Mayo clinic handbook article: Clinical neurophysiology of postural tachycardia syndrome (Sandroni 2019)

[Murph]

Handb Clin Neurol. 2019;161:429-445. doi: 10.1016/B978-0-444-64142-7.00066-7.
Clinical neurophysiology of postural tachycardia syndrome.
Cutsforth-Gregory JK1, Sandroni P2.
Author information

Abstract
Postural tachycardia syndrome (POTS) is one of several disorders of orthostatic intolerance (OI). It is defined by the development of symptoms of cerebral hypoperfusion or sympathetic activation and a sustained heart rate increment of 30 beats/min or more (40 beats/min for teenagers) within 10min of standing or head-up tilt in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. POTS is approximately five times more common in women than men.

This heterogeneous syndrome is caused by several pathophysiologic mechanisms (limited autonomic neuropathy, hyperadrenergic state, hypovolemia, venous pooling, deconditioning), which are not mutually exclusive. Anxiety and somatic hypervigilance play significant roles in POTS. Common comorbidities include visceral pain and dysmotility, chronic fatigue and fibromyalgia, migraine, joint hypermobility, mitral valve prolapse, and inappropriate sinus tachycardia.

Patients with suspected POTS should undergo comprehensive cardiac and neurologic examinations and autonomic and laboratory tests to determine the most likely pathophysiologic basis of OI. The objectives of POTS management are to (1) increase the time that patients can stand, perform daily activities, and exercise and (2) avoid syncope. Management involves nonpharmacologic (fluid and salt loading, physical countermaneuvers, compression garments, exercise training) and pharmacologic (β-blockers, pyridostigmine, fludrocortisone, midodrine) approaches.
Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS:
Autonomic neuropathy; Chronic fatigue syndrome; Deconditioning; Ehlers–Danlos syndrome; Hyperadrenergic; Inappropriate sinus tachycardia; Mitral valve prolapse; Orthostatic intolerance; Postural tachycardia syndrome; Venous pooling
PMID: 31307619 DOI: 10.1016/B978-0-444-64142-7.00066-7

 

[pattismith]

It's a pity so few studies got interest into OI and Autonomic Nervous System dysfunction in Cervical Compression Myelopathy...

"Patients with CCM have definite ANS dysfunction as compared to healthy age- and sex-matched controls. There is significant improvement in 30:15 ratio after surgery."

https://www.researchgate.net/public...ysfunction_in_Compressive_Cervical_Myelopathy

"Conclusions Cervical decompression operation could improve both somatic neurological function and cardiac autonomic regulation in CSM patients, and achieved JOA score was significantly positively correlated with improvement in HRV and cardiac parasympathetic activity."

https://www.researchgate.net/public...ressure_heart_rate_and_heart_rate_variability

"Findings: In the preoperative assessment, 14 of 19 (73.7%) patients had bladder dysfunction and orthostatic hypotension. Sympathetic Skin Response was absent in 13 (68.4%) patients preoperatively. At a mean follow-up of 14.5 months after CC, SSR was present in 12 of the 14 patients available for follow-up. SSR returned postoperatively in 9 of the 11 patients in whom it was absent preoperatively.
Conclusions: Dysfunction of the autonomic pathways as determined by the SSR is seen in nearly 70% of patients with moderate and severe CSM but did not correlate with other autonomic functions, suggesting possibly different pathways for different autonomic functions. Following uninstrumented CC, SSR returned in almost 80% of patients in whom it was absent preoperatively and this correlated significantly with improvement in functional grade. Decompressive surgery can reverse autonomic dysfunction in most of these patients."

https://www.tandfonline.com/doi/abs/10.1080/02688697.2016.1206178

 

[Judee]

Anxiety and somatic hypervigilance play significant roles in POTS.

I love how they always have to introduce that into the subject (not).

Of course, always feeling like one is going to faint would tend to make them feel anxious and hypervigilant, wouldn't you think?

 

[Belbyr]

I saw Dr Sandroni at my Mayo Clinic visit back in 2015. It would really be mean of me to call that visit a joke, so I won't say it...

POTS research is like watching a tree grow. This report mimics that of papers back in the 80's.

 

[Inara]

Anxiety and somatic hypervigilance play significant roles in POTS.

Sure.

Edit: Oops, saw your post @Judee afterwards.