New type of nerve cell in brain. POTSers, take note… and hope

This article discusses the discovery of a new type of neuron in the hypothalamus. 

A new type of nerve cell found in the brain

This specific type of nerve cell handles cardiovascular functions, playing some sort of role in regulating heart rate and blood pressure. The cardiovascular system being the interlocked system  that it is, this presumably also includes force of heart contractions, tension of the vessels, and other autonomically-driven activities.

The autonomic part of the nervous system is supposed to be the ring-master for the automatic functions of life, everything that has an up and a down: blood pressure, heart rate, sleeping/waking, appetite and thirst, and so on. Its dysregulation in CRPS is probably one of the most stubborn problems in treating and managing this disease. Finding a type of nerve that so explicitly  handles one part of that extraordinarily complex set of inter-relating functions is fascinating enough, but the ramifications are tremendous.

Here they discuss it in terms of its relationship to the thyroid, an endocrine organ that’s an important part of those regulatory mechanisms, on the chemical-messenger side. The thyroid drives the creation and balance of these types of nerves; these types of nerves then influence the output of the thyroid. It’s a metabolic two-step, a mutual relationship characteristic of nearly every chemical/physical connection in the human body.

Those who have POTS and other forms of autonomically-driven cardiovascular problems might have a new cause for hope. Being able to separate out that particular set of mechanisms from the rest of the nervous system, at least to some degree, may give them a chance of managing their disease better without throwing the rest of their autonomic functions further off.

Anyone who has been that nauseously dizzy and that weak for that long would be terribly glad of the chance. This is great science, and not just for those with thyroid disorders.

“A new type of nerve cell found in the brain”
Eurekalert press release on these findings
Wikipedia on CRPS
What is dysautonomia? – with a focus on cardiovascular issues
CRPS, ANS dysfunction, and chronic vertigo


Blood sugar and mood

“ScienceDaily (2012-01-10) — Patients simultaneously treated for both Type 2 diabetes and depression improve medication compliance and significantly improve blood sugar and depression levels compared to patients receiving usual care, according to a new study.”

In plain English, this means that people with non-insulin-dependent diabetes need to be treated both for diabetes and depression; when that happens, twice as many get stable.

This falls under the Department of the Blitheringly Obvious, because — as anyone who has hypoglycemia, or has dealt with diabetics knows — depression is the first sign of low blood sugar; low or unstable blood sugar leads to poor decision-making, notably poor food choices; poor food choices lead to unstable blood sugar, and round and round we go.

To break the cycle, both must be addressed. Otherwise, the cycle continues feeding on itself… er, unfeeding on itself. Or something.

As anyone with common sense who has dealt with the mentally ill knows, the first intervention is a proper meal. It’s simply amazing how things improve with a little real food inside.

Unstable blood sugar worsens pain, impairs memory, and limits cognitive function. Low blood sugar specifically creates an unhappy state.

A hungry brain is not a happy brain!

Treating type II diabetes without treating depression, or treating depression without treating underlying type II diabetes, is not a recipe for success. The fact that as many as one third of these diabetic patients even get better, is pretty remarkable. Treat both, and over 60% of these people go back to cheerful, stable, productive lives — not needing sickleave, additional benefits, or other direct and indirect expenses.

Sounds like a good cost/benefit profile to me!


CRPS, HPA axis, and a remarkable void in the science

I just went looking for scholarly articles linking chronic CRPS to the HPA axis damage that has been such a feature of my life. Though me, my cohorts and all my providers have been talking freely about this for years, there was nothing on PubMed and nothing of value in the Google search.

It’s possible to chain together articles that make the point — one on stress and adrenal function, one on stress and pituitary dysregulation, one on chronic neurogenic pain and hypothalamic oddness, one on constant pain as a causor of physiologic stress, and one on CRPS as a source of pain — but academics get squirrelly when you make them link the logic. They don’t want to think; it makes them feel exposed.

Nevertheless, me and my providers, me and my cohorts online, me and hundreds and thousands of people with chronic CRPS, have been taking it for granted all this time that there was a link — because it is so bloody obvious that there is.

However, the studies don’t exist.

The connection is obvious, but unwritten.

The data are sitting there, waiting to be captured.

The study subjects are right there for the recruiting.

It’s like the topic is standing there with its pants down and its pockets full. An easy target — and a rich one!

This is ridiculously obvious, and you know that all the subsequent work on CRPS and anything related to the adrenals, hypothalamus and pituitary would have to quote whoever documented it. Tenure, much?

Who wants to find the funding and put together a team? I would be happy to help. If I had the MD and the university contacts, I’d already be making calls. Please, whatever I can do to help, just let me know. Make it happen.