Reduced pain and analgesic use after acoustic binaural beats therapy in chronic pain - A double-blind randomized control cross-over trial.

BACKGROUND: Binaural Beats (BB) consist of two artificial acoustic stimuli with different frequency, presented simultaneously but independently to each ear. The human brain perceives and synchronizes to this frequency difference (entrainment). Aim of this study was to test the hypothesis that brain entrainment to a lower function rhythm, with BB application, can decrease pain perception and analgesic medication use, in chronic pain patients. METHODS: In a double blind, randomized, cross-over trial, BB at 5Hz (theta rhythm) were applied for 30 minutes, under simultaneous electroencephalogram recordings, followed by liberal, on demand use by chronic pain patients for a week, compared to sham stimulation (SS). Pain as the main outcome (numeric scale, NRS), stress (STAI) and medication usage (defined daily doses, DDD) were assessed at baseline, 30 minutes and week's end. RESULTS: Perceived pain (NRS) was significantly reduced in BB intervention (5.6±2.3 to 3.4±2.6, p<0.001), compared to SS (5.2±2.1 to 4.8±2.3, p=0.78), during the first 30-minute phase, as well as at the week's end (to 3.9±2.5 compared to 5.5±2.6 respectively, p<0.001). The mean EEG theta power at 5Hz was significantly increased only during BB application. Stress was significantly reduced at 30 minutes in both interventions but remained reduced only in the BB group at the week's end. Analgesic medication consumption (DDD, g) during the week was significantly less in the BB intervention (3.9±3.7 vs. 4.6±4.1, p<0.05), while reporting equal to SS mean levels of pain. CONCLUSIONS: Acoustic BB reduced pain intensity, stress and analgesic use, compared to SS, in chronic pain patients. SIGNIFICANCE: This study provides evidence that theta rhythm binaural beats can alleviate pain intensity, both after a brief 30 minute and a longer one week on-demand intervention. The subsequent significant reduction in analgesic medication consumption in chronic pain patients' daily living could offer a valuable tool, augmenting the effect of existing pain therapies.

Association of Urinary Sodium Excretion with Vascular Damage: A Local Kidney Effect, Rather Than a Marker of Generalized Vascular Impairment.

Evidence suggests that increased salt consumption induces blood pressure- (BP) mediated organ damage, yet it remains unclear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. We studied 197 newly diagnosed and never-treated individuals with hypertension, intermediate hypertensive phenotypes, and normal BP, classified by use of 24-hour ambulatory BP monitoring. Sodium excretion and microalbuminuria were estimated in 24-hour urine samples, dermal capillary density was estimated from capillaroscopy, and arterial stiffness was estimated with pulse wave velocity (PWV) and augmentation index (AIx). Sodium excretion correlated with microalbuminuria (p<0.001) and 24-hour and day- and nighttime systolic BP, but not with office blood pressure, arterial stiffness, or capillary density. In the multivariate analysis, the association with microalbuminuria was maintained (p=0.007). In a population free from the long-standing effects of hypertension, increased salt intake appears to be associated with early signs of vascular kidney damage, rather than a diffuse micro- and macrovascular impairment.

Association between retinal vessel caliber and arterial stiffness in a population comprised of normotensive to early-stage hypertensive individuals.

BACKGROUND: Although impairment of the micro- and macrocirculation is considered inherent to sustained hypertension, there is a substantial lack of studies investigating whether an association exists between micro- and macrovascular damage, especially in early-stage hypertension. METHODS: We studied a meticulously selected population, free of diabetes and cardiovascular disease, of 223 individuals: 137 never-treated, newly diagnosed patients with recent onset of hypertension and 86 normotensive individuals. Nonmydriatic retinal photography was used to assess retinal microvascular diameters, including central retinal arteriolar (CRAE) and venular equivalent and arteriovenous ratio (AVR). Arterial stiffness was evaluated by measurement of pulse wave velocity (PWV) and aortic augmentation index (AIx). RESULTS: Compared with normotensive subjects, hypertensive patients exhibited significantly increased PWV (8.1 vs. 7.1 m/sec; P < 0.001) and AIx (23.86% vs. 18.8%; P = 0.01) and decreased CRAE (86.47 vs. 91.44 µm; P = 0.001) and AVR (0.74 vs. 0.78; P = 0.007). A significant inverse association was demonstrated between PWV and CRAE (r = -0.205; P = 0.002), which remained significant after multivariable analysis. Likewise, CRAE (P = 0.04) and AVR (P = 0.02) were independent predictors of AIx. CONCLUSIONS: This study shows for the first time an association between quantitatively assessed retinal abnormalities and increased arterial stiffness in a sample of early-stage hypertensive and normotensive individuals, suggesting that micro- and macrocirculation impairment in hypertension is a dynamic, mutual, interdependent process present from its very early stages. Given the predictive value of both retinal arteriolar narrowing and arterial stiffness in terms of cardiovascular mortality and morbidity, identification of combined micro- and macrovascular damage might be helpful in cardiovascular risk stratification of hypertensive patients.

Divergent retinal vascular abnormalities in normotensive persons and patients with never-treated, masked, white coat hypertension.

BACKGROUND: Hypertensive patients with retinal arteriolar abnormalities are at increased risk for cardiovascular events. However, the extent of retinal microvascular changes in naïve, never-treated patients with hypertension of short duration has not been established. In addition to this, the lack of relevant data about other phenotypes of hypertension (masked and white-coat hypertension) determined by ambulatory blood-pressure measurement (ABPM) is notable, despite their relationship to increased cardiovascular risk mediated by underlying target-organ and vascular damage. METHODS: We conducted a study in which nonmydriatic retinal photography was used to assess central retinal artery equivalent (CRAE) and central retinal vein equivalent (CRVE) diameters and the retinal arteriovenus ratio (AVR) in a group of 103 individuals with never-treated hypertension of recent (< 1 year) appearance, 28 individuals with masked and 20 with white-coat hypertension, and 50 normotensive individuals, as appropriately classified by ABPM. RESULTS: Patients with sustained and masked hypertension had narrower values of CRAE than did normotensive individuals (86.7±10.1 and 87.6±9.2 vs. 94.8±10.6, P < 0.001 and P = 0.02, respectively). The AVR was lower in patients with sustained hypertension (0.736±0.102), masked hypertension (0.716±0.123), and white-coat hypertension (0.739±0.127) than in normotensive subjects (0.820±0.095), P < 0.001, P < 0.001, and P = 0.03, respectively. Both AVR and CRAE were negatively associated with mean systolic and diastolic daytime, nighttime, and 24-hour blood pressures, even after adjustment for other factors. CONCLUSIONS: Subtle retinal microvascular signs of pathology are observed in hypertensive patients at early stages of hypertension and in patients with both masked and white coat hypertension. These changes may be indicative or may mediate the differences in cardiovascular mortality in persons with masked and white-coat hypertension, and relevant information about this can be easily accessed with retinal photography.