Chronic fatigue syndrome and idiopathic intracranial hypertension

JaimeS

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Just saw this in medical hypotheses: http://www.medical-hypotheses.com/article/S0306-9877(17)30418-8/pdf

Though not discussed in the medical literature or considered in clinical practice, there are similarities between chronic fatigue syndrome and idiopathic intracranial hypertension (IIH) which ought to encourage exploration of a link between them. The cardinal symptoms of each – fatigue and headache – are common in the other and their multiple other symptoms are frequently seen in both. The single discriminating factor is raised intracranial pressure, evidenced in IIH usually by the sign of papilloedema, regarded as responsible for the visual symptoms which can lead to blindness. Some patients with IIH, however, do not have papilloedema and these patients may be clinically indistinguishable from patients with chronic fatigue syndrome. Yet IIH is rare, IIH without papilloedema (IIHWOP) seems rarer still, while chronic fatigue syndrome is common. So are the clinical parallels spurious or is there a way to reconcile these conflicting observations?

We suggest that it is a quirk of clinical measurement that has created this discrepancy. Specifically, that the criteria put in place to define IIH have led to a failure to appreciate the existence, clinical significance or numerical importance of patients with lower level disturbances of intracranial pressure. We argue that this has led to a grossly implausible distortion of the epidemiology of IIH such that the milder form of the illness (IIHWOP) is seen as less common than the more severe and that this would be resolved by recognising a connection with chronic fatigue syndrome.

We hypothesise, therefore, that IIH, IIHWOP, lesser forms of IIH and an undetermined proportion of chronic fatigue cases are all manifestations of the same disorder of intracranial pressure across a spectrum of disease severity, in which this subset of chronic fatigue syndrome would represent the most common and least severe and IIH the least common and most extreme.
 

kangaSue

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I've seen it suggested that left renal vein compression (Renal Nutcracker Syndrome) can cause a slight increase in intracranial pressure so maybe that leads to intracranial hypertension too. It's certainly known to be a cause of POTS

When the left renal vein is compressed, the blood flow from the kidney that usually drains into the inferior vena cava can reflux into the spinal canal to cause the increased intracranial pressure, something called midline congestion syndrome I think.
 
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Two of the researchers of this study have tried treatments for this on me. I had a lumber puncture, and I felt better for a few days after that. They said that this suggests I have brain inflammation as the drained cerebral spinal fluid creates more space for the brain. But there was no way to make the effects permanent.

They also did a jugular venoplasty on me, because scans showed there was a slight narrowing of my veins. This is where they insert balloons inside the vein to make it widen to increase blood flow. The first time they did it I thought I felt a mild improvement but felt nothing the second time.

In the end we gave up though I was left with the offer of having a neck stent put in. I decided not to having not fet enough improvement from the venoplasties.

I'm lucky they tried it out on me but unfortunately it didn't work.
 

pibee

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Two of the researchers of this study have tried treatments for this on me. I had a lumber puncture, and I felt better for a few days after that. They said that this suggests I have brain inflammation as the drained cerebral spinal fluid creates more space for the brain. But there was no way to make the effects permanent.

They also did a jugular venoplasty on me, because scans showed there was a slight narrowing of my veins. This is where they insert balloons inside the vein to make it widen to increase blood flow. The first time they did it I thought I felt a mild improvement but felt nothing the second time.

In the end we gave up though I was left with the offer of having a neck stent put in. I decided not to having not fet enough improvement from the venoplasties.

I'm lucky they tried it out on me but unfortunately it didn't work.

whee did you do jugular procedure? do they have experience w other ME patients? i guess you'e speaking of CCSVI?
 

pattismith

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this paper is really interesting, so many ME patients have head pressure, they may have undiagnosed low grade IHH, it makes sense.

I did myself a trial with Diamox (acetazolamide), a drug used to treat IHH and I got clear improvement, I gave some details here.
 

pattismith

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This is a working theory by Dr Driscoll in Ehlers Danloss Syndrome too;
https://slingsandarrowsofoutrageousfortune.wordpress.com/the-driscoll-theory/
Thank you, this "theory" seems to me a mixing of things with some lack of evidences. but I notice that again the vascular theory is showing up:

"CCSVI (Chronic Cerebrospinal Venus Insufficiency) Stenosed (narrowed) veins in the cervical region result in poor blood and CSF drainage, contributing to the cycle of building pressure above the brain. Angioplasty can open the narrowed veins and restore proper drainage. This is a big area of research in MS"

this theory seems to be better supported by studies and may be present at less in a CFS/ME subgroup suffering with head pressure.

This what Dr Higgins seems to be thinking at less.

Here the full scientific publication from him ( he is the doc who also wrote the article at the top of this thread) where he found focal narrowing in jugular veins from CFS/ME patients with headache (see attached file).

The problem is that all the patient he has treated with venoplasty found some improvement but relapsed more or less quickly, so this surgery doesn't seem to be the right answer.

I used Diamox and found improvement (although I don't know if it will work on the long run), but I wonder if some venodilatator could do the job...

I wish to add that high vitamine A intake has previously shown to trigger intracranial hypertension, so when a supplement makes you worse, better not insist on it...
 

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Not sure if it could cause IHH, but at the onset of my symptoms I asked to have my serum renin drawn and it was triple what it ought to be. Renin stimulates angiotensin and vasoconstriction, correct? What could cause such high renin? Does anyone else have this lab anomaly as well? Could this cause IHH?
 

kangaSue

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Not sure if it could cause IHH, but at the onset of my symptoms I asked to have my serum renin drawn and it was triple what it ought to be. Renin stimulates angiotensin and vasoconstriction, correct? What could cause such high renin? Does anyone else have this lab anomaly as well? Could this cause IHH?
If it's causing hypertension too, renal artery stenosis or Fibromuscular Dysplasia (FMD) as a cause of secondary aldosteronism (and cause renovascular hypertension).
The most important cause of secondary aldosteronism is narrowing of the blood vessels that supply the kidney, renal artery stenosis. This causes high blood pressure due to high renin and aldosterone and may be cured by surgery or angioplasty. FMD can cause a narrowing of the renal arteries
Sometimes only one kidney is affected and an angiogram (catheter inserted through the groin) to collect blood directly from the veins draining the kidney (renal vein renin levels) can be done to see If the value is significantly higher in one side or the other to then indicates where the narrowing of the artery is present.
https://www.ncbi.nlm.nih.gov/pubmed/28060190
 

Wayne

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I had a lumber puncture, and I felt better for a few days after that. They said that this suggests I have brain inflammation as the drained cerebral spinal fluid creates more space for the brain.
I experienced a lot of head pressure for many years, and tried many different things to try to relieve some of that pressure. A number of manipulative techniques helped me, but the thing that I use on a daily basis to relieve this pressure is DMSO. I wrote fairly extensively about my DMSO experiences over on HR this past year on this thread:

POTS Inexplicably Improves After Topical DMSO Applications


I got inspired to use DMSO after reading that conventional medicine has discovered it to be the best therapy for people who experience closed head injuries. Reducing the intracranial pressure as quickly as possible is of the utmost importance, and many people die before being able to accomplish that. DMSO starts working within minutes to reduce that pressure.

I figured if it is so good for a critical head injury, it just might be helpful for the chronic pressure and inflammation I've experienced for years. It did, and even improved my POTS at the same time. The two main qualities of DMSO is that it improves circulation and reduces inflammation, so it's not surprising that it would be helpful for OI.​
 
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pattismith

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Diamox (acetazolamide) also efficient in reducing migraines!

extract:

"One study has investigated acetazolamide efficacy in sporadic migraine with and without aura, demonstrating a reduction in the frequency of attacks in both migraine types [21].

This effect is explained by two possible mechanisms. The first one sees migraine deriving from cerebral oligemia [22, 23], and acetazolamide acting through vasodilatation.

The second attributes migraine to a possible disorder of neuronal ion channels [21]. This last mechanism is the one thought to be responsible for the acetazolamide mechanism of action in familial ion channels disorders, such as familial hemiplegic migraine, hypokalemic periodic paralysis and episodic ataxia type 2 [2426]. One can hypothesize that one of the above-mentioned mechanisms or even both are present also in CADASIL migraine."
 
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I just read this article. My husband has CFS sleep apnea and narcolepsy. Spinal stenosis We have struggled to get help with his illness and it just seems to be progressing. All of the bloodwork you have suggested, he has never had. The doctors here are really doing nothing for him. Dr .Charles Lapp was his last doctor, whose now retired. We travel to MD to see a internal medicine doctor. I am in search of a neurologist who is willing to think outside of the box to try to figure out what's going on with him. From the beginning I have wanted him to have a spinal tap to get some real answers. We are in Virginia, but willing to travel. There are no doctors or hospitals in this state who can help us that I know of. One doctor did suggest Vanderbilt. In Tennessee. Anyone been there? Do any of you have any suggestions? I would not be surprised if he had idiopathic intracranial hypertension. Thank you for your support. Anne
 

HowToEscape?

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I know that there's an #MEAction Tennessee group, @Pscook93, and they're pretty active -- they might be able to help you figure this out.

https://www.facebook.com/groups/MEActionTN/
There's an "#MEaction" group in NYC, which is imho sketchy. I'd rather not go into many details in public, I will give one as an example. The host/leader/whatever asked "why isn't there a list of MDs who can treat M.E.", despite NYC having 3 (now 2) of the very few practitioners. There were other signs that the individual and those who hung around had agendas other than helping M.E. Other groups flying under the same banner may be different, the attitude seems to come from an HQ in San Francisco
 

pattismith

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Another article from Belgium this time:

The link between idiopathic intracranial hypertension, fibromyalgia, and chronic fatigue syndrome: exploration of a shared pathophysiology

sept 2018

Plain language summary

The pathological mechanisms that cause both fibromyalgia (FM) and chronic fatigue syndrome (CFS) are incompletely understood. FM and CFS share very similar symptoms with idiopathic intracranial hypertension (IICH), a condition characterized by an increase in intracranial pressure (ICP) due to an unknown cause. The authors reviewed the literature to explore these common symptoms and to link them to the hypothesis that increased intracranial and spinal fluid pressure is the possible mechanism that initiates the multitude of symptoms in these conditions. The symptoms include neck pain, back pain, pain in arms and legs, numbness/tingling, headaches, fatigue, cognitive impairment, gradual loss of gray matter, in addition to symptoms involving cranial nerves, overload of the lymphatic system in the nasal mucosa and disturbance of the autonomic nervous system. Other shared characteristics include higher frequency in females and family members, and an association with obesity and Ehlers Danlos syndrome (a connective tissue disorder).
These findings are relevant as they provide an alternative hypothesis concerning the pathological mechanisms in FM and CFS.

Purpose:
Idiopathic intracranial hypertension (IICH) is a condition characterized by raised intracranial pressure (ICP), and its diagnosis is established when the opening pressure measured during a lumbar puncture is elevated >20 cm H2O in nonobese patients or >25 cm H2O in obese patients. Papilledema is caused by forced filling of the optic nerve sheath with cerebrospinal fluid (CSF). Other common but underappreciated symptoms of IICH are neck pain, back pain, and radicular pain in the arms and legs resulting from associated increased spinal pressure and forced filling of the spinal nerves with CSF. Widespread pain and also several other characteristics of IICH share notable similarities with characteristics of fibromyalgia (FM) and chronic fatigue syndrome (CFS), two overlapping chronic pain conditions. The aim of this review was to compare literature data regarding the characteristics of IICH, FM, and CFS and to link the shared data to an apparent underlying physiopathology, that is, increased ICP.

Methods:
Data in the literature regarding these three conditions were compared and linked to the hypothesis of the shared underlying physiopathology of increased cerebrospinal pressure.

Results:
The shared characteristics of IICH, FM, and CFS that can be caused by increased ICP include headaches, fatigue, cognitive impairment, loss of gray matter, involvement of cranial nerves, and overload of the lymphatic olfactory pathway. Increased pressure in the spinal canal and in peripheral nerve root sheaths causes widespread pain, weakness in the arms and legs, walking difficulties (ataxia), and bladder, bowel, and sphincter symptoms. Additionally, IICH, FM, and CFS are frequently associated with sympathetic overactivity symptoms and obesity. These conditions share a strong female predominance and are frequently associated with Ehlers-Danlos syndrome.

Conclusion:
IICH, FM, and CFS share a large variety of symptoms that might all be explained by the same pathophysiology of increased cerebrospinal pressure.

Keywords: chronic pain, fatigue, headache, Ehlers-Danlos, sympathetic activity, lymphatic olfactory pathway, small fiber neuropathy, Ménière’s disease, Tarlov cysts

(full text for free)
 
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