose level lowered. The mean of it was 63+/-8.02 sec at 30 mg/dl and 77.1+/-22.0 sec with the blood glucose falling below 20 mg/dl. The same delay in the recovery time as seen in the hypogylcemia group was observed in rats treated with hypothermia. The recovery time of DC shift was 39.4+/-3.02 sec in normothermia(36.5degrees C), but it was delayed to 61.15+/-4.15 sec at 30degrees C and 96.67+/-14.92 sec at 26degrees C body temperature. This study suggested that each condition of profound hypoglycemia below 30 mg/dl and hypothermia below 30degrees C was to be harmful to the ion homeostasis and the integrity of the cell membrane and it may lead neurons to death.
Animals ; Blood Glucose ; Body Temperature ; Cell Membrane ; Cortical Spreading Depression* ; Frontal Lobe ; Homeostasis ; Hypoglycemia* ; Hypothermia* ; Ice ; Insulin ; Microelectrodes ; Neurons ; Parietal Lobe ; Rats*

Vestibular migraine (VM) is an increasingly recognized cause of episodic recurrent vertigo. However, the pathophysiology of VM is still a matter of speculation. An understanding of the relationship between migraine and the vestibular system increases knowledge of the pathogenesis of both migraine and vertigo. The pathophysiology of VM has been known to be related to cortical spreading depression, neurotransmitters (i.e., serotonin, noradrenaline, dopamine, calcitonin gene-related peptide) and calcium ion channel disorder. Moreover, VM is related with Meniere's disease, benign paroxysmal positional vertigo, motion sickness, cerebellar dysfunction, or comorbid psychotic disorder. This review refines recently proposed pathophysiological concept for VM and relationships between migraine and other related disorders.
Calcitonin ; Calcium Channels ; Cerebellar Diseases ; Cortical Spreading Depression ; Dopamine ; Meniere Disease ; Migraine Disorders ; Motion Sickness ; Neurotransmitter Agents ; Norepinephrine ; Psychotic Disorders ; Serotonin ; Vertigo ; Vestibular Neuronitis

BACKGROUND AND PURPOSE: Migraine has been shown to increase cerebral excitability, promote rapid infarct expansion into tissue with perfusion deficits, and result in larger infarcts in animal models of focal cerebral ischemia. Whether these effects occur in humans has never been properly investigated. METHODS: In a series of consecutive patients with acute ischemic stroke, enrolled in the setting of the Italian Project on Stroke at Young Age, we assessed acute as well as chronic infarct volumes by volumetric magnetic resonance imaging, and compared these among different subgroups identified by migraine status. RESULTS: A cohort of 591 patients (male, 53.8%; mean age, 37.5±6.4 years) qualified for the analysis. Migraineurs had larger acute infarcts than non-migraineurs (median, 5.9 cm³ [interquartile range (IQR), 1.4 to 15.5] vs. 2.6 cm³ [IQR, 0.8 to 10.1], P<0.001), and the largest volumes were observed in patients with migraine with aura (median, 9.0 cm³ [IQR, 3.4 to 16.6]). In a linear regression model, migraine was an independent predictor of increased log (acute infarct volumes) (median ratio [MR], 1.64; 95% confidence interval [CI], 1.22 to 2.20), an effect that was more prominent for migraine with aura (MR, 2.92; 95% CI, 1.88 to 4.54). CONCLUSIONS: These findings reinforce the experimental observation of larger acute cerebral infarcts in migraineurs, extend animal data to human disease, and support the hypothesis of increased vulnerability to ischemic brain injury in people suffering migraine.
Animals ; Brain Injuries ; Brain Ischemia ; Brain ; Cohort Studies ; Cortical Spreading Depression ; Humans ; Linear Models ; Magnetic Resonance Imaging ; Migraine Disorders ; Migraine with Aura ; Models, Animal ; Perfusion ; Risk Factors ; Stroke

The author has examined the effect of cortical spreading depression(CSD) on the changes in extracellular concetration of aspartate and glutamate in the neocortex of anesthetized rats using microdialysis and high performance liquid chromatography(HPLC). The rats were prepared by halothane anesthesia and artificial ventilation. Rats were placed in a stereotaxic frame, and craniotomies were performed over the frontal and parietal cortexes on one side. The CSD was elicited by local application of KCI-soaked small pellets to the frontal cortex. The CSD was monitored by the changes of direct current(DC) potential in the parietal cortex. The microdialysis probe was implanted in the anterior part of the parietal cortex. Amino acids were analyzed by HPLC and fluorescence detection. Baseline concentration of the aspartate was 34.9+/-15.9nM and that of glutamate was 189.8+/-29.1nM(mean standard deviation). The perfusate for analysis was obtained 30 minutes after the beginning of the 300mM KCl induced CSD. Aspartate was found to increase to 146+/-55% baseline, glutamate up to 173+/-30% baseline(mean standard deviation). The increment of glutamate was statistically significant(p<0.05). Then 2M KCI-doaked pellets were applied for more frequent CSD amd the samples were collected. Aspartate increased up to 258+/-97% baseline, glutamate up to 174+/-57% baseline(mean standard deviation), The increment of glutamate and aspartate accompanying 2M KCI induced CSD were also statistically significant(p<0.05). These data suggest that the excitatory amino acids were released during the CSD and this may explain the various aspects of CSD that could contribute to the secondary neuronal damage in the compromised nerve cell.
Amino Acids ; Anesthesia ; Animals ; Aspartic Acid* ; Cerebral Cortex* ; Chromatography, High Pressure Liquid ; Cortical Spreading Depression* ; Craniotomy ; Excitatory Amino Acids ; Fluorescence ; Glutamic Acid* ; Halothane ; Microdialysis ; Neocortex ; Neurons ; Rabeprazole ; Rats* ; Ventilation