Evoked Pain Analgesia in Chronic Pelvic Pain Patients using Respiratory-gated Auricular Vagal Afferent Nerve Stimulation

april 3, 2014 av Marius

I medisinsk sammenheng benyttes ofte elektrisk stimuli i øret for å styrke vagusnerven gjennom dens forbindelse til huden i øret. I denne studien viser de at vagus nerven stimuleres best om man synkroniserer stimulien med utpust. Denne kobler altså medisinsk stimuli med pustens stimuli. Men de har ingen oppmerksomhet på mulighetene ved å senke pustefrekvens samtidig.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376238/

Chronic pain disorders such as CPP are in great need of effective, non-pharmacological options for treatment. RAVANS (Respiratory-gated Auricular Vagal Afferent Nerve Stimulation) produced promising anti-nociceptive effects for QST outcomes reflective of the noted hyperalgesia and central sensitization in this patient population. Future studies should evaluate longer-term application of RAVANS to examine its effects on both QST outcomes and clinical pain.

The analgesic mechanisms of VNS have not been fully elucidated, but are likely mediated by afferent (not efferent) input to supraspinal brain regions [16]. Vagal afference is relayed to the nucleus tractus solitarious (NTS) in the medullary brainstem. Importantly, the NTS also receives somatosensory afference via the auricular branch of the vagus (ABV) nerve from specific portions of the auricle [17]. ABV afference is transmitted to both the NTS [17] and the spinal trigeminal nucleus (SpV) [18], by neurons located in the superior (jugular) ganglion of the vagus nerve. Respiration can modulate NTS activity directly (the lungs are innervated by the vagus nerve) and indirectly. In regard to the latter, inspiration increases venous return to the thorax, which increases arterial pressure, and hence vagal (and glossopharyngeal n.) afference to the NTS via aortic and carotid baroreceptors, respectively [19]. The NTS then inhibits efferent vagal outflow to the heart [20, 21], leading to a transient inspiratory tachycardia with every breath. This feedback loop is termed “respiratory sinus arrhythmia” [22]. Hence, the dorsal medullary vagal system operates in tune with respiration, and we propose that supplying vagal afferent stimulation gated to the exhalation phase of respiration (i.e. when thoracic baroreceptor afference does not enter the NTS), will optimize t-VNS therapy (see Figure 1 for schematic). Furthermore, such intermittent, irregular stimulation (i.e., varying with respiration) will also mitigate classical neuronal adaptation/accomodation, which can occur with continuous stimulation of NTS neurons [23].

Autonomic system modification in zen practitioners

april 3, 2014 av Marius

Nevner mye om hvordan pustefrekvens påvirker HRV og andre faktorer. Og spesielt hvordan dette endrer den normale pusten på lang sikt.

http://www.ncbi.nlm.nih.gov/pubmed/24469560

http://www.indianjmedsci.org/article.asp?issn=0019-5359;year=2013;volume=67;issue=7;spage=161;epage=167;aulast=Fiorentini

Background: Meditation in its various forms is a traditional exercise with a potential benefit on well-being and health. On a psychosomatic level these exercises seem to improve the salutogenetic potential in man.Especially the cardiorespiratory interaction seems to play an important role since most meditation techniques make use of special low frequency breathing patterns regardless of whether they result from a deliberate guidance of breathing or other mechanisms, for example, the recitation of specific verse. During the different exercises of Zen meditation the depth and the duration of each respiratory cycle is determined only by the process of breathing. Respiratory manoeuvres during Zazen meditation may produce HR variability changes similar to those produces during biofeedback.Recognition that the respiratory sinus arrhythmia (RSA) was mediated by efferent vagal activity acting on the sinus node led investigators to attempt to quantify the fluctuations in R-R intervals that were related to breathing. Materials and Methods: Nine Zen practitioners with five years of experience took part in the study. Autonomic nervous system function was evaluated by heart rate variability (HRV) analysis during 24-hours ECG recording during zen meditation and at rest. Results: The data of this small observational study confirm that ZaZen breathing falls within the range of low frequency HR spectral bands. Our data suggest that the modification of HR spectral power remained also in normal day when the subject have a normal breathing. Conclusion: We suggest that the changes in the breathing rate might modify the chemoreflex and the continuous practice in slow breathing can reduce chemoreflex. This change in the automonic control of respiration can be permanent with a resetting of endogenous circulatory rhythms.

Figure 1: Power spectrum analysis of heart rate variability during zen meditation

Figure 2: Power spectrum analysis of heart rate variability to rest

In conclusion, repeated training to slow down breathing reduces the spontaneous breathing rate with long term effects on the cardiovascular control mechanisms. Indeed, when respiration slows to about 6 cycles/min, as in Zen practitioners and in the frequency range of the spontaneous LF oscillation, the cardiovascular fluctuations become maximal. The changes in the breathing rate might modify the chemoreflex and the continuous practice in slow breathing can reduce chemoreflex. This change in the autonomic control of respiration can be permanent with a resetting of endogenous circulatory rhythms.

Relationship between dysfunctional breathing patterns and ability to achieve target heart rate variability with features of «coherence» during biofeedback.

april 3, 2014 av Marius

Nevner hvordan en topp-pust relateres til lav HRV og problemer i hjerte/kar systemet.

http://www.ncbi.nlm.nih.gov/pubmed/22164811

Abstract

BACKGROUND:

Heart rate variability (HRV) biofeedback is a self-regulation strategy used to improve conditions including asthma, stress, hypertension, and chronic obstructive pulmonary disease. Respiratory muscle function affects hemodynamic influences on respiratory sinus arrhythmia (RSA), and HRV and HRV-biofeedback protocols often include slow abdominal breathing to achieve physiologically optimal patterns of HRV with power spectral distribution concentrated around the 0.1-Hz frequency and large amplitude. It is likely that optimal balanced breathing patterns and ability to entrain heart rhythms to breathing reflect physiological efficiency and resilience and that individuals with dysfunctional breathing patterns may have difficulty voluntarily modulating HRV and RSA. The relationship between breathing movement patterns and HRV, however, has not been investigated. This study examines how individuals’ habitual breathing patterns correspond with their ability to optimize HRV and RSA.

METHOD:

Breathing pattern was assessed using the Manual Assessment of Respiratory Motion (MARM) and the Hi Lo manual palpation techniques in 83 people with possible dysfunctional breathing before they attempted HRV biofeedback. Mean respiratory rate was also assessed. Subsequently, participants applied a brief 5-minute biofeedback protocol, involving breathing and positive emotional focus, to achieve HRV patterns proposed to reflect physiological «coherence» and entrainment of heart rhythm oscillations to other oscillating body systems.

RESULTS:

Thoracic-dominant breathing was associated with decreased coherence of HRV (r = -.463, P = .0001). Individuals with paradoxical breathing had the lowest HRV coherence (t(8) = 10.7, P = .001), and the negative relationship between coherence of HRV and extent of thoracic breathing was strongest in this group (r = -.768, P = .03).

CONCLUSION:

Dysfunctional breathing patterns are associated with decreased ability to achieve HRV patterns that reflect cardiorespiratory efficiency and autonomic nervous system balance. This suggests that dysfunctional breathing patterns are not only biomechanically inefficient but also reflect decreased physiological resilience. Breathing assessment using simple manual techniques such as the MARM and Hi Lo may be useful in HRV biofeedback to identify if poor responders require more emphasis on correction of dysfunctional breathing.

Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

april 1, 2014 av Marius

Nevner hvordan 6 pust i minuttet øker HRV og vagus nervens effekt på hjertet. Nevner også hvordan CO2 synker ved 15 pust i minuttet og holdes normalt ved 6 pust i minuttet. De med hjerteproblemer har mye større reaksjon på CO2 enn andre, og generelt lavere nivå.

http://hyper.ahajournals.org/content/46/4/714.full

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO₂ (CO₂-et) were monitored in 20 subjects with essential hypertension (56.4±1.9 years) and in 26 controls (52.3±1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and “alpha angle” method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7±3.7 to 141.1±4 mm Hg, P<0.05; and from 82.7±3 to 77.8±3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8±3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and controls (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO₂ and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

However, breathing at 6 breaths/min significantly increased the baroreflex sensitivity in hypertensive (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and control subjects (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001;Figure 2).

Hypertensive subjects showed a significantly higher resting respiratory rate (14.55±0.82 versus 11.76±1.00; P<0.05) and a significantly lower CO₂-et values compared with control subjects (Figure 3). During controlled breathing at 6/min, there were no significant changes in CO₂-et and in Vm. The lack of change in Vm, despite lower breathing rate, was attributable to a significant increase in Vt in hypertensives and controls. Controlled breathing at 15/min induced a marked decrease in CO₂-et, particularly in hypertensive subjects, and a marked relative increase in Vm and Vt (Figure 3).

We found that paced breathing, and particularly slow breathing at 6 cycle/min, reduces blood pressure in hypertensive patients. The reduction in blood pressure during slow breathing is associated with an increase in the vagal arm of baroreflex sensitivity, indicating a change in autonomic balance, related to an absolute or relative reduction in sympathetic activity.

This demonstrated that slow breathing is indeed capable of inducing a modification in respiratory and cardiovascular control, and that appropriate training could induce a long-term effect. In subjects with chronic congestive heart failure, a condition known to induce sympathetic and chemoreflex activation, slow breathing induced a reduction in chemoreflexes and an increase in baroreflex.^10,25 We have also shown that in these patients, 1-month training in slow breathing could induce prolonged benefits, even in terms of exercise capacity.²⁵

Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure

april 1, 2014 av Marius

Nevner at 6 pust i minuttet gir beste respons på HRV og vagusnerven. I tillegg til å dempe blodtrykk markant. Studien ga disse resultatene med en bare 4 minutters pustesession.

http://circ.ahajournals.org/content/105/2/143.full

Background— It is well established that a depressed baroreflex sensitivity may adversely influence the prognosis in patients with chronic heart failure (CHF) and in those with previous myocardial infarction.

Methods and Results— We tested whether a slow breathing rate (6 breaths/min) could modify the baroreflex sensitivity in 81 patients with stable (2 weeks) CHF (age, 58±1 years; NYHA classes I [6 patients], II [33], III [27], and IV [15]) and in 21 controls. Slow breathing induced highly significant increases in baroreflex sensitivity, both in controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) and in CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025), which correlated with the value obtained during spontaneous breathing (r=+0.202, P=0.047). In addition, systolic and diastolic blood pressure decreased in CHF patients (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02).

Conclusions— These data suggest that in patients with CHF, slow breathing, in addition to improving oxygen saturation and exercise tolerance as has been previously shown, may be beneficial by increasing baroreflex sensitivity.

Breathing at 6 breaths/min, compared with spontaneous breathing, slightly increased overall spontaneous fluctuations in RR interval, reduced fluctuations in blood pressure, and significantly increased the baroreflex sensitivity in both CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025) and controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) (Figure 1).

The slow breathing rate in the CHF group also produced an increase in mean RR interval of 20 ms and a decrease in both systolic and diastolic blood pressure (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02) (Figure 2).

The vagus nerve and the inflammatory reflex: wandering on a new treatment paradigm for systemic inflammation and sepsis.

mars 30, 2014 av Marius

Mer om vagusnerven og betennelsesdemping

http://www.ncbi.nlm.nih.gov/pubmed/22913335

Abstract
BACKGROUND:
The immune system protects the host against dangerous pathogens and toxins. The central nervous system is charged with monitoring and coordinating appropriate responses to internal and external stimuli. The inflammatory reflex sits at the crossroads of these crucial homeostatic systems. This review highlights how the vagus nerve-mediated inflammatory reflex facilitates rapid and specific exchange of information between the nervous and immune systems to prevent tissue injury and infection.
METHODS:
Review of the pertinent English-language literature. Nearly two decades of research has elucidated some of the essential anatomic, physiologic, and molecular connections of the inflammatory reflex. The original descriptions of how these key components contribute to afferent and efferent anti-inflammatory vagus nerve signaling are summarized.
RESULTS:
The central nervous system recognizes peripheral inflammation via afferent vagus nerve signaling. The brain can attenuate peripheral innate immune responses, including pro-inflammatory cytokine production, leukocyte recruitment, and nuclear factor kappa β activation via α7-nicotinic acetylcholine receptor subunit-dependent, T-lymphocyte-dependent, vagus nerve signaling to spleen. This efferent arm of the inflammatory reflex is referred to as the «cholinergic anti-inflammatory pathway.» Activation of this pathway via vagus nerve stimulation or pharmacologic α7 agonists prevents tissue injury in multiple models of systemic inflammation, shock, and sepsis.
CONCLUSIONS:
The vagus nerve-mediated inflammatory reflex is a powerful ally in the fight against lethal tissue damage after injury and infection. Further studies will help translate the beneficial effects of this pathway into clinical use for our surgical patients.

You May Need a Nerve to Treat Pain: The Neurobiological Rationale for Vagal Nerve Activation in Pain Management.

mars 20, 2014 av Marius

Alt om hvordan vagus nerven demper smerte gjennom 5 mekanismer samtidig: dempe betennelser, dempe sympaticus aktivitet (fight-or-flight), redusere oksidativt stress, aktivere smertedempende områder i hjernen og utløse smertedempende opioider og cannabinoider i kroppen. Den bekrefter også at pusten stimulerer vagusnerven, spesielt når man puster med HRV-synkron pust slik vi gjør i Verkstedet Breathing System Autonom Pust.

http://www.ncbi.nlm.nih.gov/pubmed/24451632

Mer fra Studien her.