Acute EEG Research Articles

Correlation of continuous electroencephalogram with clinical assessment scores in acute stroke patients

To compare electroencephalogram (EEG) symmetry values between stroke patients with different 28-day outcomes, and to assess correlations between clinical characteristics and 28-day outcomes. Twenty-two patients presenting with acute ischemic stroke and persistent neurological deficits at EEG recording were incrementally included. At 28 days after admission, the modified Rankin scale (mRS) was used to evaluate the outcomes, based on which the patients were divided into two a posteriori groups, mRS = 6 and mRS <6. Student's t-test was used to compare these two groups in terms of brain symmetry index (BSI), National Institutes of Health stroke scale (NIHSS), Glasgow coma scale (GCS) and acute physiology and chronic health evaluation II (APACHE II) assessed at admission. Then EEG parameters, NIHSS, GCS and APACHE II were correlated with the mRS. There were significant differences in BSI, NIHSS, GCS, and APACHE II between the two groups. Survivors had lower BSI, NIHSS and APACHE II, and higher GCS values, compared with patients who died within 28 days after admission. Besides, BSI at admission had a positive correlation with mRS at 28 days (r = 0.441, P = 0.040). NIHSS and APACHE II were also correlated with mRS (r = 0.736, P <0.000 1; r = 0.667, P = 0.001, respectively). GCS at admission had a negative correlation with mRS (r = -0.656, P = 0.001). A higher BSI predicts a poorer short-term prognosis for stroke patients. Acute EEG monitoring may be of prognostic value for 28-day outcomes. The early prediction of functional outcomes after stroke may enhance clinical management and minimize short-term mortality.

Human herpesvirus 6 and 7 in febrile status epilepticus: The FEBSTAT study

In a prospective study, Consequences of Prolonged Febrile Seizures in Childhood (FEBSTAT), we determined the frequency of human herpesvirus (HHV)-6 and HHV-7 infection as a cause of febrile status epilepticus (FSE). Children ages 1 month to 5 years presenting with FSE were enrolled within 72 h and received a comprehensive assessment including specimens for HHV-6 and HHV-7. The presence of HHV-6A, HHV-6B, or HHV-7 DNA and RNA (amplified across a spliced junction) determined using quantitative polymerase chain reaction (qPCR) at baseline indicated viremia. Antibody titers to HHV-6 and HHV-7 were used in conjunction with the PCR results to distinguish primary infection from reactivated or prior infection. Of 199 children evaluated, HHV-6 or HHV-7 status could be determined in 169 (84.9%). HHV-6B viremia at baseline was found in 54 children (32.0%), including 38 with primary infection and 16 with reactivated infection. No HHV-6A infections were identified. HHV-7 viremia at baseline was observed in 12 children (7.1%), including eight with primary infection and four with reactivated infection. Two subjects had HHV-6/HHV-7 primary coinfection at baseline. There were no differences in age, characteristics of illness or fever, seizure phenomenology or the proportion of acute EEG or imaging abnormalities in children presenting with FSE with or without HHV infection. HHV-6B infection is commonly associated with FSE. HHV-7 infection is less frequently associated with FSE. Together, they account for one third of FSE, a condition associated with an increased risk of both hippocampal injury and subsequent temporal lobe epilepsy.

Effect of intravenous sodium salicylate administration prior to castration on plasma cortisol and electroencephalography parameters in calves

Nociception is an unavoidable consequence of many routine management procedures such as castration in cattle. This study investigated electroencephalography (EEG) parameters and cortisol levels in calves receiving intravenous sodium salicylate in response to a castration model. Twelve Holstein calves were randomly assigned to the following groups: (i) castrated, untreated controls, (ii) 50 mg/kg sodium salicylate IV precastration, were blood sampled at 0, 5, 10, 20, 30, 45, 60, 90, 120, 150, 180, 240, 360, and 480 min postcastration. The EEG recording included baseline, castration, immediate recovery (0-5 min after castration), middle recovery (5-10 min after castration), and late recovery (10-20 min after castration). Samples were analyzed by competitive chemiluminescent immunoassay and fluorescence polarization immunoassay for cortisol and salicylate, respectively. EEG visual inspection and spectral analysis were performed. Statistical analyses included anova repeated measures and correlations between response variable. No treatment effect was noted between the two groups for cortisol and EEG measurements, namely an attenuation of acute cortisol response and EEG desynchronization in sodium salicylate group. Time effects were noted for EEG measurements, cortisol and salicylates levels. Significant correlations between cortisol and EEG parameters were noted. These findings have implications for designing effective analgesic regimens, and they suggest that EEG can be useful to monitor pain attributable to castration.

Platform Session B: Clinical Neurophysiology/Clinical Epilepsy 3:00 p.m.–6:00 p.m.

Platform Session B: Clinical Neurophysiology/Clinical Epilepsy 3:00 p.m.–6:00 p.m.

Electroencephalography and brain damage in preterm infants

Electroencephalography (EEG) is a sensitive method for detection of brain injury in preterm infants. Although the acute and chronic EEG changes are mainly non-specific regarding type of damage, they correlate with later neurological and cognitive function. In infants developing brain white matter damage, acute EEG findings include depression of background activity and presence of epileptic seizure activity. The chronic EEG changes associated with white matter injury and abnormal neurological development include delayed maturation, and presence of abundant Rolandic sharp waves. Cognitive limitations in preterm infants have been associated with changes in various sleep measures in EEG's recorded at full term. Continuous EEG-monitoring during neonatal intensive care shows that cerebral electrical activity during this vulnerable period can be affected by several extracerebral factors, e.g. cerebral blood flow, acidosis and some commonly used medications. For diagnosis of brain damage in preterm infants with neurophysiological methods, a combination of early continuous EEG monitoring during the initial intensive care period and full EEG, performed at later stages, is probably optimal.

Increase in delta- and beta-wave activity of the EEG during rapid opiate detoxification (ROD)-reversal by administration of the non-specific NMDA-antagonist S(+) ketamine-

Little is known on effects taking place in the CNS during rapid opioid detoxification (ROD) while the patient is under anesthesia. We therefore measured EEG-power spectra in the β, α, Θ, and δ-band in 36 patients undergoing ROD. Measurements were taken before, during steady-state anesthesia and following administration of the antagonist naltrexone. In addition, the non-specific NMDA-antagonist S(+) ketamine was given for reduction of CNS-hyperexcitation, while the efficacy of this adjunct was determined using EEG power spectra analysis. Compared to steady-state anesthesia, EEG power spectra were characterized by a marked decrease of power by 251% in the delta (0.5–3 Hz) and an increase by 209% in the beta- (13–30 Hz) domain when withdrawal was induced with naltrexone. Subsequent administration of S(+)-ketamine induced a reversal of acute abstinence-related EEG power changes: compared to anesthesia with naltrexone on board, power in the EEG increased by 65% in the delta- and decreased by 723% in the beta-band. While sympathetically induced hemodynamic alterations in anesthesia-assisted opioid detoxification can be attenuated by the α 2-agonist clonidine and sedation, central nervous sensory activation can be attenuated by the administration of S(+)-ketamine (1.5 mg/kg). Since EEG alterations during acute withdrawal with naltrexone can be controlled by the non-specific NMDA-antagonist S(+)-ketamine, this latter presents a useful adjunct during ROD management.

Intermittent clobazam therapy in febrile seizures

To evaluate the efficacy of intermittent clobazam therapy in preventing the recurrence of febrile seizures and to assess its safety. The study was a prospective, randomized, double-blind placebo-controlled trial conducted in the Department of Child Health, Christian Medical College Hospital, Vellore between July 2001 and September 2002. Neurologically normal children between 6 months and 3 years of age with a history of febrile seizures and no evidence of acute CNS infection or EEG abnormality were included into the study. 19 children in a clobazam group and 20 in the placebo group were randomly allocated. Temperature reduction measures with paracetamol and tepid sponging were advised to all children. In addition the dispensed medication was to be administered at the onset of fever and continued for 48 hours irrespective of the duration of fever. The children were then monitored for seizures and adverse effects of clobazam. The children were followed up for a mean period of 9.9 months. The analysis was done on the number of febrile episodes in both the groups. There were a total of 110 episodes of fever during the study period. Mean number of febrile episodes in the clobazam group was 3.1 and in placebo group 2.56. Six (12.5%) of the 48 episodes in placebo group and one (1.7%) of 60 episodes in clobazam group had seizure recurrence. This was statistically significant (p = 0.01). Drowsiness and weakness were present equally in both clobazam and placebo groups whereas ataxia was present only in the clobazam group, the difference being statistically significant (p=0.04). Intermittent clobazam therapy is an effective measure in the prevention of recurrence of febrile seizures. The ataxia due to clobazam was much lower than that reported with diazepam.

Clonidine pre-treatment fails to block acute smoking-induced EEG arousal/mood in cigarette smokers

Given the arousal eliciting actions of smoking and nicotine, and the contributing role of noradrenaline in brain arousal systems, this study examined the neuroelectric and affective correlates of cigarette smoking following acute pre-treatment with the alpha 2-noradrenergic auto-receptor agonist, clonidine. In a double-blind placebo-controlled crossover design, quantitative electroencephalography (EEG), mood, and smoking withdrawal symptoms were assessed in 12 overnight smoking abstinence smokers, before and after sham and cigarette smoking. Orally administered clonidine (0.1 mg) failed to alter overnight smoking abstinence symptoms or the EEG arousal and mood-elevating response seen with the smoking of a single cigarette. The results are discussed in relation to neural mechanisms underlying the acute reinforcement maintaining nicotine use.

Electroencephalographic aspects of periventricular hemorrhagic infarction in preterm infants.

The aim of this study was to investigate electroencephalographic aspects of periventricular hemorrhagic infarction (PVHI) in preterm infants. The subjects were 11 preterm infants with PVHI, who were admitted to the Neonatal Intensive Care Unit of Anjo Kosei Hospital from April 1985 through December 1997. The patients underwent serial cranial ultrasonography and were diagnosed as having PVHI. An EEG was recorded at least once within 1 week after PVHI and then recorded at 1- to 4-week intervals until 40 weeks of postconceptional age. The EEG findings were classified into acute and chronic stage abnormalities. Acute stage EEG abnormalities were seen in 5 infants after PVHI, which were symmetrical in all infants. Among them, 3 infants died during the early neonatal period. The infants who had a higher grade of acute stage EEG abnormalities showed significantly higher mortality. Among the surviving 8 infants, chronic stage EEG abnormalities were seen in 3 predominantly in the ipsilateral side of PVHI, and all of them developed hemiplegia. The sensitivity and specificity of chronic stage EEG abnormalities to predict outcome were 0.75 and 1.0, respectively. Acute and chronic stage EEG abnormalities give valuable information for short-term and long-term outcome in preterm infants with PVHI.

Carbamazepine for acute psychosis with eeg abnormalities

To investigate the efficacy of carbamazepine as adjuvant drug therapy in acute paranoid psychosis with associated EEG abnormalities, compared to sole antipsychotic treatment. Eleven medication-naive patients, diagnosed with acute paranoid psychosis with associated EEG abnormalities, were divided into two treatment groups: sole fluphenazine group, with flexible dosing of 5-10 mg/day (n=6), and carbamazepine group (n=5) with the addition of carbamazepine (600 mg/day) to fluphenazine treatment. Clinical Global Impression (CGI), Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS), and EEG were assessed on the baseline and after 6 weeks of treatment. Paired and two-tailed t-tests were used for statistical significance. All the patients showed significant improvement of mental state after 6 weeks of treatment with no significant differences in CGI, BPRS, and total SANS scores in relation to the therapy with carbamazepine. Nevertheless, after 6 weeks of the treatment, EEG findings were significantly better in carbamazepine group, in relation to the findings from the onset of the treatment, as well as in comparison to sole fluphenazine group. Although carbamazepine stabilized abnormal brain electrical activities it seemed that the associated EEG abnormalities were not significant for acute psychosis observed. These preliminary results suggested that there was no convincing evidence that carbamazepine was efficient as the augmentation of antipsychotic treatment for patients with both acute paranoid psychosis and EEG abnormalities.

EEG changes with vagus nerve stimulation.

Vagus nerve stimulation (VNS) has been shown to induce EEG changes in animals, but human studies have not shown any significant acute EEG changes. This study is to determine the long-term effect of VNS on EEG. Twenty-one patients aged 4 to 31 years (mean: 14.1 +/- 7.0 years) were studied for a mean duration of 16.8 months with serial EEGs performed at baseline and at 3 months, 6 months, and 12 months after receiving a VNS implant. Five patients who showed active spikes/spike and wave activity on baseline EEGs were found to have synchronization of epileptiform activity, progressive increase in duration of spike-free intervals (P < 0.05), and progressive decrease in duration and frequency of spikes/spike and wave activity (P < 0.01) with time. The remaining 16 patients with less active baseline EEGs did not show obvious synchronization or clustering of spikes but also showed a statistically significant progressive decrease in the number of spikes on EEG with time (P < 0.004 at 3 months, P < 0.008 at 6 months, and P < 0.004 at 1 year). Vagus nerve stimulation induces progressive EEG changes in the form of clustering of epileptiform activity followed by progressively increased periods of spike-free intervals. This may reflect the mechanism of action of VNS in achieving seizure control: alternating synchronization and desynchronization of EEG, with the latter being progressively the dominant feature.

Proof of principle trials: EEG surrogate endpoints

Pivotal studies in man require prolonged administration to demonstrate efficacy for most seizure types. Earlier evidence of human efficacy can be of value for decision making, and EEG surrogate endpoints can be of value in this respect. Studies of spontaneous EEG discharges under standard recording conditions can demonstrate meaningful acute EEG effects of antiepileptic drugs (AEDs). These require a rapidly effective formulation of the product, preferably intravenous. The EEG recording conditions are standardised and the subject is required to perform a task to maintain a constant level of vigilance. The outcome measure of efficacy is spike count per minute or, if the discharges are more protracted (as generalised no spike and wave), the percentage of recording time occupied by discharges. Sub-acute experiments are conducted under less rigorously standardised conditions, but over longer periods, using ambulatory monitoring or telemetry to record the EEG. The photoparoxysmal responses (PPRs) of photosensitive subjects, evoked using a standardised stimulation protocol, are subject to less variability than spontaneous epileptiform activity. The PPR is elicited over a range of flash rates that can be used as a measure of sensitivity, and an effective treatment will reduce the range or abolish the PPR. Reduction in photosensitivity is demonstrable after a single dose of various AEDs, at clinically relevant plasma concentrations, even using drugs that are not generally effective for long-term treatment of photosensitive epilepsy. Evoked potential and nerve conduction studies and electronystagmography can be used to assess possible neurotoxicity, and quantitative EEG analysis can be employed to assess sedative effects.

Acute behavioral and EEG effects of NW-1015 on electrically-induced afterdischarge in conscious monkeys

NW-1015 is a novel Na + and Ca 2+ channel blocker with broad spectrum anticonvulsant activity and an excellent safety margin. As the compound also shows sigma-1 receptor ligand properties it was deemed important to determine whether it possesses anticonvulsant properties in primates without causing behavioral and EEG abnormalities. Thus, the effects of NW-1015 on limbic electrically-induced afterdischarge (AD) were evaluated in four cynomolgus monkeys, and its activity compared to a single effective dose of phenytoin (PHT). The four male cynomolgus monkeys were chronically implanted for EEG recordings, from cortex and limbic structures. AD was induced in limbic areas by electrical stimulation. The effects of NW-1015 on the duration and the behavioral component of the AD were randomly tested at doses from 25 to 75 mg/kg and compared with the effects of PHT 50 mg/kg. Similarly to PHT, 50 mg/kg of NW-1015 significantly shortened the EEG AD and almost abolished AD elicited behavioral seizure. Only the behavioral effects of AD were reduced after administration of 25 mg/kg p.o. NW-1015 did not cause EEG or interictal behavioral alterations at doses up to 75 mg/kg p.o. These data further confirm the broad-spectrum anticonvulsant activity and a good safety profile of NW-1015 even in a primate model of complex partial seizures and suggest that its affinity for sigma-1 receptors is behaviorally irrelevant.

Positive rolandic sharp waves in preterm infants with periventricular leukomalacia: their relation to background electroencephalographic abnormalities.

The aim of this study was to clarify the significance of positive rolandic sharp waves (PRS) in preterm infants with periventricular leukomalacia (PVL) and their relation to background electroencephalographic (EEG) abnormalities. We retrospectively evaluated EEG findings of 93 preterm infants; 31 infants in the PVL group and 62 in the control group. PVL was diagnosed on the basis of ultrasonographic findings. We evaluated the EEG within 3 weeks of life in this study. PRS were defined as sharp transients of positive polarity appearing in the rolandic regions with an amplitude of more than 100 microV, sharply differentiated from the background activities. The number of PRS per minute was calculated over each record. PRS were defined as present when their frequency was beyond 0.1 per minute. PRS were observed in 14 (45%) and disorganized patterns in 27 (87%) of 31 infants in the PVL group, but both were not recognized in any infants in the control group. PRS were always associated with disorganized patterns. In the first EEG, PRS were absent in 8 of 11 infants with more than two recordings, although at least one of acute or chronic stage EEG abnormalities were already present. PRS were observed in 9 of 10 infants with severe diplegia, in 5 of 11 infants with moderate diplegia and none in 10 infants with mild diplegia. The average age of the first appearance of PRS was 7.6 days. The average age of the first appearance of periventricular echodensity and cyst was 4.2 days and 21.1 days, respectively. In conclusion, PRS are related to severe deep white matter injury and could be an early marker of severe PVL. PRS appeared in combination with disorganized patterns and were considered to be incorporated into chronic-stage EEG abnormalities. Detailed evaluation of background EEG activities can be helpful in detecting PVL with a high sensitivity from the early neonatal period.

Neonatal EEG: a powerful tool in the assessment of brain damage in preterm infants.

Serial EEG recordings beginning immediately after birth are not only of great diagnostic and prognostic value but also useful to elucidate the timing and the mode of brain injuries in the preterm newborn. It is extremely useful to distinguish between acute stage and chronic stage EEG abnormalities. The former is characterized by findings of acute depression such as increased discontinuity, decreased faster frequency activities, and lowered amplitudes. The latter mainly includes dysmature patterns and disorganized patterns. The timing of brain insult can be assessed by considering EEG findings in relation to the time of birth. Different modes of brain injury are associated with different types of EEG abnormalities and different types of neurological outcome. Sudden strong brain insults are usually associated with findings of severe depression followed by disorganized pattern and later cerebral palsy, while persistent mild insults are usually associated with prolonged mild depression followed by dysmature pattern and later mental retardation. Routine serial EEG studies in preterm infants demonstrated that one fourth of cerebral palsies in these infants were of antenatal origin, two thirds of perinatal origin and postnatal injuries played the least role. Periventricular leucomalacia (PVL) manifesting itself on the ultrasound in the late neonatal period and suggesting postnatal origin was often found to be of antenatal origin with an EEG soon after birth. PVL without apparent causes was often associated with abnormal fetal heart rate patterns and early neonatal EEG abnormalities, and considered to have originated in the antepartum period.

Cyclosporin A acute encephalopathy and seizure syndrome in childhood: clinical features and risk of seizure recurrence.

Cyclosporin A is associated with an acute encephalopathy including seizures and alterations in mental status, herein referred to as cyclosporin A acute encephalopathy and seizure syndrome. The clinical history, electroencephalogram (EEG), and neuroimaging findings in 19 children with cyclosporin A acute encephalopathy and seizure syndrome over a 10-year period were reviewed in order to delineate clinical characteristics, imaging features, and to determine the risk of seizure recurrence in this population. All 19 had motor seizures associated with other features of cortical and subcortical dysfunction. The acute mean cyclosporin A level was 342 microg/L, but was within the "therapeutic" range in five cases. Brain imaging by computed tomography (CT) or magnetic resonance imaging (MRI) in the acute or subacute phase revealed lesions characteristic of cyclosporin A toxicity in 14 cases. Acute EEG abnormalities were present in all and included epileptiform discharges or focal slowing. Patients were followed for a median of 49 months (1-9 years). Follow-up imaging (n = 10) showed lesion resolution or improvement in the majority while EEG (n = 10) had normalized in only three. Seizures recurred in six patients and only in those with persistent EEG or imaging abnormalities. No patient had a second episode of cyclosporin A associated neurotoxicity or seizure. It appears that a significant risk of seizure recurrence exists following cyclosporin A acute encephalopathy and seizure syndrome and primarily in those children with persistent EEG or imaging abnormalities.

Acute intraoperative EEG changes during cartoid endarterectomy

Acute intraoperative EEG changes during cartoid endarterectomy

Cognitive and EEG recovery following bolus intravenous administration of anesthetic agents.

Bolus intravenous (IV) administration of commonly used IV anesthetic agents such as fentanyl and the fentanyl analogues, alfentanil, remifentanil, and sufentanil, etomidate and propofol, produced anesthesia in rats as measured by the loss of righting (LOR) with calculated ED150 doses of 0.06, 0.09, 0.037, 0.007, 2.51 and 6.12 mg/kg, respectively. Animals trained in an eight arm radial maze (RAM) were assessed for cognitive recovery, as measured by response efficiency (percentage of correct arm entries within 10 min), immediately, 15 min and 30 min following IV administration of the calculated ED150 dose of each of these agents, and the subsequent return of righting (ROR). Animals administered fentanyl or sufentanil were unable to successfully complete the maze throughout the testing periods. Animals receiving remifentanil showed cognitive recovery within the first testing interval (immediately following the return of righting), while animals receiving alfentanil, etomidate or propofol showed recovery at the 15-min testing interval following ROR. In a separate experiment, bolus IV administration of the ED150 dose of these agents was evaluated in an acute rat EEG model. Following ROR, return to baseline EEG levels occurred at 0.30, 2.88, 5.06, 16.25, 31.29 and 43.98 min for remifentanil, propofol, alfentanil, etomidate, fentanyl and sufentanil, respectively. These data show that the return to efficient cognitive functioning corresponds to the return to normal baseline EEG waveforms.

Acute, Subchronic and Withdrawal Sleep EEG Changes During Treatment With Paroxetine and Amitriptyline: A Double-Blind Randomized Trial in Major Depression

Paroxetine (30 mg), a selective serotonin (5-HT) reuptake inhibitor, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 40 inpatients aged 18-65 years who fulfilled Research Diagnostic Criteria for major depression. Patients were studied after a placebo drug washout period of 10 days and after an active 4-week treatment period. Sleep EEG recordings were performed before and at the end of the study as well as during acute treatment (first 2 days) and following withdrawal of active medication. Paroxetine shows an antidepressant effect similar to amitriptyline with a different side-effect profile typical of 5-HT reuptake inhibition. Paroxetine and amitriptyline decreased the amount of REM sleep, a well-known effect of classical antidepressants. Paroxetine also shared with other 5-HT reuptake inhibitors an alerting effect on sleep that was not shown to be detrimental on subjective sleep quality.

Acute vs. chronic EEG effects in maprotiline- and in clomipramine-treated depressive inpatients and the prediction of therapeutic outcome

Patients treated with the norepinephrine uptake inhibitor maprotiline showed an opposite tendency between acute and chronic effect of EEG. Whereas the acute effect indicated a decrease upon EEG vigilance, the chronic effect indicated an increase. Under clomipramine which acts upon different transmitter systems in a complex, up to now not fully understood way, acute and chronic EEG effects could not be differentiated.