Diagnosis is made by functional testing of the ANS, focusing on the affectedorgan system. Investigations may be performed to identify underlying disease processes that may have led to the development of symptoms or autonomic neuropathy.Symptomatic treatment is available for many symptoms associated with dysautonomia, and some disease processes can be directly treated. Depending on the severity of the dysfunction, dysautonomia can range from being nearly symptomless and transient to disabling and/or life-threatening.[12]
Dysautonomia, a complex set of conditions characterized by autonomic nervous system (ANS) dysfunction, manifests clinically with a diverse array of symptoms of which postural orthostatic tachycardia syndrome (POTS) stands out as the most common.[11]
The symptoms of dysautonomia, which are numerous and vary widely for each person, are due to inefficient or unbalancedefferent signals sent via both systems.[medical citation needed] Symptoms in people with dysautonomia include:
Dysautonomia may be due toinherited or degenerativeneurologic diseases (primary dysautonomia)[5] or injury of the autonomic nervous system from an acquired disorder (secondary dysautonomia).[1][14] Its most common causes include:
In addition to sometimes being a symptom of dysautonomia,anxiety can sometimes physically manifest symptoms resembling autonomic dysfunction.[29][30][31] A thorough investigation ruling out physiological causes is crucial, but in cases where relevant tests are performed and no causes are found or symptoms do not match any known disorders, a primary anxiety disorder is possible but should not be presumed.[32] For such patients, theanxiety sensitivity index may have better predictivity for anxiety disorders while theBeck Anxiety Inventory may misleadingly suggest anxiety for patients with dysautonomia.[33]
Theautonomic nervous system is a component of theperipheral nervous system and comprises two branches: the sympathetic nervous system (SNS) and theparasympathetic nervous system (PSNS). The SNS controls the more active responses, such as increasing heart rate and blood pressure. The PSNS, for example, slows down the heart rate and aids digestion. Symptoms typically arise from abnormal responses of either the sympathetic or parasympathetic systems based on situation or environment.[5][36][26]
Diagnosis of dysautonomia depends on the overall function of three autonomic functions—cardiovagal, adrenergic, and sudomotor. A diagnosis should, at a minimum, include measurements ofblood pressure andheart rate while lying flat and after at least three minutes of standing. The best way to make a diagnosis includes a range of testing, notably an autonomic reflex screen,tilt table test, and testing of thesudomotor response (ESC, QSART or thermoregulatory sweat test).[37]
Additional tests and examinations to diagnose dysautonomia include:
Despite official recognition by the medical institutions in the USSR and some otherWarsaw-pact countries (and their successor countries), it has also been described as a form ofculture-bound syndrome.[38]
Treatment of dysautonomia can be difficult; since it is made up of many different symptoms, a combination of drug therapies is often required to manage individual symptomatic complaints. In the case of autoimmune neuropathy, treatment with immunomodulatory therapies is done. Ifdiabetes mellitus is the cause, control ofblood glucose is important.[1] Treatment can includeproton-pump inhibitors andH2 receptor antagonists used for digestive symptoms such asacid reflux.[43]
The prognosis of dysautonomia depends on several factors; people with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration such as Parkinson's disease or multiple system atrophy generally have poorer long-term prognoses. Dysautonomia can be fatal due topneumonia,acute respiratory failure, or suddencardiopulmonary arrest.[5] Autonomic dysfunction symptoms such as orthostatic hypotension,gastroparesis, andgustatory sweating are more frequently identified in mortalities.[46]
^Sakakibara R, Uchiyama T, Kuwabara S, Mori M, Ito T, Yamamoto T, Awa Y, Yamaguchi C, Yuki N, Vernino S, Kishi M, Shirai K (2009). "Prevalence and mechanism of bladder dysfunction in Guillain-Barre Syndrome".Neurourol Urodyn.28 (5):432–437.doi:10.1002/nau.20663.PMID19260087.S2CID25617551.
^Aiba Y, Sakakibara R, Tateno F, Shimizu N (May 2021). "Orthostatic hypotension possibly caused by vincristine".Neurology and Clinical Neuroscience.9 (4):365–366.doi:10.1111/ncn3.12517.S2CID235628396.
^Loganovsky K (1999). "Vegetative-Vascular Dystonia and Osteoalgetic Syndrome or Chronic Fatigue Syndrome as a Characteristic After-Effect of Radioecological Disaster".Journal of Chronic Fatigue Syndrome.7 (3):3–16.doi:10.1300/J092v07n03_02.
^Ivanova ES, Mukharliamov FI, Razumov AN, Uianaeva AI (2008). "[State-of-the-art corrective and diagnostic technologies in medical rehabilitation of patients with vegetative vascular dystonia]".Voprosy Kurortologii, Fizioterapii, I Lechebnoi Fizicheskoi Kultury (1):4–7.PMID18376477.
Brading A (1999).The autonomic nervous system and its effectors. Oxford: Blackwell Science.ISBN978-0-632-02624-1.
Goldstein D (2016).Principles of Autonomic Medicine(PDF) (free online version ed.). Bethesda, Maryland: National Institute of Neurological Disorders and Stroke, National Institutes of Health.ISBN978-0-8247-0408-7. Archived fromthe original(PDF) on December 6, 2018.
Jänig W (2008).Integrative action of the autonomic nervous system : neurobiology of homeostasis (Digitally printed version. ed.). Cambridge: Cambridge University Press.ISBN978-0-521-06754-6.
Media related toDysautonomia at Wikimedia Commons
