Tilt Table Testing

Number: 0299

Table Of Contents

Policy
Applicable CPT / HCPCS / ICD-10 Codes
Background
References


Policy

Scope of Policy

This Clinical Policy Bulletin addresses tilt table testing.

  1. Medical Necessity

    Aetna considers tilt table testing (TTT), alone or in combination with administration of provocative agents (e.g., isoproterenol, sublingual nitroglycerin), medically necessary for the following indications when criteria are met:

    1. As part of a diagnostic workup for individual with suspected postural orthostatic tachycardia syndrome (POTS); or
    2. For evaluation of unexplained syncope or near syncope (including suspected or delayed orthostatic hypotensionFootnote*) when all of the following criteria are met:

      1. Member has recurrent episodes of syncope or presyncope, or has experienced a single episode considered high risk of physical injury if episode were to recur; and
      2. Initial evaluation is inconclusive or equivocal, including:
        1. History and physical examination;
        2. Medication review;
        3. Orthostatic vitals or standing test, if safely obtainable;
        4. 12-lead electrocardiogram (ECG);
        5. Laboratory testing
      3. Noninvasive cardiac testing (e.g., echocardiogram, ambulatory ECG monitoring, exercise stress test) excludes ischemia, tachyarrhythmia, or bradyarrhythmia requiring pacemaker as an etiology for the episode(s); and 
      4. Member has no contraindication to TTT (e.g., severe coronary or cerebrovascular disease in which induced hypotension may provoke ischemia, or pregnancy).

        Footnote1*Delayed orthostatic hypotension (dOH) is defined as a sustained decrease in systolic blood pressure (SBP) of at least 20 mmHg or a diastolic blood pressure (DBP) of at least 10 mmHg occurring after 3 minutes of standing.
  2. Experimental, Investigational, or Unproven

    The use of tilt table testing is considered experimental, investigational, or unproven for all other indications, including any of the following (not an all-inclusive list) because there is little support in the peer-reviewed medical literature for tilt table testing for these indications:

    1. Determining the effectiveness of medications in treating recurrent unexplained syncope; or
    2. Diagnosing joint hypermobility syndrome; or
    3. Differential diagnosis of parkinsonian syndromes (e.g., Parkinson's disease, multiple system atrophy and progressive supranuclear palsy); or
    4. Evaluating autonomic dysfunction in childhood hypersomnia disorders; or
    5. Evaluating dizziness alone when orthostatic hypotension is not suspected; or
    6. Evaluating vertigo; or
    7. Evaluating post-concussion syndrome; or
    8. Guiding surgical decision-making as well as predicting the clinical response to surgical decompression of Chiari type I-malformation (Chiari drop attacks); or;
    9. Identifying members with chronic fatigue syndrome and/or evaluating treatment effectiveness of this condition.
  3. Related Policies


Table:

CPT Codes / HCPCS Codes / ICD-10 Codes

Code Code Description

CPT codes covered if selection criteria are met:

93660 Evaluation of cardiovascular function with tilt table evaluation, with continuous ECG monitoring and intermittent blood pressure monitoring, with or without pharmacological intervention

Other CPT codes related to the CPB:

93000 Electrocardiogram, routine ECG with at least 12 leads; with interpretation and report
93005      tracing only, without interpretation and report
93010      interpretation and report only
93303 – 93356 Echocardiogram
93224 – 93278 Cardiovascular monitoring services
93015 – 93018 Cardiovascular stress test

HCPCS codes covered if selection criteria are met:

Sublingual nitroglycerin – no specific code
J7657 Isoproterenol hcl, inhalation solution, compounded product, administered through dme, concentrated form, per milligram
J7658 Isoproterenol hcl, inhalation solution, fda-approved final product, non-compounded, administered through dme, concentrated form, per milligram
J7659 Isoproterenol hcl, inhalation solution, fda-approved final product, non-compounded, administered through dme, unit dose form, per milligram
J7660 Isoproterenol hcl, inhalation solution, compounded product, administered through dme, unit dose form, per milligram

ICD-10 codes covered if selection criteria are met:

G90.A Postural orthostatic tachycardia syndrome [POTS]
I49.5 Sick sinus syndrome
I49.8 Other specified cardiac arrhythmias [postural orthostatic tachycardia syndrome]
I95.1 Orthostatic hypotension
R00.0 Tachycardia, unspecified [postural orthostatic tachycardia syndrome]
R55 Syncope and collapse

ICD-10 codes not covered for indications listed in the CPB (not all-inclusive):

F07.81 Postconcussional syndrome
G20.A1 - G20.C Parkinson's disease
G21.11 - G21.9 Secondary parkinsonism
G47.10 – G47.19 Hypersomnia [including childhood hypersomnia disorders]
G60.8 Other hereditary and idiopathic neuropathies [supranuclear palsy]
G93.5 Compression of the brain [Chiari type I-malformation (Chiari drop attacks)]
G96.810, G96.811, G96.819, G96.89 Other specified disorders of central nervous system [multiple system atrophy]
G98.8 Other disorders of nervous system
M35.7 Hypermobility syndrome
R42 Dizziness and giddiness
R53.0 - R83.8 Malaise and fatigue
Z79.890 - Z79.899 Other long term (current) drug therapy [Determining the effectiveness of medications in treating recurrent unexplained syncope]

ICD-10 codes contraindicated for indications listed in the CPB:

I20.0 – I25.110 Ischemic heart diseases
I60.00 – I69.998 Cerebrovascular diseases
O00.101 – O9A.519 Pregnancy, Childbirth and the puerperium

Background

Tilt table testing (TTT) is a standardized diagnostic procedure designed to evaluate autonomic and cardiovascular responses to positional changes, particularly in patients with unexplained syncope. During the test, the patient is secured on a motorized table, which is gradually tilted from a supine to an upright position while continuously monitoring heart rate, blood pressure, rhythm, and symptoms. If the baseline tilt does not elicit diagnostic responses, pharmacologic agents such as isoproterenol (to increase sympathetic stimulation) or sublingual nitroglycerin (to promote venous pooling and vasodilation) may be administered to enhance the test's sensitivity. These medications help provoke reflex-mediated changes in hemodynamics, aiding clinicians in identifying patterns consistent with vasovagal syncope, orthostatic hypotension, or autonomic dysfunction.

There is sufficient evidence that tilt table testing, with or without isoproterenol, is safe and effective as a diagnostic tool for the evaluation of patients with recurrent unexplained syncope. The reported sensitivity, specificity, and reproducibility of tilt table testing ranged from 65 to 87%, 55 to 96%, and 71 to 88%, respectively. This procedure helps to identify a largely benign disorder and, indirectly, exclude other possibly life-threatening conditions. Tilt table testing performed early in the evaluation may obviate extensive and expensive tests such as intra-cardiac electrophysiological studies, CAT scans, and MRIs of the brain. In contrast, there is insufficient evidence that tilt table testing following intravenous infusion of metoprolol can accurately predict the effectiveness of oral metoprolol therapy in treating patients with recurrent unexplained syncope. This procedure has not been shown to provide any additional information than would have been obtained from a trial of oral therapy.

Ringer et al. (2025) describe orthostatic hypotension, or postural hypotension, as a condition characterized by a sudden drop in blood pressure when an individual stands from a sitting or supine position. This condition can be classified into neurogenic and non-neurogenic types and is clinically diagnosed when systolic blood pressure decreases by at least 20 mm Hg or diastolic pressure by 10 mm Hg within three minutes of standing or being tilted at a 60-degree angle. The drop in blood pressure is often attributed to autonomic reflex failure, central or peripheral nervous system lesions, cardiac dysfunction, volume depletion, or medication side effects. Orthostatic hypotension significantly impacts quality of life and is associated with increased risks of falls, cardiovascular disease, dementia, depression, and mortality. Symptoms typically arise from cerebral hypoperfusion, although some patients may remain asymptomatic. The condition is prevalent among older adults, affecting about one in five individuals aged 60 and older, and can manifest as acute or chronic episodes.

Orthostatic hypotension can be further categorized into classic, delayed, initial, and delayed blood pressure recovery types. Classic orthostatic hypotension occurs within three minutes of standing, while delayed orthostatic hypotension manifests after three minutes. Initial orthostatic hypotension lasts less than 15 seconds following postural changes, and delayed blood pressure recovery refers to a drop that takes longer than 15 seconds to return to baseline levels. Studies indicate that over 95% of patients can be diagnosed based on systolic hypotension alone, making it the most commonly reported metric for this condition. The underlying causes can be neurogenic, stemming from conditions like Parkinson's disease or peripheral neuropathy, or non-neurogenic, often linked to volume depletion or cardiac issues. Medications, particularly in older patients with polypharmacy, can also contribute to the condition. Differentiating orthostatic hypotension from related conditions such as vasovagal syncope and postural tachycardia syndrome (POTS) is necessary, as both can present with similar symptoms of autonomic dysfunction. Diagnosis involves a comprehensive history, physical examination, and orthostatic vital signs, which are essential yet frequently overlooked in clinical practice. Moreover, patients at risk for cardiac disease should undergo a comprehensive cardiac evaluation, starting with an electrocardiography (ECG). Further testing, such as a Holter monitor, echocardiogram, or additional diagnostics, should be considered if the history suggests a cardiogenic origin. Laboratory tests should assess for anemia, dehydration, diabetes, alcohol use disorder, or heart failure. Treatment focuses on identifying and addressing the underlying causes, with behavioral modifications and pharmacological options considered as needed. Tilt table testing serves as a valuable tool in diagnosing orthostatic hypotension and related conditions, helping to provoke symptoms and assess the physiological responses to postural changes (Ringer et al., 2025).

Postural orthostatic tachycardia syndrome (POTS), also known as postural tachycardia syndrome, is a type of orthostatic intolerance characterized by excessive tachycardia and decreased cerebral blood flow in the upright position. This can result in significant symptoms of dizziness and light-headedness that can eventually lead to syncope. Symptoms of POTS include light-headedness, visual blurring, palpitations, and weakness upon assuming an upright posture; these symptoms are relieved by resuming a supine position. Tilt table testing has been used to aid in the diagnosis of POTS.

An UpToDate review on "Postural Tachycardia Syndrome" (Freeman and Kaufmann, 2012) states that: "The diagnosis of POTS is established from the history and head-up tilt testing, which demonstrates a heart rate increase of >30 bpm over baseline or to >120 bpm. Dehydration, prolonged bed rest, medications, and other dysautonomias should be excluded as etiologies."

Grubb et al. (1997) stated that head-up tilt (HUT) testing has emerged as an accepted modality for identifying an individual's predisposition to episodes of autonomically mediated hypotension and bradycardia that are sufficiently profound to cause transient loss of consciousness (neuro-cardiogenic syncope [NCS]). However, it has also become apparent that less dramatic falls in blood pressure, while not sufficient to cause full syncope, may produce symptoms such as near syncope, vertigo, dizziness, and transient ischemic attack-like episodes. These investigators have identified a subgroup of individuals with a mild form of autonomic dysfunction who experience symptoms of postural tachycardia, light-headedness, disabling fatigue, exercise intolerance, dizziness, and near syncope. During baseline tilt table testing, these patients demonstrated a heart rate increase of greater than or equal to 30 beats per minute (bpm) (or a maximum heart rate of 120 bpm) within the first 10 minutes upright (unassociated with profound hypotension), which reproduced their symptom complex. In addition, these patients exhibited an exaggerated response to isoproterenol infusions. Similar observations have been made by others who have dubbed this entity POTS. The authors concluded that POTS represents a mild (and potentially treatable) form of autonomic dysfunction that can be readily diagnosed during HUT testing.

Novak et al. (1998) identified clinical and laboratory indices that improve the diagnosis of the POTS. These investigators assessed associations of orthostatic intolerance (OI) by using multi-variate regression analysis. They evaluated autonomic symptoms and autonomic function in 30 patients with POTS, 30 patients with mild OI, and 19 age- and gender-matched control subjects. Indices of para-sympathetic and sympathetic functions were analyzed on the basis of

  1. autonomic function tests (HUT test),
  2. oscillations at respiratory and non-respiratory frequencies (0.01 to 0.09 Hz) in R-R interval and BP (Wigner distribution), and
  3. deterministic component (re-scaled range analysis).

The 4 clinical and laboratory indices that independently supported the diagnosis of POTS are as follows:

  1. orthostatic HR during the 1st minute of the HUT test,
  2. autonomic deficit (adrenergic autonomic score),
  3. loss of spectral powers in R-R interval during the HUT test at the 5th minute, and
  4. severity of orthostatic dizziness, fatigue, palpitations, and shortness of breath.

The authors concluded that enhancing the sensitivity and specificity of the diagnosis of POTS should be possible by using these 4 indices.

Lamarre-Cliche and Cusson (2001) stated that the HUT test is used primarily for the investigation of orthostatic symptoms. Although this test is frequently the gold standard for the evaluation of NCS, dysautonomia, and POTS, there is a debate over its diagnostic value and method. The authors reviewed the physiologic basis of the HUT test, the method, patterns of response, indications and contraindications, and diagnostic validity. They concluded that despite its limitations, the HUT test is useful in patients with a variety of clinical manifestations induced by orthostatism. It is most useful in documenting objective measures of orthostatic hypertension (OH) that cannot be obtained in a clinical setting.

In a prospective study, Singer et al. (2002) examined whether an intrinsic sinus node abnormality is involved in the pathophysiology of POTS. These researchers compared the relationship between P-wave axis (PWA) and heart rate (HR) in 11 healthy controls and 14 patients with POTS by obtaining 12-lead electrocardiographic recordings during supine rest and during gradual HUT testing. The HR of controls was titrated with isoproterenol infusion to match the HR of patients. The PWA was compared at different HR levels, and the relationship between HR and PWA was assessed for patients and controls. Primary endpoints were the PWA-HR relationship in healthy controls, comparison of these data with data from patients with POTS as a group, and identification of a possible subgroup of patients with POTS with an irregular PWA-HR relationship. The PWA increased with increasing HR following a similar logarithmic trend line in both groups. The PWA of patients was significantly lower at the lowest comparable HR level but not different at faster HR levels. Three patients (21%) had a clearly abnormal HR-PWA relationship with a substantial shift toward lower PWA. The authors concluded that these findings supported the hypothesis of a primary sinus node abnormality in a subset of patients with POTS.

In their 2005 study, Winker et al. evaluated the effectiveness of the Schellong test (ST) for diagnosing various forms of orthostatic dysregulation compared to the tilt-table test (TT), which served as the gold standard. The study involved 67 young males from military service, with a mean age of 22 ± 4 years, representing two different cohorts. Among the participants, 32 were asymptomatic, while 35 sought medical attention for orthostatic issues. Based on the results of the TT, subjects were classified into categories including normal TT, orthostatic hypotension (OH), postural orthostatic tachycardia syndrome (POTS), and neuro-cardiogenic syncope (NCS). A chi-square test was used to calculate the sensitivity and specificity of ST in detecting forms of orthostatic dysregulation. The TT identified 23 recruits with POTS, 16 with NCS, and 2 with OH. Of the 32 asymptomatic subjects, only one was diagnosed with POTS by both TT and ST, while the others had normal results on both tests. The sensitivity of ST for detecting POTS was 61% with a specificity of 100%, while for NCS, the sensitivity was 31% and specificity was 100% compared to TT. Data on OH could not be analyzed due to the small number of cases. The authors concluded that these findings suggest ST can be used as a first-line diagnostic tool for patients with orthostatic symptoms; however, if the ST result is normal, further evaluation with TT is essential, as the sensitivity of ST for POTS and NCS is relatively low.

Qingyou et al. (2008) stated that orthostatic intolerance (OI) is a common clinical manifestation in pediatrics. The HUT test is considered the standard for orthostatic assessment, but the physiologic neuro-circulatory profile during HUT has not been fully realized in children with OI. The present study, therefore, was designed to investigate the physiologic patterns that occur during HUT in children with OI. A total of 90 children (56 girls; mean age of 11.6 ± 2.3 years) with OI underwent HUT testing under quiet circumstances; blood pressure (BP) and heart rate (HR) were monitored simultaneously. A total of 49 children with OI (54.4%) had a vaso-vagal response during HUT testing; 33 (36.7%) had a vasodepressor response; 6 (6.7%) had a cardio-inhibitory response; and 10 (11.1%) had a mixed response. Twenty-eight children (31.1%) had POTS; 1 (1.1%) had OH; and 12 (13.3%) had a normal physiologic response. Patterns of cerebral syncope response and chronotropic incompetence were not observed. The authors concluded that the classical vaso-vagal response was the major physiologic pattern seen in children with OI during HUT testing, and the POTS response ranked second.

In a case-control study, Carew and colleagues (2009) defined the optimal duration of TT for the assessment of patients with suspected POTS. Cases were identified retrospectively from a database of patients referred with OI, all of whom met the diagnostic criteria for POTS. Controls were enrolled prospectively. All subjects underwent tilting to 70 degrees for 40 minutes if tolerated. Continuous monitoring was provided by a Finometer. Analysis of responses to TT was performed on 28 cases and 28 controls. The mean age in the case group was 23.6 years, and in the control group, it was 26.2 years. The majority were female in both groups (cases = 4 females and 3 males; controls = 2 females and 1 male). All cases met the criteria for POTS within 7 minutes of orthostasis. No controls demonstrated a sustained tachycardia. The prevalence of vaso-vagal syncope (VVS) was 36% in cases versus 7% in controls (p = 0.02) and 25% in the remaining patients (n = 233) on the OI database (p = 0.259). The authors concluded that a 10-minute TT will diagnose POTS in the majority of patients; however, it will not be sufficient to identify the overlap that exists between POTS and VVS. The optimal duration of TT in patients suspected of POTS is 40 minutes.

Singer et al. (2012) examined whether the use of adult heart rate criteria is appropriate for diagnosing OI POTS in children and adolescents and established normative data and diagnostic criteria for pediatric OI and POTS. A total of 106 normal controls aged 8 to 19 years (mean age of 14.5 ± 3.3 years) underwent standardized autonomic testing, including 5 minutes of 70-degree HUT testing. The orthostatic HR increment and absolute orthostatic HR were assessed and retrospectively compared with values in 654 pediatric patients of similar age (mean age of 15.5 ± 2.3 years) who were referred to the Clinical Autonomic Laboratory with symptoms of OI. The HR increment was mildly higher in patients referred for OI/POTS, but there was considerable overlap between the patient and control groups. Approximately 42% of the normal controls had an HR increment of greater than or equal to 30 bpm. The 95th percentile for the orthostatic HR increment in the normal controls was 42.9 bpm. There was a greater and more consistent difference in absolute orthostatic HR between the two groups, although there was still considerable overlap. The authors concluded that the diagnostic criteria for OI and POTS in adults are unsuitable for children and adolescents. Based on the normative data from this study, the authors proposed new criteria for the diagnosis of OI and POTS in children and adolescents.

The 2017 ACC/AHA/HRS guidelines for the evaluation and management of patients with syncope recommend tilt-table testing for patients with suspected vasovagal syncope (VVS) when the diagnosis remains unclear after initial evaluation, as it can be particularly useful in cases of recurrent syncope (COR IIa, LOE B-R). However, the role of tilt-table testing has diminished due to its moderate sensitivity, specificity, and reproducibility, the occurrence of false-positive responses in control subjects, the increasing ability to identify VVS through structured history taking, and the availability of long-term cardiac monitoring. Additionally, tilt-table testing is not recommended for predicting responses to medical treatments for VVS (COR III; No Benefit), despite some small studies suggesting potential benefits, which were limited by the lack of reproducibility. For patients with syncope and suspected delayed orthostatic hypotension (OH) when initial evaluations are inconclusive, tilt-table testing may also be beneficial (COR IIa, LOE B-NR). Delayed OH can lead to syncopal episodes or symptoms of orthostatic intolerance after prolonged standing; a retrospective study indicated that only 46% of patients experienced OH within 3 minutes of head-up tilt, while 15% had OH between 3 and 10 minutes, and 39% only after 10 minutes. Follow-up data over 10 years showed that 54% of individuals with delayed OH progressed to classic OH, with a 10-year death rate of 29% in those with delayed OH, compared to 64% in individuals with baseline OH and 9% in controls (Shen et al., 2017).

The 2018 European Society of Cardiology (ESC) guidelines for the diagnosis and management of syncope recommend considering tilt testing in patients with suspected reflex syncope, orthostatic hypotension (OH), postural orthostatic tachycardia syndrome (POTS), or postprandial syncope (PPS) (Class IIa, LOE B). Tilt testing may also be considered to educate patients on recognizing symptoms and performing physical maneuvers (Class IIb, LOE B). Reflex syncope, OH, POTS, or PPS should be deemed likely if tilt testing reproduces symptoms along with the characteristic circulatory patterns of these conditions (Class IIa, LOE B). The guidelines further note that a negative tilt table response does not exclude a diagnosis of reflex syncope. While the sensitivity and specificity of tilt testing are acceptable when assessed in patients with vasovagal syncope and healthy controls, in typical clinical settings where the cause of syncope is uncertain, tilt testing may indicate hypotensive susceptibility, which can be relevant for other causes of syncope, including certain cardiac conditions. This concept of hypotensive susceptibility is important for guiding pacemaker therapy in patients with reflex syncope and managing hypotensive treatments, particularly in the elderly. A positive cardioinhibitory response during tilt testing is a strong predictor of spontaneous asystolic syncope, which has significant therapeutic implications for cardiac pacing. Conversely, a positive vasodepressor response, a mixed response, or a negative response does not exclude the possibility of asystole during spontaneous syncope. Additionally, tilt testing may help differentiate syncope with abnormal movements from epilepsy, distinguish syncope from falls, and separate syncope from PPS, ideally when performed alongside EEG monitoring to confirm the diagnosis. However, tilt testing should not be used to assess the efficacy of drug treatments (Brignole et al., 2018).

A 2021 consensus statement from the European Federation of Autonomic Societies (EFAS), supported by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN), established an expert committee to reach a consensus on the use of tilt table testing (TTT) for diagnosing disorders that may lead to transient loss of consciousness (TLOC) and to determine when additional provocative cardiovascular autonomic tests are necessary. While TTT can enhance the diagnostic process, it should not replace thorough history taking. An abnormal TTT result is most significant when the provoked event is recognized by patients or witnesses as resembling spontaneous episodes. The essential requirements for conducting TTT include a tilt table, continuous beat-to-beat blood pressure monitoring, at least one ECG lead, established protocols for indicated tests, and trained personnel. This basic setup allows for the performance of additional provocation tests, such as active standing tests, carotid sinus massage, and autonomic function tests, as well as supplementary measurements like video, EEG, transcranial Doppler, NIRS, end-tidal CO2, or neuro-endocrine tests. It also enables customized provocation procedures for individuals with specific and consistent TLOC triggers. TTT and other provocative cardiovascular autonomic tests are warranted when initial evaluations do not provide a definitive or highly likely diagnosis but suggest conditions such as reflex syncope, the three types of orthostatic hypotension (initial, classic, and delayed), postural orthostatic tachycardia syndrome, or psychogenic pseudo-syncope. Additionally, TTT can serve a therapeutic purpose by helping patients with reflex syncope and orthostatic hypotension recognize hypotensive symptoms and perform physical counter maneuvers (Thijs et al., 2021).

The EFAS/AAS/EAN 2021 Consensus on tilt table testing (TTT) recommends its use in the following scenarios:

  • To increase the probability of a diagnosis of reflex syncope when initial evaluation and noninvasive testing is inconclusive
  • To assess classic orthostatic hypotension (OH) and delayed OH (i.e., those with a sustained blood pressure fall of the magnitude of classic OH, but occurring later than 3 min upon standing)
  • To support a clinical diagnosis of postural orthostatic tachycardia syndrome (POTS)
  • To differentiate between syncope with myoclonus (‘convulsive’ syncope) and tonic–clonic seizures
  • To discriminate between neurogenic and non-neurogenic classic OH. A blunted heart rate increase during classic OH makes a neurogenic cause more likely
  • To differentiate between vasovagal syncope and psychogenic transient loss of consciousness (TLOC)
  • To study the timing between asystole and the onset of TLOC. Asystole in vasovagal syncope (VVS) may occur too late to have been the prime cause of TLOC, making pacemaker implantation likely ineffective.

According to Kim and Farrell (2022), orthostatic hypotension is characterized by a drop in blood pressure of 20 mm Hg or more systolic or 10 mm Hg or more diastolic within three minutes of standing from a supine position or assuming a head-up position of at least 60 degrees during tilt table testing. Symptoms arise from inadequate physiological compensation and organ hypoperfusion, manifesting as headache, lightheadedness, shoulder and neck pain (often referred to as coat hanger syndrome), visual disturbances, dyspnea, and chest pain. The prevalence of orthostatic hypotension is approximately 20% among older adults and 5% among middle-aged adults, with risk factors like diabetes mellitus increasing its occurrence across all age groups. This condition is linked to a significant rise in cardiovascular risk, falls, and up to a 50% increase in the relative risk of all-cause mortality. Diagnosis is typically confirmed through a bedside simplified Schellong test, which involves measuring blood pressure and heart rate after five minutes in a supine position and three minutes after standing. If a patient cannot stand safely or if there is a strong clinical suspicion of orthostatic hypotension despite normal bedside test results, head-up tilt table testing is recommended. Orthostatic hypotension can be classified as neurogenic or nonneurogenic based on its etiology and heart rate response. Treatment aims to alleviate symptoms and enhance quality of life, initially focusing on addressing the underlying cause and adjusting any potentially causative medications. Nonpharmacologic strategies may include dietary changes, compression garments, physical maneuvers, and avoiding situations that worsen symptoms, while first-line medications include midodrine and droxidopa; although fludrocortisone can improve symptoms, it raises concerns regarding long-term effects.

According to van Zanten et al. (2024), tilt table testing (TTT) has been utilized for decades to examine short-term blood pressure (BP) and heart rate regulation during orthostatic challenges, often provoking a vasovagal reflex in many patients with syncope due to its widespread use. Despite the existence of evidence-based syncope guidelines, the proper application and interpretation of TTT in everyday clinical practice remain challenging. The authors' review provides practical insights on the requirements for conducting TTT, how to interpret the results—including the Vasovagal Syncope International Study classification—and the necessity of inducing syncope during TTT for patients with unexplained syncope, as well as the indications for TTT in syncope management. The authors state that essential requirements for performing TTT include a tilt table with an appropriate tilt-down time, a continuous beat-to-beat BP monitor with at least three ECG leads, and trained personnel. They emphasize that while TTT is a valuable tool that contributes to the diagnostic process, it cannot replace thorough history taking, and recognizing abnormal TTT results is necessary, even in the absence of syncope. Patient or eyewitness acknowledgment of the reproducibility of the induced event is essential for confirming a diagnosis. TTT may be warranted when initial evaluations do not provide a definitive, highly likely, or possible diagnosis but raise clinical suspicion of conditions such as reflex syncope, orthostatic hypotension (OH), postural orthostatic tachycardia syndrome, or psychogenic pseudo-syncope. Additionally, TTT can serve a therapeutic purpose for patients with a likely diagnosis of reflex syncope by educating them about prodromal symptoms, and in cases of reflex syncope with OH, TTT can help patients recognize hypotensive symptoms that lead to near-syncope, enabling them to perform physical countermeasures for syncope prevention (biofeedback). Identifying hypotensive susceptibility that requires treatment is particularly valuable.

In an UpToDate review on "Upright tilt table testing in the evaluation of syncope," Benditt (2025) summarizes several recommendations regarding tilt table testing (TTT). The authors states that TTT is indicated as part of the evaluation for selected patients with syncope, although its role is limited since initial diagnostic evaluations often suffice for diagnosing vasovagal syncope (VVS), and TTT has variable reproducibility and diagnostic accuracy. A positive test that reproduces symptoms can be diagnostically helpful and may enhance patient confidence in the diagnosis. TTT may be included in the comprehensive evaluation of syncope for patients with unknown causes of recurrent syncope or a single episode with a high risk of injury, provided that cardiac causes are ruled out if structural heart disease is present. It can also help confirm suspected vasovagal or orthostatic syncope when the diagnosis remains uncertain and can identify the mechanism of syncope, which influences treatment. Additionally, TTT may be used to evaluate autonomic system function. However, TTT is contraindicated in patients with severe coronary or cerebrovascular disease or those who are pregnant. The procedure is typically conducted in an electrophysiology lab using a specialized motorized tilt table, with a passive phase lasting 20 to 45 minutes, followed by a drug provocation phase if necessary. Interpretation of TTT findings should consider all relevant clinical data, as the test is not the gold standard for diagnosing vasovagal syncope due to its limited sensitivity and specificity. The review also outlines various symptomatic responses, including postural tachycardia syndrome (POTS), possible vasovagal responses, and nonspecific responses, as well as patterns associated with syncope, such as vasovagal responses, orthostatic hypotension, and psychogenic pseudosyncope. The sensitivity and specificity of TTT are uncertain, with reported sensitivity rates for the passive phase ranging from 13 to 75 percent and specificity potentially exceeding 90 percent. While drug provocation may enhance sensitivity, it can lower specificity. Complications from TTT are rare but can include prolonged asystole, hypotension, and, in patients with heart disease, the rare induction of ventricular fibrillation during isoproterenol administration.

Abbreviated Tilt Table Testing for Diagnosing Postural Tachycardia Syndrome in Adults with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

van Campen and colleagues (2018) noted that orthostatic intolerance is common among individuals with myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). In some ME/CFS case definitions, orthostatic intolerance is considered a core feature of the disorder. Some studies have employed tilt table tests lasting 2 to 5 minutes to diagnose one common form of orthostatic intolerance, POTS. These investigators examined the diagnostic yield of abbreviated durations of tilt table testing in adults meeting criteria for ME/CFS and identified the proportion with POTS misdiagnosed using testing of less than 10 minutes. Eligible participants were consecutive individuals satisfying study criteria for ME/CFS and POTS evaluated at the Stichting CardioZorg (SCZ, Hoofddorp, NL) between November 2012 and August 2018. Individuals being treated with medications commonly used to manage orthostatic intolerance were excluded. Head-up tilt table testing involved 15 minutes of supine posture followed by 20 minutes at 70 degrees upright. Only the data from the first 10 minutes upright were used. POTS was defined as an increase in heart rate (HR) during a maximum of 10 minutes of upright tilt of at least 30 beats per minute (bpm), in the absence of either classical or delayed orthostatic hypotension. These investigators measured the time until HR criteria for POTS were reached using survival curves and compared survival curves between subgroups divided by age, sex, disease duration, and degree of hypocapnia during the test. Of 627 individuals with ME/CFS evaluated during the study period, 155 met criteria for POTS. The median time to reaching HR criteria for POTS was 3 minutes. A 2-minute tilt table test would miss 55% (95% confidence interval [CI]: 48 to 63%) of those meeting POTS criteria over the course of 10 minutes upright. The median time to reaching HR criteria for POTS did not differ by sex, age, duration of ME/CFS, or hypocapnia during tilt. The authors concluded that abbreviated tilt table testing missed a substantial proportion of those ultimately diagnosed with POTS during a 10-minute tilt table test and should be abandoned for clinical diagnosis and in epidemiologic studies designed to estimate the prevalence of POTS among those with ME/CFS.

Nelson and colleagues (2019) noted that ME/CFS is a complex condition with no reliable diagnostic biomarkers. Studies have shown evidence of autonomic dysfunction in patients with ME/CFS, but results have been equivocal. Heart rate parameters can reflect changes in autonomic function in healthy individuals; however, this has not been thoroughly evaluated in ME/CFS. These researchers carried out a systematic database search for case-control literature. A meta-analysis was conducted to determine differences in HR parameters between ME/CFS patients and controls. A total of 64 articles were included in the systematic review. HR parameters assessed in ME/CFS patients and controls were grouped into 10 categories: resting heart rate (RHR), maximal heart rate (HRmax), HR during submaximal exercise, HR response to head-up tilt testing (HRtilt), resting HR variability (HRVrest), HR variability during head-up tilt testing (HRVtilt), orthostatic HR response (HROR), HR during mental task(s) (HRmentaltask), daily average HR (HRdailyaverage), and HR recovery (HRR). Meta-analysis revealed that RHR (MD ± 95% CI: 4.14 ± 1.38, p < 0.001), HRtilt (SMD ± 95% CI: 0.92 ± 0.24, p < 0.001), HROR (0.50 ± 0.27, p < 0.001), and the ratio of low-frequency power to high-frequency power of HRVrest (0.39 ± 0.22, p < 0.001) were higher in ME/CFS patients compared to controls, while HRmax (MD ± 95% CI: -13.81 ± 4.15, p < 0.001), HR at anaerobic threshold (SMD ± 95% CI: -0.44 ± 0.30, p = 0.005), and the high-frequency portion of HRVrest (-0.34 ± 0.22, p = 0.002) were lower in ME/CFS patients. The authors concluded that numerous HR parameters have been reported in ME/CFS patients, with wide variations in study design and data acquisition methods, including body position and the duration/intensity of interventions (HUTT, exercise, etc.). Meta-analysis revealed significant differences between patients and controls in several parameters, including patients having higher RHR, HRtilt, orthostatic HR response, and LF/HF ratio, and lower HRmax, HRthreshold, HFP, and RMSSD. These differences suggested an altered regulation of HR in ME/CFS patients that is indicative of reduced vagal and increased sympathetic modulation of heart rate. However, it does not appear that any of the currently used HR parameters have the sensitivity to detect the presence of ME/CFS on their own, as demonstrated by the presence of high levels of statistical heterogeneity and methodological issues that limit the usefulness of these parameters. The findings of this review suggested that there are quantifiable differences in autonomic HR regulation in ME/CFS patients, and future research in ME/CFS populations should therefore focus on determining if there are additional HR parameters that have diagnostic utility in this group.

van Campen and colleagues (2020) noted that in a study of 429 adults with ME/CFS, these researchers showed that 86% had symptoms of orthostatic intolerance in daily life. By means of extra-cranial Doppler measurements of the internal carotid and vertebral arteries during a 30-minute head-up tilt to 70 degrees, 90% had an abnormal reduction in cerebral blood flow (CBF). A standard head-up tilt test of this duration might not be tolerated by the most severely affected bedridden ME/CFS patients. These investigators examined if a shorter 15-minute test at a lower 20-degree tilt angle would be sufficient to provoke reductions in CBF in severe ME/CFS patients. A total of 19 severe ME/CFS patients with OI complaints in daily life were studied: 18 women. The mean (SD) age was 35 (14) years, body surface area (BSA) was 1.8 (0.2) m², and body mass index (BMI) was 24.0 (5.4) kg/m². The median disease duration was 14 (inter-quartile range [IQR] 5 to 18) years. Heart rate increased, and stroke volume index and end-tidal CO2 decreased significantly during the test (p ranging from < 0.001 to < 0.0001). The cardiac index decreased by 26 (7)% (p < 0.0001). CBF decreased from 617 (72) to 452 (63) ml/min, a 27 (5)% decline. All 19 severely affected ME/CFS patients met the criteria for an abnormal CBF reduction. The authors concluded that using a less demanding 20-degree tilt test for 15 minutes in severe ME/CFS patients resulted in a mean CBF decline of 27%. This was comparable to the mean 26% decline previously noted in less severely affected patients studied during a 30-minute, 70-degree head-up tilt. These observations have implications for the evaluation and treatment of severely affected individuals with ME/CFS.

The authors stated that this study had several drawbacks. It only included ME/CFS patients who were bedridden, and these researchers cautioned that the 20-degree head-up tilt angle needs further study before it can replace longer 70-degree tilt angles for evaluating less severely impaired ME/CFS patients. Comparisons of the hemodynamic and CBF abnormalities of 20 and 70 degrees of tilting are needed. In addition, these researchers did not include healthy controls for comparison. It was possible that healthy controls would have little or no perturbation in response to a 20-degree head-up angle, which would have the effect of widening the physiologic differences between ME/CFS patients and controls. Whether disease severity differences led to differences in CBF reduction needs to be examined in future trials. Finally, while it was reasonable to expect that the 20-degree abbreviated tilt test would be less taxing than a longer 70-degree tilt test, thus less likely to provoke post-exertional malaise, this hypothesis remains to be tested.

Active Standing in the Diagnosis of Postural Tachycardia Syndrome (POTS) in the Young

Stewart and Medow (2025) compared standing and upright tilt in patients with postural orthostatic tachycardia syndrome (POTS) and healthy volunteers to examine if standing accurately tests for POTS in individuals under 19 years of age. POTS in adolescents is defined by orthostatic intolerance plus sustained excessive upright tachycardia, without hypotension during upright tilt. These investigators examined whether active standing is a valid classifier for POTS in adolescents compared to tilt. Patients with POTS (n = 36, aged 12.2 to 18.8 years) and healthy volunteers (n = 39, aged 13.1 to 18.9 years) stood for a minimum of 5 minutes and were tilted to 70° for 10 minutes. Receiver operating characteristic analyses (ROC) were carried out at 5-minute stand and at 5- and 10-minute tilt to determine the optimal threshold for heart rate increase (ΔHR), as well as test sensitivity and specificity. Most participants were unable to stand for 10 minutes; ΔHRs at 5-minute stand were higher in POTS (31 ± 3) compared with controls (21 ± 2) and elevated at 5- or 10-minute tilt in POTS (51 ± 3 and 51 ± 2) versus controls (26 ± 2 and 25 ± 2) compared with standing. ΔHR in POTS and controls for 10 minutes was not different from 5 minutes. For the 5-minute stand, the ROC threshold was 26 beats per minute (bpm), with a sensitivity of 70.6% and specificity of 68.2%, compared with 39 bpm, 88.2%, and 95.1% for 5-minute tilt, and 40 bpm, 94.1%, and 95.1% for 10-minute tilt. A precision-recall graph confirmed the superior discriminating ability of 5-minute and 10-minute tilt compared to 5-minute stand. The authors concluded that the stand test was relatively non-specific and imprecise compared to tilt and did not satisfactorily distinguish POTS from controls in patients aged under 19 years.

Carotid Sinus Massage During Head-up Tilt Testing as a Screening Tool in Patients with Unexplained Syncope

Prakash et al. (2024) stated that head-up tilt table testing (HUTT) has been employed for decades in the work-up of patients presenting with syncope and a suspected reflex etiology. Different protocols have been used with varying sensitivity and specificity. The standard protocols are relatively long, involving various maneuvers to elicit a response and potentially abbreviate the test. The role of carotid sinus massage (CSM) as a provocative maneuver has not been well-studied. In a prospective, single-center study, these researchers examined whether CSM could predict the outcome of the HUTT. A total of 50 consecutive patients who had been referred for HUTT were enrolled in this trial. All participants underwent an identical protocol that entailed provocation with CSM both initially in the supine posture and at the end of 30 minutes of HUTT. Seventeen out of 50 (34%) patients ultimately had a positive tilt table test result—15 of these 17 patients exhibited a significant vasodepressor response (symptomatic blood pressure drop of more than 20 mmHg) without significant bradycardia (heart rate of less than 50 bpm) during the initial CSM in the supine posture. Of the 33 patients with a negative tilt table result, none had a vasodepressor response to CSM. The sensitivity of CSM in detecting a patient who would ultimately have a positive tilt table test was 88.24% (95% CI: 63.56% to 98.54%), while the specificity was 100% (95% CI: 89.42% to 100.00%). CSM conducted in the supine posture at the beginning of a tilt table test was highly sensitive and specific for the outcome of the test after completion of the entire protocol. The authors concluded that based on these findings, CSM may obviate the need for completion of the protocol for diagnostic reasons.

The authors acknowledged several drawbacks of the study. First, the sensitivity and specificity have not been calculated concerning clinical disease status, but rather in relation to another, more cumbersome test. Second, the population in the study included patients whose symptoms were not diagnostic of a reflex, which may explain the low incidence of a positive result upon completion of the test. Third, patients with a high likelihood of carotid sinus hypersensitivity based on history were not included. Fourth, episodes of syncope and pre-syncope were not numerically quantified, as the intention was to examine the role of CSM rather than to determine the outcome. The researchers noted that with a small sample size (n = 50 subjects) and the study being a single-center study, there is a need for a larger study to derive definitive conclusions.

Furthermore, an UpToDate review on "Syncope in Adults: Risk Assessment and Additional Diagnostic Evaluation" (Benditt, 2025) states that "Carotid sinus syndrome (CSS) is an infrequent cause of collapse in older patients (generally males > 60 years of age) and/or individuals who have had prior head/neck surgery or irradiation. Careful massage of the neck at the angle of the mandible by an experienced clinician (both sides at separate times) may unmask carotid sinus hypersensitivity. CSS is diagnosed if carotid sinus hypersensitivity is present (usually a sinus pause > 3 to 5 seconds and/or a blood pressure fall of > 50 mmHg) with reproduction of symptoms (which usually requires the patient to be upright [usually seated or on a tilt table] when tested). Although there is little evidence of risk, most guidelines indicate that practitioners should avoid CSM in patients with a history of transient ischemic attack or stroke within the past 3 months and in patients with carotid bruits (except if carotid Doppler studies have previously excluded significant carotid stenosis). For patients with multiple recurrences of syncope and an unexplained diagnosis in the absence of structural heart disease, and who have a normal ECG, reflex syncope remains the most probable diagnosis. At this stage, if the etiology is in doubt, tilt-table testing and carotid sinus massage (CSM) may be helpful. CSM is exclusively directed to assessing the possibility of carotid sinus hypersensitivity (CSH) and carotid sinus syndrome (CSS). The presence of CSH (i.e., > 3- to 5-second pause with CSM) is not sufficient to conclude that the diagnosis is CSS. Carotid sinus syndrome is usually a condition of older (i.e., over 60 years, mainly male) persons unless the patient has had prior neck surgery or irradiation. Diagnosis is best established if CSM, undertaken with the subject in an upright posture, such as seated in a chair, results in reproduction of syncope symptoms." Moreover, carotid sinus massage (CSM) is not mentioned in the "Summary and Recommendations" section of this UpToDate review.

Chronic Fatigue Syndrome

There is inadequate evidence of the effectiveness of tilt table testing for identifying chronic fatigue syndrome (CFS) patients who would respond to medications to increase their blood pressure. Several case series have shown that patients with known CFS frequently have abnormal responses to tilt table testing, and CFS patients in these series also frequently appear to respond to anti-hypotensive medications commonly used in patients with neurally mediated hypotension. These case studies fail to demonstrate, however, any value of tilt table testing in distinguishing CFS patients who would respond to these medications from those who would not.

Diagnosis of Joint Hypermobility Syndrome

Joint hypermobility syndrome (JHS) is a chronic disorder characterized by arthralgia, myalgia, and periodic visceral manifestations, including postural orthostatic tachycardia syndrome (POTS). Patients with JHS are more likely to be diagnosed with chronic fatigue syndrome (CFS) or fibromyalgia compared to the general population (Mandel et al., 2017).

In a prospective study, Adamec and colleagues (2018) examined the association of autonomic nervous system (ANS) abnormalities on head-up tilt table test (HUTT) with generalized joint hypermobility, as expressed by the Beighton score (BS). This trial enrolled 115 consecutive patients (91 women; mean age of 34.35 ± 14.11 years) referred either for the HUTT or for testing of cardiovascular autonomic reflexes alongside HUTT. Generalized joint hypermobility was evaluated according to the BS system, after which HUTT was performed. Clinical significance was considered if the BS was greater than or equal to 4. A total of 15 patients (15.1%) had a BS greater than or equal to 4. Results of the HUTT were normal in 58 (50.4%) patients, while 57 (49.6%) had abnormal results; 15 (13.0%) patients fulfilled criteria for orthostatic hypotension, 30 (26.1%) for reflex syncope, and 21 (18.3%) for POTS. Patients with pathological findings on HUTT had significantly higher BS compared to those with normal HUTT (median of 1 versus 0, p = 0.001). There was a significant association between participants with BS greater than or equal to 4 and pathological HUTT (χ[1] = 6.392, p = 0.011). Results of the multivariate regression analysis revealed that an increase in the BS was associated with an increased likelihood of HUTT pathology (Exp[B] 1.44, 95% confidence interval [CI]: 1.084 to 1.922, p = 0.012), while an increase in age was associated with a lower risk of HUTT pathology (Exp[B] 0.968, 95% CI: 0.939 to 0.998, p = 0.036). The authors concluded that there was an association between ANS abnormalities on the HUTT and generalized joint hypermobility, and they emphasized that the clinical significance of this association needs further investigation.

The British Society for Paediatric and Adolescent Rheumatology’s guidelines for "Management of Joint Hypermobility Syndrome in Children and Young People" (BSPAR, 2012) stated that "Diagnosis of POTS is not easy, and though it is often done by performing a tilt table test (or standing and lying heart rate if tilt table unavailable), this is not validated in children and adolescents, so the results of the tilt table test have to be interpreted carefully."

Furthermore, an UpToDate review on "Joint Hypermobility Syndrome" (Grahame and Hakim, 2019) does not mention tilt table testing as a management tool.

Diagnosis of Parkinsonian Syndromes

Riley and Chelimsky (2003) stated that formal laboratory testing of autonomic function is reported to distinguish between patients with Parkinson's disease (PD) and those with multiple system atrophy (MSA), but such studies segregated patients according to clinical criteria that select those with autonomic dysfunction for the MSA category. These researchers attempted to characterize the profiles of autonomic disturbances in patients in whom the diagnosis of PD or MSA used criteria other than autonomic dysfunction. A total of 47 patients with parkinsonism and autonomic symptoms who had undergone autonomic laboratory testing were identified and their case records reviewed for non-autonomic features. They were classified clinically into 3 diagnostic groups:

  1. PD (n = 19),
  2. MSA (n = 14),and
  3. uncertain (n = 14).

The performance of the patients with PD was compared with that of the MSA patients on 5 autonomic tests:

  1. R-R interval variations during deep breathing,
  2. heart rate changes with the Valsalva maneuver,
  3. tilt table testing,
  4. the sudomotor axon reflex test, and
  5. thermoregulatory sweat testing.

None of the tests distinguished one group from the other with any statistical significance, alone or in combination. Parkinson's disease and MSA patients showed similar patterns of autonomic dysfunction on formal testing of cardiac sympathetic and parasympathetic, vasomotor, and central and peripheral sudomotor functions. The authors concluded that these findings supported the clinical observation that PD is often indistinguishable from MSA when it involves the autonomic nervous system. The clinical combination of parkinsonism and dysautonomia is as likely to be caused by PD as by MSA. Current clinical criteria for PD and MSA that direct patients with dysautonomia into the MSA group may be inappropriate.

Reimann et al. (2010) stated that differential diagnosis of parkinsonian syndromes is a major challenge in movement disorders. Dysautonomia is a common feature but may vary in clinical severity and onset. These investigators attempted to find a pattern of autonomic abnormalities discriminative for patients with different parkinsonian syndromes. The cross-sectional study included 38 patients with MSA, 32 patients with progressive supranuclear palsy (PSP), 26 patients with idiopathic PD (IPD), and 27 age-matched healthy controls. Autonomic symptoms were evaluated by a standardized questionnaire.  The performance of patients and controls was compared on 5 autonomic function tests:

  1. deep breathing,
  2. Valsalva maneuvre,
  3. tilt-table testing,
  4. sympathetic skin response,
  5. pupillography, as well as 24-hr ambulatory BP monitoring (ABPM).

Disease severity was significantly lower in IPD than PSP and MSA. Except for pupillography, none of the laboratory autonomic tests distinguished one patient group from the other alone or in combination. The same was observed on the questionnaire. Receiver operating characteristic curve revealed discriminating performance of pupil diameter in darkness and nocturnal BP change. The composite score of urogenital and vasomotor domains significantly distinguished MSA from IPD patients but not from PSP. These findings supported the observation that even mild IPD is frequently indistinguishable from more severe MSA and PSP. Thus, clinical combination of motor and non-motor symptoms does not exclusively point at MSA. Pupillography, ABPM and the questionnaire may assist in delineating the 3 syndromes when applied in combination.

Diagnosis of Unexplained Syncope in Patients with Hypertrophic Cardiomyopathy

Bozyel et al. (2025) noted that conflicting results have been published regarding the diagnostic performance of head-up tilt table testing (HUTT) in patients with hypertrophic cardiomyopathy (HCM). In a meta-analysis, these investigators examined the diagnostic value of HUTT in the evaluation of unexplained syncope in patients with HCM. They conducted a structured systematic database search using the following keywords: hypertrophic cardiomyopathy, syncope, unexplained syncope, head-up tilt test, tilt table test, tilt testing, orthostatic stress, autonomic function, and autonomic response. Studies in which HUTT was used to define autonomic dysfunction in patients with syncope at baseline or without syncope were included in the final analysis. A total of 252 HCM patients from six studies were evaluated, comprising 159 patients without a history of syncope and 93 with a history of syncope. HUTT was positive in 50 (19.84%) of the 252 patients, with 21 of 93 patients (22.58%) with a history of syncope and 29 of 159 patients (18.24%) without a history of syncope testing positive. The pooled total sensitivity and specificity of HUTT for detecting syncope were 22.1% (95% CI: 14.8% to 35.1%) and 83.6% (95% CI: 73.2% to 91.6%), respectively. The summary receiver operating characteristic (ROC) curve indicated that HUTT had only modest discriminative ability for syncope, with an area under the curve (AUC) value of 0.565 (95% CI: 0.246 to 0.794). The authors concluded that although HUTT exhibited significant limitations in diagnosing unexplained syncope in patients with HCM, it may still be useful for determining hypotensive susceptibility. They suggested that other autonomic tests could be incorporated into the diagnostic workflow for this population.

Evaluation of Autonomic Dysfunction in Childhood Hypersomnia Disorders

Jagadish and colleagues (2021) noted that orthostatic intolerance (OI) is a common manifestation of autonomic dysfunction. It is characterized by light-headedness and palpitations in the upright position, with relief when supine. OI can affect the quality of life (QOL). Other symptoms that may accompany OI include headache, fatigue, nausea, palpitations, and abdominal pain. The prevalence and characteristics of autonomic symptoms in childhood hypersomnia disorders have not been examined, and hence were studied. The medical records of children and adolescents with hypersomnia disorders were reviewed. Subjects had been diagnosed with narcolepsy types 1 or 2 (NT1 or NT2), idiopathic hypersomnia (IH), Kleine-Levin syndrome (KLS), or hypersomnia related to medical conditions, were under 18 years of age at sleep diagnosis, and had been evaluated at the authors’ sleep center between 2000 and 2018. Those with comorbidities such as obstructive sleep apnea (OSA) and major depression were excluded. The medical records were reviewed for symptoms at initial presentation suggestive of autonomic dysfunction, such as OI, headache, fatigue, nausea, palpitations, and abdominal pain. If these symptoms had been recorded, the chart was examined further to determine if an autonomic reflex screen (ARS) battery had been conducted. The ARS battery examines both sympathetic and parasympathetic function. It is composed of a tilt table test, heart rate and blood pressure responses to the Valsalva maneuver and deep breathing, a quantitative sudomotor axon reflex test, and beat-to-beat blood pressure measurements during the Valsalva maneuver. Results of the ARS battery were interpreted by an autonomic neurology specialist (WS), who was not otherwise involved in the care of the patients. Medications taken at the time of autonomic testing were recorded. There were 89 patients with hypersomnia disorders; 46 had NT1, 17 had NT2, 18 had IH, 1 had KLS, and 7 had hypersomnia associated with medical disorders. Thirty-three of the 89 subjects (37%) had the symptom of OI at initial presentation and hence underwent autonomic reflex screen testing. The median age at diagnosis of hypersomnia in the 33 subjects with the OI symptom was 14.5 years (IQR 12 to 16), which was similar (14.5 years, IQR 11.5 to 16) in the 56 subjects without OI. In the group with OI, 25 out of 33 had not received medications for treating hypersomnia at the time of autonomic testing. OI was not related to the degree of sleepiness; the mean sleep latency in the subjects with OI was 5.3 ± 2.9 minutes, while in those without OI, it was 4.5 ± 3.8 minutes. The symptom of OI was not more likely to occur in any specific type of hypersomnia. However, OI tended to occur predominantly in females—the female-to-male ratio in the OI subgroup was 2:1 (n = 33), while in the subgroup without OI, it was 1:2.1 (n = 56; p = 0.0015). Additional symptoms recorded in the OI subgroup included lightheadedness in 25 out of 33, palpitations in 6 out of 33, nausea and vomiting in 4 out of 33, fatigue in 25 out of 33, headache in 15 out of 33, and constipation in 3 out of 33. The symptoms of OI were reproduced during the tilt table test in 17 out of 33 subjects; 5 of these patients had a rise in heart rate consistent with POTS. The authors concluded that in this retrospective study, one-third of children with hypersomnia disorders exhibited the symptom of OI at initial presentation, with a female predominance. A smaller subgroup met criteria for POTS.

Furthermore, an UpToDate review on "Idiopathic Hypersomnia" (Chervin, 2021) does not mention tilt table testing as a management tool.

Evaluation of Autonomic Dysfunction in Obstructive Sleep Apnea Syndrome

Uno and colleagues (2009) noted that although it is well known that autonomic dysfunction in obstructive sleep apnea syndrome (OSAS) is associated with hypertension, its relationship to hypotension and orthostatic dysregulation is still unclear. These investigators examined the response of blood pressure (BP) and cardiovascular autonomic function to the head-up tilt (HUT) test in patients with OSAS. In this study, a total of 14 patients (mean age of 65 ± 2 years, male/female: 11/3) with diagnosed OSAS by overnight polysomnography and 84 healthy subjects (mean age of 62 ± 1 years, male/female: 46/38) underwent the HUT test (from 5 to 10 minutes at 45 degrees). Autonomic functions were evaluated by spectrum analysis of BP and heart rate variability. In healthy subjects, systolic BP was unchanged by the HUT test due to the enhancement of sympathetic nerve activity and the inhibition of parasympathetic nerve activity. In contrast, autonomic responses were unchanged, and systolic BP tended to decrease during the HUT test in OSAS patients. The authors concluded that the findings of this study suggested that baroreflex function is impaired in patients with OSAS. Furthermore, the HUT test with spectrum analysis may be useful to evaluate autonomic functions in OSAS patients.

Evaluation of Autonomic Dysfunction in Paroxysmal Atrial Fibrillation

Oliveira et al. (2009) stated that the autonomic nervous system (ANS) is known to be an important modulator in the pathogenesis of paroxysmal atrial fibrillation (PAF). Changes in ANS control of heart rate variability (HRV) occur during orthostatism to maintain cardiovascular homeostasis. Wavelet transform has emerged as a useful tool that provides time-frequency decomposition of the signal under investigation, enabling intermittent components of transient phenomena to be analyzed. These investigators studied HRV during the HUT test with wavelet transform analysis in PAF patients and healthy individuals (normals). A total of 21 patients with PAF (8 men; age of 58 ± 14 years) were examined and compared with 21 normals (7 men; age of 48 ± 12 years). After a supine resting period, all subjects underwent passive HUT (60 degrees) while in sinus rhythm. Continuous monitoring of electroencephalography and BP was carried out. Acute changes in RR intervals were assessed by wavelet analysis, and low-frequency power (LF: 0.04 to 0.15 Hz), high-frequency power (HF: 0.15 to 0.60 Hz), and LF/HF (sympatho-vagal) were calculated for

  1. the last 2 mins of the supine period;
  2. the 15 secs of tilting movement (TM); and
  3. the 1st (TT1) and 2nd (TT2) min of HUT.

Data were expressed as means +/- SEM. Baseline and HUT RR-intervals were similar for the 2 groups. Supine basal BP was also similar for the 2 groups, with a sustained increase in PAF patients, and a decrease followed by an increase and then recovery in normals. Basal LF, HF and LF/ HF values in PAF patients were 632 +/- 162 ms2, 534 +/- 231 ms2 and 1.95 +/- 0.39, respectively, and 1,058 +/- 223 ms2, 789 +/- 244 ms2 and 2.4 +/- 0.36, respectively, in normals (p = NS). During TM, LF, HF and LF/HF values for PAF patients were 747 +/- 277 ms2, 387 +/- 94 ms2 and 2.9 +/- 0.6, respectively, and 1316 +/- 315 ms2, 698 +/- 148 ms2 and 2.8 +/- 0.6, respectively, in normals (p < 0.05 for LF and HF). During TF1, LF, HF and LF/ HF values for PAF patients were 1,243 +/- 432 ms2, 302 +/- 88 ms2 and 7.7 +/- 2.4, respectively, and 1,992 +/- 398 ms2, 333 +/- 76 ms2 and 7.8 +/- 0.98, respectively, for normals (p < 0.05 for LF).  During TF2, LF, HF and LF/HF values for PAF patients were 871 +/- 256 ms2, 242 +/- 51 ms2 and 4.7 +/- 0.9, respectively, and 1263 +/- 335 ms2, 317 +/- 108 ms2 and 8.6 +/- 0.68, respectively, for normals (p < 0.05 for LF/HF). The dynamic profile of HRV showed that LF and HF values in PAF patients did not change significantly during TM or TT2, and LF/HF did not change during TM but increased in TT1 and TT2. The authors concluded that patients with PAF present alterations in HRV during orthostatism, with decreased LF and HF power during TM, without significant variations during the first minutes of HUT. These findings suggested that wavelet transform analysis may provide new insights when assessing autonomic heart regulation and highlight the presence of ANS disturbances in PAF. The findings of these small preliminary studies need to be validated by well-designed studies.

Evaluation of Post-Concussion Syndrome

Heyer et al. (2016) examined HUT signs of autonomic dysfunction in a cohort of youth with persistent post-concussion symptoms (PCSs) that include light-headedness and to correlate repeat tilt table results with symptom improvements for those patients found to have POTS on initial testing. A total of 34 patients (13 to 18 years of age) with persistent PCSs participated in this study. All patients underwent at least 1 tilt table test. The PCS Interview (PCS-I) and patient ratings of light-headedness and vertigo were used to measure symptom burden. Patients found to have POTS were asked to repeat tilt table testing when PCSs improved or 3 to 6 months after the initial test if symptoms persisted. Overall, 24 of the 34 (70.6%) patients had abnormal tilt table results with patients categorized as normal (n = 10), isolated syncope (n = 10), and POTS (n = 14). Patients with POTS had higher PCS-I scores than normal patients (p < 0.001) and higher ratings of light-headedness than both normal patients (p = 0.015) and syncope patients (p = 0.04); 12 POTS patients underwent repeat tilt table testing, and 9 of 12 (75%) no longer met POTS diagnostic criteria. All patients with resolution of POTS had corresponding improvements in PCSs, including light-headedness and vertigo. The authors concluded that the findings of this study demonstrated a high rate of tilt table abnormalities among youth with persistent PCSs. Several patients with POTS had normalization of tilt table testing when PCSs improved. They stated that these findings warrant further research of autonomic dysfunction related to concussion.

Furthermore, an UpToDate review on "Postconcussion syndrome’ (Evans, 2016) does not mention tilt table testing as a management tool.

Guidance of Pacing Therapy for Reflex Syncope

Furukawa (2017) stated that the tilt table test (TTT) is a method used for the management of reflex syncope. However, the TTT is incomplete and has several problems. The TTT is unsuitable for all syncopal patients. Several questions on this technology remain unclear: When should the TTT be used; for which types of patients TTT should be performed; and does the TTT provide useful information to guide indication for pacing therapy for reflex syncope. The answers to these questions appear in recent reports from 2 guidelines published by the European Society of Cardiology and the Japan Circulation Society. The indications for TTT do not apply to all syncopal patients, but selected patients. For patients with low risks and rare syncopal events, the TTT is not necessary, even when diagnoses are unconfirmed. The TTT is used not only for diagnosis of reflex syncope, but also for many clinical management of several conditions (i.e., exclusion of cardiac syncope). The author stated that positive TTT results cannot predict the effects of pacing therapy for reflex syncope; pacing therapy should be administered based on documented electrocardiograms, TTT results (negative or positive), and other findings.

In Chiari type I-Malformation (Chiari Drop Attacks)

Straus and colleagues (2009) stated that Chiari I malformation (CM1) is characterized by impaired cerebrospinal fluid flow through the foramen magnum. Dysfunctional autonomic cardiovascular regulation may result in syncope, which may be the primary presenting symptom of CM1 (a syndrome termed Chiari drop attack). It has been postulated that Chiari drop attack is secondary to dysautonomia caused by hind-brain compression. These researchers studied patients with Chiari drop attacks who had negative work-ups for cardiac syncope, followed by tilt table testing and subsequent surgical decompression. They reported test results and clinical outcomes following CM1 decompression. A total of 10 patients met the inclusion criteria: 5 patients had positive and 5 negative tilt table tests. Following decompression, 7 had symptomatic improvement or resolution, and 3 failed to improve. The sensitivity and specificity of the tilt table test for detecting clinical improvement with surgical decompression were 43% and 33%, respectively. Tilt table testing had 40% accuracy in predicting clinical response to decompression. The authors concluded that in this short series, surgical decompression of CM1 has a high success rate (70%) for patients with Chiari drop attacks. Moreover, tilt table testing has poor predictive value in judging the clinical response to surgical decompression and is not a useful test to guide surgical decision-making.


References

The above policy is based on the following references:

  1. Adamec I, Junakovic A, Krbot Skorić M, Habek M. Association of autonomic nervous system abnormalities on head-up tilt table test with joint hypermobility. Eur Neurol. 2018;79(5-6):319-324.
  2. Arnold M. In adult patients presenting with syncope, how effective is tilt table testing in diagnosing psychogenic blackout?  BestBETS Best Evidence Topics. July 21, 2011. 
  3. Baschetti R. Chronic fatigue syndrome and neurally mediated hypotension. JAMA. 1996;275(5):359; author reply 360.
  4. Benditt D. Syncope in adults: Risk assessment and additional diagnostic evaluation. UpToDate [online serial] Waltham, MA: UpToDate; updated January 2025.
  5. Benditt D. Upright tilt table testing in the evaluation of syncope. UpToDate [online serial]. Waltham, MA: UpToDate; updated December 2025.
  6. Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing syncope. American College of Cardiology. J Am Coll Cardiol. 1996;28(1):263-275.
  7. Bou-Holaigah I, Rowe PC, Kan J, et al. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA. 1995;274(12):961-967.
  8. Bozyel S, Saylık F, DalgıC N, et al. Diagnostic yield of head-up tilt table test in hypertrophic cardiomyopathy and unexplained syncope: the knot does not seem to be unraveling. J Interv Card Electrophysiol. 2025;68(2):267-276.
  9. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J. 2001;22(15):1256-1306.
  10. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948.
  11. British Society for Paediatric and Adolescent Rheumatology (BSPAR). Guidelines for management of joint hypermobility syndrome in children and young people. London, UK: BSPAR; 2012. Available at: https://www.sparn.scot.nhs.uk/wp-content/uploads/2017/01/Guidelines-for-Management-of-Joint-Hypermobility-Syndrome-v1.1-June-2013.pdf. Accessed February 4, 2019.
  12. Carew S, Cooke J, O'Connor M, et al. What is the optimal duration of tilt testing for the assessment of patients with suspected postural tachycardia syndrome? Europace. 2009;11(5):635-637.
  13. Chervin RD. Idiopathic hypersomnia. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed January 2021.
  14. Edfors R, Erdal J, A-Rogvi-Hansen B. Tilt table testing in patients with suspected epilepsy. Acta Neurol Scand. 2008;117(5):354-358.
  15. Evans RW. Postconcussion syndrome. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed January 2016.
  16. Faddis MN, Rich MW. Pacing interventions for falls and syncope in the elderly. Clin Geriatr Med. 2002;18(2):279-294.
  17. Freeman R, Kaufmann H. Postural tachycardia syndrome. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed December 2012.
  18. Freeman R. Assessment of cardiovascular autonomic function. Clin Neurophysiol. 2006;117(4):716-730. 
  19. Furukawa T. Role of head-up tilt table testing in patients with syncope or transient loss of consciousness. J Arrhythm. 2017;33(6):568-571.
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  21. Grahame R, Hakim AJ. Joint hypermobility syndrome. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed January 2019.
  22. Grubb BP, Kosinski D. Current trends in etiology, diagnosis, and management of neurocardiogenic syncope. Curr Opin Cardiol. 1996;11(1):32-41.
  23. Grubb BP, Kosinski DJ, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: A neurocardiogenic variant identified during head-up tilt table testing. Pacing Clin Electrophysiol. 1997;20(9 Pt 1):2205-2212.
  24. Hamer AWF, Menahem S. Upright tilt table testing in children and adolescents: An aid to the clinical diagnosis of postural orthostatic tachycardia syndrome. Paediatr Child Health. 2025;61(1):124-126.
  25. Heyer GL, Fischer A, Wilson J, et al. Orthostatic intolerance and autonomic dysfunction in youth with persistent postconcussion symptoms: A head-upright tilt table study. Clin J Sport Med. 2016;26(1):40-45.
  26. Jagadish S, Singer W, Kotagal S. Autonomic dysfunction in childhood hypersomnia disorders. Sleep Med. 2021;78:43-48.
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  28. Kim MJ, Farrell J. Orthostatic hypotension: A practical approach. Am Fam Physician. 2022;105(1):39-49.
  29. Kirsch P, Mitro P, Mudrakova K, Valocik G. Diagnostic yield of adenosine and nitroglycerine stimulated tilt test in patients with unexplained syncope. Bratisl Lek Listy. 2007;108(6):259-264.
  30. Klonoff D. Chronic fatigue syndrome and neurally mediated hypotension. JAMA. 1996;275(5):359-360.
  31. Lamarre-Cliche M, Cusson J. The fainting patient: Value of the head-upright tilt-table test in adult patients with orthostatic intolerance. CMAJ. 2001;164(3):372-376.
  32. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med. 1997;127(1):76-86.
  33. Luria DM, Shen WK. Syncope in the elderly: New trends in diagnostic approach and nonpharmacologic management. Am J Geriatr Cardiol. 2001;10(2):91-96.
  34. Mandel D, Askari AD, Malemud CJ, Kaso A. Joint hypermobility syndrome and postural orthostatic tachycardia syndrome (HyPOTS). Biomed Res Clin Prac. 2017;2(1): 1-4.
  35. Mehlsen AB, Mehlsen J. Investigation in suspected syncope. A study of more than 1,174 consecutively referred patients. Ugeskr Laeger. 2008;170(9):723-727.
  36. Miller TH, Kruse JE. Evaluation of syncope. Am Fam Physician. 2005;72(8):1492-1500.
  37. Morillo CA, Klein GJ, Gersh BJ. Can serial tilt testing be used to evaluate therapy in neurally mediated syncope? Am J Cardiol. 1996;77(7):521-523.
  38. Nelson MJ, Bahl JS, Buckley JD, et al. Evidence of altered cardiac autonomic regulation in myalgic encephalomyelitis/chronic fatigue syndrome: A systematic review and meta-analysis. Medicine (Baltimore). 2019;98(43):e17600.
  39. Novak V, Novak P, Opfer-Gehrking TL, et al. Clinical and laboratory indices that enhance the diagnosis of postural tachycardia syndrome. Mayo Clin Proc. 1998;73(12):1141-1150.
  40. Oliveira MM, da Silva N, Timóteo AT, et al. Alterations in autonomic response head-up tilt testing in paroxysmal atrial fibrillation patients: A wavelet analysis. Rev Port Cardiol. 2009;28(3):243-257.
  41. Parry SW, Kenny RA. Tilt table testing in the diagnosis of unexplained syncope. QJM. 1999;92(11):623-629.
  42. Prakash A, Truong J, Adelakun A, Singh R. Carotid sinus massage during head-up tilt testing can predict the test outcome: Implications for its use as a screening tool in patients with unexplained syncope. J Innov Card Rhythm Manag. 2024;15(10):6047-6051.
  43. Qingyou Z, Karmane SI, Junbao D. Physiologic neurocirculatory patterns in the head-up tilt test in children with orthostatic intolerance. Pediatr Int. 2008;50(2):195-198.
  44. Reimann M, Schmidt C, Herting B, et al. Comprehensive autonomic assessment does not differentiate between Parkinson's disease, multiple system atrophy and progressive supranuclear palsy. J Neural Transm. 2010;117(1):69-76.
  45. Riley DE, Chelimsky TC. Autonomic nervous system testing may not distinguish multiple system atrophy from Parkinson's disease. J Neurol Neurosurg Psychiatry. 2003;74(1):56-60.
  46. Ringer M, Hashmi MF, Lappin SL. Orthostatic hypotension. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; updated January 17, 2025.
  47. Rowe PC, Bou-Holaigah I, Kan JS, et al. Is neurally mediated hypotension an unrecognized cause of chronic fatigue? Lancet. 1995;345(8950):623-624.
  48. Ruiz GA, Scaglione J, Gonzalez-Zuelgaray J. Reproducibility of head-up tilt test in patients with syncope. Clin Cardiol. 1996;19(3):215-220.
  49. Ruzieh M, Ghahramani M, Nudy M, et al. The benefit of closed loop stimulation in patients with cardioinhibitory vasovagal syncope confirmed by head-up tilt table testing: A systematic review and meta-analysis. J Interv Card Electrophysiol. 2019;55(1):105-113.
  50. Saengsuwan J, Berger L, Schuster-Amft C, et al. Test-retest reliability and four-week changes in cardiopulmonary fitness in stroke patients: Evaluation using a robotics-assisted tilt table. BMC Neurol. 2016;16(1):163.
  51. Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients With syncope: A report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines and the Heart Rhythm Society. Circulation. 2017;136(5):e60-e122.
  52. Singer W, Shen WK, Opfer-Gehrking TL, et al. Evidence of an intrinsic sinus node abnormality in patients with postural tachycardia syndrome. Mayo Clin Proc. 2002;77(3):246-252.
  53. Singer W, Sletten DM, Opfer-Gehrking TL, et al. Postural tachycardia in children and adolescents: What is abnormal? J Pediatr. 2012;160(2):222-226.
  54. Steinberg LA, Knilans TK. Syncope in children: Diagnostic tests have a high cost and low yield. J Pediatr. 2005;146(3):355-358.
  55. Stewart JM, Medow MS. Can standing replace upright tilt table testing in the diagnosis of postural tachycardia syndrome (POTS) in the young? Clin Auton Res. 2025;35(2):257-266. 
  56. Straus D, Foster K, Zimmerman F, Frim D. Chiari drop attacks: Surgical decompression and the role of tilt table testing. Pediatr Neurosurg. 2009;45(5):384-389.
  57. Sutton R, Bloomfield DM. Indications, methodology, and classification of results of tilt-table testing. Am J Cardiol. 1999;84(8A):10Q-19Q.
  58. Tang S, Calkins H, Petri M. Neurally mediated hypotension in systemic lupus erythematosus patients with fibromyalgia. Rheumatology (Oxford). 2004;43(5):609-614.
  59. Thijs RD, Brignole M, Falup-Pecurariu C, et al. Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness: Consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN). Auton Neurosci. 2021;233:102792.
  60. Timoteo AT, Oliveira MM, Antunes E, et al. Tilt test in elderly patients with syncope of unknown etiology: Experience with pharmacological stimulation with nitroglycerin. Rev Port Cardiol. 2005;24(7-8):945-953.
  61. Uno C, Fukuda C, Tanaka N, et al. Study of autonomic dysfunction in patients with obstructive sleep apnea syndrome to head-up tilt test. Rinsho Byori. 2009;57(12):1164-1169.
  62. van Campen CLMC, Rowe PC, Visser FC. Cerebral blood flow is reduced in severe myalgic encephalomyelitis/chronic fatigue syndrome patients during mild orthostatic stress testing: An exploratory study at 20 degrees of head-up tilt testing. Healthcare (Basel). 2020;8(2):169.
  63. van Campen CLMC, Rowe PC, Visser FC. Low sensitivity of abbreviated tilt table testing for diagnosing postural tachycardia syndrome in adults with ME/CFS. Front Pediatr. 2018;6:349.
  64. van Zanten S, Sutton R, Hamrefors V, et al. Tilt table testing, methodology and practical insights for the clinic. Clin Physiol Funct Imaging. 2024;44(2):119-130. 
  65. Vlahos AP, Tzoufi M, Katsouras CS, et al. Provocation of neurocardiogenic syncope during head-up tilt testing in children: Comparison between isoproterenol and nitroglycerin. Pediatrics. 2007;119(2):e419-e425.
  66. Voice RA, Lurie KG, Sakaguchi S, et al. Comparison of tilt angles and provocative agents (edrophonium and isoproterenol) to improve head-upright tilt-table testing. Am J Cardiol. 1998;81(3):346-351.
  67. Wessely S. Is neurally mediated hypotension an unrecognized cause of chronic fatigue? Lancet. 1995;345:1112; discussion 1112-1113.
  68. Winker R, Prager W, Haider A, et al. Schellong test in orthostatic dysregulation: A comparison with tilt-table testing. Wien Klin Wochenschr. 2005;117(1-2):36-41.