Physical Countermaneuvers Research Articles

Non-Pharmacological Treatment of Autonomic Dysfunction in Parkinson's Disease and Other Synucleinopathies.

Symptoms of autonomic dysfunction are prevalent and can be very debilitating, reducing the quality of life in patients with Parkinson's disease (PD) and other synucleinopathies such as dementia with Lewy bodies and multiple system atrophy. Non-pharmacological therapies are key to effective management and are frequently used alone in patients with mild autonomic symptoms, or in combination with pharmacological therapies in patients with moderate and severe symptoms. This article focuses on non-pharmacological approaches. Our objective was to review the non-drug and non-surgical approaches to treating autonomic symptoms in patients with PD and other synucleinopathies, focusing on cardiovascular, gastrointestinal, and genitourinary autonomic dysfunction. Evidence supporting the effectiveness of non-pharmacological treatment for the management of neurogenic orthostatic hypotension, supine hypertension, constipation, and bladder and sexual dysfunction is available. High-quality prospective trials are scarce, yet some non-pharmacological interventions (e.g., physical counter maneuvers) can be evaluated relatively quickly on an individual basis and often seem effective. The emerging variety of clinical presentations advocates for a stepwise, individualized, and non-pharmacological approach for the management of autonomic symptoms. Often, the first step is to reduce or discontinue drugs that cause or aggravate autonomic symptoms followed by lifestyle measures. While non-pharmacological and non-surgical treatments are available and, in many cases, effective to improve symptoms of autonomic dysfunction in PD and other synucleinopathies, they are often overlooked. Large randomized trials testing and comparing non-pharmacological approaches are warranted.

Management of vasovagal syncope.

Vasovagal syncope (VVS) is a very common form of fainting. Treatment begins with patient education about the mechanism of fainting, and the non-lethal nature of vasovagal syncope. In this article, we review several non-pharmacological approaches that form the foundation of our current treatments. These include increases in dietary salt and water intake, the use of compression garments, physical counter-maneuvers and tilt-training. When these approaches are inadequate, medications can sometimes be effective. While the evidence base for the pharmacological treatment of VVS is modest, recent trial data have found drugs to be useful in placebo-controlled randomized trials. For select patients, and those patients more refractory to medications, procedural treatments may be an option. In this review, we discuss the current state of evidence for the non-pharmacological and pharmacological treatments for VVS, as well as some novel, emerging therapies for VVS.

Effectiveness of non-pharmacological interventions to treat orthostatic hypotension in elderly people and people with a neurological condition: a systematic review.

The objective of this review was to summarize the best available evidence regarding the effectiveness of non-pharmacological interventions to treat orthostatic hypotension (OH) in elderly people and people with a neurological condition. Orthostatic hypotension is common in elderly people and people with a neurological condition and can interfere with or limit rehabilitation. Non-pharmacological interventions to treat OH could allow for longer and earlier mobilization, which is recommended in national clinical guidelines for rehabilitation in the acute or sub-acute phase following stroke or other neurological conditions. The review considered people aged 50 years and older, and people aged 18 years and elderly people with a neurological condition. Non-pharmacological interventions to treat OH included compression garments, neuromuscular stimulation, physical counter-maneuvers, aerobic or resistance exercises, sleeping with head tilted up, increasing fluid and salt intake, and timing and size of meals. The comparator was usual care, no intervention, pharmacological interventions, or other non-pharmacological interventions. Outcome measures included systolic blood pressure, diastolic blood pressure, heart rate, cerebral blood flow, observed/perceived symptoms, duration of standing or sitting in minutes, tolerance of therapy, functional ability, and adverse events/effects. Databases for published and unpublished studies available in English up to April 2018 with no lower date limit were searched. Critical appraisal was conducted using standardized instruments from JBI. Data were extracted using standardized tools designed for quantitative studies. Where appropriate, studies were included in a meta-analysis; otherwise, data were presented in a narrative form due to heterogeneity. Forty-three studies - a combination of randomized controlled trials (n = 13), quasi-experimental studies (n = 28), a case control study (n = 1), and a case report (n = 1) - with 1069 participants were included. Meta-analyses of three interventions (resistance exercise, electrical stimulation, and lower limb compression bandaging) showed no significant effect of these interventions. Results from individual studies indicated physical maneuvers such as leg crossing, leg muscle pumping/contractions, and bending forward improved orthostatic hypotension. Abdominal compression improved OH. Sleeping with head up in combination with pharmacological treatment was more effective than sleeping with head up alone. Eating smaller, more frequent meals was effective. Drinking 480 mL of water increased blood pressure. The review found mixed results for the effectiveness of non-pharmacological interventions to treat OH in people aged 50 years and older, and people with a neurological condition. There are several non-pharmacological interventions that may be effective in treating OH, but not all have resulted in clinically meaningful changes in outcome. Some may not be suitable for people with moderate to severe disability; therefore, it is important for clinicians to consider the patient's abilities and impairments when considering which non-pharmacological interventions to implement.

19 The Efficacy, Safety and Acceptability of Non-Pharmacologic Therapy for Orthostatic Hypotension in Older People: A Mixed Methods Study

Abstract Introduction First-line treatment for OH is typically with non-pharmacologic therapy. However, the current evidence base is poor, particularly in older people. Aim Determine the safety, efficacy and acceptability of single and combination therapies for OH in older people. Methods A three-stage, mixed-methods study consisting of a phase 2 efficacy study with a nested qualitative study. Stage One calculated response rates to therapy (defined as an improvement in standing systolic blood pressure (SSBP) by ≥10 mmHg). Stage Two explored the tolerability of therapies in qualitative interviews. Stage Three evaluated response rates to combinations of the most efficacious and tolerable therapies. All participants were aged ≥60 years, had OH and were recruited from a UK Falls and Syncope Service. Results Stage One. Response rates to therapies were evaluated in 25 older people (74 years, 60-92): Bolus-water drinking 56% (95%CI 35, 76); abdominal compression 52% (95%CI 31, 72), physical counter-maneuvers 44% (PCM, 95%CI 24, 65), full-leg length compression 32% (95%CI 15, 54). Stage Two. PCM was considered an acceptable therapy as no equipment is required, is only needed during postural change and can be performed conspicuously. Water was largely acceptable but there were concerns around urinary frequency. Compression stockings were considered unacceptable due to cosmesis, practicalities and discomfort. There were mixed views on the tolerability of abdominal compression. There were no adverse events. Stage Three. Response rates to combination therapy were evaluated in 37 older people (71 years, 60-94). Bolus water drinking + PCM 38% (95%CI 22, 55); water + PCM + abdominal compression 46% (95%CI 29, 63). Conclusions Due to its superior efficacy, safety and acceptability, bolus water drinking should become standard first-line therapy. Conversely, compression stockings should be disregarded in this population, as they are the least efficacious and most unacceptable treatment. Surprisingly, there is no additional benefit of combining therapies.

Chapter 29 - Clinical neurophysiology of postural tachycardia syndrome

Postural tachycardia syndrome (POTS) is one of several disorders of orthostatic intolerance (OI). It is defined by the development of symptoms of cerebral hypoperfusion or sympathetic activation and a sustained heart rate increment of 30 beats/min or more (40 beats/min for teenagers) within 10min of standing or head-up tilt in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. POTS is approximately five times more common in women than men. This heterogeneous syndrome is caused by several pathophysiologic mechanisms (limited autonomic neuropathy, hyperadrenergic state, hypovolemia, venous pooling, deconditioning), which are not mutually exclusive. Anxiety and somatic hypervigilance play significant roles in POTS. Common comorbidities include visceral pain and dysmotility, chronic fatigue and fibromyalgia, migraine, joint hypermobility, mitral valve prolapse, and inappropriate sinus tachycardia. Patients with suspected POTS should undergo comprehensive cardiac and neurologic examinations and autonomic and laboratory tests to determine the most likely pathophysiologic basis of OI. The objectives of POTS management are to (1) increase the time that patients can stand, perform daily activities, and exercise and (2) avoid syncope. Management involves nonpharmacologic (fluid and salt loading, physical countermaneuvers, compression garments, exercise training) and pharmacologic (β-blockers, pyridostigmine, fludrocortisone, midodrine) approaches.

Orthostatic Hypotension: Mechanisms, Causes, Management.

Orthostatic hypotension (OH) occurs when mechanisms for the regulation of orthostatic BP control fails. Such regulation depends on the baroreflexes, normal blood volume, and defenses against excessive venous pooling. OH is common in the elderly and is associated with an increase in mortality rate. There are many causes of OH. Aging coupled with diseases such as diabetes and Parkinson's disease results in a prevalence of 10-30% in the elderly. These conditions cause baroreflex failure with resulting combination of OH, supine hypertension, and loss of diurnal variation of BP. The treatment of OH is imperfect since it is impossible to normalize standing BP without generating excessive supine hypertension. The practical goal is to improve standing BP so as to minimize symptoms and to improve standing time in order to be able to undertake orthostatic activities of daily living, without excessive supine hypertension. It is possible to achieve these goals with a combination of fludrocortisone, a pressor agent (midodrine or droxidopa), supplemented with procedures to improve orthostatic defenses during periods of increased orthostatic stress. Such procedures include water bolus treatment and physical countermaneuvers. We provide a pragmatic guide on patient education and the patient-orientated approach to the moment to moment management of OH.

Blood pressure regulation X: what happens when the muscle pump is lost? Post-exercise hypotension and syncope

Syncope which occurs suddenly in the setting of recovery from exercise, known as post-exercise syncope, represents a failure of integrative physiology during recovery from exercise. We estimate that between 50 and 80% of healthy individuals will develop pre-syncopal signs and symptoms if subjected to a 15-min head-up tilt following exercise. Post-exercise syncope is most often neurally mediated syncope during recovery from exercise, with a combination of factors associated with post-exercise hypotension and loss of the muscle pump contributing to the onset of the event. One can consider the initiating reduction in blood pressure as the tip of the proverbial iceberg. What is needed is a clear model of what lies under the surface; a model that puts the observational variations in context and provides a rational framework for developing strategic physical or pharmacological countermeasures to ultimately protect cerebral perfusion and avert loss of consciousness. This review summarizes the current mechanistic understanding of post-exercise syncope and attempts to categorize the variation of the physiological processes that arise in multiple exercise settings. Newer investigations into the basic integrative physiology of recovery from exercise provide insight into the mechanisms and potential interventions that could be developed as countermeasures against post-exercise syncope. While physical counter maneuvers designed to engage the muscle pump and augment venous return are often found to be beneficial in preventing a significant drop in blood pressure after exercise, countermeasures that target the respiratory pump and pharmacological countermeasures based on the involvement of histamine receptors show promise.

Current Concepts in Orthostatic Hypotension Management

Orthostatic hypotension is a condition commonly affecting the elderly and is often accompanied by disabling presyncopal symptoms, syncope and impaired quality of life. The pathophysiology of orthostatic hypotension is linked to abnormal blood pressure regulatory mechanisms and autonomic insufficiency. As part of its diagnostic evaluation, a comprehensive history and medical examination focused on detecting symptoms and physical findings of autonomic neuropathy should be performed. In individuals with substantial falls in blood pressure upon standing, autonomic function tests are recommended to detect impairment of autonomic reflexes. Treatment should always follow a stepwise approach with initial use of nonpharmacologic interventions including avoidance of hypotensive medications, high-salt diet and physical counter maneuvers. If these measures are not sufficient, medications such as fludrocortisone and midodrine can be added. The goals of treatment are to improve symptoms and to make the patient as ambulatory as possible instead of targeting arbitrary blood pressure values.

Orthostatic Hypotension in the Elderly: Diagnosis and Treatment

Orthostatic hypotension is a common problem among elderly patients, associated with significant morbidity and mortality. While acute orthostatic hypotension is usually secondary to medication, fluid or blood loss, or adrenal insufficiency, chronic orthostatic hypotension is frequently due to altered blood pressure regulatory mechanisms and autonomic dysfunction. The diagnostic evaluation requires a comprehensive history including symptoms of autonomic nervous system dysfunction, careful blood pressure measurement at various times of the day and after meals or medications, and laboratory studies. Laboratory investigation and imaging studies should be based upon the initial findings with emphasis on excluding diagnoses of neurodegenerative diseases, amyloidosis, diabetes, anemia, and vitamin deficiency as the cause. Whereas asymptomatic patients usually need no treatment, those with symptoms often benefit from a stepped approach with initial nonpharmacological interventions, including avoidance of potentially hypotensive medications and use of physical counter maneuvers. If these measures prove inadequate and the patient remains persistently symptomatic, various pharmacotherapeutic agents can be added, including fludrocortisone, midodrine, and nonsteroidal anti-inflammatory drugs. The goals of treatment are to improve symptoms and to make the patient as ambulatory as possible rather then trying to achieve arbitrary blood pressure goals. With proper evaluation and management, the occurrence of adverse events, including falls, fracture, functional decline, and myocardial ischemia, can be significantly reduced.

Current Management of Syncope

Syncope is defined as transient loss of consciousness as a result of inadequate cerebral perfusion. The causes of syncope fall into five broad categories: neurally mediated, orthostatic (the most frequent causes), cardiac arrhythmias, structural cardiovascular (relatively uncommon cause), and cerebrovascular (very rare). The initial evaluation of the syncope patient includes a detailed medical history and physical exam, and usually an ECG and echocardiogram. Thereafter, selected additional testing (e.g. ambulatory ECG recording, autonomic function testing, electrophysiologic study) may be needed on a case-by-case basis. Neurally mediated and orthostatic syncope should first be treated by conservative therapies including hydration/volume expanders and physical counter-maneuvers. Various drugs may play a role as second-line of treatment. However, apart from midodrine, randomized studies of drug therapy are largely lacking, and most agents have not proved to be predictably effective. For syncope due to cardiac arrhythmias, treatment options (depending on the specific circumstance) include ablation of the arrhythmia origin, antiarrhythmic drugs, and/or implantable devices (pacemakers and defibrillators). In the case of syncope due to structural cardiovascular defects (e.g. acute myocardial ischemia, pulmonary hypertension, obstructive cardiomyopathy), treatment is aimed at ameliorating the underlying structural defect. In brief, establishing a specific cause(s) for syncope is crucial. Only then can a potentially effective treatment strategy be contemplated.

Improved orthostatic tolerance by leg crossing and muscle tensing: indisputable evidence for the arteriovenous pump existence

The following is the abstract of the article discussed in the subsequent letter: Tensing of lower body muscles without or with leg crossing (LBMT, LCMT), whole body tensing (WBT), squatting, and sitting with the head bent between the knees (“crash position,” HBK) are believed to abort vasovagal

Leg crossing improves orthostatic tolerance in healthy subjects: a placebo-controlled crossover study

Vasovagal syncope is the most common cause of transient loss of consciousness, and recurrent vasovagal fainting has a profound impact on quality of life. Physical countermaneuvers are applied as a means of tertiary prevention but have so far only proven useful at the onset of a faint. This placebo-controlled crossover study tested the hypothesis that leg crossing increases orthostatic tolerance. Nine naïve healthy subjects [6 females, median age 25 yr (range 20-41 yr), mean body mass index 23 (SD 2)] were subjected to passive head-up tilt combined with a graded lower body negative pressure challenge (20, 40, and 60 mmHg) determining orthostatic tolerance thrice, in randomized order: 1) control, 2) with leg crossing, and 3) with oral placebo. Blood pressure (Finometer), heart rate, and changes in thoracic blood volume (impedance), stroke volume, and cardiac output (Modelflow) were followed during orthostatic stress. Primary outcome was time to presyncope (systolic blood pressure </=85 mmHg, heart rate >/=140 beats/min). With leg crossing, orthostatic tolerance increased from 26 +/- 2 to 34 +/- 2 min (placebo 23 +/- 3 min, P < 0.001). During leg crossing, mean arterial pressure (81 vs. 81 mmHg) and cardiac output (95 vs. 94% supine) remained unchanged; heart rate increase was lower (13 vs. 18 beats/min, P < 0.05); stroke volume was higher (79 vs. 74% supine, P < 0.05); and there was a trend toward lower thoracic impedance. Leg crossing increases orthostatic tolerance in healthy human subjects. As a measure of prevention, it is a worthwhile addition to the management of vasovagal syncope.

Effect of physical countermaneuvers on orthostatic hypotension in familial dysautonomia

Familial dysautonomia (FD) patients frequently experience debilitating orthostatic hypotension. Since physical countermaneuvers can increase blood pressure (BP) in other groups of patients with orthostatic hypotension, we evaluated the effectiveness of countermaneuvers in FD patients. In 17 FD patients (26.4 +/- 12.4 years, eight female), we monitored heart rate (HR), blood pressure (BP), cardiac output (CO), total peripheral resistance (TPR) and calf volume while supine, during standing and during application of four countermaneuvers: bending forward, squatting, leg crossing, and abdominal compression using an inflatable belt. Countermaneuvers were initiated after standing up,when systolic BP had fallen by 40mmHg or diastolic BP by 30mmHg or presyncope had occurred. During active standing, blood pressure and TPR decreased, calf volume increased but CO remained stable. Mean BP increased significantly during bending forward (by 20.0 (17 - 28.5) mmHg; P = 0.005) (median (25(th) - 75(th) quartile)), squatting (by 50.8 (33.5 - 56) mmHg; P = 0.002), and abdominal compression (by 5.8 (-1 - 34.7) mmHg; P = 0.04) - but not during leg-crossing. Squatting and abdominal compression also induced a significant increase in CO (by 18.1 (-1.3 - 47.9) % during squatting (P = 0.02) and by 7.6 (0.4 - 19.6) % during abdominal compression (P=0.014)). HR did not change significantly during the countermaneuvers. TPR increased significantly only during squatting (by 37.2 (11.8 - 48.2) %; P = 0.01). However, orthopedic problems or ataxia prevented several patients from performing some of the countermaneuvers. Additionally, many patients required assistance with the maneuvers. Squatting, bending forward and abdominal compression can improve orthostatic BP in FD patients, which is achieved mainly by an increased cardiac output. Squatting has the greatest effect on orthostatic blood pressure in FD patients. Suitability and effectiveness of a specific countermaneuver depends on the orthopedic or neurological complications of each FD patient and must be individually tested before a therapeutic recommendation can be given.

Pharmacological treatment of reflex syncope.

Patient education, identification of possible triggers of syncope and reassurance are a central feature of the management of patients with reflex syncope. Patients should be advised as to the importance of adequate hydration and taught physical countermaneuvers to enhance cardiac venous return. These maneuvers are sufficient for most patients, however, for a small number of patients who continue to have recurrent syncopal events, pharmacological intervention may be considered. Volume expansion can be enhanced with salt and fludrocortisone. Agents from diverse pharmacological classes have been used to attenuate the reflex response, enhance vasoconstriction and attenuate vagal outflow. Alpha adrenoreceptor agonists, anticholinergic agents, theophylline, beta adrenoreceptor antagonists, serotonin reuptake inhibitors and disopyramide are the most widely studied. None of these agents has shown a consistent therapeutic benefit in clinical trials.

Treatment of orthostatic hypotension.

Orthostatic hypotension (OH) is a fall in blood pressure after assuming an upright position. Whereas asymptomatic patients usually need no treatment, the majority of symptomatic patients can be cured by avoidance of trigger mechanisms and the use of physical countermaneuvers and non-pharmacological interventions. Several pharmacological therapies are available and generally fludrocortisone and midodrine are the drugs of first choice. Recently, highly individualized therapy with ambulatory norepinephrine therapy was able to mobilize otherwise immobile patients.

Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome.

A variety of approaches have been used to alleviate symptoms in postural tachycardia syndrome (POTS). Drugs reported to be of benefit include midodrine, propranolol, clonidine, and phenobarbital. Other measures used include volume expansion and physical countermaneuvers. These treatments may influence pathophysiologic mechanisms of POTS such as alpha-receptor dysfunction, beta-receptor supersensitivity, venous pooling, and brainstem center dysfunction. The authors prospectively studied hemodynamic indices and symptom scores in patients with POTS who were acutely treated with a variety of interventions. Twenty-one subjects who met the criteria for POTS were studied (20 women, 1 man; mean age, 28.7 +/- 6.8 y; age range, 14-39 y). Patients were studied with a 5-minute head-up tilt protocol, ECG monitoring, and noninvasive beat-to-beat blood pressure monitoring, all before and after the administration of an intervention (intravenous saline, midodrine, propranolol, clonidine, or phenobarbital). The hemodynamic indices studied were heart rate (ECG) and systolic, mean, and diastolic blood pressure. Patients used a balanced verbal scale to record any change in their symptoms between the tilts. Symptom scores improved significantly after the patients received midodrine and saline. Midodrine and propranolol reduced the resting heart rate response to tilt (p <0.005) and the immediate and 5-minute heart rate responses to tilt (p <0.002). Clonidine accentuated the immediate decrease in blood pressure on tilt up (p <0.05). It was concluded that midodrine and intravenous saline are effective in decreasing symptoms on tilt in patients with POTS when given acutely. Effects of treatments on heart rate and blood pressure responses generally reflected the known pharmacologic mechanisms of the agents.

Role of Physical Countermaneuvers in the Management of Orthostatic Hypotension: Efficacy and Biofeedback Augmentation

To evaluate the efficacy of various physical countermaneuvers in reducing orthostatic hypotension and its associated symptoms and to assess the efficacy of biofeedback training in enhancing the effectiveness of physical countermaneuvers. In nine study subjects with neurogenic orthostatic hypotension, four training sessions on physical countermaneuvers were performed after tilt-up, three with visual feedback on the effect of physical countermaneuvers on blood pressure and other cardiovascular variables. Blood pressure change and orthostatic symptoms during tilt-up were determined, as were the changes in total peripheral resistance, stroke index, and heart rate. The five female and four male patients had a mean age of 53 years and a mean duration of symptoms of 4.2 years. On an orthostatic symptom scale of 0 to 10, these patients had a mean symptom score of 7.3. The increment in systolic blood pressure was better for some maneuvers (such as leg crossing and a combination) than others (such as neck flexion and abdominal contraction). Three patterns of responses to biofeedback were found. Simple maneuvers such as squatting did not improve with training; visual feedback was needed for maneuvers such as thigh contraction, and performance declined without biofeedback; the third pattern, seen in maneuvers such as leg crossing, showed continued improvement with training, even without biofeedback. A survey at 3 to 4 months after training revealed continued use of physical maneuvers (3.8 +/- 3.1 per day), increased standing time with each episode of presyncopal symptoms (8.3 +/- 5.8 minutes), and continued global symptomatic improvement. Total peripheral resistance, but not heart rate or stroke index, showed significant regression with blood pressure improvement. Physical countermaneuvers are efficacious in reducing orthostatic hypotension, can be augmented by use of biofeedback, and may significantly improve the functional outcome. The major mechanism of improvement is an increase in total peripheral resistance, presumably by reducing the vascular capacitance.