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PubMed2006

Haemodynamic and neural responses to hypercapnia in the awake rat.

The relationship between localized changes in brain activity and metabolism, and the blood oxygenation level-dependent (BOLD) signal used in functional magnetic resonance imaging studies is not fully understood. One source of complexity is that stimulus-elicited changes in the BOLD signal arise both from changes in oxygen consumption due to increases in activity and purely 'haemodynamic' changes such as increases in cerebral blood flow. It is well established that robust cortical haemodynamic changes can be elicited by increasing the concentration of inspired CO(2) (inducing hypercapnia) and it is widely believed that these haemodynamic changes occur without significant effects upon neural activity or cortical metabolism. Hypercapnia is therefore commonly used as a calibration condition in functional magnetic resonance imaging studies to enable estimation of oxidative metabolism from subsequent stimulus-evoked functional magnetic resonance imaging BOLD signal changes. However, there is little research that has investigated in detail the effects of hypercapnia upon all components of the haemodynamic response (changes in cerebral blood flow, volume and oxygenation) in addition to recording neural activity. In awake animals, we used optical and electrophysiological techniques to measure cortical haemodynamic and field potential responses to hypercapnia (60 s, 5% CO(2)). The main findings are that firstly, in the awake rat, the temporal structure of the haemodynamic response to hypercapnia differs from that reported previously in anaesthetized preparations in that the response is more rapid. Secondly, there is evidence that hypercapnia alters ongoing neural activity in awake rats by inducing periods of cortical desynchronization and this may be associated with changes in oxidative metabolism.

Animals↗
PubMed2006

Annotation: Tourette syndrome: a relentless drumbeat--driven by misguided brain oscillations.

OBJECTIVE: This annotation reviews recent evidence that points to the likely role of aberrant neural oscillations in the pathogenesis of Tourette syndrome (TS). METHODS: The available anatomic and electrophysiological findings in TS are reviewed in the context of an emerging picture of the crucial role that neural oscillations play in maintaining normal central nervous system (CNS) function. RESULTS: Neurons form behavior-dependent oscillating networks of various sizes and frequencies that bias input selection and facilitate synaptic plasticity, mechanisms that cooperatively support temporal representation as well as the transfer and long-term consolidation of information. Coherent network activity is likely to modulate sensorimotor gating as well as focused motor actions. When these networks are dysrhythmic, there may be a loss of control of sensory information and motor action. The known electrophysiological effects of medications and surgical interventions used to treat TS likely have an ameliorative effect on these aberrant oscillations. Similarly, a strong case can be made that successful behavioral treatments involve the willful training regions of the prefrontal cortex to engage in tic suppression and the performance of competing motor responses to unwanted sensory urges such that these prefrontal regions become effective modulators of aberrant thalamocortical rhythms. CONCLUSIONS: A deeper understanding of neural oscillations may illuminate the complex, challenging, enigmatic, internal world that is TS.

Basal Ganglia↗
PubMed1996

Enhanced psychophysiological signs of attention after angiotensin-converting enzyme inhibition by captopril.

Complementary to its essential role in the central nervous control of cardiovascular activity, the neuropeptide angiotensin II may regulate attentional processes. The present study evaluated central nervous, cardiovascular, and sympathetic indicators of attention after inhibition of angiotensin II synthesis by captopril (50 mg vs. placebo) in 14 men. Event-related potentials (ERPs) and stimulus-related electroencephalographic (EEG) activity were recorded while the subject performed an auditory oddball task. Captopril increased both the N1-P2 component of the ERP (p < .05) and--following the first tone of the task--the EEG desynchronization in the lower alpha frequency band (p < .05). Although blood pressure remained unchanged, heart rate was lowered (p < .05) and plasma norepinephrine concentrations increased (p < .01) after captopril. The effects suggest that inhibition of angiotensin II synthesis enhances an attentional state typically present during sensory intake.

Acoustic Stimulation↗
PubMed1977

A presynaptic site of action within the mesencephalic reticular formation for (+)-amphetamine-induced electrocortical desynchronization.

1. Changes induced in the electrocorticogram by the bilateral perfusion of (+)-amphetamine into the mesencephalic reticular formation (MRF) have been studied in cat encéphale isolé preparations. 2. (+)-Amphetamine, applied for 5 min in the MRF, mimicked the electrocortical desynchronization induced by the perfusion of (-)-noradrenaline (NA) or (-)-alpha-methylnoradrenaline (AMNA) into the same sites. 3. Perfusion of 6-hydroxydopamine (6-OHDA) also induced desynchronization but, over the 1 h perfusion period, slow wave activity gradually returned to the electrical record. 4. Following the application of 6-OHDA the effect of (+)-amphetamine was abolished or significantly attenuated, whereas the effect of NA or AMNA was not affected. 5. The electrocortical desynchronization induced by (+)-amphetamine could be restored if its application was preceded by perfusion with NA or AMNA. 6. Fluorescence studies using AMNA indicated that 6-OHDA depleted noradrenergic nerve terminals near the cannulae tips. However, the terminals were still capable of taking up exogenously applied AMNA. 7. These results suggest that (+)-amphetamine has a presynaptic action on noradrenergic nerve terminals within the MRF.

Animals↗
PubMed1988

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine.

1. The behavioural and electrocortical (ECoG) power spectrum effects of clonidine, and yohimbine, an agonist and an antagonist at alpha 2-adrenoceptors, after their unilateral microinfusion into the rat locus coeruleus (LC) in young (50-70 days old) and old (13-15 months old) rats were studied. 2. Clonidine (0.09, 0.19, 0.28 and 0.56 nmol) microinfused into the LC of young rats induced dose-dependent behavioural and ECoG slow wave sleep (SWS) with a significant increase in total voltage power and power in the lower frequency bands. In contrast, yohimbine (1.3 and 2.6 nmol) infused into the LC of young rats produced ECoG desynchronization and a significant decrease in total voltage power. 3. In contrast to young rats, clonidine (0.19 and 0.28 nmol) given into the LC did not affect behaviour and the ECoG power spectrum in old rats. However, after higher doses of clonidine (0.56 and 1.2 nmol) a small and short-lasting period of behavioural and ECoG SWS was still evident. Similarly, in old rats yohimbine, at a dose (1.3 nmol) which was stimulative in young animals, did not significantly affect behaviour and ECoG power spectrum. Higher doses of yohimbine (2.6 and 5.2 nmol) were required to induce behavioural and ECoG changes similar to those observed with lower doses of yohimbine in young rats. 4. Chronic treatment with phosphatidylserine (30 mg kg-1, orally, daily for 21 and 30 days), was able gradually to restore in old rats, in comparison with a vehicle-treated group, the responsiveness of alpha 2-adrenoceptors to clonidine and yohimbine given into the LC.

Aging↗
PubMed1993

Inhibition by N omega-nitro-L-arginine methyl ester of the electrocortical arousal response in rats.

In rats chronically implanted with cannulae into one lateral cerebral ventricle and recording electrodes onto the fronto-parietal cortex, the effects of systemic or intraventricular administration of the nitric oxide (NO) synthesis inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), on electrocortical (ECoG) arousal response evoked by sound stimulation were studied. In control animals, a single acoustic stimulation (80 dB for 15 s) produced a significant decrease in ECoG total voltage power lasting approximately 25 s. No tolerance developed after repeating the same sound stimulation at 15, 30, 60 min and 24 h intervals. Under these experimental conditions, pretreatment with L-NAME, given systemically (10 mg kg-1, i.p.) or intracerebroventricularly (300 micrograms), significantly reduced the sound-evoked arousal response 1 h and 15 min later, respectively. In conclusion, the present data are in favour of a physiological role of NO in the control of arousal mechanisms.

Acoustic Stimulation↗
PubMed2004

Spatio-temporal imaging of cortical desynchronization in migraine visual aura: a magnetoencephalography case study.

OBJECTIVE: To determine cortical oscillatory changes involved in migraine visual aura using magnetoencephalography (MEG). BACKGROUND: Visual aura in the form of scintillating scotoma precedes migraine in many cases. The involvement of cortical spreading depression within striate and extra-striate cortical areas is implicated in the generation of the disturbance, but the details of its progression, the effects on cortical oscillations, and the mechanisms of aura generation are unclear. METHODS: We used MEG to directly image changes in cortical oscillatory power during an episode of scintillating scotoma in a patient who experiences aura without subsequent migraine headache. Using the synthetic aperture magnetometry method of MEG source imaging, focal changes in cortical oscillatory power were observed over a 20-minute period and visualized in coregistration with the patient's magnetic resonance image. RESULTS: Alpha band desynchronization in both the left extra-striate and temporal cortex persisted for the duration of reported visual disturbance, terminating abruptly upon disappearance of scintillations. Gamma frequency desynchronization in the left temporal lobe continued for 8 to 10 minutes following the reported end of aura. CONCLUSIONS: Observations implicate the extra-striate and temporal cortex in migraine visual aura and suggest involvement of alpha desynchronization in generation of phosphenes and gamma desynchronization in sustained inhibition of visual function.

Cortical Synchronization↗
PubMed1977

EEG operant conditioning in a monkey model: I. Seizure data.

EEG operant conditioning in an alumina-gel monkey model (N = 14) to decrease EMG, to increase 9 Hz or decrease 9 Hz, and to increase 23 Hz (18 Hz and 26 Hz in 2 pilot monkeys), respectively, was not consistently beneficial in reducing seizures. The data suggested: (1) that desynchronization of the EEG by reinforcing 18-26 Hz decreased in some animals the extent and severity of seizures while increasing seizure frequency; (2) that attending during conditioned EMG suppression reduced seizures somewhat; and (3) that the operant conditioning setting became stressful to the majority of monkeys under certain conditions, precipitating status epilepticus, gastrointestinal disturbances, and shock, which culminated in the death of 3 animals. Certain precautions are discussed in the therapeutic application of this technique to epileptic patients.

Animals↗
PubMedDate not supplied

Effect of chronic electrical stimulation of the centromedian thalamic nuclei on various intractable seizure patterns: I. Clinical seizures and paroxysmal EEG activity.

Twenty-three patients with various intractable seizure patterns were divided into four groups based on their most frequent seizure type and their clinical and EEG response to chronic electrical stimulation of the centromedian thalamic nuclei (ESCM): group A, generalized tonic-clonic (GTC, n = 9); group B, partial motor (Rasmussen type) (n = 3); group C, complex partial seizures (CPS, n = 5); and group D, generalized tonic seizures (Lennox-Gastaut type) (n = 6). CM were radiologically and electrophysiologically localized by means of stereotaxic landmarks and by thalamically induced scalp recruiting-like responses and desynchronization. ESCM consisted of daily 2-h stimulation sessions for 3 months. Each stimulus consisted of a 1-min train of square pulses with a 4-min interstimulus interval, alternating right and left CM. Each pulse was 1.0 ms in duration at 60/s frequency and 8-15 V (400-1,250 microA) amplitude. Voltage (V), current flow (microA) and impedance (k omega) at the electrode tips were kept constant. A significant decrease in the number of seizures per month and paroxysmal EEG waves per 10-s spochs occurred in group A patients between the baseline period (BL) and the ESCM period. These changes persisted for > 3 months after discontinuation of ESCM (poststimulation period, Post). Post was accompanied by a significant decrease in the number of paroxysmal EEG discharges. A substantial decrease in seizures and paroxysmal discharges was also observed in patients of group B. In contrast, patients of groups C and D showed no significant changes from BL to ESCM and Post periods, except for a significant decrease in the number of seizures in group D patients from BL to Post periods.

Adolescent↗
PubMedDate not supplied

Evaluation of the hypothesis that hippocampal interictal spikes are caused by long-term potentiation.

Hippocampal spontaneous interictal spikes (SISs) occur in the EEG after repeated afterdischarges (ADs) induced by high-frequency (200 Hz) stimulation trains. Because SISs resemble population excitatory postsynaptic potentials (EPSPs), and SISs persist for several days like some types of hippocampal long-term potentiation (LTP), LTP has been suggested as a mechanism for SISs. We specifically examined the hypothesis that SISs are caused by basal-dendritic LTP in CA1. Rats were chronically implanted with bilateral electrodes in the hippocampal CA1 region. In the first experiment, 10-18 patterned primed burst (PB) stimulations were delivered hourly for 2-3 days to activate the commissural basal-dendritic EPSP in CA1. Robust LTP of the basal-dendritic CA1 synapse was detected, typically saturating at 100% enhancement after five stimulations. However, few SISs were detected if ADs were not elicited. In the second experiment, repeated commissurally evoked ADs induced a high rate of SISs, together with LTP of the basal-dendritic and apical-dendritic EPSP in CA1, but the SIS rate was not necessarily related to the level of LTP. In the third experiment, an intraventricular dose (20 micrograms) of an N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovalerate (APV) was used to block the basal-dendritic LTP in CA1. The increase in SISs induced by a single AD was not blocked, however, suggesting that NMDA receptors were not critical in generation of SISs. In the fourth experiment, PBs (that induced LTP but no ADs) were able to increase the rate of SISs marginally when SISs were already present. In all, the experiments suggest that LTP at the basal dendrites of CA1 is not critical in generation of hippocampal SISs, although an increase in LTP may increase the rate of SISs marginally when SISs are already present.

Animals↗
PubMedDate not supplied

Ictal video-EEG analysis of infantile neuroaxonal dystrophy.

A 4-year-old boy with infantile neuroaxonal dystrophy (INAD) showed gradual deterioration from age 9 months with seizure development at age approximately 36 months. Sural nerve biopsy performed at age 42 months confirmed INAD. The seizure, recorded by video-EEG, consisted of a series of symmetrical tonic spasms of both upper extremities after a prodrome period of staring and akinesis. Each spasm had phonation, and episodic autonomic symptoms such as hypertension and flushing of the face occurred throughout the seizure. Ictal EEG with each tonic spasm, showed diffuse 1-s, irregular sharp and high-voltage slow wave complexes followed by desynchronization.

Axons↗
PubMed1997

Abnormal cortical activation during planning of voluntary movement in patients with epilepsy with focal motor seizures: event-related desynchronization study of electroencephalographic mu rhythm.

PURPOSE: The spatiotemporal distribution of EEG mu rhythm desynchronization was analyzed in patients with partial epilepsy to determine whether frequent focal motor seizures could induce a change of cortical activation during the planning of a voluntary movement. METHODS: The event-related desynchronization (ERD) of the mu rhythm was quantified during a self-paced voluntary movement of the thumb. The results were compared between two groups of patients with epilepsy: in one group (n = 12), the patients had frontal lobe epilepsy with frequent focal motor seizures (FMS); in the second group (n = 12), they had temporal lobe epilepsy (TLE) with complex partial seizures but no ictal movement disorder. The results were also compared with those of control subjects of same age (n = 10). RESULTS: In the control group, desynchronization of mu rhythm began over the contralateral central region 2,000 ms before the movement onset. In the FMS group, the desynchronization of mu rhythm was delayed, appearing only 500 ms before the movement onset, and the amplitude of ERD was increased over the frontocentral region. In the TLE group, the spatiotemporal pattern of ERD was the same as in normal subjects, but the amplitude of ERD was increased. CONCLUSIONS: These results indicate that there is a change of reactivity of mu rhythm in patients with partial epilepsy. The change in spatiotemporal pattern of ERD in patients with frequent focal motor seizures suggests that there is an abnormal cortical activation during the planning of a voluntary movement.

Adult↗
PubMed2000

The clinical usefulness of ictal surface EEG in neocortical epilepsy.

PURPOSE: Localizable scalp EEGs, during ictal episodes, appear to be rare in neocortical epileptic syndromes. However, studies based on large numbers of patients are also rare. This study aims to identify the characteristic patterns of variable neocortical epilepsies and to evaluate their clinical usefulness in the localization of epileptogenic focuses. METHODS: We retrospectively assessed 394 noninvasive ictal recordings from 86 patients who subsequently underwent invasive study and resective surgery. Ictal EEGs were recorded using a video-EEG monitoring system with electrodes placed according to the International 10-20 system, with additional anterior temporal electrodes. The ictal recordings were analyzed according to localizing accuracy and frequency characteristics. The durations of discrete or regional ictal rhythms were also measured. RESULTS: The percentage of discrete or regional EEGs was 23% in frontal lobe epilepsy, 52% in lateral temporal lobe epilepsy, 70% in occipital lobe epilepsy, and 10% in parietal lobe epilepsy. In order of frequency, the localizable ictal rhythms were theta, beta, alpha, delta, and rhythmic spike-and-wave. The duration of discrete or regional ictal rhythms was significantly shorter in frontal lobe epilepsy and parietal lobe epilepsy than in other epilepsies. Ictal beta activity was the most common rhythm in discrete-patterned EEGs. Structural lesions found on MRI did not significantly affect the localization of epileptogenic focuses in the patients. The type of seizure was not related to the degree of localization, with the exception of simple partial seizure. CONCLUSIONS: Ictal surface EEG was clinically helpful in the localization of epileptogenic focuses in at least some neocortical epileptic syndromes.

Adult↗