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.

Links:
“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

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Makes my brain explode — but now it can be repaired

It’s almost impossible to discuss this article without leaping out of the chair and waving my arms around, squealing with the sheer thrill of its deep and wide implications for treatment and understanding:

Precisely Engineering 3-D Brain Tissues

Using a 3-D printer, transparencies, and binder clips, these wunderkinder can create neural tissues that mimic the cellular proportions and relationships of real, living brains.

On this basis, here are some possibilities discussed in the article:

  • Watch how brain tissue responds under different circumstances, leading to new understanding of brain growth, disease progression and structure-dependent brain abnormalities.
  • Repair damaged brain tissue. With historic rates of traumatic brain injury in the most productive age group, this alone is world-changing.
  • With samples from patients, custom brain cultures can be grown, and drugs tested against them, targeting drug treatment that works on the first trial. This saves people who need CNS-affecting drugs countless weeks and months — even years — of untold misery, as different drugs get pushed through their systems in an effort to find one that works.

Harvard Med and MIT at their collective finest.

The great challenge, of course, is getting this OUT of the lab and INTO the populations that need it. I hope it’s not kyboshed by those whose profits depend on the current ineffective, inefficient, expensive, and unspeakably brutal systems of CNS treatment.

Let good medicine prevail.

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Re-myelination from stem cells

Scientists at Case Western Reserve have found a way to persuade pluripotent stem cells to become the specific type of cell that produces myelin and to re-myelinate living mice:

Mice stem cells guided into myelinating cells by the trillions

For once, I’ve got no logical criticisms to make. This is brilliant work which fills me with hope for those of us dealing with demyelination and all the havoc it causes. Here’s hoping it translates well into human models, and soon.

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Assessing live myelination — and dead CRPS!

Fortunately, I’m bright enough to evaluate this extraordinary new method:

http://www.sciencedaily.com/releases/2011/09/110913103211.htm#.TnDL-iVvIQs.mailto

There are vague mentions in the literature of myelination in CRPS, but researchers are so busy trying to figure out how to pill CRPS — a highly pillable disease — that such mechanistic issues get surprisingly little play.

Myelin is the protective sheath of fat that keeps your neurons safe and warm, so they can do their work. Without myelin, your nerves can’t fire properly — or else they can’t stop firing. They need the myelin sheath. Little kids need to take in a certain amount of cholesterol so their growing bodies can build good myelination. Demyelination, that is, the loss of that sheath, is most famously known for its role in Lou Gherig’s disease.

I’ve long suspected that demyelination is both an important sign of disease progress and a powerful contributing factor to further degeneration of the peripheral, if not the central, nervous system in CRPS. However, there’s not much in the literature, probably because it’s a useless treatment marker in someone who’s beyond treatment.

This brings us to the particularly delightful issue of finding corpses to study, since until now we could only check myelination after autopsy, and those who donate their bodies to science are filed under what took their lives.

People with CRPS develop heart disease, cardiovascular disease, bleeding disorders, organ failure, vision impairment, and staggering depression as a direct consequence of CRPS. However, when they drop dead, get struck by a bus they couldn’t see, or take their own lives, we don’t say “They died of CRPS.” We say, “They died of heart disease, organ failure etc., traffic accident, or suicide” (– if we’re feeling kindly, “or depression.”)

Thus, there’s no way to identify the actual mortality rate of CRPS, although there unquestionably is one.

Diabetes, cancer, and AIDS get more dignity than this. I’d like to see our mortality rate properly attributed, not swept under the enormous rug of opportunistic conditions. This would contribute hugely to better medicine.

Doctors hate seeing patients hurt, but after awhile they can turn away from that, in order to drag themselves back to the office; they hate to see them die on their watch, and it makes them apply upward pressure on the reimbursement and legislative aspects of the care system.

There’s nothing like a mortality rate among those in their “productive years” to make legislators sit up and take notice.

I started nursing within a decade of the first AIDS diagnosis; my first job was on an AIDS unit. I’ve seen it work.

Let’s get our deaths properly attributed. It’s one last gift we can give our compatriots as we head out the door. I’m going to put it in my will.

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Proportional monocytes and CRPS, translated

Today’s translation from medspeak to English: Inflammatory white blood cells and inflammatory nerve cells, in relation to CRPS.

Elevated blood levels of inflammatory monocytes (CD14+ CD16+ ) in patients with complex regional pain syndrome

Here’s what the jargon means.
// ed. note: my comments and clarifications are picked out by those two slashes and the contraction for “editorial notation.”

One important factor in CRPS is inflammation that starts in the nerves. Microglia and astrocytes, which are the inflammatory and immune cells of the nervous system, get active enough to cause worse pain by themselves.

That’s a sparking astrocyte. Pretty, eh?

// ed. note:  The inflammatory and immune responses are mixed blessings throughout the body.  An immune response is uncomfortable; think about the last time you had the flu — sucked, huh?  An inflammatory response can cause pain due solely to the inflammation, like with some kinds of arthritis.  So, for the microglia and astrocytes to make pain worse is not a surprise, since that’s what immune response and inflammation can do anywhere.

One type of immune cells normally floating in your blood, called monocytes, can get into the brain and spinal cord and turn themselves into the nervous system’s immune cells, microglia. The added level of inflammatory/immune response leads to more pain.

// ed. note: Again, not as strange as it sounds.  The body’s living cells all contain complete DNA, and they are designed to be both helpful and appropriate; heart cells transplanted into muscles become muscle cells, and muscle cells transplanted in the heart become very much like heart cells.  So, for this type of small white blood cells to turn into microglia is reasonable.

These are microglia in various active states.

// ed. note: The inflammatory response releases cytokines.  Cytokines are the chemical widgets, produced in inflammation, that serve as the chemical messengers running around the cells screaming that the sky is falling.  Some cytokines increase inflammatory pain, some cytokines reduce it.

This study looked for particular kinds of inflammatory monocytes in the blood, to test the assumption that higher levels of these particular types of monocytes (which can then turn into microglia, making the inflammation and pain worse, etc.) are related specifically to CRPS.

Now here’s the fun part.  The basic blood-borne indicators of inflammation and illness were no different in those with CRPS than in normal people. That’s why conventional lab results, like “complete” blood counts, come back normal for us.  However, the proportion of the particular types of monocytes associated with CRPS, were significantly higher in those with CRPS.  The type of cytokine that reduces inflammatory pain, was also significantly lower in people with CRPS.

That means the inflammatory process screws us coming and going, and screws specifically us, the people with CRPS, in ways that can be checked in a lab.

OK, GTK.

These are sensible scientists: they state that they don’t know if the monocyte proportions changed before or after the onset of CRPS, or both before and after.  If before, it might indicate a predisposition to CRPS, in which case surgeries and accidents have to be handled with specific care for antioxidant therapy and aggressive pain control. If after, it might be relevant in figuring out how things are going and if what the doc is doing works.

Also, some drug company could make a staggering fortune off of new meds that mess with this process. They actually mention that at the end of the article, which means someone has to fund their work.

// ed. note: Be fair. We have a profit-based health care system driven by enormous corporations that are traded on the stock exchange, and the Sarbanes-Oxley laws mean that their first obligation is to their shareholders. Not patients. Not customers. But shareholders.

Conventional medicine has to come back to profitability.  There are more direct ways to address these immune and inflammatory issues by existing means, which could be further developed, but they don’t sustain the pharma industry’s usual annual returns of 20-40% — a rate of stock profitability matched only by oil companies.

… On your pain.

If you have something to say about that, you can contact your political representatives here: http://www.usa.gov/Contact/Elected.shtml

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Spinal cord changes in longstanding CRPS

This is brilliant:

Spinal cord histopathological alterations in a patient with longstanding complex regional pain syndrome

The authors did an autopsy on one person with longstanding CRPS and did comparative autopsies on 4 people who did not have CRPS. They checked samples from the neck, thorax, and low-back for microglia and astrocytes. These are the kinds of cells that not only are part of the nervous system’s immune response, but also increase the transmission of pain signals. That means, inflammation plus more pain! They found plenty in the CRPS patient’s spine.

They also found that the normal cells in the dorsal horn of the spine – the ones that carry sensations of light touch, vibration, and proprioception (the sense of the body in space) – are significantly fewer in the CRPS patient. This makes sense of the fact that allodynia (light touch) gets worse, vibration is so agonizing (making both riding public transit and holding a steering wheel pretty horrible), and we get clumsy over time because we can’t quite feel where our bodies are in space.

These strange cellular changes were found “most prominently at the level of the original injury, but extending throughout the entire length of the spinal cord.” That means that the allodynia, diminished balance, etc. physically spread from the original dorsal root, all the way up and down the spine, affecting the whole physical self.

So, with more cells for pain and immune attack, and fewer cells to transport normal messages of light touch, vibration, and proprioception, we have some stunningly clear evidence that the spreading allodynia, clumsiness, and intolerance to vibration is NOT IMAGINARY.

Given how many people get told that it’s all in their heads, they’re hurting because they’re thinking wrong or because they were abused as children, etc., this is an important thing to keep in mind. Let’s keep the cart behind the horse.

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