Autonomic Testing / Sudomotor Tests

Number: 0485

  1. Aetna considers autonomic testing such as quantitative sudomotor axon reflex test (QSART), silastic sweat imprint, and thermoregulatory sweat test (TST) medically necessary for use as a diagnostic tool for any of the following conditions/disorders:

    1. Amyloid neuropathy
    2. Diabetic autonomic neuropathy
    3. Distal small fiber neuropathy
    4. Idiopathic neuropathy
    5. Multiple system atrophy
    6. Pure autonomic failure
    7. Reflex sympathetic dystrophy or causalgia (sympathetically maintained pain)
    8. Sjogren’s syndrome.

    Aetna considers autonomic testing experimental and investigational for all other indications (e.g., chronic fatigue syndrome/myalgic encephalomyelitis, postural tachycardia syndrome, Raynaud phenomenon, and predicting foot ulcers) because its effectiveness for indications other than the ones listed above has not been established.

  2. Aetna considers sympathetic skin response testing experimental and investigational for any indications because it has a relatively low sensitivity and uncertain specificity, and the peer-reviewed medical literature does not support its effectiveness.

  3. Aetna considers the use of quantitative direct and indirect reflex testing (QDIRT) of sudomotor function experimental and investigational because its clinical value has not been established.

  4. Aetna considers quantitative pilomotor axon reflex test (QPART) for evaluating pilomotor function experimental and investigational because its clinical value has not been established.

  5. Aetna considers ANSAR (ANX 3.0) test experimental and investigational in the evaluation of paradoxical parasympathetic syndrome because its clinical value has not been established. 

  6. Aetna considers measurement of cardiac baroreflex sensitivity for assessing cognitive function experimental and investigational because its clinical value for this indication has not been established.


Sudomotor testing is used in the clinical setting to evaluate and document neuropathic disturbances that may be associated with pain. The quantitative sudomotor axon reflex test (QSART), thermoregulatory sweat test (TST), sympathetic skin responses, and silastic sweat imprints are tests of sympathetic cholinergic sudomotor function. All of these tests measure only post-ganglionic sudomotor function.

The QSART device was first reported in detail in 1983 and its clinical use has spread since that time for the evaluation of autonomic dysfunction (Low, et al., 1983; Kennedy, et al., 1984; Low, et al., 1985; Cohen, et al., 1987; Fealey, et al., 1989; Maselli, et al., 1989; Low, et al., 1990; Kahara, et al., 1991; Levy, et al., 1992; Kihara, et al., 1983; Crandall, et al., 1995; Lang, et al., 1995; Sandroni, et al., 1998; O'Suilleabhain, et al., 1998; Birklein, et al., 1998; Hoeldtke et al., 2001; Vinik, et al., 2003; Low, 2003; Bickel, et al., 2004; Singer, et al., 2004; Low, 2004; Low, et al., 2004; Hilz, et al., 2006; Smith, et al., 2006; Low, et al., 2006; Nolano, et al., 2006). The QSART measures axon reflex-mediated sudomotor responses quantitatively and evaluates post-ganglionic sudomotor function.  Recording is usually carried out from the forearm and 3 lower extremity skin sites to assess the distribution of post-ganglionic deficits. Normative values for QSART have been established. 

The sympathetic skin response is another test of sudomotor function (Maselli, et al., 1989; Levy, et al., 1992; Fagias & Wallin, 1980a; Fagias & Wallin, 1980b; Lidberg & Wallin, 1981; Shahani, et al., 1984; Soliven, et al., 1987; Uncini, et al., 1988; Niakan & Harati, 1988; Dellantonio, et al., 1989; Elie & Guihaneus, 1990; Baser, et al., 1991; Caccia, et al., 1991; Berne, et al., 1992; Drory & Korczyn, 1993; Paresi, et al., 1995; Linden & Berlit, 1995; Abbott, et al., 1996; Baron & Maier, 1996; Magerl, et al., 1996; Shivji, et al., 1999; Illigens & Gibbons, 2008). Widely used in the past, sympathetic skin response measures change in skin resistance following a random electric stimulation, and provides an index of sweat production.  However, this is non-thermoregulatory sweat that occurs on the palms and soles, is of different pharmacological and physiologic properties, and involves somatic afferents.  The medical literature proves that this test is of relatively low sensitivity and uncertain specificity, as compared to QSART.

The thermoregulatory sweat test (TST) is another widely used clinical test for evaluating sudomotor function (Hilz & Dutch, 2006; Nolano, et al., 2006; Illigens & Gibbons, 2009; Cheshire & Freeman, 2003; Lipp, et al., 2009; Stewart, et al., 1992; Jacobson & Hiner, 1998; Birklein, et al., 2001; Atkinson & Fealey, 2003; Schiffmann, et al., 2003; Nakazato, et al., 2004; Kimpinski, et al., 2009). The TST evaluates the distribution of sweating by a change in color of an indicator powder.  The test is sensitive, and its specificity for delineating the site of lesion is greatly enhanced when used in conjunction with QSART.

QDIRT and silastic sweat imprint methods are also widely used, but do not have the same level of clinical data supporting their use (Kihara, et al., 1993; Illigens & Gibbons, 2009; Gibbons, et al., 2001; Perretti, et al., 2003; Berghoff, et al., 2006; Manganelli, et al., 2007). Sweat imprints are formed by the secretion of active sweat glands into a plastic (silastic) imprint.  The test can determine sweat gland density, a histogram of sweat droplet size and sweat volume per area. . 

Presently, post-ganglionic sudomotor function is assessed by means of QSART or silicone impressions.  Quantitative direct and indirect reflex testing (QDIRT) is a technique for assessing post-ganglionic sudomotor function.  This technique combines some of the advantages of silicone impressions and QSART by providing data on droplet number, droplet topographic distribution, and temporal resolution in direct and axon reflex-mediated regions.

Gibbons et al (2008) described their findings on the use of QDIRT for evaluating sudomotor function.  In this study, sweating in 10 healthy subjects (3 women and 7 men) was stimulated on both forearms by iontophoresis of 10 % acetylcholine.  Silicone impressions were made and topical indicator dyes were digitally photographed every 15 seconds for 7 minutes after iontophoresis.  Sweat droplets were quantified by size, location, and percent surface area.  Each test was repeated eight times in each subject on alternating arms over 2 months.  Another 10 subjects (5 women and 5 men) had silicone impressions, QDIRT, and QSART performed on the dorsum of the right foot.  The percent area of sweat photographically imaged correlated with silicone impressions at 5 minutes on the forearm (r = 0.92, p < 0.01) and dorsal foot (r = 0.85, p < 0.01).  The number of sweat droplets assessed with QDIRT correlated with the silicone impression, although the droplet number was lower (162 +/- 28 versus 341 +/- 56, p < 0.01, r = 0.83, p < 0.01).  The sweat response and sweat onset latency assessed by QDIRT correlated with QSART measured at the dorsum of the foot (r = 0.63, p < 0.05; r = 0.52, p < 0.05).  The authors concluded that QDIRT measured both the direct and the indirect sudomotor response with spatial resolution similar to that of silicone impressions, and with temporal resolution similar to that of QSART.  They noted that QDIRT provides a novel tool for the evaluation of post-ganglionic sudomotor function.  Furthermore, they stated that more research is needed to ascertain the utility of QDIRT in disease states that alter sudomotor structure or function.

One limitation of QDIRT is that ambient room temperature and humidity need to be controlled to prevent cool dry air from causing evaporation of sweat production.  Furthermore, normative values for QDIRT need to be established to avoid over-diagnosis of sudomotor dysfunction.

Sudomotor testing has data to suggest it may be the most sensitive means to detect a peripheral small fiber neuropathy (Low, et al., 2006). Hoitsma et al (2003) reported that sympathetic skin responses testing appeared to be of little value in diagnosing small-fiber neuropathy in patients with sarcoidosis.  On the other hand, Hoitsma et al (2004) noted that QSART is useful for diagnosing small fiber neuropathy.

Sudomotor testing is also the only way to detect isolated damage to sudomotor nerves in a number of different disease states such as Ross Syndrome, Harlequin Syndrome, diabetes, multiple system atrophy, Parkinson’s disease, autoimmune autonomic ganglionopathy, and pure autonomic failure (Low, et al., 1983; Kennedy, et al, 1984; Low, et al., 1990; Kihara, et al., 1991; Kihara, et al., 1993; Sandroni, et al., 1998; O'Suilleabhan, et al., 1998; Low, 2003; Bickel, et al., 2004; Low, 2004; Low, et al., 2006; Niahan & Harati, 1998; Baser, et al., 1991; Illigen & Gibbons, 2009; Cheshire & Freeman, 2003; Stewart, et al., 1992; Ross, 1958; Petagan, et al., 1965; Schondorf & Low, 1993; Kihara, et al., 1993; Wolfe, et al., 1995; Rex, et al., 1998). The clinical implications of testing and outcomes are reviewed in detail in a number of different studies across different diseases (Cheshire & Freeman, 2003).

Autonomic testing (including sudomotor testing) is recommended for all patients with type 2 diabetes at the time of diagnosis and 5 years after diagnosis in individuals with type 1 diabetes (Boulton, et al., 2005; Tesfaye, et al., 2010; Spallone, et al., 2011a; Bernardi, et al., 2011; Spallone, et al., 2011b; Spallone, et al., 2011c). Individuals with diabetes that have autonomic neuropathy have a significantly higher mortality, and guidelines for anesthesia, surgery and medical therapies to affect outcomes have been established (Boulton, et al., 2005; Spallone, et al., 2011a; Vinik & Ziegler, 2007).

Argiana et al (2011) noted that diabetic foot ulcers affect almost 5 % of the patients with diabetes and carry a huge physical, emotional, and financial burden.  Almost 80 % of amputations in patients with diabetes are preceded by a foot ulcer.  Simple tests (e.g., monofilament, tuning fork, vibration perception threshold determination, ankle reflexes, and pinprick sensation), alone or in combination, have been studied prospectively and can be used for identification of patients at risk.  Newer tests examining sudomotor dysfunction and skin dryness have been introduced in recent years.  In cross-sectional studies, sudomotor dysfunction assessed by either sympathetic skin response or Neuropad (Miro Verbandstoffe GmbH, Wiehl-Drabenderhöhe, Germany) testing has been consistently associated with foot ulceration.  The authors concluded that prospective studies are needed to establish if sudomotor dysfunction can predict foot ulcers and if simple methods assessing sudomotor dysfunction (e.g., Neuropad testing) can be included in the screening tests for the prevention of this complication.

Peltier and colleagues (2010) stated that postural tachycardia syndrome (POTS) is a heterogeneous disorder characterized by excessive orthostatic tachycardia in the absence of orthostatic hypotension and by sympathetic nervous system activation.  Post-ganglionic sudomotor deficits have been used to define a neurogenic POTS subtype.  Norepinephrine levels above 600 pg/ml have also been used to delineate patients with a hyperadrenergic state.  These reseachers determined the relationship of sudomotor abnormalities to other aspects of dysautonomia in POTS.  Autonomic function was quantified in 30 women through tests of cardio-vagal, adrenergic, and sudomotor function including QSART and spectral indices.  Differences between patients with and without sudomotor dysfunction as defined by QSART and between patients with and without hyperadrenergic POTS were assessed with Mann-Whitney U test and Mantel-Haenszel Chi-Square test using a p value of 0.01 for significance.  Spearman correlation coefficients were used to test raw sweat volume correlations with other variables.  Of 30 women (aged 20 to 58), 17 patients (56 %) had an abnormal QSART that was typically patchy and involved the lower extremity, while 13 patients had normal QSART results.  Other autonomic tests, catecholamines or spectral indices did not correlate with QSART results.  No differences in autonomic tests or spectral indices were observed between hyperadrenergic and non-hyperadrenergic POTS.  The authors concluded that these findings confirmed that a large subset of POTS patients have sudomotor abnormalities that are typically patchy in distribution but do not correlate with other tests of autonomic function.  They stated that further studies are needed to determine the best method of endophenotyping patients with POTS.

Manek and associates (2011) stated that the pathophysiological factors of primary Raynaud phenomenon (RP) are unknown.  Preliminary evidence from skin biopsy suggests small-fiber neuropathy (SFN) in primary RP.  In a pilot study, these investigators aimed to quantitatively assess SFN in patients with primary RP.  Consecutive subjects with an a priori diagnosis of primary RP presenting to the authors' outpatient rheumatology clinic over a 6-month period were invited to participate.  Cases of secondary RP were excluded.  All participants were required to have normal results on nail-fold capillary microscopy.  Assessment for SFN was performed with autonomic reflex screening, which includes QSART, and cardiovagal and adrenergic function testing, TST, and quantitative sensory test (QST) for vibratory, cooling, and heat-pain sensory thresholds.  A total of 9 female subjects with a median age of 38 years (range of 21 to 46 years) and a median symptom duration of 9 years (range of 5 months to 31 years) were assessed.  Three participants had abnormal results on QSART, indicating peripheral sudomotor autonomic dysfunction; 2 participants had evidence of large-fiber involvement with heat-pain thresholds on QST.  Heart rate and blood pressure responses to deep breathing, Valsalva maneuver, and 70-degree tilt were normal for all participants.  Furthermore, all participants had normal TST results.  In total, 3 of the 9 participants had evidence of SFN.  The presence of SFN raises the possibility that a subset of patients with primary RP have an underlying, subclinical small-fiber dysfunction.  The authors concluded that these data open new avenues of research and therapeutics for this common condition.  The findings of this small, pilot study need to be validated by well-designed studies.

Guidelines from the American College of Occupational and Environmental Medicine (2008) make no recommendation for use of Quantitative Sudomotor Axon Reflex Test (QSART) to assist in the diagnostic confirmation of CRPS because of insufficient evidence. 

An International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis’s practice guideline on “Chronic fatigue syndrome/myalgic encephalomyelitis” (2012) stated that “No specific diagnostic laboratory test is currently available for ME/CFS, although potential biomarkers are under investigation”.

Siepmann et al (2012) noted that although piloerector muscles are innervated by the sympathetic nervous system, there are at present no methods to quantify pilomotor function.  In a pilot study, these researchers quantified piloerection using phenylephrine hydrochloride in humans.  A total of 22 healthy volunteers (18 males, 4 females) aged 24 to 48 years participated in 6 studies.  Piloerection was stimulated by iontophoresis of 1 % phenylephrine.  Silicone impressions of piloerection were quantified by number and area.  The direct and indirect responses to phenylephrine iontophoresis were compared on both forearms after pre-treatment to topical and subcutaneous lidocaine and iontophoresis of normal saline.  Iontophoresis of phenylephrine induced piloerection in both the direct and axon reflex-mediated regions, with similar responses in both arms.  Topical lidocaine blocked axon reflex-mediated piloerection post-iontophoresis (mean [SD], 66.6 [19.2] for control impressions versus 7.2 [4.3] for lidocaine impressions; p < 0.001).  Subcutaneous lidocaine completely blocked piloerection. The area of axon reflex-mediated piloerection was also attenuated in the lidocaine-treated region post=iontophoresis (mean [SD], 46.2 [16.1]cm2 versus 7.2 [3.9]cm2; p < 0.001).  Piloerection was delayed in the axon reflex region compared with the direct region.  Normal saline did not cause piloerection.  The authors concluded that phenylephrine provoked piloerection directly and indirectly through an axon reflex-mediated response that is attenuated by lidocaine.  Piloerection is not stimulated by iontophoresis of normal saline alone.  They stated that the quantitative pilomotor axon reflex test (QPART) may complement other measures of cutaneous autonomic nerve fiber function.

Quattrini et al (2007) measured foot skin vasodilator responses to acetylcholine (Ach) and sodium nitroprusside (SNP) and vasoconstrictor responses to sympathetic stimulation in 5 healthy control subjects, 10 non-neuropathic diabetic (NND) patients, 10 diabetic patients with painless neuropathy (PLDN), and 8 diabetic patients with painful diabetic neuropathy (PDN).  In PDN, there were significantly reduced responses to Ach (ANOVA, p = 0.003) and vasoconstrictor inspiratory gasp (ANOVA, p < 0.001) but not to SNP (not significant).  Post-hoc analysis showed significant differences in Ach-induced vasodilation between PDN and non-diabetic control subjects (p < 0.05) as well as between PDN and NND (p < 0.05) but not PDN and PLDN (not significant).  There were no significant differences for SNP-induced vasodilation.  However, there were significant differences in the vasoconstrictor response between PDN and control, NND, and PLDN (p < 0.01).  This study found an impairment of cutaneous endothelium-related vasodilation and C-fiber-mediated vasoconstriction in PDN.  Inappropriate local blood flow regulation may have a role in the pathogenesis of pain in diabetic neuropathy.  The authors stated that prospective studies are needed to determine the temporal relationship of these changes in relation to the emergence of neuropathic pain.

The use of autonomic nervous system function testing for cardiovagal innervation has clinical data supporting its use.  It is the only way to measure the function of the parasympathetic, or cardiovagal, nervous system (O'Suilleabhain, et al., 1998; Low, 2003; Singer, et al., 2004; Low, et al., 2004; Low & Opfer-Gehrking, 1993; Salo, et al., 1996; Novak, et al., 1996; Low, et al., 1997; Wright, et al., 1999; Benarroch, 2002; Goldstein, et al., 2003; Thaisetthawatkul, et al., 2004; Sanya, et al., 2005; Benarrach, et al., 2006; Wang, et al., 2008; Goldstein, et al., 2010).

Autonomic testing (including cardiovagal testing) is recommended for all patients with type 2 diabetes at the time of diagnosis and 5 years after diagnosis in individuals with type 1 diabetes (Boulton, et al., 2005; Tesfaye, et al., 2010; Spallone, et al., 2011a; Bernardi, et al., 2011; Spallone, et al., 2011b; Spallone, et al., 2011c). Individuals with diabetes that have cardiac autonomic neuropathy have a significantly higher mortality, and guidelines for anesthesia, surgery and medical therapies to affect outcomes have been established (Boulton, et al., 2005; Spallone, et al., 2011a; Vinik & Ziegler, 2007). Cardiovagal testing has been demonstrated in a number of disease states as an early marker of autonomic parasympathetic dysfunction (O'Suilleabhain, et al., 1998; Low, et al., 2004; Novak, et al., 1996; Thaisetthawatkur, et al., 2004; Beske, et al., 2002; Gibbons & Freeman, 2006; Goldstein, et al., 2009). Some disorders preferentially affect autonomic nerve fibers, such as amyloidosis and autoimmune autonomic ganglionopathy, and do not exhibit abnormalities of somatic nerve fiber tests (Low, et al., 2003). Heart rate variability is a simple and reliable test of cardiovagal function.  It has a sensitivity of 97.5% for detection of parasympathetic dysfunction in diabetes when age related normative values are used (Low, et al., 1997; Dyck, et al., 1992). The heart rate response to deep breathing, tilt table test and the heart rate response to the Valsalva maneuver are considered standard clinical tests of autonomic function and are sensitive, specific and reproducible methods for grading the degree of autonomic dysfunction (Low, 1993).

Freeman and Chapleau (2013) stated that autonomic testing is used to define the role of the autonomic nervous system in diverse clinical and research settings.  Because most of the autonomic nervous system is inaccessible to direct physiological testing, in the clinical setting the most widely used techniques entail the assessment of an end-organ response to a physiological provocation.  The non-invasive measures of cardiovascular parasympathetic function involve the assessment of heart rate variability while the measures of cardiovascular sympathetic function assess the blood pressure response to physiological stimuli.  Tilt-table testing, with or without pharmacological provocation, has become an important tool in the assessment of a predisposition to neurally mediated (vasovagal) syncope, the postural tachycardia syndrome, and orthostatic hypotension.  Distal, post-ganglionic, sympathetic cholinergic (sudomotor) function may be evaluated by provoking axon reflex mediated sweating, e.g., the quantitative sudomotor axon reflex test (QSART) or the quantitative direct and indirect axon reflex test (QDIRT).  The thermoregulatory sweat test provides a non-localizing measure of global pre- and post-ganglionic sudomotor function.  Frequency domain analyses of heart rate and blood pressure variability, microneurography, and baroreflex assessment are currently research tools but may find a place in the clinical assessment of autonomic function in the future.

Siepmann et al (2013) noted that among the few well-established techniques to diagnose autonomic dysfunction are head-up-tilt table testing, heart rate variability measurement and axon-reflex based sudomotor testing.  Recent research focused on the development of novel techniques to assess autonomic function based on axon-reflex testing in both vasomotor and pilomotor nerve fibers.  However, these techniques are clinically not widely used due to technical limitations and the lack of data on their utility to detect autonomic dysfunction in patients with neuropathy.

In a community-based cross-sectional study, Saint Martin et al (2013) evaluated the role of the cardiac autonomic nervous system (ANS), as measured according to spontaneous cardiac baroreflex sensitivity (BRS), in the type and degree of cognitive performance in healthy young-elderly individuals, taking into account the presence of other vascular risk factors.  A subset of participants, aged 66.9 ± 0.9, from a prospective study that aimed to assess the influence of ANS activity on cardiovascular and cerebrovascular morbidity and mortality (n = 916) were included in this study.  All subjects underwent a clinical interview, neuropsychological testing, and autonomic and vascular measurements.  Three cognitive domains were defined: (i) attentional (Trail-Making Test Part A, (ii) Stroop code and parts I & II), and (iii) executive (Trail-Making Test Part B, Stroop part III, verbal fluency and similarity tests), and memory (Benton visual retention test, Grober and Buschke procedure).  Subjects were stratified according to their scores into normal, low, and impaired performers.  After adjustments to demographic and vascular data, participants with moderate autonomic dysregulation (3 < BRS ≤ 6) were determined to be 1.82 times as likely to have memory impairment (odds ratio (OR) = 1.82, 95 % confidence interval (CI): 1.13 to 3.17, p = 0.02) and those with severe autonomic dysregulation (BRS ≤ 3) to be 2.65 as likely (OR = 2.65, 95 % CI: 1.40 to 5.59, p = 0.006) as participants with normal BRS (> 6).  The authors concluded that in older individuals without dementia, autonomic dysregulation seems to have a direct, gradual, and independent effect on memory.  Moreover, they stated that future studies are needed to evaluate the long-term effects of BRS and other markers of the ANS on cognitive decline.

Testing sympathetic adrenergic function is the primary method for evaluating patients with syncope, orthostatic hypotension, postural tachycardia syndrome and postural dizziness (Gibbons & Freeman, 2006; Faraji, et al., 2011; Sundkvist, 1981; Sundkvist, et al., 1981; Abraham, et al., 1986; Kenny, et al., 1986; Turkka, et al., 1987; Bergstrom, et al., 1987; Abi Samra, 1988; Ruviele, et al., 1990; Thilenius, et al., 1991; Grubb, et al., 1991; Sra, et al., 1991; Benditt, et al., 1991; Navarro, et al., 1991; Kupoor, 1992; Fouad, et al., 1993; Calkins, et al., 1993; Mathias, et al., 2001; Lahrmann, et al., 2006). Testing is sensitive, specific, and is useful across diseases to diagnose patients with autonomic dysfunction.  Sympathetic adrenergic testing (in conjunction with cardiovagal and sudomotor function testing) has been shown to aid in diagnosis, management and outcomes in patients with autonomic dysfunction or syncope of unexplained cause(Gibbons & Freeman, 2006; Faraji, et al., 2011; Sundkvist, 1981; Sundkvist, et al., 1981; Abraham, et al., 1986; Kenny, et al., 1986; Turkka, et al., 1987; Bergstrom, et al., 1987; Abi Samra, 1988; Ruviele, et al., 1990; Thilenius, et al., 1991; Grubb, et al., 1991; Sra, et al., 1991; Benditt, et al., 1991; Navarro, et al., 1991; Kupoor, 1992; Fouad, et al., 1993; Calkins, et al., 1993; Mathias, et al., 2001; Lahrmann, et al., 2006' Freeman, 2006; Oka, et al., 2007; Low, 2008; Gibbons, et al., 2011).  

Autonomic testing (including adrenergic testing) is recommended for all patients with type 2 diabetes at the time of diagnosis and 5 years after diagnosis in individuals with type 1 diabetes (Boulton, et al., 2005; Tesfaye, et al., 2010; Spallone, et al., 2011a; Bernardi, et al., 2011; Spallone, et al., 2011b; Spallone, et al., 2011c). Individuals with diabetes that have cardiac autonomic neuropathy have a significantly higher mortality, and guidelines for anesthesia, surgery and medical therapies to affect outcomes have been established (Boulton, et al., 2005; Spallone, et al., 2011a; Vinik & Ziegler, 2007).

There are studies that support the role of autonomic testing in improving clinical outcomes (Low, et al., 2006; Nolano, et al., 2006; Illigens & Gibbons, 2009; Gibbons & Freeman, 2006; Low, 1993; Mathias, et al., 2001; Gibbons, et al., 2001; Gibbons, et al., 2008; Gibbons & Freeman, 2010; Gibbons & Freeman, 2005, Maguire, et al., 20008; Schurmann, et al., 2000; Donadio, et al., 2008). One of the longest running and most detailed examples includes the DCCT trial of diabetic autonomic neuropathy where cardiovagal function was better in individuals with tight glycemic control even 13 years after the end of the study (Pop-Busui, et al., 2009). This data strongly supports the utility of autonomic testing to impact clinical outcomes.  Patients with cardiac autonomic neuropathy have an increased risk of silent myocardial ischemia (Vinik, et al., 2003), major cardiac events (Vinik & Ziegler, 2007) and is a predictor of cardiovascular mortality (Vinik & Ziegler, 2007; Maser, et al., 2003).

There are studies of the impact of autonomic testing on clinical treatment.  A few examples of the many situations where autonomic testing is of clinical use include: 

  1. Patients with syncope –autonomic testing is necessary to differentiate neurally mediated syncope from neurogenic orthostatic hypotension and other causes of syncope (Lahrmann, et al., 2006; Abi-Samra, et al, 1988; Kaufmann, 1997; Kochiadakis, et al., 1997; Stewart, 2000; Karas, et al., 2000; Freeman, et al., 2011; Baker, et al., 2009; Iodice, et al., 2009).
  2. Patients with diabetes – all patients with diabetes are recommended to have autonomic testing (sudomotor, cardiovagal and adrenergic) at diagnosis (type 1 diabetes) or 5 years after diagnosis (type 2 diabetes) (Boulton, et al., 2005; Tesfaye, et al., 2010; Spallone, et al., 2011a; Bernardi, et al., 2011; Spallone, et al., 2011b; Spallone, et al., 2011c). In diabetes there is a high prevalence of cardiovascular autonomic neuropathy in this population (Low, et al., 1983; Kennedy, et al., 1984). The relationship between autonomic dysfunction and cardiovascular risk has been well documented and is important to monitor for patients planning major surgical procedures or considering moderate to high intensity physical exercise. This is the reason that the ADA recommends autonomic testing for all patients with type 2 diabetes at the time of diagnosis, and all patients with type 1 diabetes 5 years after diagnosis.  The perioperative mortality in cardiovascular autonomic neuropathy is linked to greater blood pressure instability and hypothermia (Low, et al., 1985; Cohen, et al., 1987; Fealey, et al., 1989; Maselli, et al., 1989). This information may prompt high-risk patients to forgo an elective procedure or allow the anesthesiologist to prepare for potential hemodynamic changes, thereby reducing morbidity and mortality (Kennedy, et al., 1984: Low, et al., 1985; Cohen, et al., 1987; Fealey, et al., 1989; Maselli, et al., 1989).
  3. Patients with orthostatic dizziness – patients with recurrent dizziness with standing may have autonomic dysfunction, postural tachycardia syndrome or other autonomic neuropathy that can be treated if a diagnosis is made (Singer, et al., 2004; Gibbons, et al., 2011; Baker, et al., 2001; Iodice, et al., 2009; Vernino, et al., 1998; Vernino, et al., 2000; Low, et al., 1995; Gordon, et al., 2000; Sandvani, et al., 2000; Low, et al., 2001; Thieben, et al., 2007). All autonomic tests (sudomotor, cardiovagal and adrenergic) are appropriate to use in forming a differential diagnosis.
  4. Patients with disorders of sweating – autonomic testing can provide a diagnosis which can lead to treatment of the underlying disorder and improvements in clinical outcomes (Fealey, et al., 1989; Nolano, et al., 2006; Cheshire & Freeman 2003; Kimpinski, et al., 2009; Fisher & Maibach, 1970; Spector & Bachman, 1984; Kang, et al., 1987; Mitchell, et al., 1987; Weller, et al., 1992; Gibbons & Freeman, 2009). Although sudomotor testing will provide specific information about the problem with sweating, cardiovagal and adrenergic testing will narrow the differential diagnosis and are therefore integral parts of the autonomic test (i.e. is this an autonomic ganglionopathy, an isolated autonomic neuropathy such as Ross syndrome, is this a peripheral neuropathy causing distal anhidrosis and proximal hyperhidrosis etc).
  5. Patients with peripheral neuropathy from a number of different causes such as (but not limited to) amyloidosis, Fabry’s disease, sjogren’s syndrome, autoimmune neuropathies (Wang, et al., 2008; Low, et al., 2003; Kang, et al., 1987; Sung, 1979; Kaye, et al., 1988; Mutoh, et al., 1988; Kovacs, et al., 2004; Sakakibora, et al., 2004; Mori, et al., 2005; Lopate, et al., 2006; Seldin, et al., 2004; Delanaye, et al., 2006; Shimojima, et al., 2008). All tests of autonomic function (sudomotor, cardiovagal and adrenergic) can provide utility in making a diagnosis, defining the severity of autonomic dysfunction and aiding in treatment of the underlying disorder. The autonomic phenotype can be relatively specific for some neuropathies such as amyloid (Wang, et al., 2008)) and autoimmune autonomic neuropathy (Kimpinski, et al.,, 2009; Sandroni, et al., 2004; Manganelli, et al., 2011).
  6. In Parkinson’s disease (or other synucleinopathies): Many patients are on a variety of medications that may exacerbate, or cause, autonomic dysfunction (such as levodopa).  Patients may be having falls for a variety of reasons, and it is important to distinguish the underlying cause before major injury occurs.   Autonomic testing can quickly help distinguish whether there is a primary underlying autonomic disorder that is causing the problem (and therefore result in a change in diagnosis or management) or the medication is actually causing the problem thereby leading to a change in pharmacotherapy.
  7. Patients with neurogenic orthostatic hypotension, especially if due to a treatable etiology such as drug-induced or autoimmune. Testing, for instance in autoimmune autonomic ganglionopathy, can help the clinician evaluate response to therapy (Manganelli, et al., 2011; Gibbons, et al., 2011; Gibbons, et al., 2008; Gibbons & Freeman, 2009).

There are several devices on the market (e.g., ANSAR, Critical Care Assessment) that state that they offer complete autonomic assessment in 10-15 minutes. In contrast to standard autonomic testing (as described above), the use of “autonomic testing” by these automated devices has not been validated, nor is there data to show they are clinically meaningful. This testing is typically performed without a 5 minute tilt table test and beat-to-beat blood pressure monitoring. These automated testing devices have been promoted for use by physicians with little or no training in autonomic testing, and little understanding of autonomic nervous system physiology.

Many of the references to ANSAR testing offered by the manufacturer are in abstract form or are published in journals that are not indexed by the National Library of Medicine's PubMed database of peer-reviewed medical publications. Of the full-length articles that were published in peer-reviewed journals indexed in PubMed, three are to animal studies, one is a case report, four are to review articles and not primary research studies, and two are to studies that observe autonomic activity following trauma. One of the references is to a study that reports on changes in management of subjects with ANSAR testing; however, there is no comparison group managed without ANSAR testing.

None of the articles in peer-reviewed publications index in PubMed are of clinical studies proving the value of ANSAR testing. Of the peer-reviewed published evidence, one of the references is to a case report (Turner & Colombo, 2004); case reports do not provide high quality evidence.

Three of the ANSAR references in peer-reviewed publications indexed in PubMed are to animal studies: Akselrod, et al., 1981; Akselrod, et al., 1985; Akselrod, et al., 1987.

A study by Arora, et al. (2008) documents changes in alpha-1 agonist (midodrine) with ANSAR testing in persons with diabetes; however, there is no comparison group of subjects managed without ANSAR testing. Thus, this study does not provide evidence that clinical outcomes were improved with ANSAR testing compared to management without ANSAR testing in persons with diabetes.

Two of the studies of ANSAR testing in peer-reviewed publications indexed by the National Library of Medicine (PubMed) are to observations of autonomic activity following trauma. A study by Fathizadeh, et al. (2004) reports on cardiovascular changes and autonomic activity (by ANSAR testing) in trauma subjects. However, ANSAR testing results were not used in managing patients in this study. A study by Colombo, et al. (2008) is also a descriptive study, reporting on changes in autonomic activity in trauma subjects. 

Several of the ANSAR references are to review articles, and not primary clinical studies. A reference from Vinik & Ziegler, et al. (2007) is a review of diabetic cardiovascular autonomic neuropathy. The authors mention ANSAR testing as a method of autonomic nervous system functioning; however, the article was not a clinical study of ANSAR testing. An additional reference from Akselrod, et al. (1988) is a review article and is not primary research. An editorial from Vinik (2010) reviews the relationships between neuropathy and cardiovascular disease in diabetes; this is not a clinical study, and no specific reference is made to ANSAR testing. The reference to Vinik (2003) is also a review article and not a clinical study.

Several references to ANSAR testing are abstracts, rather than full-length peer-reviewed publications: Waheed, et al., 2006; Arora, et al., 2008; Aysin & Aysin, 2006; Aysin, et al., 2007; Vinik, et al., 2004; Boyd, et al., 2010; Boyd, et al., 2010; Nemechek, et al., 2009; Nemechek, et al., 2009; Pereira, et al., 2011, Baker, et al., 2011; Rothstein, et al., 2011. Abstracts do not undergo the level of peer-review as full-length publications, and provide insufficient information to adequately evaluate the clinical study. 

Several of the references to ANSAR are to the Touchpoint Briefings in U.S. Cardiology, U.S. Neurology, and U.S. Endocrinology; these journals are not of sufficient quality to be indexed by the National Library of Medicine in the PubMed database of peer-reviewed published medical literature: Vinik & Murray, 2008; Vinik, et al., 2007; Tobias, et al., 2010; Nanavanti, et al., 2010. An article by Vinik & Murray (2008) is a review article that includes case reports. An article by Vinik, et al. (2007) is also a review article, and is not a clinical study. An article by Nanavanti, et al. (2010) described a study where therapies in atrial fibrillation were changed based upon ANSAR testing; however, there is no comparison group of subjects managed without ANSAR testing, so no conclusions about the benefits of ANSAR testing can be drawn from this study. A study by Tobias, et al. (2010) reports on observations regarding a large number of subjects who underwent ANSAR testing at six primary care ambulatory clinics, and those with parasympathetic excess were treated according to certain protocols; this study did not include a comparison group of subjects managed without ANSAR testing, so no conclusions can be drawn on the effectiveness of ANSAR testing in improving clinical outcomes.

CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
95921 Testing of autonomic nervous system function; cardiovagal innervation (parasympathetic function), including two or more of the following: heart rate response to deep breathing with recorded R-R interval, Valsalva ratio, and 30:15 ratio
95922     vasomotor adrenergic innervation (sympathetic adrenergic function), including beat-to beat blood pressure and R-R interval changes during Valsalva maneuver and at least five minutes of passive tilt
95923     sudomotor, including one or more of the following: quantitative sudomotor axon reflex test (QSART), silastic sweat imprint, thermoregulatory sweat test, and changes in sympathetic skin potential
95924 Testing of autonomic nervous system function; combined parasympathetic and sympathetic adrenergic function testing with at least 5 minutes of passive tilt
CPT codes not covered for indications listed in the CPB:
95943 Simultaneous, independent, quantitative measures of both parasympathetic function and sympathetic function, based on time-frequency analysis of heart rate variability concurrent with time-frequency analysis of continuous respiratory activity, with mean heart rate and blood pressure measures, during rest, paced (deep) breathing, Valsalva maneuvers, and head-up postural change
ICD-9 codes covered if selection criteria are met:
250.60 - 250.63 Diabetes with neurological manifestations
277.30 - 277.39 Amyloidosis
337.20 - 337.29 Reflex sympathetic dystrophy
356.4 Idiopathic progressive polyneuropathy
356.8 Other specified idiopathic peripheral neuropathy
356.9 Unspecified idiopathic peripheral neuropathy
357.2 Polyneuropathy in diabetes
357.4 Polyneuropathy in diseases classified elsewhere
710.2 Sicca syndrome
ICD-9 codes not covered for indications listed in the CPB::
323.9 Unspecified causes of encephalitis, myelitis, and encephalomyelitis [myalgic encephalomyelitis]
337.9 Unspecified disorder of autonomic nervous system [POTS syndrome]
443.0 Raynaud's syndrome
780.71 Chronic fatigue syndrome

The above policy is based on the following references:
    1. American Academy of Neurology. Assessment: Clinical autonomic testing report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 1996;46(3):873-880.
    2. Ravits JM. AAEM minimonograph #48: Autonomic nervous system testing. Muscle Nerve. 1997;20(8):919-937.
    3. American College of Occupational and Environmental Medicine (ACOEM). Chronic pain. In: Occupational Medicine Practice Guidelines: Evaluation and Management of Common Health Problems and Functional Recovery in Workers. Elk Grove Village, IL: ACOEM; 2008.
    4. England JD, Gronseth GS, Franklin G, et al; American Academy of Neurology; American Association of Neuromuscular and Electrodiagnostic Medicine; American Academy of Physical Medicine and Rehabilitation. Evaluation of distal symmetric polyneuropathy: The role of autonomic testing, nerve biopsy, and skin biopsy (an evidence-based review). Muscle Nerve. 2009;39(1):106-115.
    5. International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME). Chronic fatigue syndrome/myalgic encephalomyelitis. A primer for clinical practitioners. Chicago (IL): International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME); 2012. Available at: Accessed May 1, 2013.
    6. Abbot NC, Beck JS, Mostofi S, Weiss F. Sympathetic vasomotor dysfunction in leprosy patients: Comparison with electrophysiological measurement and qualitative sensation testing. Neurosci Lett. 1996;206(1):57-60.
    7. Abi-Samra F, Maloney JD, Fouad-Tarazi FM, Castle LW. The usefulness of head-up tilt testing and hemodynamic investigations in the workup of syncope of unknown origin. Pacing Clin Electrophysiol. 1988;11(8):1202-1214.
    8. Abraham RR, Abraham RM, Wynn V. Autonomic and electrophysiological studies in patients with signs or symptoms of diabetic neuropathy. Electroencephalogr Clin Neurophysiol. 1986;63(3):223-230.
    9. Amoiridis G, Tzagournissakis M, Christodoulou P, et al. Patients with horizontal gaze palsy and progressive scoliosis due to ROBO3 E319K mutation have both uncrossed and crossed central nervous system pathways and perform normally on neuropsychological testing. J Neurol Neurosurg Psychiatry. 2006;77(9):1047-1053.
    10. Argiana V, Eleftheriadou I, Tentolouris N. Screening for the high-risk foot of ulceration: Tests of somatic and autonomic nerve function. Curr Diab Rep. 2011;11(4):294-301.
    11. Atkinson JL, Fealey RD. Sympathotomy instead of sympathectomy for palmar hyperhidrosis: Minimizing postoperative compensatory hyperhidrosis. Mayo Clin Proc. 2003;78(2):167-172.
    12. Baker SK, Morillo C, Vernino S. Autoimmune autonomic ganglionopathy with late-onset encephalopathy. Auton Neurosci. 2009;146(1-2):29-32.
    13. Baron R, Maier C. Reflex sympathetic dystrophy: skin blood flow, sympathetic vasoconstrictor reflexes and pain before and after surgical sympathectomy. Pain.  1996;67(2-3):317-326.
    14. Baser SM, Meer J, Polinsky RJ, Hallett M. Sudomotor function in autonomic failure. Neurology. 1991;41(10):1564-1566.
    15. Benarroch EE, Schmeichel AM, Sandroni P, et al. Involvement of vagal autonomic nuclei in multiple system atrophy and Lewy body disease. Neurology. 2006;66(3):378-383.
    16. Benarroch EE. New findings on the neuropathology of multiple system atrophy. Auton Neurosci. 2002;96(1):59-62.
    17. Benditt DG, Remole S, Bailin S, et al. Tilt table testing for evaluation of neurally-mediated (cardioneurogenic) syncope: Rationale and proposed protocols. Pacing Clin Electrophysiol. 1991;14(10):1528-1537.
    18. Berghoff M, Kilo S, Hilz MJ, Freeman R. Differential impairment of the sudomotor and nociceptor axon-reflex in diabetic peripheral neuropathy. Muscle Nerve. 2006;33(4):494-499.
    19. Bergström B, Lilja B, Osterlin S, Sundkvist G. Autonomic neuropathy in type I diabetes: Influence of duration and other diabetic complications. Acta Med Scand. 1987;222(2):147-154.
    20. Bernardi L, Spallone V, Stevens M, et al.; on behalf of the Toronto Consensus Panel on Diabetic Neuropathy*. Investigation methods for cardiac autonomic function in human research studies. Diabetes Metab Res Rev. 2011 Jun 21. [Epub ahead of print]
    21. Berne C, Fagius J, Pollare T, Hjemdahl P. The sympathetic response to euglycaemic hyperinsulinaemia. Evidence from microelectrode nerve recordings in healthy subjects. Diabetologia. 1992;35(9):873-879.
    22. Beske SD, Alvarez GE, Ballard TP, Davy KP. Reduced cardiovagal baroreflex gain in visceral obesity: Implications for the metabolic syndrome. Am J Physiol Heart Circ Physiol. 2002;282(2):H630-H635.
    23. Bickel A, Axelrod FB, Marthol H, et al. Sudomotor function in familial dysautonomia. J Neurol Neurosurg Psychiatry. 2004;75(2):275-279.
    24. Birklein F, Künzel W, Sieweke N. Despite clinical similarities there are significant differences between acute limb trauma and complex regional pain syndrome I (CRPS I). Pain. 2001;93(2):165-171.
    25. Birklein F, Riedl B, Claus D, Neundörfer B. Pattern of autonomic dysfunction in time course of complex regional pain syndrome. Clin Auton Res. 1998;8(2):79-85.
    26. Boulton AJ, Vinik AI, Arezzo JC, et al.; American Diabetes Association. Diabetic neuropathies: A statement by the American Diabetes Association. Diabetes Care. 2005;28(4):956-962.
    27. Caccia MR, Dezuanni E, Salvaggio A, et al. Sympathetic skin response versus maximum motor and sensory conduction velocity to detect subclinical neuropathy in non-insulin-dependent diabetics. Acta Neurol Belg. 1991;91(4):213-222.
    28. Calkins H, Byrne M, el-Atassi R, et al. The economic burden of unrecognized vasodepressor syncope. Am J Med. 1993;95(5):473-479.
    29. Chan RC, Chuang TY, Chiu FY. Sudomotor abnormalities in reflex sympathetic dystrophy. Zhonghua Yi Xue Za Zhi (Taipei). 2000;63(3):189-195.
    30. Chelimsky TC, Low PA, Naessens JM, et al. Value of autonomic testing in reflex sympathetic dystrophy. Mayo Clin Proc. 1995;70(11):1029-1040.
    31. Cheshire WP, Freeman R. Disorders of sweating. Semin Neurol. 2003;23(4):399-406.
    32. Cohen J, Low P, Fealey R, et al. Somatic and autonomic function in progressive autonomic failure and multiple system atrophy. Ann Neurol. 1987;22(6):692-699.
    33. Crandall CG, Musick J, Hatch JP, et al. Cutaneous vascular and sudomotor responses to isometric exercise in humans. J Appl Physiol (1985). 1995;79(6):1946-1950.
    34. De Marinis M, Stocchi F, Testa SR, et al. Alterations of thermoregulation in Parkinson's disease. Funct Neurol. 1991;6(3):279-283.
    35. Delahaye N, Rouzet F, Sarda L, et al. Impact of liver transplantation on cardiac autonomic denervation in familial amyloid polyneuropathy. Medicine (Baltimore). 2006;85(4):229-238.
    36. Dellantonio R, Paladini D, Carletti P, et al. Sympathetic skin response in chronic renal failure and correlation with sensorimotor neuropathy. Funct Neurol. 1989;4(2):173-175.
    37. Donadio V, Nolano M, Elam M, et al. Anhidrosis in multiple system atrophy: A preganglionic sudomotor dysfunction? Mov Disord. 2008;23(6):885-888.
    38. Dotson RM. Clinical neurophysiology laboratory tests to assess the nociceptive system in humans. J Clin Neurophysiol. 1997;14(1):32-45.
    39. Drory VE, Korczyn AD. Sympathetic skin response: Age effect. Neurology. 1993;43(9):1818-1820.
    40. Dyck PJ, Karnes JL, O'Brien PC, et al. The Rochester Diabetic Neuropathy Study: Reassessment of tests and criteria for diagnosis and staged severity. Neurology. 1992;42(6):1164-1170.
    41. Elie B, Guiheneuc P. Sympathetic skin response: normal results in different experimental conditions. Electroencephalogr Clin Neurophysiol. 1990;76(3):258-267.
    42. Fagius J, Wallin BG. Sympathetic reflex latencies and conduction velocities in patients with polyneuropathy. J Neurol Sci. 1980;47(3):449-461.
    43. Fagius J, Wallin BG. Sympathetic reflex latencies and conduction velocities in normal man. J Neurol Sci. 1980;47(3):433-448.
    44. Faraji F, Kinsella LJ, Rutledge JC, Mikulec AA. The comparative usefulness of orthostatic testing and tilt table testing in the evaluation of autonomic-associated dizziness. Otol Neurotol. 2011;32(4):654-659.
    45. Fealey RD, Low PA, Thomas JE. Thermoregulatory sweating abnormalities in diabetes mellitus. Mayo Clin Proc. 1989;64(6):617-628.
    46. Fisher DA, Maibach HI. Postural hypotension and anhidrosis. The autonomic insufficiency syndrome. Arch Dermatol. 1970;102(5):527-531.
    47. Fouad FM, Sitthisook S, Vanerio G, et al. Sensitivity and specificity of the tilt table test in young patients with unexplained syncope. Pacing Clin Electrophysiol. 1993;16(3 Pt 1):394-400.
    48. Freeman R. Assessment of cardiovascular autonomic function. Suppl Clin Neurophysiol. 2004;57:369-375.
    49. Freeman R, Chapleau MW. Testing the autonomic nervous system. Handb Clin Neurol. 2013;115:115-136.
    50. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neutrally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011;21(2):69-72.
    51. Gibbons CH, Centi J, Vernino S, Freeman R. Autoimmune autonomic ganglionopathy with reversible cognitive impairment. Arch Neurol. 2012r;69(4):461-466.
    52. Gibbons CH, Freeman R. Treatment-induced diabetic neuropathy: A reversible painful autonomic neuropathy. Ann Neurol. 2010;67(4):534-541.
    53. Gibbons CH, Freeman R. Antibody titers predict clinical features of autoimmune autonomic ganglionopathy. Auton Neurosci. 2009;146(1-2):8-12.
    54. Gibbons CH, Illigens BM, Centi J, Freeman R. QDIRT: quantitative direct and indirect test of sudomotor function. Neurology. 2008;70(24):2299-2304.
    55. Gibons CH, Vernino SA, Freeman R. Combined immunomodulatory therapy in autoimmune autonomic ganglionopathy. Arch Neurol. 2008;65(2):213-217.
    56. Gibbons CH, Freeman R. Delayed orthostatic hypotension: A frequent cause of orthostatic intolerance. Neurology. 2006;67(1):28-32.
    57. Goldstein DS, Sewell L, Holmes C. Association of anosmia with autonomic failure in Parkinson disease. Neurology. 2010;74(3):245-251.
    58. Goldstein DS, Sharabi Y, Karp BI, et al. Cardiac sympathetic denervation preceding motor signs in Parkinson disease. Cleve Clin J Med. 2009;76 Suppl 2:S47-S50.
    59. Goldstein DS, Pechnik S, Holmes C, et al. Association between supine hypertension and orthostatic hypotension in autonomic failure. Hypertension. 2003;42(2):136-142.
    60. Gordon VM, Opfer-Gehrking TL, Novak V, Low PA. Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome. Clin Auton Res. 2000;10(1):29-33.
    61. Grubb BP, Gerard G, Roush K, et al. Differentiation of convulsive syncope and epilepsy with head-up tilt testing. Ann Intern Med. 1991;115(11):871-876.
    62. Hilz MJ, Dütsch M. Quantitative studies of autonomic function. Muscle Nerve. 2006;33(1):6-20.
    63. Hoeldtke RD, Bryner KD, Horvath GG, et al. Redistribution of sudomotor responses is an early sign of sympathetic dysfunction in type 1 diabetes. Diabetes. 2001;50(2):436-443.
    64. Hoeldtke RD, Davis KM, Hshieh PB, et al. Autonomic surface potential analysis: Assessment of reproducibility and sensitivity. Muscle Nerve. 1992;15(8):926-931.
    65. Hoitsma E, Drent M, Verstraete E, et al. Abnormal warm and cold sensation thresholds suggestive of small-fibre neuropathy in sarcoidosis. Clin Neurophysiol. 2003;114(12):2326-2333.
    66. Hoitsma E, Reulen JP, de Baets M, et al. Small fiber neuropathy: A common and important clinical disorder. J Neurol Sci. 2004;227(1):119-130.
    67. Huang YN, Jia ZR, Shi X, Sun XR. Value of sympathetic skin response test in the early diagnosis of diabetic neuropathy. Chin Med J (Engl). 2004;117(9):1317-1320.
    68. Humm AM, Mathias CJ. Unexplained syncope--is screening for carotid sinus hypersensitivity indicated in all patients aged >40 years? J Neurol Neurosurg Psychiatry. 2006;77(11):1267-1270.
    69. Illigens BM, Gibbons CH. Sweat testing to evaluate autonomic function. Clin Auton Res. 2009;19(2):79-87.
    70. Iodice V, Kimpinski K, Vernino S, et al. Immunotherapy for autoimmune autonomic ganglionopathy. Auton Neurosci. 2009;146(1-2):22-25.
    71. Jacobson DM, Hiner BC. Asymptomatic autonomic and sweat dysfunction in patients with Adie's syndrome. J Neuroophthalmol. 1998;18(2):143-147.
    72. Jaradeh SS, Prieto TE. Evaluation of the autonomic nervous system. Phys Med Rehabil Clin N Am. 2003;14(2):287-305.
    73. Kang WH, Chun SI, Lee S. Generalized anhidrosis associated with Fabry's disease. J Am Acad Dermatol. 1987;17(5 Pt 2):883-887.
    74. Kapoor WN. Evaluation and management of the patient with syncope. JAMA. 1992;268(18):2553-2560.
    75. Karas B, Grubb BP, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: A potentially treatable cause of chronic fatigue, exercise intolerance, and cognitive impairment in adolescents. Pacing Clin Electrophysiol. 2000;23(3):344-351.
    76. Kaufmann H. Neurally mediated syncope and syncope due to autonomic failure: Differences and similarities. J Clin Neurophysiol. 1997;14(3):183-196.
    77. Kaye EM, Kolodny EH, Logigian EL, Ullman MD. Nervous system involvement in Fabry's disease: Clinicopathological and biochemical correlation. Ann Neurol. 1988;23(5):505-509.
    78. Kennedy WR, Sakuta M, Sutherland D, Goetz FC. Quantitation of the sweating deficiency in diabetes mellitus. Ann Neurol. 1984;15(5):482-488.
    79. Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: A useful test for investigating unexplained syncope. Lancet. 1986;1(8494):1352-1355.
    80. Kihara M, Opfer-Gehrking TL, Low PA. Comparison of directly stimulated with axon-reflex-mediated sudomotor responses in human subjects and in patients with diabetes. Muscle Nerve. 1993;16(6):655-660.
    81. Kihara M, Kihara Y, Tukamoto T, et al. Assessment of sudomotor dysfunction in early Parkinson's disease. Eur Neurol. 1993;33(5):363-365.
    82. Kihara M, Sugenoya J, Takahashi A. The assessment of sudomotor dysfunction in multiple system atrophy. Clin Auton Res. 1991;1(4):297-302.
    83. Kimpinski K, Iodice V, Burton DD, et al. The role of autonomic testing in the differentiation of Parkinson's disease from multiple system atrophy. J Neurol Sci. 2012;317(1-2):92-96.
    84. Kimpinski K, Iodice V, Sandroni P, et al. Sudomotor dysfunction in autoimmune autonomic ganglionopathy. Neurology. 2009;73(18):1501-1506.
    85. Kochiadakis GE, Rombola AT, Kanoupakis EM, et al. Assessment of autonomic function at rest and during tilt testing in patients with vasovagal syncope. Am Heart J. 1997;134(3):459-466.
    86. Kovács L, Paprika D, Tákacs R, et al. Cardiovascular autonomic dysfunction in primary Sjögren's syndrome. Rheumatology (Oxford). 2004;43(1):95-99.
    87. Lacomis D. Small-fiber neuropathy. Muscle Nerve. 2002;26(2):173-188.
    88. Lahrmann H, Cortelli P, Hilz M, et al. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur J Neurol. 2006;13(9):930-936.
    89. Lang E, Spitzer A, Claus D, et al. Stimulation of sudomotor axon reflex mechanism by carbachol in healthy subjects and patients suffering from diabetic polyneuropathy. Acta Neurol Scand. 1995;91(4):251-254.
    90. Levy DM, Reid G, Rowley DA, Abraham RR. Quantitative measures of sympathetic skin response in diabetes: Relation to sudomotor and neurological function. J Neurol Neurosurg Psychiatry. 1992;55(10):902-908.
    91. Lidberg L, Wallin BG. Sympathetic skin nerve discharges in relation to amplitude of skin resistance responses. Psychophysiology. 1981;18(3):268-270.
    92. Linden D, Berlit P. Sympathetic skin responses (SSRs) in monofocal brain lesions: Topographical aspects of central sympathetic pathways. Acta Neurol Scand. 1995;91(5):372-376.
    93. Lipp A, Sandroni P, Ahlskog JE, et al. Prospective differentiation of multiple system atrophy from Parkinson disease, with and without autonomic failure. Arch Neurol. 2009;66(6):742-750.
    94. Lopate G, Pestronk A, Al-Lozi M, et al. Peripheral neuropathy in an outpatient cohort of patients with Sjögren's syndrome. Muscle Nerve. 2006;33(5):672-676.
    95. Low PA. Prevalence of orthostatic hypotension. Clin Auton Res. 2008;18 Suppl 1:8-13.
    96. Low PA. Evaluation of sudomotor function. Clin Neurophysiol. 2004;115(7):1506-1513.
    97. Low PA, Benrud-Larson LM, Sletten DM, et al. Autonomic symptoms and diabetic neuropathy: A population-based study. Diabetes Care. 2004;27(12):2942-2947.
    98. Low PA, Vernino S, Suarez G. Autonomic dysfunction in peripheral nerve disease. Muscle Nerve. 2003;27(6):646-661.
    99. Low PA. Testing the autonomic nervous system. Semin Neurol. 2003;23(4):407-421.
    100. Low PA, Schondorf R, Rummans TA. Why do patients have orthostatic symptoms in POTS? Clin Auton Res. 2001;11(4):223-224.
    101. Low PA, Denq JC, Opfer-Gehrking TL, et al. Effect of age and gender on sudomotor and cardiovagal function and blood pressure response to tilt in normal subjects. Muscle Nerve. 1997;20(12):1561-1568.
    102. Low PA, Opfer-Gehrking TL, Proper CJ, Zimmerman I. The effect of aging on cardiac autonomic and postganglionic sudomotor function. Muscle Nerve. 1990;13(2):152-157.
    103. Low PA, Opfer-Gehrking TL, Textor SC, et al. Postural tachycardia syndrome (POTS). Neurology. 1995;45(4 Suppl 5):S19-S25.
    104. Low PA. Composite autonomic scoring scale for laboratory quantification of generalized autonomic failure. Mayo Clin Proc. 1993 Aug;68(8):748-752.
    105. Low PA, Opfer-Gehrking TL. Differential effects of amitriptyline on sudomotor, cardiovagal, and adrenergic function in human subjects. Muscle Nerve. 1992;15(12):1340-1344.
    106. Low PA, Opfer-Gehrking TL, Proper CJ, Zimmerman I. The effect of aging on cardiac autonomic and postganglionic sudomotor function. Muscle Nerve. 1990;13(2):152-157.
    107. Low PA, Fealey RD, Sheps SG, et al. Chronic idiopathic anhidrosis. Ann Neurol. 1985;18(3):344-348.
    108. Low PA, Caskey PE, Tuck RR, et al. Quantitative sudomotor axon reflex test in normal and neuropathic subjects. Ann Neurol. 1983;14(5):573-580.
    109. Low VA, Sandroni P, Fealey RD, Low PA. Detection of small-fiber neuropathy by sudomotor testing. Muscle Nerve. 2006;34(1):57-61.
    110. Magerl W, Koltzenburg M, Schmitz JM, Handwerker HO. Asymmetry and time-course of cutaneous sympathetic reflex responses following sustained excitation of chemosensitive nociceptors in humans. J Auton Nerv Syst. 1996;57(1-2):63-72.
    111. Maguire AM, Craig ME, Craighead A, et al. Autonomic nerve testing predicts the development of complications: A 12-year follow-up study. Diabetes Care. 2007;30(1):77-82.
    112. Manek NJ, Holmgren AR, Sandroni P, et al. Primary Raynaud phenomenon and small-fiber neuropathy: Is there a connection? A pilot neurophysiologic study. Rheumatol Int. 2011;31(5):577-585.
    113. Manganelli F, Dubbioso R, Nolano M, et al. Autoimmune autonomic ganglionopathy: A possible postganglionic neuropathy. Arch Neurol. 2011;68(4):504-507.
    114. Manganelli F, Iodice V, Provitera V, et al. Small-fiber involvement in spinobulbar muscular atrophy (Kennedy's disease). Muscle Nerve. 2007;36(6):816-820.
    115. Maselli RA, Jaspan JB, Soliven BC, et al. Comparison of sympathetic skin response with quantitative sudomotor axon reflex test in diabetic neuropathy. Muscle Nerve. 1989;12(5):420-423.
    116. Maser RE, Mitchell BD, Vinik AI, Freeman R. The association between cardiovascular autonomic neuropathy and mortality in individuals with diabetes: A meta-analysis. Diabetes Care. 2003;26(6):1895-1901.
    117. Mathias CJ, Deguchi K, Schatz I. Observations on recurrent syncope and presyncope in 641 patients. Lancet. 2001;357(9253):348-353.
    118. Mitchell J, Greenspan J, Daniels T, et al. Anhidrosis (hypohidrosis) in Sjögren's syndrome. J Am Acad Dermatol. 1987;16(1 Pt 2):233-235.
    119. Mori K, Iijima M, Koike H, et al. The wide spectrum of clinical manifestations in Sjögren's syndrome-associated neuropathy. Brain. 2005;128(Pt 11):2518-2534.
    120. Mutoh T, Senda Y, Sugimura K, et al. Severe orthostatic hypotension in a female carrier of Fabry's disease. Arch Neurol. 1988;45(4):468-472.
    121. Nakazato Y, Tamura N, Ohkuma A, et al. Idiopathic pure sudomotor failure: Anhidrosis due to deficits in cholinergic transmission. Neurology. 2004;63(8):1476-1480.
    122. Navarro X, Kennedy WR, Ferrer MT. Cardiovascular responses to tilting in healthy and diabetic subjects. J Neurol Sci. 1991;104(1):39-45.
    123. Niakan E, Harati Y. Sympathetic skin response in diabetic peripheral neuropathy. Muscle Nerve. 1988;11(3):261-264.
    124. Nolano M, Provitera V, Perretti A, et al. Ross syndrome: A rare or a misknown disorder of thermoregulation? A skin innervation study on 12 subjects. Brain. 2006;129(Pt 8):2119-2131.
    125. Novak V, Novak P, Opfer-Gehrking TL, Low PA. Postural tachycardia syndrome: Time frequency mapping. J Auton Nerv Syst. 1996;61(3):313-320.
    126. O'Suilleabhain P, Low PA, Lennon VA. Autonomic dysfunction in the Lambert-Eaton myasthenic syndrome: Serologic and clinical correlates. Neurology. 1998;50(1):88-93.
    127. Oka H, Yoshioka M, Onouchi K, et al. Characteristics of orthostatic hypotension in Parkinson's disease. Brain. 2007;130(Pt 9):2425-2432.
    128. Opfer-Gehrking TL, Low PA. Impaired respiratory sinus arrhythmia with paradoxically normal Valsalva ratio indicates combined cardiovagal and peripheral adrenergic failure. Clin Auton Res. 1993;3(3):169-173.
    129. Pavesi G, Medici D, Gemignani F, et al. Sympathetic skin response (SSR) in the foot after sural nerve biopsy. Muscle Nerve. 1995;18(11):1326-1328.
    130. Peltier AC, Garland E, Raj SR, et al. Distal sudomotor findings in postural tachycardia syndrome. Clin Auton Res. 2010;20(2):93-99.
    131. Perretti A, Nolano M, De Joanna G, et al. Is Ross syndrome a dysautonomic disorder only? An electrophysiologic and histologic study. Clin Neurophysiol. 2003;114(1):7-16.
    132. Petajan JH, Danforth RC, D’Allesio D, Lucas GH. Progressive sudomontor denervation and Aidie’s syndrome. Neurology. 1965;15:172-166.
    133. Pop-Busui R, Low PA, Waberski BH, et al.; DCCT/EDIC Research Group. Effects of prior intensive insulin therapy on cardiac autonomic nervous system function in type 1 diabetes mellitus: The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study (DCCT/EDIC). Circulation. 2009;119(22):2886-2893.
    134. Quattrini C, Harris ND, Malik RA, Tesfaye S. Impaired skin microvascular reactivity in painful diabetic neuropathy. Diabetes Care. 2007;30(3):655-659.
    135. Raviele A, Gasparini G, Di Pede F, et al. Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study. Am J Cardiol. 1990;65(20):1322-1327.
    136. Rex L, Claes G, Drott C, et al. Vasomotor and sudomotor function in the hand after thoracoscopic transection of the sympathetic chain: Implications for choice of therapeutic strategy. Muscle Nerve. 1998;21(11):1486-1492.
    137. Ross AT. Progressive selective sudomotor denervation; A case with coexisting Adie's syndrome. Neurology. 1958;8(11):809-817.
    138. Saint Martin M, Sforza E, Thomas-Anterion C, et al. Baroreflex sensitivity, vascular risk factors, and cognitive function in a healthy elderly population: The PROOF cohort. J Am Geriatr Soc. 2013;61(12):2096-2102.
    139. Sakakibara R, Hirano S, Asahina M, et al. Primary Sjogren's syndrome presenting with generalized autonomic failure. Eur J Neurol. 2004;11(9):635-638.
    140. Salo TM, Viikari JS, Antila KJ, et al. Antihypertensive treatment and heart rate variability in diabetic patients: Role of cardiac autonomic neuropathy. J Auton Nerv Syst. 1996;60(1-2):61-70.
    141. Sandroni P, Vernino S, Klein CM, et al. Idiopathic autonomic neuropathy: Comparison of cases seropositive and seronegative for ganglionic acetylcholine receptor antibody. Arch Neurol. 2004;61(1):44-48.
    142. Sandroni P, Novak V, Opfer-Gehrking TL, et al. Mechanisms of blood pressure alterations in response to the Valsalva maneuver in postural tachycardia syndrome. Clin Auton Res. 2000;10(1):1-5.
    143. Sandroni P, Low PA, Ferrer T, et al. Complex regional pain syndrome I (CRPS I): prospective study and laboratory evaluation. Clin J Pain. 1998;14(4):282-289.
    144. Sanya EO, Tutaj M, Brown CM, et al. Abnormal heart rate and blood pressure responses to baroreflex stimulation in multiple sclerosis patients. Clin Auton Res. 2005;15(3):213-218.
    145. Schiffmann R, Floeter MK, Dambrosia JM, et al. Enzyme replacement therapy improves peripheral nerve and sweat function in Fabry disease. Muscle Nerve. 2003;28(6):703-710.
    146. Schondorf R, Low PA. Idiopathic postural orthostatic tachycardia syndrome: An attenuated form of acute pandysautonomia? Neurology. 1993 Jan;43(1):132-137.
    147. Schürmann M, Gradl G, Zaspel J, et al. Peripheral sympathetic function as a predictor of complex regional pain syndrome type I (CRPS I) in patients with radial fracture. Auton Neurosci. 2000;86(1-2):127-134.
    148. Seldin DC, Anderson JJ, Sanchorawala V, et al. Improvement in quality of life of patients with AL amyloidosis treated with high-dose melphalan and autologous stem cell transplantation. Blood. 2004;104(6):1888-1893.
    149. Shahani BT, Halperin JJ, Boulu P, et al. Sympathetic skin response--a method of assessing unmyelinated axon dysfunction in peripheral neuropathies. J Neurol Neurosurg Psychiatry. 1984;47:536-542.
    150. Shimojima Y, Morita H, Kobayashi S, et al. Ten-year follow-up of peripheral nerve function in patients with familial amyloid polyneuropathy after liver transplantation. J Neurol. 2008;255(8):1220-1225.
    151. Shivji ZM, Ashby P. Sympathetic skin responses in hereditary sensory and autonomic neuropathy and familial amyloid neuropathy are different. Muscle Nerve. 1999;22(9):1283-1286.
    152. Siepmann T, Gibbons CH, Illigens BM, et al. Quantitative pilomotor axon reflex test: A novel test of pilomotor function. Arch Neurol. 2012;69(11):1488-1492.
    153. Siepmann T, Penzlin AI, Illigens BM. Autonomic neuropathies--diagnosis and evidence based treatment. Dtsch Med Wochenschr. 2013;138(30):1529-1532.
    154. Singer W, Spies JM, McArthur J, et al. Prospective evaluation of somatic and autonomic small fibers in selected autonomic neuropathies. Neurology. 2004;62(4):612-618.
    155. Smith AG, Russell J, Feldman EL, et al. Lifestyle intervention for pre-diabetic neuropathy. Diabetes Care. 2006;29(6):1294-1299.
    156. Soliven B, Maselli R, Jaspan J, et al. Sympathetic skin response in diabetic neuropathy. Muscle Nerve. 1987;10(8):711-716.
    157. Spallone V, Ziegler D, Freeman R, et al.; on behalf of the Toronto Consensus Panel on Diabetic Neuropathy*. Cardiovascular autonomic neuropathy in diabetes: Clinical impact, assessment, diagnosis, and management. Diabetes Metab Res Rev. 2011 Jun 22.[Epub ahead of print]
    158. Spallone V, Bellavere F, Scionti L, et al.; Diabetic Neuropathy Study Group of the Italian Society of Diabetology. Recommendations for the use of cardiovascular tests in diagnosing diabetic autonomic neuropathy. Nutr Metab Cardiovasc Dis. 2011;21(1):69-78.
    159. Spallone V, Morganti R, D'Amato C, et al. Clinical correlates of painful diabetic neuropathy and relationship of neuropathic pain with sensorimotor and autonomic nerve function. Eur J Pain. 2011;15(2):153-160.
    160. Spector RH, Bachman DL. Bilateral Adie's tonic pupil with anhidrosis and hyperthermia. Arch Neurol. 1984;41(3):342-343.
    161. Sra JS, Anderson AJ, Sheikh SH, et al. Unexplained syncope evaluated by electrophysiologic studies and head-up tilt testing. Ann Intern Med. 1991;114(12):1013-1019.
    162. Stewart JD, Low PA, Fealey RD. Distal small fiber neuropathy: Results of tests of sweating and autonomic cardiovascular reflexes. Muscle Nerve. 1992;15(6):661-665.
    163. Stewart JM. Autonomic nervous system dysfunction in adolescents with postural orthostatic tachycardia syndrome and chronic fatigue syndrome is characterized by attenuated vagal baroreflex and potentiated sympathetic vasomotion. Pediatr Res. 2000;48(2):218-226.
    164. Sundkvist G. Autonomic nervous function in asymptomatic diabetic patients with signs of peripheral neuropathy. Diabetes Care. 1981;4(5):529-534.
    165. Sundkvist G, Almér LO, Lilja B. A sensitive orthostatic test on tilt table, useful in the detection of diabetic autonomic neuropathy. Acta Med Scand Suppl. 1981;656:43-45.
    166. Sung JH. Autonomic neurons affected by lipid storage in the spinal cord in Fabry's disease: Distribution of autonomic neurons in the sacral cord. J Neuropathol Exp Neurol. 1979;38(2):87-98.
    167. Tesfaye S, Boulton AJ, Dyck PJ, et al.; Toronto Diabetic Neuropathy Expert Group. Diabetic neuropathies: Update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes Care. 2010;33(10):2285-2293.
    168. Thaisetthawatkul P, Boeve BF, Benarroch EE, et al. Autonomic dysfunction in dementia with Lewy bodies. Neurology. 2004;62(10):1804-1809.
    169. Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic tachycardia syndrome: The Mayo clinic experience. Mayo Clin Proc. 2007;82(3):308-313.
    170. Thilenius OG, Quinones JA, Husayni TS, Novak J. Tilt test for diagnosis of unexplained syncope in pediatric patients. Pediatrics. 1991;87(3):334-338.
    171. Turkka JT, Tolonen U, Myllylä VV. Cardiovascular reflexes in Parkinson's disease. Eur Neurol. 1987;26(2):104-112.
    172. Uncini A, Pullman SL, Lovelace RE, Gambi D. The sympathetic skin response: Normal values, elucidation of afferent components and application limits. J Neurol Sci. 1988;87(2-3):299-306.
    173. Vernino S, Low PA, Fealey RD, et al. Autoantibodies to ganglionic acetylcholine receptors in autoimmune autonomic neuropathies. N Engl J Med. 2000;343(12):847-855.
    174. Vernino S, Adamski J, Kryzer TJ, et al. Neuronal nicotinic ACh receptor antibody in subacute autonomic neuropathy and cancer-related syndromes. Neurology. 1998;50(6):1806-1813.
    175. Vinik AI, Ziegler D. Diabetic cardiovascular autonomic neuropathy. Circulation. 2007;115(3):387-397.
    176. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care. 2003;26(5):1553-1579.
    177. Wang AK, Fealey RD, Gehrking TL, Low PA. Patterns of neuropathy and autonomic failure in patients with amyloidosis. Mayo Clin Proc. 2008;83(11):1226-1230.
    178. Weller M, Wilhelm H, Sommer N, et al. Tonic pupil, areflexia, and segmental anhidrosis: Two additional cases of Ross syndrome and review of the literature. J Neurol. 1992;239(4):231-234.
    179. Wolfe GI, Galetta SL, Teener JW, et al. Site of autonomic dysfunction in a patient with Ross' syndrome and postganglionic Horner's syndrome. Neurology. 1995;45(11):2094-2096.
    180. Wright RA, Grant IA, Low PA. Autonomic neuropathy associated with sicca complex. J Auton Nerv Syst. 1999;75(1):70-76.
    181. Akselrod S, Gordon D, Ubel FA, et al. Power spectrum analysis of heart fluctuations: A quantitative probe of beat to beat cardiovascular control. Science. 1981;213:220-222.
    182. Arora RR, Bulgarelli RJ, Gosh-Dastidar S, Colombo J. Autonomic mechanisms and therapeutic implications of postural diabetic cardiovascular abnormalities. J Diabetes Science and Technology. 2008;2(4):568-571.
    183. Arora RR, Gosh Dastidar S, Colombo J. Autonomic balance is associated with decreased morbidity. American Autonomic Society, 17th International Sympsium, Kauai, HI, 29 Oct - 1 Nov, 2008.
    184. Askelrod S, Gordon D, Madwed JB, et al. Hemodynamic regulation by SHR: Investigation by spectral analysis. Am J Physiol. 1987;253:H176-83.
    185. Askelrod S, Gordon D, Madwed JB, et al. Hemodynamic regulation: Investigation by spectra analysis. Am J Physiol. 1985;249:H867-75.
    186. Askelrod S. Spectral analysis of fluctuations in cardiovascular parameters: A quantitative tool for the investigation of autonomic control. Trends Pharmacol Sci. 1988;9:6-9.
    187. Aysin B, Aysin E, Colombo J. Comparison of HRV analysis methods during orthostatic challenge: HRV with respiration or without? IEEE Engineering in Medicine and Biology Conference, Lyons, France, 2007.
    188. Aysin B, Aysin E. Effect of respiration in heart rate variability (HRV) analysis. IEEE Engineering in Medicine and Biology Society Conference, New York, NY, 2006.
    189. Baker S, Pereira E, Rothstein M, Arora R, Bhatkar V, Colombo J. Parasympathetic Involvement in Sleep Medicine, Cardiovascular Implications. Accepted abstract, Autonomic Society, 2011.
    190. Boyd G, Stout D, Aultman M, Wyatt K, Vetter T, et al. Are there reliable clinical predictors of cardiac autonomic neuropathy in diabetic patients? American Society of Anesthesiologists, Annual Meeting, San Diego 16-20 Oct 2010.
    191. Boyd G, Stout D, Morris R, Witherspoon CD, Vetter T, et al. Prevalance and severity of autonomic dysfunction in diabetic patients presenting for retinal surgery. American Society of Anesthesiologists, Annual Meeting, San Diego, 16-20 Oct 2010.
    192. Colombo J, Shoemaker WC, Belzberg H, Hatzakis G, Fathizadeh P, Demetriades D.  Noninvasive monitoring of the autonomic nervous system and hemodynamics of patients with blunt and penetrating trauma. J Trauma. 2008 Dec;65(6):1364-73.
    193. Fathizadeh P, Shoemaker WC, Woo CCJ, Colombo J. Autonomic activity in trauma patients based on variability of heart rate and respiratory rate. Crit Care Med. 2004;32(5):1300-5.
    194. Nanavanti SH, Bulgarelli RJ, Vazquez-Tanus J, Gosh-Dastidar S, Colombo J, Arora RR. Altered autonomic activity with atrial fibrillation as demonstrated by non-invasive autonomic monitoring. US Cardiol. 2010;7(1):47-50.
    195. Nemechek P, Gosh Dastidar S, Colombo J. Early autonomic dysfunction is associated with secondary hypertension in HIV/AIDS patients. American Autonomic Society, St. Thomas, Virgin Islands, 31 Oct - 3 Nov 2009.
    196. Nemechek P, Gosh Dastidar S, Colombo J. HIV/AIDS leads to early cardiovascular autonomic neuropathy. American Autonomic Society, St. Thomas, Virgin Islands, 31 Oct - 3 Nov, 2009.
    197. Pereira E, Baker S, Rothstein M, Arora R, Bhatkar V, Colombo J. Sympathetic Involvement in Sleep Medicine, Cardiovascular Implications. Accepted abstract, Autonomic Society, 2011.
    198. Rothstein M, Pereira E, Baker S, Arora R, Bhatkar V, Colombo J. Parasympathetic and Sympathetic Involvement in Obstructive Sleep Apnea. Accepted abstract, Autonomic Society, 2011.
    199. Tobias H,Vinitsky A, Bulgarelli RJ, Gosh-Dastidar S, Colombo J. Autonomic nervous system monitoring of patients with excess parasympathetic responses to sympathetic challenges - clinical observations. US Neurol. 2010;5(2):62-66.
    200. Turner IM, Colombo J. Autonomic dysfunction in migraine: A case study. Headache and Pain. 2004 Nov;15(4):185-93.
    201. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care. 2003;26:1553-1579.
    202. Vinik AI, Maser RE, Ziegler D. Neuropathy. The crystal ball for cardiovascular disease. Diabetes Care. 2010;33(7):1-3.
    203. Vinik AI, Maser, RE, Nakave AA. Diabetic cardiovascular autonomic nerve dysfunction. US Endocrine Disease. 2007; Dec: 2-9.
    204. Vinik AI, Murray GL. Autonomic neuropathy is treatable. US Endocrinol. 2008;2:82-84.
    205. Vinik AI, Ziegler D. Diabetic cardiovascular autonomic neuropathy. Circulation. 2007;115:387-397.
    206. Vinik, AI, Aysin B, Colombo J. Enhanced frequency domain analysis replaces older heart rate variability methods. Fourth Annual Diabetes Technology Meeting, Philadelphia, PA, 28-30 October, 2004.
    207. Waheed A, Ali MA, Jurivich DA, Colombo J, Singer DH. Gender differences in longevity and autonomic function. Geriatric Medicine Society Meeting, Chicago, IL, May 200

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