6th International Symposium on regional analgesia musculoskeletal and interventional pain medicine. November 2015

DYSAUTONOMIA = Autonomic Dysfunction = CHRONIC

Phillips C – DMA Clinical Pilates & Physiotherapy Melbourne, Australia

The missing link in a majority of Chronic & Complex patient presentations is the role that the Autonomic Nervous System plays. When aggravated the symptoms are generally seen as separate issues rather than a series of connected issues.

Dysautonomia refers to a dysfunction of the autonomic nervous system involving one or more of the following symptoms:

– Postural Dizziness (also referred to as syncope)

– Bowel dysfunction, gut disturbance , nausea

– Abnormalities of sweating

– Central / peripheral vasomotor and circulatory abnormalities

– Sexual dysfunction in males and females

– Urinary tract dysfunction

Patients with a dysautonomia are typically unaware of their condition given that most functions of the autonomic nervous system are involuntary and many of the symptoms are not easily perceived.

Postural dizziness, also known as postural orthostatic Intolerance, is a commonly reported symptom and can be diagnosed by an impaired heart rate response to moving from a recumbent to an upright posture. This problem typically results due to a failure in the baroreflex, an autonomic response to the change in blood pressure which occurs when standing from lying. Patients will typically describe a sensation of transient dizziness and weakness accompanied by a drop in blood pressure when rising from a supine posture.

The majority of patients with an autonomic dysautonomia will also experience urinary tract dysfunction. Bladder symptoms are typically non-specific and can include nocturnal frequency without associated urinary frequency, increasing susceptibility to overflow incontinence.

Bowel dysfunction, a less common symptom of an autonomic dysautonomia, is characterised by increased bowel movement frequency and a less solid stool and when severe can manifest with uncontrollable flatulence, diarrhoea and stool incontinence.

Sexual dysfunction is also a very common in dysautonomia. The key to identifying sexual dysfunction caused by an autonomic dysautonomia is the presence or absence of a morning erection. The morning erection, which occurs as a result of sympathetic nervous activity during REM sleep, will be absent in patients presenting with a true autonomic dysautonomia.

Vascular disturbances are also extremely common given the key role of the autonomic nervous system in regulating blood pressure and the circulation. Altered autonomic nervous system activation can result in sustained increases or decreases in blood pressure.

Increases in sympathetic output should result in net increase in blood pressure and heart rate and increases in parasympathetic output in a net decrease in blood pressure and heart rate. Deregulation of these autonomic vasomotor responses can result in malfunctioning of this vascular control system and altered blood pressure and heart rate responses to normal physiological stimuli. Clinically patients will present with elevated or lowered blood pressure and/or heart rate as well as an absence of normal physiological responses to postural stimuli.

Circulatory responses to normal physiological stimuli may also malfunction in a dysautonomic individual, with patients experiencing heat flushes due to increased perfusion to the extremities and scalp. Normal peripheral responses to exercise can also be affected leading to the loss of autoregulatory vasodilatory responses leading to exertion-mediated syncope.

The autonomic nervous system also has an important role in the regulation of glandular secretions. Dysautonomia is also commonly associated with loss of sweating responses however these are less commonly reported and will often affect the lower limbs.

Confirmation of a diagnosis of autonomic dysautonomia requires careful consideration of the patient history and presenting signs and symptoms, inparticular the physical findings as outlined above.

Many conditions have been shown to be associated with the development and coexistence of autonomic dysautonomias. Notable examples of conditions with associated dysautonomias include:

– Traumatic Brain Injury

– Familial Dysautonomia

– Diabetes Mellitus

– Fibromyalgia

– Trauma

– Joint hypermobility

Physical trauma to the nervous system is a common cause of dysautonomia and the syndrome has been well documented in survivors of acquired brain injury (ABI) (Perkes & Baguley, 2008). Elevations in heart rate, respiratory rate, body temperature, increased sweating and muscular overactivity related to autonomic malfunction have all been associated with ABI.

Conditions such as familial dysautonomia, result in an almost complete loss of somatosensory function and present with symptoms of glandular disturbances affecting the digestive and circulatory systems. Symptoms include lack of tears, drooling, vomiting, abdominal distension, constipation, diarrhoea, enuresis and overflow incontinence.

Diabetes Mellitus, a common systemic illness, is also susceptible to the development of autonomic dysautonomia. Diabetics may demonstrate some visceral effects including nocturnal diarrhoea, constipation and impaired bowel function. They are also prone to developing impotence and retrograde ejaculation as well as postural syncope and related blood pressure problems.

Alterations in the body’s response to stress have also been documented in conditions such as fibromyalgia An increase in resting sympathetic tone with associated blunted responses to stressors have been found to exist in a subgroup of patients with fibromyalgia (Nielsen & Henriksson, 2007).

There are multiple approaches to the management of autonomic dysautonomia depending on the cause and associated symptoms.

Medical approaches to management include the prescription of adrenergic and cholingeric acting medications which act at the pre and post synaptic neural synapses of the autonomic nervous system. Surgical intervention to decompress the spinal cord, brain stem and sympathetic trunk can also be effective in the instance of physical impairment to the autonomic nervous system.

Physical interventions which both directly and indirectly disinhibit the sympathetic nervous system have been shown to result in instant and major improvements in patient symptoms (Tullock & Phillips, 2008). Mechanical compression of brainstem & / or thoracic cord through trauma, postural deficits or conditions including myelopathy , stenosis, or space occupying lesions will trigger episodic autonomic symptoms. Exercise specific to unloading central spinal canal structures do have predictable outcomes.

Dysautonomia is an oft missed co mornbidity in chronic & complex patient presentations that does have a simple management process to reduce the impact of symptoms.

REFERENCES:

Goldstein, D.S., & Smith L. The NDRF Handbook for Patients with Dysautonomias, Medtronic Foundation , Retrieved January 16th 2015, from http://www.ndrf.org/NDRFHandbook.htm Gazit, Y., Nahir, A. M., Grahame, R., & Jacob, G. (2003). Dysautonomia in the joint hypermobility syndrome. The American Journal of Medicine, 115(1), 33-40.

Holman A, (2008) Positional Cervical Spinal Cord Compression and Fibromyalgia: A Novel Comorbidity With Important Diagnostic and Treatment Implications The Journal of Pain, Vol 9, No 7 (July), 2008: pp 613-622

Goldman, J. M., et al (2003) Joint Hypermobility Syndrome: an update for clinicians. International Journal for Advances in Rheumatic Disease ; 1 (4): Grahame, R., & Pyerttz, R. E. (1995). The Marfan Syndrome: Joint and skin manifestations are prelevant and correlated. Rheumatology, 34(2), 126-131.

Grahame, R. (2001). Time to take hypermobility seriously (in adults and children). Rheumatology, 40(5), 485-487.

Gerrity TR, Bates J, Bell DS et al. (2002) Chronic Fatigue Syndrome: What Role Does the Autonomic Nervous System Play in the Pathophysiology of This Complex Illness? Neuroimmunomodulation ;10:134-41

Goldstein et al. (2002) Dysautonomias: clinical disorders of the autonomic nervous system. Annals of Internal Hakim, A., & Grahame, R. (2003). Joint hypermobility. Best Practice & Research Clinical Rheumatology, 17(6), 989-1004.

Hakim, A. J., & Grahame, R. (2004). Non-musculoskeletal symptoms in joint hypermobility syndrome. Indirect evidence for autonomic dysfunction? Rheumatology, 43(9), 1194-1195.

Nielsen, L.A. & Henriksson, K.G. (2007), Pathophysiological mechanisms in chronic musculoskeletal pain (fibromyalgia): the role of central and peripheral sensitization and pain disinhibition, Best Practice & Research Clinical Rheumatology, Vol 21, No 3, pp 465-480.

Perkes, I.E. & Baguley I.J. (2008), Current Understanding of Dysautonomia after severe Aquired Brain Injury, ACNR, Vol 8, No. 1 pp 10-11.

Tulloch, E., & Phillips, C. (2008), Chronic fatigue syndrome: a possible role of mechanical treatment? Physical Therapy Reviews, Vol13, No 2, pp. 111-118.