Skip to comments.Reduced Cardiac Vagal Modulation Impacts on Cognitive Performance in Chronic Fatigue Syndrome
Posted on 12/30/2012 7:18:29 AM PST by Seizethecarp
Cognitive difficulties and autonomic dysfunction have been reported separately in patients with chronic fatigue syndrome (CFS). A role for heart rate variability (HRV) in cognitive flexibility has been demonstrated in healthy individuals, but this relationship has not as yet been examined in CFS. The objective of this study was to examine the relationship between HRV and cognitive performance in patients with CFS.
Patients with CFS showed no deficits in performance accuracy, but were significantly slower than healthy controls. CFS was further characterized by low and unresponsive HRV; greater heart rate (HR) reactivity and prolonged HR-recovery after cognitive challenge. Fatigue levels, perceived effort and distress did not affect cognitive performance. HRV was consistently associated with performance indices and significantly predicted variance in cognitive outcomes.
These findings reveal for the first time an association between reduced cardiac vagal tone and cognitive impairment in CFS and confirm previous reports of diminished vagal activity.
(Excerpt) Read more at plosone.org ...
Tell me about it!
I suddenly feel sleepy ... I’ll read this later ....
Hold-outs for the “its all in the mind” (big fakers, big whiners) theory of ME/CFS will be hard-pressed to explain how “chronic sympathetic hyper-arousal...persists even during sleep,” but old prejudices die hard for some.
It took a whole study with some long, stupid name to tell that people who can’t sleep have slower reaction times?
That’s why I wouldn’t feel safe driving until my parathyroid surgery.
Maybe the government should give me millions of dollars to find out why Liberals are so stupid...
You believe this crap, Jane?
CFS isn’t about people who can’t sleep, although some folks with CFS may also have sleep disorders or develop sleep disorders.
I hope you never have to experience it.
Too small a study to be useful
Hold-outs for the its all in the mind (big fakers, big whiners) theory of ME/CFS will be hard-pressed to explain how chronic sympathetic hyper-arousal...persists even during sleep, but old prejudices die hard for some.
But... Doesn't this study show strong evidence that it *is* all in the mind? It's all that nervous system involvement, you know.
Another thing, of course, the endocrine system is forgotten about.
“Patients with CFS showed no deficits in performance accuracy, but were significantly slower than healthy controls. CFS was further characterized by low and unresponsive HRV; greater heart rate (HR) reactivity and prolonged HR-recovery after cognitive challenge. Fatigue levels, perceived effort and distress did not affect cognitive performance. HRV was consistently associated with performance indices and significantly predicted variance in cognitive outcomes”
I already have primary hyperparathyroid disease. I’ve been experiencing it since 2002.
We’ve already decided that Liberals are moronic, at least Conservatives have. I figure that since the government gives out grants to study the sex habits of a Polish frog, then yeah, I believe taxpayer money goes to Liberal orgs as payback ... :)
another thing is if you are smoking like a chimney you are unlikely to get well under any circumstances—little frustration with my sibling here
I’ve never smoked anything at all and don’t have any plans to start smoking anything.
Studying the sex habits of a Polish frog... it kinda makes me vaguely regret being a taxpayer.
“It took a whole study with some long, stupid name to tell that people who cant sleep have slower reaction times?”
The study validates the CFS diseased state of the autonomic heart-brain feedback loop that ultimately regulates blood flow to the brain. This defective mechanism is NOT a function of lack of sleep per se, although poor sleep quality contributes to background fatigue level for CFS patients, I am sure.
Here is a 1997 John’s Hopkins paper that explains better what this Australian study is confirming:
GENERAL INFORMATION BROCHURE ON NEURALLY MEDIATED HYPOTENSION AND ITS TREATMENT
Neurally Mediated Hypotension Working Group
Johns Hopkins Hospital
Revised January 1997
This document has been prepared for those who have requested further information about neurally mediated hypotension.
What is neurally mediated hypotension?
Neurally mediated hypotension is also known by the following names: the fainting reflex, neurocardiogenic syncope, vasodepressor syncope, the vaso-vagal reflex, and autonomic dysfunction. Hypotension is the formal medical term for low blood pressure, and syncope is the term for fainting. Neurally mediated hypotension occurs when there is an abnormal reflex interaction between the heart and the brain, both of which usually are structurally normal.
When does neurally mediated hypotension lead to symptoms?
Neurally mediated hypotension occurs in susceptible individuals in the following settings:
after prolonged periods of quiet upright posture (such as standing in line, standing in a shower, or even sitting up for long periods),
after being in a warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath),
immediately after exercise,
after emotionally stressful events (seeing blood or gory scenes, being scared or anxious).
some individuals get symptoms soon after eating, when blood flow has shifted to the intestinal circulation during the process of digestion.
We are all susceptible to activation of the vaso-vagal reflex that results in a lowered blood pressure (NMH), but each person’s susceptibility is affected by his or her genetic make-up, dietary factors, psychological make-up, and acute triggers such as infection and allergy. The clinical problem of NMH occurs when there is sufficiently early triggering of this reflex to cause symptoms.
How does upright posture lead to these problems?
After a normal individual stands up, blood pools in the legs through the effect of gravity. To compensate for the lower amount of blood returning to the heart immediately after standing, the body has a surge of adrenaline (epinephrine). This adrenaline surge leads to a faster heart rate and to more vigorous heart beats (a familiar feeling we all experience when we are frightened, for example). The faster heart rate and more vigorous heart contractions allow the reduced amount of blood returning to the heart to be pumped more efficiently to vital organs (especially the brain).
In individuals with neurally mediated hypotension, there is a Amiscommunication@ between the heart and the brain. Just when the heart needs to beat faster, (to pump blood to the brain and prevent fainting), the brain sends out the message that the heart rate should be slowed down, and that the blood vessels in the arms and legs should dilate. These actions take even more blood away from the central part of the circulation where it is needed. In response, individuals feel lightheaded or may faint because not enough blood is getting to the brain. Fainting is helpful, in that it restores a person to the flat position, removing the pooling effect of gravity on the blood, and allowing more blood to return to the heart. Following the lightheadedness or syncope, most individuals feel tired and their mental abilities are somewhat foggy.
Which symptoms can be caused by the neurally mediated hypotension?
Recurrent lightheadedness and fainting are common symptoms, as is an unusual difficulty with prolonged fatigue after a modest amount of physical activity. This post-exertional fatigue can last 24-72 hours, and interferes with many daily activities.
We have also observed that chronic fatigue, muscle aches (or fibromyalgia), headaches, and mental confusion can be prominent symptoms of neurally mediated hypotension even in individuals who do not faint. The mental confusion takes the form of difficulty concentrating, staying on task, paying attention, or finding the right words.