A Hypothalamus Fix for Closed Head Injury?
As 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
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