PTSD Survivors Speak: Closed Head Injury Hypothalamus Fix

This guest post, about regulating stress originally appeared on Shireen Jeejeebhoy’s blog, 

ptsd brainAs I wrote earlier, I had suffered from various metabolic issues that the medical community was either unable or unwilling to understand and to treat. Over the years, I sought understanding, using what I remembered of my pre-injury knowledge of physiology, neurophysiology, and research skills. As I got better cognitively, especially this past year with more spontaneous healing that restored some knowledge, it became clearer to me that the problems stemmed from the hypothalamus, rather than just the pituitary, and I came to a decision: to fix it myself. This is the last part of a three-part series on the hypothalamus and brain injury or closed head injury.

Hypothesis

A closed head injury somehow alters the functioning of the hypothalamus. The question is, is the body responding normally and chronically to an extreme stressor(s) or is the body responding in an extreme way to stress? Given that my need for atenolol increases at night and my symptoms are worse at night, a time when stress drops, I concluded that it was the latter. Furthermore, in my mind, it seemed that the issue was low serotonin levels in the hypothalamus and that generally speaking, treatment needed to reset the hypothalamus to a normal, balanced state. The beta blockers I was on only controlled some of the symptoms, and with a half-life of 6 hours, required a “top-up” dose at midnight and/or a morning dose about 5:00 am, further interrupting already fractured sleep. In addition, beta blockers are known for their fatiguing side effects; sometimes it’s so bad, it knocks me out for the whole day. Fatigue on top of brain-injury and fibromyalgia-induced fatigue is not good, and it diminishes any sense of well being.

I needed a treatment that addressed all of the symptoms, did not cause added fatigue, improved sense of well being, and allowed me to become more functional so that ultimately, combined with other therapies and improvements, I could reintegrate into society and become a productive contributing member of it. I decided to do a single-subject research study on myself to gauge the effectiveness of Audiovisual Entrainment and Cranial Electrical Stimulation on hypothalamus function. I call it the “hypothalamus fix.”

Method

On 16 August 2010 I began using the sub-delta session of Mind Alive‘s Audiovisual Entrainment (AVE) unit almost every night, with some nights off. I then began using it nightly on 28 August 2010. This session emits visual pulses from 0.5 to 1Hz and back again, along with binaural beats, for 24 minutes. It is a passive session and does not entrain the brain. I kept both the auditory and visual intensities at 4. Any lower on the visual intensity, and I found it had no effect. There is little research on the effects of this session but what evidence exists shows it calms the hypothalamus. That is why I chose it. I also decided to use it just before going to sleep in order to facilitate falling asleep.

About the same time, I began using the Oasis II Cranial Electrical Stimulation (CES) device from Mind Alive. This device directs a microcurrent, through clips attached to the earlobes, into the brain. It has three settings: Sleep at 100Hz (short pulses), Relief at 0.5-3.0Hz (long pulses), and micro-TENS at 0.5-3.0Hz (short pulses). Being unfamiliar with the device, I experimented with the various settings before settling on a pattern of use that seemed to have an effect. I used the Sleep session every morning, beginning on 17 September 2010, right after awakening, which varied from 5:30 to 9:00 am (depending on how fractured my sleep was through the night) for one hour at the highest point of the low intensity level (there are four intensity levels, each of which rises in intensity as well).

A month later I began experimenting with evening times. From 16 October 2010 on, I used the CES device nightly at 10:00 pm for 30 minutes at the highest point of the low intensity level. I also upped the intensity level of the morning session to the lowest point of the second intensity level.

Results

I was looking for changes in body temperature, water retention, sleep, and skin health and a reduction in the dosage of atenolol. (I am not equipped to take any objective measurements, obviously.) I should note here that typically, I need twice the dose of atenolol in the winter than I do in the summer. Beginning this regimen in the summer gave me a heads-start to hopefully ensure I didn’t have to increase my morning dose as the weather got cooler, from either 0 in the heat of the summer or 12.5mg to 25mg by January. Evening dose has remained consistent at 25mg for the last 3 years.

After three sub-delta AVE sessions on 16- 17- and 20 August 2010, I began to be cooler. By the fourth session on 21 August 2010, I began to fall asleep near the end of the session. And overall I was falling asleep within about 30 minutes (though it’s hard to be exact when you cannot use objective measures like a sleep study), instead of my usual 1 to 2 hours. After the 6th session on 25 August 2010, I started turning the volume down on the television  (volume is not a function of deafness but of comprehension). By the 7th session on 26 August 2010, my speech became more animated. Speech improvements are usually the first thing I note whenever I start a new treatment modality.

I had been using CES sleep alternating with relief at various times beginning on 13 August 2010 to see what the effects were. Even though use was not daily or sometimes two or three times a day, depending on pain levels, and variable, by 5 September 2010 I was feeling calmer after use, and I had also begun dreaming again. On the second morning I began to use the 1-hour Sleep session consistently, the edema or water retention started to go down, as evidenced by looser rings, a thinner face, thinner nose, and being able to feel my bones from my shoulders to my knuckles to my feet. By the third session on 19 September 2010, I reduced the morning dose of atenolol (normally 12.5mg). However, that smaller dose was still too much as it put me to sleep. Overall night-time sleep was becoming more consistent, including at times wake-up time. By 21 September 2010, my neck thinned and began to show a normal hollow at the base.

On 30 September 2010, my acupuncturist confirmed that I was significantly less hyperthermic, though still producing some heat. And she noted my mood was elevated; for the first time in over 10 years, I looked happy. She recommended reducing acupuncture frequency. However, about the same time I became aware that I had started to forget my regular daytime AVE sessions of alpha and beta waves; I was becoming more and more distracted. I resumed those sessions on 7 October 2010.

On 4 October 2010, I had my first hot shower in years and years, and my skin did not react nor did I overheat. Normally, my skin develops hot spots, which turn red and swell up and spread unless I pour cold water on them and moisturize with melaleuca-oil cream. Having a hot shower with no need to cool my skin down is a very big deal.

There was a hiccup in my study as the outside temperature dropped and my home got cold the first week of October. Environmental temperature affects my internal temperature as my body cannot regulate its own temperature very well. The optimum environmental temperature for me is about 22C. With each degree below 20C or above 26C, I retain more water and become hotter, yet I can at times feel the outside cold (or heat). But because of my skin reaction I cannot wear long-sleeved shirts, only loose sweatshirts and T-shirts. I also become more fatigued, reducing my functionality.

On 7 October 2010, I saw my behavioural cardiologist who recommended sticking with this therapy for 3 to 4 months to fully assess the effects before trying anything else.

On 8 October 2010, the evening atenolol dose of 25mg was suddenly too much. It knocked me right out. It was very unpleasant to fight sleep for 6 hours — I cannot nap otherwise it interferes with my night-time sleep. I reduced my atenolol a bit and experimented with adding an evening CES Sleep session. I tried 8:00 pm, 9:00 pm, and 10:00 pm. The 10 o’clock time seemed the best, otherwise with a reduced atenolol dose, I had started to wake up again too warm and with increased water retention.

Currently at this stage of my single-subject study — 20 October 2010 — I remain cooler and have markedly less water retention. I also have less shortness of breath. This kind of shortness of breath has nothing to do with my lungs as they are clear. I am not however, back to normal on these three indices. I am sleeping better, though have a long way to go to have normal sleep. I am sweating at more normal levels. My thinking is clearer, though processing speed remains the same. My skin is better to the point that I can wear long sleeves again and have the occasional hot shower. The results remain uneven on that score, but overall my skin is less reactive to allergens or stimulations. I do not know the effects on blood pressure, heart rate, type 2 diabetes, triglycerides or cholesterol. I may find the answers when I next see my GP.

Unexpected Results

Brain injury anger can best be described as a beast that rises suddenly, takes over, manifests with yelling or violence, and just as suddenly disappears. It’s difficult to manage by the brain-injured person as we don’t know when it will hit until it does. We learn compensating strategies to avoid it being triggered, including avoiding triggers altogether. But at best these strategies, I’m told, work only 50 percent of the time. So you’re pretty much at the mercy of this thing. Brain injury anger is a serious problem, yet no one seems to have figured out what causes it or how to cure it, only how to manage it, sort of. And even then there is no manual on how to manage this kind of anger; traditional methods do not work. The most common theory given for brain injury anger seems to be that damage to the frontal lobes removes the control over the limbic system and thus anger can have dominance over the person. Concurrent with this anger is irritability. It’s like everything is nails-on-chalkboard. I was told that the filters to outside stimulants are turned off, and so we become aware or reactive to everything. It’s unpleasant.

For me, brain biofeedback reduced and my constant irritability and then after several months, began to reduce the severity and frequency of the brain injury anger. Acupuncture also calms the irritability and anger, though doesn’t cure it. Using the 32-minute alpha-wave and 14Hz beta-wave sessions on the AVE can also calm rising irritability and anger, temporarily. However, my main triggers remained just as potent as ever. So I avoided them. Unfortunately, one of them is the TTC, and it’s not possible to avoid it altogether.

On 5 October 2010, I used the TTC subway and streetcar. It was uncomfortable but uneventful. I noted that down but didn’t really think too much of it. But the next day 6 October 2010, it started to sink in that my new therapy was positively affecting brain injury anger when I had to deal with technical support over the phone for a computer problem. I got angry — who doesn’t — but the brain injury anger did not rise. I did not feel edgy either. That is a first.  In over 10 years.

On 12 October 2010, I had to use the TTC subway and streetcar again. I was disturbed by the sensory data coming in but felt no angry reaction.

On 18 October 2010, for the first time in almost 11 years, I felt nothing, just like I used to before the brain injury, when I rode the TTC. No anger, no irritation, no annoyance, no discomfort. And I was only using one of my compensating strategies too. I usually use about three or more.

Another typical problem with brain injury is mood instability. Your mood can be fine one moment, and in the dumps the next, then fine the next, or manic the next. I’m not sure how common this is, but one guy described it as having leaky eyes. I have heard that anti-depressants are commonly given to those with brain injury to stabilize mood. My problem was I had a lack of affect interrupted occasionally by very intense moods. Brain biofeedback brought my emotions back to life, and over time the wild mood swings have settled down to regular, old instability. I don’t like the side effects of anti-depressants, and so I do not take them. Instead, I use the AVE and acupuncture to help my moods.

Concurrent with the anger reduction, mood instability has lessened in intensity markedly.

Last year I learnt that people with brain injuries can have exercise intolerance. After  I reduced my exerciseby two-thirds, I had an increase in energy, reduction in water retention, was less hyperthermic (but since I still was, shows just how hot I was), and was much less short of breath. However, I have not been able to increase my exercise beyond 15-17 minutes four times per week, despite the fact I need to do so because of my diabetes diagnosis and for general physical health. And physical stress, like walking longer than about 5 minutes, will worsen my metabolic symptoms at night. Ever since my brain injury, I cannot walk uphill or up stairs without slowing down or taking breaks.

On 14 October 2010, I climbed a long, steep set of steps out of a ravine without having to stop (I stopped only to take photos). I was able to keep up with my mother enough so that I didn’t lose sight of her. I panted like crazy, but I felt no dizziness, no shortness of breath because of my heart or brain, no increased heat. And though I was dead tired and sleepy for the rest of the day, I suffered no worsening metabolic effects that night. It was so astonishing, I still cannot believe it.

Discussion

What I call my “hypothalamus fix” has shown great promise. But it’s early days yet. I have had only about 6 weeks of combined CES-AVE therapy. And, as well, cold-weather stress has just begun and will not hit its peak for another 2 to 3 months, which will be the real test of this fix. I am increasing the intensity of the sessions and will increase the duration of the CES evening session (I’m taking it slowly) to, hopefully, compensate for the weather getting colder.

On the plus side, I have not yet had to resume morning atenolol doses, I remain cooler, my water retention continues to drop, my skin is less red and irritable, my sleep is better, my brain injury anger seems to be gone, my mood instability has diminished greatly, my exercise tolerance has begun to increase, and I need fewer acupuncture sessions.

On the remains-to-be-seen side, I do not know how my heart rate, blood pressure, and blood glucose levels have been affected. I do not know if this will help me drop weight, which I have not been able to do to any great extent with diet and exercise alone. However, I theorize that if the stress reaction drops, then insulin levels will drop, and so my weight should be more responsive to what I’m eating and doing physically. On the few times, I’ve remembered to take my pulse, it’s been variable and on the high side, though not as high as before I started taking the atenolol. I still get hot under cognitive, physical, or emotional stress, though I now have the ability to reduce it by using an extra CES sleep session. I have had reversals of the water retention improvement, though they were temporary and due to cold-weather stress. My wake-up times remain inconsistent, and I still suffer next-day fatigue from doing too much the previous day.

I also have more questions. From my experience, it is now clear to me that the hypothalamus is involved in brain injury anger. But is it the only part of the brain that is? What causes this kind of anger? What combination of therapies will cure it? And when should they be introduced in the recovery process? The hypothalamus also affects mood. But how much? Can treating only the hypothalamus stabilize mood, or are there other parts of the brain involved? Where does exercise intolerance come from? Is it because of an overactive sympathetic system and/or high cortisol release that drains the body to the point that there’s nothing left for exercise or physical activity? How does cognitive activity affect it? What else will improve exercise tolerance? And just how many people with brain injuries, especially closed head injury, suffer from these metabolic, anger, mood, and exercise tolerance issues? I have found only one study that talks about the prevalence of these things, as well as other related issues that I haven’t mentioned here. But that is insufficient to get a good picture of this issue. I plan on doing a formal survey with the Brain Injury Society of Toronto to get a sense at the local level. But if I had the means and resources, I’d do a proper research study, building on my own single-subject study. I’ll blog on that next time.

But first things first. I’ll continue my therapy, and if I remain at this level or better come January, if I no longer need the atenolol, and if the changes become permanent so at most I only need to do my “hypothalamus fix” occasionally, then I know I will have succeeded for sure.

 

For more information check out Shireen’s book, Concussion Is Brain Injury.

 
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