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Transcranial Doppler waveform of right middle cerebral artery flow recorded in a patient with postural tachycardia (panel A) and in a patient with neurocardiogenic syncope (panel B) during HUT test: (1) basal supine rest, (2) 1 min of tilt, (3) 2 min of tilt, and (4) 4 min of tilt. Notice waveform fluctuations from min to min in the recording from the patient with postural tachycardia due to the variation in the pulsatility index (PI) related to changes in diastolic velocity (ED). These oscillations were not observed in any patient with typical neurocardiogenic syncope.
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We assessed the cerebral blood flow velocity response to head-up tilt test in patients with typical neurocardiogenic syncope compared with patients showing postural tachycardia. Fifty patients (21 men) with history of orthostatic intolerance, younger than 50 years (mean 27 +/- 10), participated in the study. Transcranial Doppler sonography of the m...
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... with postural tachycardia show heart rate incre- ments of greater than 30 beats . min (bpm), accompanied by symptoms of cerebral hypoperfusion on standing [10] . Although there are systematic studies of cerebral blood flow on patients with neurocardiogenic syncope [8,11,12] and in patients with postural tachycardia [7,13,14] , to our knowledge there are no comparative studies. This study was aimed to evaluate cerebral blood flow velocity response to HUT in patients su ff ering from typical neurocardiogenic syncope compared with patients showing postural tachycardia. Fifty patients with orthostatic intolerance, accepted to participate in the study, mean age 27 10 years (21 men and 29 women). All the subjects gave their informed consent, and the Ethics Committee of the Instituto Nacional de Cardiolog ́a ‘Ignacio Ch ́vez’ approved the study protocol. Subjects were selected because they were younger than 50 years and for having a history of at least two episodes of malaise while standing up. The episodes of malaise were characterized by: weakness, sweating, pallor, palpitations, warmth, nausea, and blurred vision. Twenty-eight (44%) of them also had a history of recurrent loss of consciousness. To assess specific causes of the orthostatic intolerance, a clinical evaluation was performed in all patients. Patients with structural heart disease, sick sinus syndrome, intra- ventricular conduction disturbance, orthostatic hypotension, chronic and paroxysmal atrial fibrillation, and permanent pacemakers were excluded from the study. HUT was performed between 9:00 am and 11:00 am, in a quiet room and after overnight fasting. Subjects were tilted to 70 degrees head-up, using a motorized tilt-table with a foot-board support. During the test, electrocar- diogram leads I, II and III were continuously monitored and blood flow velocity in the middle cerebral artery was assessed by continuous transcranial Doppler sonography (DTC Multigon 500 Neurovision, Multigon Indus- tries Inc., NY, U.S.A.). A 2-MHz Doppler probe was placed over a temporal window and fixed at a constant angle and position with an adjustable headband accord- ing to standard technique [15] . Doppler signals were recorded at least at 5 min intervals or more often if symptoms developed, to evaluate systolic peak velocity, end diastolic velocity and Gosling’s pulsatility index ([(systolic velocity) (diastolic velocity)]/mean velocity). The latter is an index of vascular resistance which reflects changes in cerebral small-vessel resistance [16] . Brachial blood pressure was recorded using a standard cu ff sphygmomanometer at intervals of 5 min, whenever symptoms of malaise developed and immediately after each transcranial Doppler recording. The HUT was considered to be positive when malaise symptoms appeared accompanied by systemic hypotension (systolic BP<90 mmHg or d 30% reduction from baseline) and/or bradycardia (heart rate less than 50 bpm or d 20% reduction in heart rate from baseline) [17] . According to the heart rate response to HUT, patients were categorized in two groups, neurocardiogenic syncope and postural tachycardia. Postural tachycardia was diagnosed when during the first 10 min of HUT patients showed an increase in heart rate of more than 30 bpm [4] . For ethical reasons, all patients were rapidly returned to the supine position once systemic hypotension was evident [18] . Results are described using mean values, standard de- viation and 95% confidence intervals. Comparison between groups was performed using ANOVA and t test for independent samples. Di ff erences were considered significant when the P value was less than 0·05. The clinical history of the patients showing postural tachycardia during HUT was similar to the history of the patients with typical neurocardiogenic syncope: Twenty-one patients showed postural tachycardia, four men and 17 women (mean age 26·2 years, SD 10·4). They had a history of orthostatic intolerance of 20·8 years (SD 10·3) and 13 (38%) of them also reported a history of loss of consciousness. Twenty-nine patients were positive for typical neurocardiogenic syncope, 17 men and 12 women (mean age 27·6 years, SD 10·1). They had a history of orthostatic intolerance of 21·6 years (SD 11·4) and 15 (49%) of them also reported a history of loss of consciousness. As summarized in Table 1, during baseline in the supine position, no di ff erences in haemodynamic parameters were observed between the two groups. During tilt, just heart rate was di ff erent between the two groups ( P< 0·05), while blood pressure and absolute values of cerebral blood flow parameters were similar. The di ff erence in the heart rate response was patent throughout the HUT test, from the first min of tilt up to the occurrence of hypotension ( P< 0·01) (Table 2). During HUT, the time to develop hypotension was similar for the two groups, mean time for patients with postural tachycardia 10·28 5·01 min and for patients with neurocardiogenic syncope 14·58 6·75 min. In most patients, the symptoms related to hypotension were lightheadedness and blurred vision, followed by nausea. In the two groups, hypotension was associated with an increase of the pulsatility index (Table 3), which was mainly related to a decrease in the end diastolic blood flow velocity. During tilt, continuous observation of the Doppler recording showed that patients with postural tachycardia had intermittent fluctuations of the end diastolic blood flow velocity, with an oscillatory pattern. In these patients, a decrease of the end diastolic blood flow velocity (>20%) was evident earlier than in patients with typical neurocardiogenic syncope, mean time 3·9 3·8 min and 9·3 6·2 min respectively ( P< 0·001). Before hypotension developed, only in patients with postural tachycardia, the decrease of the end diastolic blood flow velocity was just evident during brief periods and it was associated with heart rate increase (Fig. 1). The oscillations of the blood flow velocity ...
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Citations
... The present study found results similar to others who noted that cerebral perfusion persisted after HUT (18, 41, 47). Her-mosillo et al. (18) compared CBFv of patients experiencing neurocardiogenic syncope with those diagnosed with POTS and showed that in POTS and syncope patients, CBFv did not differ significantly during HUT. They concluded that defects within the central nervous system play a crucial role in the pathology of POTS (18). ...
... Her-mosillo et al. (18) compared CBFv of patients experiencing neurocardiogenic syncope with those diagnosed with POTS and showed that in POTS and syncope patients, CBFv did not differ significantly during HUT. They concluded that defects within the central nervous system play a crucial role in the pathology of POTS (18). Razumovsky et al. (41) investigated if chronic fatigue syndrome patients, who have an exaggerated risk for POTS, experienced an abnormal CBFv response compared with healthy control subjects during HUT. ...
Cognitive deficits are characteristic of postural tachycardia syndrome (POTS). Intact nitrergic nitric oxide (NO) is important to cerebral blood flow (CBF) regulation, to neurovascular coupling, and to cognitive efficacy. POTS patients often experience defective (NO) mediated vasodilation caused by oxidative stress. We previously showed dilation of the middle cerebral artery (MCA) in response to a bolus administration of the NO donor sodium nitroprusside (SNP) in healthy volunteers. We hypothesized a blunted MCA response to SNP in POTS. Using combined transcranial-Doppler-ultrasound to measure CBF velocity (CBFv), and near-infrared spectroscopy (NIRS) to measure cerebral hemoglobin oxygenation while supine. The responses of 17 POTS patients were compared with 12 healthy controls (ages 14-28). CBFv in POTS and control were not different at baseline (75 ± 3 vs. 71 ±2 cm • s(-1) P = 0.31) and decreased to a lesser degree with SNP in POTS (to 71 ± 3 vs 62 ± 2 cm • s(-1); P = 0.02). The changes in total and oxygenated hemoglobin (8.83 ± 0.45 and 8.13 ± 0.48 µmol/kg tissue) were markedly reduced in POTS compared to control (14.2 ± 1.4 and 13.6 ± 1.6 µmol/kg tissue), primarily due to increased venous efflux. The data indicate reduced cerebral oxygenation, blunting of cerebral arterial vasodilation and heightened cerebral venodilation. We conclude based on the current study outcomes decreased bioavailability of NO is apparent in the vascular beds resulting in a down regulation of NO receptor sites, ultimately leading to blunted responses to exogenous NO.
... Similarly, Low et al. (1999) suggested that the altered CBFv in POTS was explained solely by respiratory changes and their concomitant affect on cerebrovasomotor tone. Other research suggested that ineffective cerebral autoregulation also played a role in the decreased CBFv seen in POTS (Jacob et al., 1999;Hermosillo et al., 2002). Ocon et al. (2009) found a relationship between decreased CBFv and altered cerebral autoregulation in a cohort of POTS subjects who were eucapnic during orthostatic stress. ...
Chronic Fatigue Syndrome (CFS) is defined as greater than 6 months of persistent fatigue that is experienced physically and cognitively. The cognitive symptoms are generally thought to be a mild cognitive impairment, but individuals with CFS subjectively describe them as “brain fog.” The impairment is not fully understood and often is described as slow thinking, difficulty focusing, confusion, lack of concentration, forgetfulness, or a haziness in thought processes. Causes of “brain fog” and mild cognitive impairment have been investigated. Possible physiological correlates may be due to the effects of chronic orthostatic intolerance (OI) in the form of the Postural Tachycardia Syndrome (POTS) and decreases in cerebral blood flow (CBF). In addition, fMRI studies suggest that individuals with CFS may require increased cortical and subcortical brain activation to complete difficult mental tasks. Furthermore, neurocognitive testing in CFS has demonstrated deficits in speed and efficiency of information processing, attention, concentration, and working memory. The cognitive impairments are then perceived as an exaggerated mental fatigue. As a whole, this is experienced by those with CFS as “brain fog” and may be viewed as the interaction of physiological, cognitive, and perceptual factors. Thus, the cognitive symptoms of CFS may be due to altered CBF activation and regulation that are exacerbated by a stressor, such as orthostasis or a difficult mental task, resulting in the decreased ability to readily process information, which is then perceived as fatiguing and experienced as “brain fog.” Future research looks to further explore these interactions, how they produce cognitive impairments, and explain the perception of “brain fog” from a mechanistic standpoint.
... Microvascular filtration [meaning the amount of blood within capillary vessels] increases in the legs of such patients during passive upright posture, increasing blood flow in the extremities. This induces a redistributive hypovolemia consistent with inappropriate lower-limb vasodilation (59,(63)(64)(65).This redistributive hypovolemia [thoracic hypovolemia] causes compensatory sympathetic hyperactivation that associates with sympathetic blunted response to orthostatic stress. The relative hypovolemia state and the reflex sympathetic activation could then be responsible for failure in cerebral blood flow autoregulation, leading to transient cerebral hypoperfusion. ...
Objectives: Fibromyalgia syndrome [FMS] is one of the most common causes of widespread pain and fatigue, associated with significant morbidity. It is characterized by chronic widespread body pain and a defined number of tender points, as well as multisystem-related alterations. There is considerable diagnostic overlap with chronic fatigue syndrome. Mainstay theory states that these findings could be caused by a central sensitization phenomenon that would lead to diffused hyperalgesia. Until now, however, little is known about the nature of this central sensitization and the possible causative events that lead to it. We sought to review the current evidence about FMS, its relation to cardiovascular alterations [dysautonomia], and to propose a new model upon its physiopathogenesis. Findings: Fibromyalgia syndrome patients have a greater incidence of orthostatic intolerance, characterized by pre-syncope symptoms and a relentless activated sympathetic system, perhaps causally related to FMS. Independent authors have theorized that orthostatic intolerance has a causal link to FMS. Recently it has been demonstrated that alterations in small vessel tone and endothelial function of skeletal muscle or splanchnic vascular beds are crucial to the development of orthostatic intolerance. Conclusions: We propose two novel hypotheses: FMS would be related to a derangement in cardiovascular autonomic control secondary to endothelial function disturbance and this cardiovascular derangement could correlate with attenuation of supraspinal descending nociceptive inhibition through an integrated central nervous system modulation.
This is an Accepted Manuscript of an article published by Taylor & Francis in Journal of Musculoskeletal Pain on7/9/2009, available online: http://wwww.tandfonline.com/10.1080/10582450802679904.
... Se han descrito previamente, como ya se mencionó, marcadores tempranos que sugieren el resultado de la prueba de inclinación, todos ellos se asocian con la presencia de actividad simpática temprana, que se supone genera una descarga parasimpática brusca del tipo del reflejo de Bezold-Jarish, que es la responsable de que aparezca hipotensión y bradicardia. [13][14][15] Pese a esto, los estudios con cuantificación en sangre periférica de catecolaminas muestran resultados discordantes, y es posible que sea necesario buscar cambios más sutiles o cambios regionales en las concentraciones plasmáticas de catecolaminas. Los cambios fisiológicos detectables clínicamen-te y sin métodos invasivos como la frecuencia cardíaca y la presión arterial, permiten suponer una serie de eventos complejos. ...
... Este efecto puede ser secundario a una respuesta simpática amortiguada por un tono parasimpático aumentado, o tal vez, asociado a una respuesta vascular periférica diferencial, dependiente de las concentraciones locales de catecolaminas, como podría ocurrir en el caso del STOP. 7,13 Tal vez esta explicación pueda concordar con los hallazgos previos relativos al comportamiento diferencial de la frecuencia cardíaca. Los pacientes con síncope tienen mayores elevaciones iniciales de la frecuencia cardíaca, manifestación que concuerda con el aumento de las resistencias periféricas como resultado de estimulación simpática. ...
Neurocardiogenic syncope (NCS) is diagnosed by means of a head-up tilt table tests (HUTT). This is a prolonged test although early outcome predictors are known. Methods: We conducted a study among patients engaged in a syncope study protocol. We performed HUTT in all of them and compared the basal arterial pressure with the arterial pressure at the end of a the 70° tilting. Results: We performed 185 HUTT studies. Systolic blood pressure (BP) raised 0.9% among patients with a negative test, whereas patients with a positive HUTT showed a 2.3% decrease (p = 0.2) in the same measurement. Diastolic BP increased 34% among negative HUTT patients and 14.9% among patients with positive test (p = 0.02). We calculated a relative risk of 1.45 for positive test when the combination of systolic BD decrease and dyastolic increase was present, according to the percentage of change (IC95%: 1.1 to 7.8). Conclusions: The combination of systolic BP reduction and diastolic BP elevation at the end of the 70° tilting is associated with an increased risk of having a positive HUTT. These changes might be related to differential sympathetic stimulation.
... Se han descrito previamente, como ya se mencionó, marcadores tempranos que sugieren el resultado de la prueba de inclinación, todos ellos se asocian con la presencia de actividad simpática temprana, que se supone genera una descarga parasimpática brusca del tipo del reflejo de Bezold-Jarish, que es la responsable de que aparezca hipotensión y bradicardia. [13][14][15] Pese a esto, los estudios con cuantificación en sangre periférica de catecolaminas muestran resultados discordantes, y es posible que sea necesario buscar cambios más sutiles o cambios regionales en las concentraciones plasmáticas de catecolaminas. Los cambios fisiológicos detectables clínicamen-te y sin métodos invasivos como la frecuencia cardíaca y la presión arterial, permiten suponer una serie de eventos complejos. ...
... Este efecto puede ser secundario a una respuesta simpática amortiguada por un tono parasimpático aumentado, o tal vez, asociado a una respuesta vascular periférica diferencial, dependiente de las concentraciones locales de catecolaminas, como podría ocurrir en el caso del STOP. 7,13 Tal vez esta explicación pueda concordar con los hallazgos previos relativos al comportamiento diferencial de la frecuencia cardíaca. Los pacientes con síncope tienen mayores elevaciones iniciales de la frecuencia cardíaca, manifestación que concuerda con el aumento de las resistencias periféricas como resultado de estimulación simpática. ...
Neurocardiogenic syncope (NCS) is diagnosed by means of a head-up tilt table tests (HUTT). This is a prolonged test although early outcome predictors are known.
We conducted a study among patients engaged in a syncope study protocol. We performed HUTT in all of them and compared the basal arterial pressure with the arterial pressure at the end of a the 70 degrees tilting.
We performed 185 HUTT studies. Systolic blood pressure (BP) raised 0.9% among patients with a negative test, whereas patients with a positive HUTT showed a 2.3% decrease (p = 0.2) in the same measurement. Diastolic BP increased 34% among negative HUTT patients and 14.9% among patients with positive test (p = 0.02). We calculated a relative risk of 1.45 for positive test when the combination of systolic BD decrease and dyastolic increase was present, according to the percentage of change (IC95%: 1.1 to 7.8).
The combination of systolic BP reduction and diastolic BP elevation at the end of the 70 degrees tilting is associated with an increased risk of having a positive HUTT. These changes might be related to differential sympathetic stimulation.
... The changes in cerebral perfusion during standing in patients with POTS have been measured using transcranial Doppler sonography of the middle cerebral artery (MCA). Some investigators did find that MCA cerebral blood velocity (CBV) decreased excessively during orthostatic stress (23,34), whereas others found no such change in CBV, despite the presence of symptoms suggestive of cerebral hypoperfusion (22,38). The reduction in CBV during orthostatic stress has been attributed to excessive hyperventilation (34) or to exaggerated sympathetic activity directed to cerebral vasculature (28). ...
... First, contrary to our hypothesis, patients with POTS did not have impaired cerebral perfusion compared with normal control subjects, despite the presence of a cardiovascular profile during HUT, suggestive of increased orthostatic stress. In this regard, our data confirm the observations of others who did not observe reductions in CBV during orthostatic stress in POTS (22,38) and are not consistent with other studies in which CBV was excessively reduced during HUT (23,34). ...
To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome (POTS), we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure, heart rate, and cerebral blood velocity (transcranial Doppler) were recorded at rest and during 80 degree head-up tilt (HUT). Static cerebral autoregulation, as assessed from the change in cerebrovascular resistance during HUT, was the same in POTS and in controls. The properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between blood pressure and cerebral blood velocity estimated from filtered data segments (0.02-0.8 Hz). Dynamic cerebral autoregulation of patients with POTS did not differ from that of controls. The patients' dynamic cerebral autoregulation did not change over the course of HUT, despite increased tachycardia suggestive of worsening orthostatic stress. Inflation of military anti-shock trouser pants substantially reduced the tachycardia of patients with POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in one-half of the patients following military anti-shock trouser pants inflation. We conclude that cerebral perfusion and autoregulation in many patients with POTS do not differ from that of normal control subjects.
... However, in patients with POTS, head-up tilt typically induces persistent sinus tachycardia associated with a mild reduction in systemic blood pressure [4] and a substantial decrease in cerebral blood flow velocity can occur despite a well sustained blood pressure [2,5]. In a previous study, aimed to compare cerebral blood flow velocity responses to head-up tilt in patients suffering from typical NMR-syncope and patients showing POTS, we observed that patients with POTS have larger oscillations and an earlier decrease in cerebral blood flow velocity than patients with NMR-syncope [6]. These results suggested that patients with POTS, on standing up, could have an inefficient regulation of cerebral blood vessels and the tachycardia may occur to compensate the diminished cerebral blood flow and even contribute to prevent hypotension. ...
... Few studies have compared responses to tilt in patients with POTS or NMR-syncope [6,11]. In the present study, we compared the responses of the two groups with the responses of a group of patients with dizziness but no syncope. ...
... In a previous study we observed that, during upright tilt, patients with postural tachycardia can have periods of cerebral blood flow velocity decrease related to the heart rate increase [6], suggesting that tachycardia may occur to compensate for an inefficient regulation of cerebral blood vessels. In the present study we observed that, compared with patients with NMR-syncope and with dizziness and without syncope, patients with POTS had a larger heart rate increase related to the maintenance of cerebral blood flow velocity and pulsatility index, with a larger decrease in the pulsatility index/heart rate ratio. ...
To assess the cerebral blood flow velocity during the first minute of head-up tilt in patients with postural tachycardia syndrome (POTS) or neurally-mediated reflex syncope compared with patients with dizziness.
We evaluated 120 patients selected from 470 patients who underwent head-up tilt testing: 40 with POTS, 40 with typical neurally-mediated reflex syncope and 40 who complained of dizziness with no history of loss of consciousness and a negative head-up tilt test (with and without isosorbide). Transcranial Doppler sonography of the middle cerebral artery, heart rate and brachial blood pressure were recorded during a 70 degrees head-up tilt test.
During both baseline in supine position and the first minute of upright tilt, patients with postural tachycardia syndrome showed higher heart rate and cerebral blood flow velocity than patients with dizziness and patients with neurally-mediated reflex syncope (P < 0.05, ANOVA), but no significant difference was observed on the Gosling's pulsatility index.
Patients with POTS have an autonomic dysfunction that is not triggered by upright posture but is accentuated by it.
The classic dogma of cerebral autoregulation is that cerebral blood flow is steadily maintained across a wide range of perfusion pressures. This has been challenged by recent studies suggesting little to no 'autoregulatory plateau' in the relationship between cerebral blood flow and blood pressure (BP). Therefore, the mechanisms underlying the cerebral pressure-flow relationship still require further understanding. Here we present a novel approach to examine dynamic cerebral autoregulation in conscious Wistar rats (n=16) instrumented to measure BP and internal carotid blood flow (iCBF), as an indicator of cerebral blood flow. Transient reductions in BP were induced by occluding the vena cava via inflation of a chronically implanted intravascular silicone balloon. Falls in BP were paralleled by progressive decreases in iCBF, with no evidence of a steady state plateau. No significant changes in internal carotid vascular resistance (iCVR) were observed. In contrast, intravenous infusions of the vasoactive drug sodium nitroprusside (SNP) produced a similar fall in BP but increases in iCBF and decreases in iCVR. These data suggest a considerable confounding influence of vasodilatory drugs such as SNP on cerebrovascular tone in the rat, making them unsuitable to investigate cerebral autoregulation. We demonstrate that our technique of transient vena cava occlusion produced reliable and repeatable depressor responses, highlighting the potential for our approach to permit assessment of the dynamic cerebral pressure-flow relationship over time in conscious rats.
Postural tachycardia syndrome (PoTS)Postural tachycardia syndrome is a heterogeneous clinical syndrome of orthostatic intoleranceOrthostatic intolerance. Distinct subtypes (neuropathicNeuropathic, hypovolemic, and hyperadrenergicHyperadrenergic PoTS) have been developed in an effort to better understand the physiological underpinnings of the disorder. These subtypes are problematic, due to lack of standard definitions, implied exclusivity, and poor explanatory power regarding the underlying pathophysiologyPathophysiology. Our continued investigation of PoTS has recently revealed a number of novel mechanisms, such as the involvement of the immuneImmune system (including mast cellMast cell activationActivation syndrome), physical deconditioning, norepinephrineNorepinephrine transporter deficiency, and impaired cerebral autoregulationCerebral autoregulation. A more comprehensive paradigm is needed, including a precise description of how these diverse processes might overlap, and how each contributes to the clinical presentation of a given PoTS patient. This understanding is critical to the diagnosisDiagnosis and treatment of patients with PoTS.
Objective
To study the frequency of latent and overt involuntary emotional expression disorder (IEED) in postural tachycardia syndrome (PoTS).
Methods
We compared 51 PoTS patients with 15 neurally mediated hypotension (NMH) patients and 12 control subjects using the Center for Neurologic Study-Lability Scale (CNS-LS) for latent IEED and the PHQ-9 questionnaire for depression screening before head-up tilt (HUT). Overt IEED occurrence was observed during HUT.
Results
HUT precipitated overt IEED in 11 (22%) PoTS patients but not in NMH patients or controls. CNS-LS identified latent IEED in 23 (45%) PoTS patients, 5 (33%) NMH patients, and no control subjects. The CNS-LS tearfulness subscale was elevated in PoTS patients compared with controls (P = 0.0006). The PHQ-9 questionnaire scores were elevated in 69% of PoTS patients and 47% of NMH patients. The PHQ-9 score was higher in PoTS (<0.0001) and NMH (P = 0.0002) patients compared with controls.
Conclusions
The study demonstrated frequent occurrence of latent IEED in PoTS and NMH and overt IEED in PoTS without “structural” involvement. HUT was a specific trigger for overt IEED in PoTS. Depression was co-morbid with PoTS. Neurohumoral and cerebral blood flow changes in supine position along with reduced gray matter volume in the insula and cingulate gyrus may underlie susceptibility to IEED. During HUT, cerebral hypoperfusion, rising epinephrine levels, and augmented autonomic arousal provide underpinnings for overt IEED. Clinicians should recognize this entity and counsel PoTS patients and their families. Limiting the duration of orthostatic stress may reduce morbidity.
