THE NEUROENDOCRINE THEORY – HOW I BELIEVE I DEVELOPED IIH

I’m away from my computer at the moment. Mixed feelings, that…at any rate, I wanted to start getting this idea out for discussion. I’ve been wanting to get it out for four months, but I was just too sick to drive my computer after performing the basic tasks of paying bills, laundry, opening a can of Campbell’s Kettle Cooked soup (not a plug, Campbells isn’t paying me a darn thing, but for $2.50 from Amazon, the Jambalaya and White Chicken Chili is not too bad).

I will only be posting the bullet point outline of my theory today due to limitations of typing on a phone as well as the need to present aspects of each point in greater detail in the proper order. And, while this is MY theory of how I developed “IIH”, I have witnessed it play out personally in two people I know personally (both female), as well as seen it as a theme in many other “IIH” patients in various support groups. I suspect this process may likely apply to others as well due to commonalities in physiology between human beings, but I don’t represent it as the ultimate explanation for all Adult Onset Acquired/Secondary IIH/PTC/NPH.

I put this theory together through months of research, review of my medical records, family interviews, and the following publications I urge everyone coping with this disorder to read:

1) “The Driscoll Theory” by Dr. Diana Driscoll, available on her website PrettyIll.com (thank you Renee for bringing this to my attention). While Dr. Driscoll’s focus is primarily related to complications off Ehlers-Danlos Syndrome in which altered intracranial pressure is a common symptom, I believe much of her theory applies to non-EDS patients with altered ICP as well, and will discuss this in detail in the near future.

2) “Adrenal Fatigue Syndrome” by Dr. Michael and Dorine Lam. Adrenal Fatigue Syndrome (AFS) is a condition that develops in cases of prolonged stress. This can result in a blunting of the endocrine response to stress, and Dr. Lam details what the result of this altered endocrine response can cause. I have been dealing with AFS most of my professional life, and it has been a significant obstacle in my recovery.

Even with these contributions, I still didn’t understand how stress causes increased intracranial pressure. However, shortly after reading Dr. Lam’s book, a research paper from 2013 literally fell into my lap, a veritable Rosetta Stone tying everything together.

I need to state this theory is based around my initial postulate that ICP in adult onset secondary “IIH” is governed primarily by cerebrovascular/blood dynamics. Blood is the ONLY fluid that flows into the brain/skull at a rate of 750-1000 cc/minute at rest. CSF is made from arterial blood in the brain at a mere 0.35 cc/minute. While CSF can make a significant contribution to ICP, failing to take cerebrovascular dynamics into account ignores the 800 lb gorilla in the head. I arrived at this in a rather “side-loaded” manner, but I’m not the first to make this observation:

Dr. Mark Wilson, Neurosurgeon, Royal Academy of Medicine: Monro-Kellie 2.0: The dynamic vascular and venous pathophysiological components of intracranial pressure

Thus, without further rambling, The ShuntWhisperer’s Neuroendocrine Theory of Adult Onset Acquired/Secondary Intracranial Hypertension:

IIH IS NOT A PRIMARY DISORDER. IT IS A SYMPTOM OF ENDOCRINE DYSREGULATION AS A RESULT OF PROLONGED STRESS. I don’t consider this to be the only possible cause of Acquired ICP, but I believe it is how I developed my particular disorder. Thus my contention that endocrine evaluation and stress reduction are as important to optimal treatment outcome as is reduction of pathologic ICPs.

1) Pre-existing condition(s), developmental or acquired, which predisposes a patient’s intracranial pressure physiology to be higher than “normal”. Examples include but are not limited to:

a. Underdevelopment of the Venous Sinus Network, resulting in reduced absorption of CSF

b. Reduced Intracranial Volume, including Chiari Spectrum findings with or without symptoms.

2) Past Physical Trauma, especially cervical trauma

3) Autoimmune/Inflammatory conditions with or without symptoms, especially IBS, Crohn’s Disease, gastroparesis, endometriosis, and Polycystic Ovary Disorder

4). Female Sex

5). Exposure to prolonged stress with alteration of endocrine stress response, especially “blunting” of the Recovery Phase from initial Fight/Flight Response.

and finally:

6) Precipitating Stressor. This critical event can be physical and/or emotional, and pushes a patient’s quiescently challenged physiology into an area where increased ICP and associated serious consequences develop. If, as in my case, it results in a dramatic and unexplained loss of function which threatens livelihood, relationships, and pleasure activities, this can initiate a vicious cycle of increasing intensity until the patient has very limited or no ability to function.

The Good News: based on observation of the early onset of IIH in several patients, I believe that ICP is reduced into a normal zone while the patient’s body still has the ability to heal the damage caused, remission is possible when accompanied by lifestyle changes to reduce stress, dietary changes, and monitoring. Reduction of ICP at this time may be able to accomplished with very small doses of Diamox/acetozolamide.

So there it is, for what it’s worth. Over the next few weeks I will fill out pertinent details, with research references. Again, this is my theory based on my experience; I have no idea how broadly it applies to any other patient, but I’m beginning to see similar notions from medicine.

As always, prayers for comfort and food days to all & May God Bless each of us, our families, and our doctors.

April 30, 2019

The Shunt Whisperer

2 thoughts on “THE NEUROENDOCRINE THEORY – HOW I BELIEVE I DEVELOPED IIH

  1. This speaks volumes to me…
    – Past physical trauma, yes to the head.
    – Auto-immune/Inflammatory conditions, yes, psoriasis, and I believe I have some level of metabolic disorder and/or hypothyroidism
    – female, yes
    – Exposure to prolonged stress with alteration of endocrine stress response, especially “blunting” of the Recovery Phase from initial Fight/Flight Response….. I was in a long term emotionally abusive relationship, so yes.
    – precipitating stressor… I left said relationship and changed my entire lifestyle (moved states, quit smoking, changed diet, etc) within months of my initial symptom onset….
    I look forward to reading more of your theorising 🙂

    1. Kelly: I’m sorry to hear about these challenges. An ultimate point in this theory is that I believe involvement of an endocrinologist is necessary to evaluate the FUNCTIONAL status of your endocrine system’s condition, especially the HPA Axis (Hypothalamus/PituitaryAdrenal System). The HPA Axis is the “master control” of the endocrine system, and typically the adrenal segment weakens first, taking the other systems down with it. When I say “functional” status, I’m referring to testing that assesses individual hormone levels over their particular period of normal highs and lows. One endocrine blood panel gives a “snapshot” of the endocrine system, but as the saying goes, even broken clocks show the right time twice a day. Cortisol is a critically important stress control hormone that waxes and wanes throughout the day, so proper evaluation requires measuring its levels during at least 5 critical periods in 24 hours. You might want to start looking at Dr. Lam’s website, DrLam.com, and familiarize yourself with Adrenal Fatigue; “The Driscoll Theory” addresses issues of autoimmune conditions with regards to stress as well.

      My belief is that my IIH is a symptom of Adrenal Fatigue, not a primary disorder. Treating Intracranial Pressure Dysregulation without looking at how endocrine function may have been affected by ICP alterations seems less than ideal. I will be filling in the blanks regularly, even daily if possible, in hopes that it helps others such as yourself. Prayers to you for comfort and better days.

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