Glossopharyngeal Nerve Block versus Lidocaine Spray to Improve Tolerance in Upper Gastrointestinal Endoscopy.

Aim of the Study. To compare the effect of glossopharyngeal nerve block with topical anesthesia on the tolerance of patients to upper gastrointestinal endoscopy. Methods. We performed a clinical trial in one hundred patients undergoing upper gastrointestinal endoscopy. Subjects were randomly assigned to one of the following two groups: (1) treatment with bilateral glossopharyngeal nerve block (GFNB) and intravenous midazolam or (2) treatment with topical anesthetic (TASS) and intravenous midazolam. We evaluated sedation, tolerance to the procedure, hemodynamic stability, and adverse symptoms. Results. We studied 46 men and 54 women, from 17 to 78 years of age. The procedure was reported without discomfort in 48 patients (88%) in the GFNB group and 32 (64%) in the TAAS group; 6 patients (12%) in GFNB group and 18 (36%) in TAAS group reported the procedure as little discomfort (χ (2) = 3.95, P = 0.04). There was no difference in frequency of nausea (4% in both groups) and retching, 4% versus 8% for GFNB and TASS group, respectively (P = 0.55). Conclusions. The use of glossopharyngeal nerve block provides greater comfort and tolerance to the patient undergoing upper gastrointestinal endoscopy. It also reduces the need for sedation.

Enhanced frontoparietal synchronized activation during the wake-sleep transition in patients with primary insomnia.

INTRODUCTION: Cognitive and brain hyperactivation have been associated with trouble falling asleep and sleep misperception in patients with primary insomnia (PI). Activation and synchronization/temporal coupling in frontal and frontoparietal regions involved in executive control and endogenous attention might be implicated in these symptoms. METHODS: Standard polysomnography (PSG) and electroencephalogram (EEG) were recorded in 10 unmedicated young patients (age 19-34 yr) with PI with no other sleep/medical condition, and in 10 matched control subjects. Absolute power, temporal coupling, and topographic source distribution (variable resolution electromagnetic tomography or VARETA) were obtained for all time spent in waking, Stage 1 and Stage 2 of the wake-sleep transition period (WSTP), and the first 3 consecutive min of N3. Subjective sleep quality and continuity were evaluated. RESULTS: In comparison with control subjects, patients with PI exhibited significantly higher frontal beta power and current density, and beta and gamma frontoparietal temporal coupling during waking and Stage 1. CONCLUSION: These findings suggest that frontal deactivation and disengagement of brain regions involved in executive control, attention, and self-awareness are impaired in patients with PI. The persistence of this activated and coherent network during the wake-sleep transition period (WSTP) may contribute to a better understanding of underlying mechanisms involved in difficulty in falling asleep, in sleep misperception, and in the lighter, poorer, and nonrefreshing sleep experienced by some patients with PI.

La actividad Alfa frontal en insomnes primarios con dificultad para iniciar el sueño / Frontal alpha activity in primary insomniacs with sleep onset difficulties

Difficulty in sleep initiation, with or without objective signs, is one of the most frequent complaints in primary insomniacs. The electroencephalographic (EEG) activity characteristic of waking (beta and alpha oscillations) is gradually replaced by the EEG signs of sleep (sleep spindles and theta/delta waves) during the sleep onset period (SOP) in normal subjects. The decrease in fast oscillations occurs at the first signs of stage 1, whereas theta and delta increase occurs later, indicating that waking promoting mechanisms are turned off before sleep-promoting mechanisms are fully started. It could be therefore hypothesized that difficulty in sleep initiation in insomniacs might be due to either a hyperactivation of waking promoting systems, a weakness of sleep promoting mechanisms or an imbalance between them. Quantitative EEG analysis has revealed higher beta during wakefulness, as well as during sleep and lower slow (delta) activity in insomniacs. The presence of alpha activity during cognitive information processing, especially of slow alpha activity in relation to attention, as well as in some pathologies associated to sleep disturbances, has suggested that alpha activity during sleep is a sign of activation; however, alpha activity during sleep has been less studied in insomniacs. Only broad bands have been considered in all of the aforementioned studies, and in almost all of them the analyses were restricted to central regions. It is therefore important to study the entire frequency spectrum of EEG activity in insomniacs. Sleep initiation does not occur simultaneously over the entire cortex but starts as a local process which gradually invades the rest of the cortex, in which the frontal lobes play a crucial role. Frontal and parietal regions are part of an important network involved in attention and conduction of thought. Thus, quantitative analysis of narrow EEG bands and their distribution in the cerebral cortex may contribute to a better understanding of neural mechanisms compromised in etiology of sleep initiation in primary insomnia. The main objective of the present investigation was, therefore, to analyze the spectral power of narrow EEG bands in the 19 derivations of the 10-20 International System during SOP in primary insomniacs with difficulty in sleep initiation. Given that one of the main complaints of insomniacs is the difficulty to initiate sleep and that hyperarousal is one of the factors proposed to be involved in the etiology of insomnia, EEG activity during SOP of the first night in the laboratory was analyzed to control activating effects of surrounding circumstances and isolate permanent EEG characteristics. Subjects were 19-34 years old, right-handed with primary sleep insomnia, which were thoroughly screened via structured psychiatric, medical and sleep interviews and scales. Subjects were younger and the age range was narrower than in other EEG frequency spectral content studies of primary insomniacs to avoid confounding effects of changes in sleep architecture or in EEG generated by development. All patients met the criteria for primary insomnia with sleep onset difficulty and impaired daytime function on three or more nights per week for at least six months and with no medical, psychiatric or neurological conditions; they were not medicated and had no other sleep disorders. Participants taking sleep medications or other drugs (urine test), respiratory or sleep disorders such as apnea and periodic limb movements (PSG) were excluded. The control group (n = 9) was matched for age and dexterity, but had no complaints of insomnia and reported their sleep as restorative and satisfactory. All participants underwent a single night of standard polysomnography (EEG, EOG and EMG) in the laboratory. In addition, the 19 electrode sites of the 10-20 International System referred to ipsilateral earlobes, oral-nasal airflow and anterior tibialis EMG were recorded. PSG was scored in 30 sec epochs, blind to the subject group according to Rechtschaffen and Kales criteria. EEG from SOP (lights out to consolidate sleep), defined as 3 consecutive minutes of delta sleep, was digitized at 1024 Hz with 12 bits resolution and filter settings of 0.03-70 Hz. EEG was segmented into two-sec non-overlapping epochs and inspected for artifacts. All artifact-free epochs were Fast Fourier Transformed and absolute (AP) and relative power (RP: AP in each Hz bin/total spectrum power × 100) was obtained for 1 Hz bins. AP and RP was log-transformed before statistical analysis, and was averaged over each derivation and sleep stage of SOP. Group differences were compared by means of Student's t tests and probability level was set at p<0.05. In contrast with healthy controls, insomniac patients exhibited higher alpha RP (7 and 8 Hz) over all frontal derivations during stage 2 of SOP and higher RP of isolated beta and gamma frequencies during wakefulness. PSG of both groups showed the <> with decreased total sleep time, decreased sleep efficiency index and REM sleep percentage compared to normal values for the 20-30 age decade; PSG variables were not significantly different between the two groups except for wakefulness percentage during SOP. Insomniacs did differ from controls in subjective estimation of sleep quality and continuity in spite of similar PSG. The absence of significant differences between insomniacs and controls in sleep EEG activity (delta, theta and sigma frequencies) suggests that sleep homeostatic function is preserved in insomniacs, which agrees with results obtained in other studies after partial sleep deprivation. The absence of a stronger promoting effect of insomnia in the insomniac group by the first recording night indicates that EEG characteristics found in this group cannot be attributed to external stimuli nor surrounding circumstances and rather suggests a more stable alteration; however, further studies of larger groups and other age spans are needed to confirm present results. The evidence mentioned above suggests an imbalance between waking and sleep promoting mechanisms in primary insomniacs with difficulty in sleep initiation and sleep perception. Attention depends not only on vigilance level, but also on frontal regions which, together with posterior association areas, conform an essential network for purposive endogenously guided attention. The presence in insomniacs of alpha activity in frontal regions, which is a sign of top-down control of attention, and its absence in posterior regions during stage 2 suggests the persistence of a certain level of endogenous attention during stage 2 of SOP, which contributes in turn to the subjective perception of sleep onset difficulties and bad sleep quality.

La dificultad para conciliar el sueño es uno de los síntomas más frecuentes del insomnio primario. La apreciación subjetiva de un periodo prolongado de latencia al sueño, aun en presencia de signos de sueño, puede deberse a la coexistencia de los mecanismos promotores de la vigilia y del sueño, y la lucha por el predominio de uno de ellos. La red de atención ejecutiva, conformada por las áreas de asociación frontales y parietales, cumple un papel de particular importancia en el control endógeno de la atención y en la regulación del alertamiento por parte de la corteza. Las frecuencias del EEG en el rango de actividad alfa lenta (7 y 8 Hz) participan en los procesos cognoscitivos activos de la vigilia, especialmente en la atención y la memoria, y son indicadoras del control corticofugo, o top-down, de estos procesos. Sin embargo, el análisis cuantitativo del EEG durante el proceso de conciliación del sueño en los insomnes se ha centrado fundamentalmente en la actividad delta, theta y beta, y únicamente en las regiones centrales (C3 y C4), de tal forma que el análisis de banda estrecha del EEG y su distribución en toda la corteza podría contribuir a una mejor comprensión de los mecanismos neurales comprometidos en la etiología del insomnio primario. El objetivo principal de esta investigación es, por lo tanto, analizar el espectro de frecuencias con resolución de 1 Hz en todas las derivaciones del Sistema Internacional 10-20 en insomnes primarios crónicos durante el periodo inicial del sueño (PIS) y comparar a estos últimos con un grupo control. Con el fin de aislar las características del EEG de los insomnes de causas circunstanciales, se analizará la primera noche de PSG igualando en ambos grupos el efecto activador que ejerce el medio circundante sobre el Sistema Nervioso Central, el estado psicológico y la arquitectura del sueño. Se estudiaron nueve pacientes insomnes primarios cuya queja principal era la dificultad para iniciar el sueño y nueve sujetos controles libres de problemas de sueño, diestros y entre 19-34 años de edad. Se realizó la PSG durante la primera noche en el laboratorio siguiendo los procedimientos estándar y adicionalmente se registraron las 19 derivaciones del Sistema Internacional 10-20. Se obtuvieron los espectros de potencia del EEG de todas las derivaciones con resolución de 1 Hz del PIS (tiempo comprendido entre las buenas noches y el sueño consolidado: 3 minutos consecutivos de sueño delta). Los insomnes tuvieron mayor actividad alfa lenta (7 y 8 Hz) en las regiones frontales durante la etapa 2 del PIS y de algunas frecuencias rápidas (beta y gamma) en la vigilia; subestimaron la calidad de sueño; y mostraron el mismo efecto de primera noche que los controles. La ausencia de diferencias entre los dos grupos en el EEG típico del sueño (delta, theta y sigma) sugiere que los insomnes tienen preservada la función homeostásica del sueño. La ausencia de diferencias en la PSG de los insomnes y controles indica que la dificultad para conciliar el sueño del grupo de insomnes no se encuentra en estímulos externos ambientales ni en condiciones circunstanciales y sugiere que se debe a alteraciones más permanentes. El conjunto de estas evidencias apunta hacia una alteración de la vigilia en concordancia con las hipótesis que proponen que el insomnio tiene un componente primordial de activación fisiológica y psicológica. La atención depende, además del nivel de vigilancia, de las regiones frontales que, junto con las áreas posteriores de asociación, conforman una red esencial para la atención dirigida endogenamente. La presencia de ritmo alfa en las regiones frontales y su ausencia en las áreas posteriores durante la etapa 2 en los insomnes podría reflejar la permanencia de cierto nivel de atención endógena durante la etapa 2 del PIS y podría constituir un mecanismo alterado del sistema frontal subyacente a la dificultad para iniciar el sueño.