Relationship of age to power spectrum analysis of EEG during sleep.

We describe a method of power spectrum analysis of all-night sleep EEGs in 20 normal subjects aged 18-43 years. The analysis calculates the energy of the whole sleep period, the various frequency bands, and selected sleep stages automatically. The numerical value of the energies was directly comparable between subjects, presented in numbers (microV2s) and displayed as a color density spectral array with fixed power values for each color. A significant relationship between age and power spectra was found, in that total energy/minute was higher in younger subjects than in older. The energy in delta sleep/minute also showed an inverse relationship with age.     

不同异丙酚诱导麻醉对颅内假性动脉瘤介入治疗气管插管 期心血管反应的影响

目的 观察异丙酚不同输注法行麻醉诱导对颅内假性动脉瘤介入治疗气管插管期心血管反应的影响。方法 选择2010年6月至2018年5月血管内介入治疗的颅内假性动脉瘤60例,根据麻醉诱导方 法分为三组:单次静脉推注组（A组）、血浆靶控组（B组）和效应室靶控组（C组）,每组20例。麻醉诱导方法:A组采用异丙酚2 mg/kg单次静脉推注;B组设定异丙酚血浆靶浓度为4 μg/ml;C组设定异 丙酚效应室靶浓度4 μg/ml。三组均同时采用瑞芬太尼4 ng/ml血浆靶浓度靶控输注诱导,待意识消失后静注罗库溴铵0.6 mg/kg,脑电双频谱指数在40~60并维持5s时行气管插管。记录进入手术室（T0） 、喉镜暴露声门（T1）、气管导管过声门（T2）、气管导管进入气管后1 min（T3）、2 min（T4）、3 min（T5）平均动脉压（MAP）、心率（HR）;并记录气管插管期不良反应及纠正次数。结果 与T0比 较,三组T1~T3 MAP均明显降低（P<0.05）,三组T1~T5 HR均明显减慢（P<0.05）;与B组比较,A组与C组T1 MAP明显降低（P<0.05）、HR明显减慢（P<0.05）。B组低血压、心动过缓等发生率和纠正次数 明显少于A组（P<0.05）,而且B组心动过缓发生率和纠正次数少于C组（P<0.05）。C组纠正次数明显少于A组（P<0.05）。结论 4 μg/ml异丙酚血浆药物浓度作为目标靶控输注浓度更适合颅内假性动脉 瘤介入治疗的麻醉诱导,低血压和心动过缓不良反应等发生率更低。     

Relation of frequency-analyzed EEG to monitoring behavior.

Two experiments examined the relation of prestimulus electroencephalographic (EEG) frequency to choice RT. Based on previous studies, initial analysis was concerned with 3--7 c/sec activity. In well-rested subjects (Exp. 1), trial-by-trial analyses indicated large variations in prestimulus EEG activity which were unrelated to RT and large variations in RT which were unrelated to prestimulus EEG. In Exp. 2, subjects were deprived of sleep for 1 night and within-subject comparisons made between RT and EEG activity immediately preceding the 10 shortest and 10 longest RT trials, and 10 trials where the subject failed to respond. Significant univariate correlations were found, largely between RT and the frequencies in the 15--20 c/sec range of EEG activity and not in the 3--7 c/sec activity. A multiple regression analysis using up to 5 EEG frequencies indicated significant correlations of prestimulus EEG activity with RT; but with considerable subject-to-subject variability in the EEG frequencies contributing to the multiple R. The overall results suggest that there can be considerable variation in EEG activity which is unrelated to performance, except when the EEG fluctuations are secondary to changes in arousal which, in turn, effect performance.     

Specific response of the epileptic focus to anesthesia with propofol

Twenty patients suffering from medically intractable epilepsy were submitted to invasive presurgical evaluation using subdural strip electrodes for chronic electrocorticographic (ECoG) recordings. A short anesthesia of 12–15 min was induced to ensure painless percutaneous removal of the subdural electrode strips. Anesthesia was provided by two consecutive intravenous injections of propofol (50 and 70 mg or 70 and 140 mg) preceded by fentanyl (0.1–0.15 mg) in 12 patients. In order to test whether the epileptic focus showed a specific response following application of propofol, the first 12 min of ECoG recordings, prior to removal of the subdural strip electrodes, were visually analyzed. Specific patterns of response confined to the epileptic focus (foci) were observed in 18 of 20 patients following application of at least one of the two doses of propofol. Patterns observed in the epileptogenic area consisted of (a) a loss or marked reduction of activity induced by propofol (n = 16), (b) a maximum of suppression of brain activity (n = 12), (c) suppression of spontaneous interictal activity (n = 10), (d) induction of epileptiform activity (n = 5), and (e) induction of a habitual seizure (n = 1). In summary, ECoG recordings during anesthesia with propofol provide complementary information about the epileptic focus in the process of presurgical evaluation of epileptics.     

Manipulations during forced wakefulness have differential impact on sleep architecture, EEG power spectrum, and Fos induction

We propose a hypothesis suggesting that the most prominent experiences occurring during wakefulness activate specific clusters of neurons related to such experiences. These neurons could possibly then evoke the release of various types of sleep-inducing molecules, thereby causing different patterns of sleep architecture. In this study, we therefore sought to determine whether manipulations of behavior during wakefulness, such as forced wakefulness induced by gentle handling, forced wakefulness associated with a stressful condition such as immobilization, or forced wakefulness associated with excess intake of palatable food, could result in a variation of Fos immunoreactivity in selective brain structures and could also result in different sleep and EEG power density patterns. The results showed that the sleep-wake cycle of rats after all the experimental manipulations was different not only with respect to the control group but also among themselves. Additionally, power spectrum analysis showed an increase of 0.25–4.0 Hz in all experimental manipulations, whereas the 4.25–8.0 Hz increase occurred only in the situation of forced wakefulness plus stress. The Fos induction showed activation of cell clusters in cortical areas and telencephalic centers, in several hypothalamic nuclei, in monoaminergic cell groups, and in brain stem nuclei. The density of Fos-immunoreactive neurons varied in relation to the different paradigms of forced wakefulness. These results suggest that activation of cell clusters in the brain are related to the type of manipulation imposed on the rat during wakefulness and that such variation in cell activation prior to sleep may be associated with sleep architecture and EEG power.     

EEG findings in heroin addicts during induction and maintenance on methadone.

This study investigated changes in the EEG of addicts initially on heroin as they progressed through the induction and maintenance phases of a methadone program. Spectral analysis of bipolar recordings revealed significant consistent differences only in the eyes-closed resting state. Patients under the influence of heroin showed large sharp peaks at 9-10 c/sec, particularly in the parieto-occipital recording. Methadone induction led either to marked reduction of this peak and widening of alpha band activity or to an increase in frequency of the alpha peak to 12 c/sec. After several months of methadone the alpha peak was still absent unless heroin abuse was present, a theta peak was present in three of four patients, and the alpha bandwidth remained broad. Changes in the theta band were more difficult to interpret.     

Presence of 14Hz spindle oscillations in the human EEG during deep anesthesia.

OBJECTIVE: To report on presence of human EEG spindle oscillations on the cortical level within flat periods of the burst-suppression pattern during propofol-induced anesthesia; to search for corresponding oscillations and possible functional connections. METHODS: Artefact-free epochs of spindle activation were selected from the electroencephalograms of opiate-dependent patients undergoing rapid opiate detoxification. Power spectral analysis and source localization using low-resolution-brain-electromagnetic-tomography (LORETA(Key)) were performed. RESULTS: Sinusoidal rhythms with waxing and waning amplitudes appeared after propofol-induced narcosis but no direct correlations could be determined between individual dosage and characteristic spindle attributes. The power maximum stood midline over the cortical areas, especially around C(z). We calculated a peak frequency of 14(+/-1.2) Hz. Motor fields, particularly in the frontal, parietal, and various cingulate areas, were found to be the primary sources of spindle oscillations in the cortex. CONCLUSIONS: The frequent occurrence of these localized spindle sources demonstrates the preference for motor fields. Spindle oscillations observed during propofol-induced narcosis were similar in frequency and shape to those observed in natural sleep. SIGNIFICANCE: The results lend support to models that postulate a close link between the motor system and the organization of behavior. In addition, spindle rhythms under propofol bore some resemblance to spindle types which occur during sleep.     

咪达唑仑和丙泊酚诱导麻醉对继发性癫痫 术中皮层脑电图的影响

目的 探讨咪达唑仑与丙泊酚诱导麻醉对继发性癫痫术中皮层脑电图（ECoG）的影响。方法 2013年6月至2015年9月收治非功能区占位性病变继发性癫痫180例,根据诱导麻醉方法分为咪达唑仑组（60例;0.2 mg/kg）、丙泊酚组（60例;2 mg/kg）和咪达唑仑+丙泊酚组[60例;咪达唑仑（0.05 mg/kg）+丙泊酚（1 mg/kg）]。打开硬膜后行第一次ECoG监护,病灶切除后行第二次ECoG监护。结果 从麻醉诱导至第一次监护的时间为（110.3±15.9）min。第一次ECoG监护显示,咪达唑仑组暴发抑制（BS）波形发生率（68.3%,41/60）明显高于丙泊酚组（25.0%,15/60;PP<0.05）,后两组之间无统计学差异（>P>0.05）。麻醉诱导至第一次监护时间≤120 min时,咪达唑仑组BS发生率均明显高于丙泊酚组（P<0.05）和咪达唑仑+丙泊酚组（>P<0.05）;>120 min时,3组BS发生率无统计学差异（P>0.05）。第二次ECoG监护显示,咪达唑仑组、丙泊酚组和咪达唑仑+丙泊酚组BS发生率分别为5.0%（3/60）、3.3%（2/60）和3.3%（2/30）,3组之间无统计学差异（P>0.05）。结论 继发性癫痫患者术前镇静类诱导麻醉用药宜选用小剂量咪达唑仑联合丙泊酚。     

A switch from propofol to etomidate during an ECT course increases EEG and motor seizure duration

INTRODUCTION: Of 58 patients treated at our electroconvulsive therapy (ECT) unit early in the year 2000, 12 patients under propofol did not achieve a seizure duration of >30 s [electroencephalogram (EEG)] with a maximum stimulation charge of 504.0 mC (100%). METHOD: A switch from propofol to etomidate was therefore undertaken in these patients at the next treatment to achieve longer seizure duration. RESULTS: In 11 of the 12 patients, a remarkable increase in seizure duration was recorded after the change of anesthetic. The mean seizure duration increased from 18.6 to 43.4 s and remained at that level for the following ECT session. The increase was highly significant (t11 = 3.772, p < 0.001). The mean motor seizure also changed from 11.6 to 27.5 s (t11 = 5.560, p < 0.003) and remained there for the next treatment. DISCUSSION: Our data show that the switch more than doubles EEG seizure duration and suggest that etomidate can be used instead of methohexital as an alternative in patients with short seizure duration. It is also a potential option to avoid the pain frequently associated with the injection of propofol.     

Selective loss of Purkinje and granule cell responsiveness to N-methyl-D-aspartate in rat cerebellum during development

Depolarizing responses of Purkinje and granule cells to excitatory amino acid receptor agonists were recorded from rat cerebellar slices at various stages of postnatal maturation using a gap technique. No major developmental changes in relative potency or efficacy of kainate and quisqualate were observed. However, Purkinje and granule neurones both became less responsive to N-methyl-D-aspartate (NMDA) with age, most dramatically so between 14 and 21 days. This transient chemosensitivity to NMDA may reflect a special role of the NMDA receptor system in cerebellar development.     

EEG correlates in the spectrum of cognitive decline.

OBJECTIVE: To investigate relations between EEG measures and performance on tests of global cognition, memory, language and executive functioning. METHODS: Twenty-two controls, 18 patients with mild cognitive impairment (MCI) and 16 with probable Alzheimer's disease (AD) underwent neuropsychological and EEG investigations. We used the following EEG measures: theta relative power during eyes closed, alpha reactivity during memory activation (i.e. the percentual decrease in alpha power as compared to eyes closed) and alpha coherence during eyes closed and memory activation. RESULTS: Theta relative power was increased in AD patients as compared with controls (p<0.001) and MCI patients (p<0.01) and related to decreased performance in all cognitive domains. Alpha reactivity was decreased in AD patients as compared with controls (p<0.005) and related to decreased performance on tests of global cognition, memory and executive functioning. Alpha coherence did not differ between groups and was unrelated to cognition. CONCLUSIONS: EEG power measures were associated with decreased performance on tests of global cognition, memory, language and executive functioning, while coherence measures were not. SIGNIFICANCE: The EEG yielded several power measures related to cognitive functions. These EEG power measures might prove useful in prospective studies aimed at predicting longitudinal cognitive decline and dementia.     

Connectivity changes underlying spectral EEG changes during propofol-induced loss of consciousness

The mechanisms underlying anesthesia-induced loss of consciousness remain a matter of debate. Recent electrophysiological reports suggest that while initial propofol infusion provokes an increase in fast rhythms (from beta to gamma range), slow activity (from delta to alpha range) rises selectively during loss of consciousness. Dynamic causal modeling was used to investigate the neural mechanisms mediating these changes in spectral power in humans. We analyzed source-reconstructed data from frontal and parietal cortices during normal wakefulness, propofol-induced mild sedation, and loss of consciousness. Bayesian model selection revealed that the best model for explaining spectral changes across the three states involved changes in corticothalamic interactions. Compared with wakefulness, mild sedation was accounted for by an increase in thalamic excitability, which did not further increase during loss of consciousness. In contrast, loss of consciousness per se was accompanied by a decrease in backward corticocortical connectivity from frontal to parietal cortices, while thalamocortical connectivity remained unchanged. These results emphasize the importance of recurrent corticocortical communication in the maintenance of consciousness and suggest a direct effect of propofol on cortical dynamics.     

Neonatal propofol anesthesia modifies activity-dependent processes and induces transient hyperlocomotor response to d-amphetamine during adolescence in rats

This study examined the influence of propofol anesthesia on the expression of activity-regulated molecules (BDNF and c-Fos) and synaptic plasticity markers (synaptophysin, GAP-43, drebrin) in the frontal cortex and thalamus of 7-day-old (P7) rats. Although these brain regions are the main targets of anesthetic action, they are contained in the cortico–striato–thalamo–cortical feedback loops, involved in naturally occurring and drug-induced psychoses. Therefore, functional integrity of these loops was examined in adolescent and adult rats through d-amphetamine-induced hyperactivity. Propofol treatment (25 mg/kg) decreased exon-specific and total BDNF mRNA expression in the frontal cortex and thalamus, in a time-dependent manner. BDNF protein level was increased in the frontal cortex and decreased in the thalamus, which was accompanied by the change of phospho-TrkB expression. Similarly to BDNF, the expression of c-Fos was decreased in the frontal cortex while it was changed only at the protein level in the thalamus. Synaptic plasticity markers changed in a time- and region-specific manner, indicating increased synaptogenesis in the frontal cortex and synapse elimination in the thalamus in P7 rats after the propofol anesthesia exposure. These early molecular changes were followed by time-related, increased motor reaction to d-amphetamine in adolescent, but not in adult rats. Our study revealed that exposure of immature brain to propofol anesthesia during the critical phase of development provoked immediate changes in activity-dependent processes and synaptic adjustment, influencing brain capacity to integrate later developmental events and resulting in temporary altered response to acute psychotropic stimulation during adolescence.     

Correction of muscle artefacts in the EEG power spectrum.

OBJECTIVE: To provide a method for correcting muscle artefacts in fast band power at EEG derivations. METHODS: We define an indicator of surface EMG as power in the band 51.0-69.0 Hz ('muscle power'). This indicator is used to approximately eliminate the contribution of muscle activity on fast band power via a regression model. RESULTS: (1) Patients show a larger proportion of muscle activity in fast band power. (2) There is a clear topographic pattern, frontal-temporal derivations being most susceptible to EMG artefacts. (3) The contribution of surface EMG can be drastically reduced by the proposed correction method. (4) Without correction, results for fast bands can be biased when e.g. comparing control and patient groups and the proposed correction method by and large eliminates this bias. CONCLUSIONS: It is advisable to correct the quantitative EEG reflecting fast activity for the extent of EMG artefacts. SIGNIFICANCE: To render the quantitative EEG more valid as an indicator of cerebral activity.     

α2-去甲基肾上腺素能受体对异丙酚麻醉下大鼠SEP的调节

目的探讨大鼠异丙酚麻醉中α2-去甲基肾上腺素能(NA)受体调节剂对皮层躯体感觉诱发电位(SEP) N20波的影响.方法将SD雄性大鼠30只随机分为3组.单纯异丙酚A组:微量泵以异丙酚10 mg/kg/h、60mg/kg/h的速度依次各静注45 min,停止静注异丙酚直至动物清醒.B组和C组在输注异丙酚的同时腹腔内分别注射可乐定和育亨宾各0.5 mg/kg.分别监测麻醉前、中及苏醒期的皮层SEP N20波的潜伏期和波幅.结果与基础值相比,3组药物对SEP N20波潜伏期均无显著影响;A组对SEP N20波的波幅无影响, B组降低SEP N20波的波幅, C组则增加了SEP N20波的波幅.结论异丙酚麻醉下α2-NA受体激动剂和抑制剂所引起SEP N20波波幅变化可能与镇痛机制有关.