25 January 2012

Braced and balanced

Saying that your child has no head control is a term that can mean a variety of different things. While in all instances it means that your child can not hold their head upright and independent permanently, it can mean that your child can hold their head up and in control for varying periods of time.

When I say Liam has no head control, I mean he has absolutely none. He can not balance his noggin up on his little neck. He will either let it fall back in order to keep it held up by his shoulders (called stacking) or he will fall forward where he can not pick it up to save his life. Literally. He can not pick it up (which is because of his very low trunk tone).We can shout, encourage, tease and prompt, but the muscles used to pick his head up do not respond and he will leave it down on his chest.

Liam doesn't like his head stacked or fallen forward so he tries to correct it. When it's stacked he will try to bring it in correct position and then once it gets upright it will fall forward where his head hangs down on his chest. This in turn makes him upset and he will use all the wrong muscles to try to upright himself and it just propels himself even farther forward making his body round into a ball. It makes breathing pretty difficult at that point.

We've been tossing around the idea of a neck brace for years. Therapists don't like to use them because they want the child to learn to hold their head on their own. But Liam is 4 years old and head control is still out of his grasp. We needed something to make learning in his chair easier.


We finally found this neck brace for him to be able to use. It is open at the neck front keeping his airway nice and clear. It wraps around the back with just a 2 inch piece wide of material that is soft and comfortable. We can attach it in seconds and he can then rest his chin and be upright allowing him to play.


It's been really helpful. I'm surprised at the simple construction and how well it actually supports him. We can use it in the stander and in his chair. I can actually leave him alone in his chair for the first time. He tolerates it for long periods of time. I can usually tell when he's done because he will fight against it by pushing forward with his head (which is what he does when he doesn't wear it).



We still do a lot of work with out it. Some days Liam will do well holding his head up in his chair, leaned against the head rest. But when we are working on specific tasks like communication, it's been a huge relief to take the head control out of the equation so he can work only on one task at a time.
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19 January 2012

70% success for TBI & Stem Cells

Why didn't 60 minutes show this?? They said there is no treatment for cerbral palsy with stem cells. They show the bad apple and not the encouraging, positive news coming from adult stem cells. I guess bad news makes the Nielson's even when it comes to your health.





Autologous Bone Marrow Mononuclear Cell Therapy for Severe Traumatic Brain Injury in Children.
by admin on February 7, 2011

Cox CS Jr, Baumgartner JE, Harting MT, Worth LL, Walker PA, Shah SK, Ewing-Cobbs L, Hasan KM, Day MC, Lee D, Jimenez F, Gee A.

From the University of Texas Medical School at Houston, Departments
of Pediatric Surgery, Surgery, Pediatrics, and Diagnostic & Interventional Imaging; Children’s Memorial Hermann Hospital; University of Texas M.D. Anderson Cancer Center, Department of Pediatrics, Division of Cell Therapy; Baylor College of Medicine Center for Cell and Gene Therapy.

BACKGROUND:
Severe traumatic brain injury (TBI) in
children is associated with substantial long-term morbidity and
mortality. Currently, there are no successful
neuroprotective/neuroreparative treatments for TBI. Numerous
pre-clinical studies suggest that bone marrow derived mononuclear cells
(BMMNCs), their derivative cells (marrow stromal cells), or similar
cells (umbilical cord blood cells) offer neuroprotection.

OBJECTIVE:
To determine if autologous BMMNCs are a safe treatment for severe TBI in children.

METHODS: Ten children aged 5-14 years with a post-resuscitation GCS of
5-8 were treated with 6X10 autologous BMMNCs/kg body weight delivered
intravenously within 48 hours after TBI. To determine safety of the
procedure, systemic and cerebral hemodynamics were monitored during bone
marrow harvest; infusion related toxicity was determined by pediatric
logistic organ dysfunction (PELOD) scores, hepatic enzymes, Murray lung
injury scores, and renal function. Conventional magnetic resonance
imaging (cMRI) data were obtained at 1 and 6 months post-injury, as were
neuropsychologic and functional outcome measures.


****RESULTS: All patients survived. There were no
episodes of harvest related depression of systemic or cerebral
hemodynamics. There was no detectable infusion related toxicity as
determined by PELOD score, hepatic enzymes, Murray lung injury scores,
or renal function. cMRI imaging comparing gray matter, white matter, and
cerebrospinal fluid (CSF) volumes showed no reduction from 1-6 months
post injury. Dichotomized Glasgow Outcome Score (GOS) at 6 months showed
70% with good outcomes and 30% with moderate to severe disability.



****CONCLUSION
: Bone marrow harvest and intravenous
mononuclear cell infusion as treatment for severe TBI in children is
logistically feasible and safe.

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16 January 2012

How stem cells heal.

Scientists are learning so much about stem cells and how they are healing victims of TBI- traumatic brain injury.



How Stem Cell Implants Help Heal Traumatic Brain Injury

ScienceDaily (Jan. 12, 2012) --- For years, researchers seeking new
therapies for traumatic brain injury have been tantalized by the results
of animal experiments with stem cells. In numerous studies, stem cell
implantation has substantially improved brain function in experimental
animals with brain trauma. But just how these improvements occur has
remained a mystery.

Now, an important part of this puzzle has been pieced together by
researchers at the University of Texas Medical Branch at Galveston. In
experiments with both laboratory rats and an apparatus that enabled them
to simulate the impact of trauma on human neurons, they identified key
molecular mechanisms by which implanted human neural stem cells -- stem
cells that are in the process of developing into neurons but have not
yet taken their final form -- aid recovery from traumatic axonal injury.

A significant component of traumatic brain injury, traumatic axonal
injury involves damage to axons and dendrites, the filaments that extend
out from the bodies of the neurons. The damage continues after the
initial trauma, since the axons and dendrites respond to injury by
withdrawing back to the bodies of the neurons.

"Axons and dendrites are the basis of neuron-to-neuron communication,
and when they are lost, neuron function is lost," said UTMB professor
Ping Wu, lead author of a paper on the research appearing in the
/Journal of Neurotrauma/. "In this study, we found that our stem cell
transplantation both prevents further axonal injury and promotes axonal
regrowth, through a number of previously unknown molecular mechanisms."

The UTMB researchers began their investigation with a clue from their
previous work: they had determined that their neural stem cells secreted
a substance called glial derived neurotrophic factor, which seemed to
help injured rat brains recover from injury. As a first step toward
identifying the processes by which GDNF and neural stem cell
transplantation produced their beneficial effects, Wu enlisted UTMB
professors Larry Denner, Douglas Dewitt and Dr. Donald Prough to use
proteomic techniques to compare injured rat brains with injured rat
brains into which neural stem cells had been transplanted.

"We identified about 400 proteins that respond differently after injury
and after grafting with neural stem cells," Wu said. "When we grouped
them using a state-of-the-art Internet database, we found that a group
of cytoskeleton proteins was being changed, and in particular one called
alpha-smooth muscle actin, which had never been reported in the neurons
before."

Because so many of the proteins that changed were related to axonal
structure and function, the UTMB scientists then focused on traumatic
axonal injury. Initially working with rats, they confirmed that axons
and dendrites suffered damage from trauma; implanted neural stem cells
reduced this harm, as well as lowering levels of alpha-smooth muscle
actin inside neurons that were raised after trauma.

To probe further into the molecular details of GDNF's role in reducing
traumatic axonal injury, the researchers used a system in which human
neurons were placed on a flexible membrane that was then suddenly
distended with a precisely calibrated puff of gas. Their goal was to
simulate the sudden compression and stretching forces exerted on brain
cells by a blow to the head.

Initial results from this "rapid stretch injury model" matched those
seen in rat experiments, with GDNF protecting axons and dendrites from
additional damage in the period after trauma and significantly reducing
alpha-smooth muscle actin levels boosted by the simulated injury. In
addition, they found evidence linking alpha-smooth muscle actin with
RhoA, a small protein that blocks axonal growth after injury. Finally,
again taking a cue from their proteomic study, they turned their
attention to one component of a protein known as calcineurin, finding
that it interacted with GDNF to protect axons and dendrites in the RSI
model.

"We're quite excited about these discoveries, because they're highly
novel -- we now know much more about how GDNF protects axons and
dendrites from further injury and promotes their re-growth after
trauma," Wu said. "This kind of detailed study is essential to
developing safe and effective therapies for traumatic brain injury."

Other authors of the Journal of Neurotrauma paper include graduate
students Enyin Wang, Junling Gao and Tiffany Dunn; assistant research
lab director Margaret Parsley; Qin Yang of Huazhong University of
Science and Technology in Wuhan, China, Lin Zhang of Sichuan University
in Chengdu, China; and professors Douglas DeWitt, Larry Denner and
Donald Prough. Support for this research was provided by the U.S. Army,
the Coalition for Brain Injury Research, the Moody Center for Traumatic
Brain and Spinal Cord Injury Research, Mission Connect, the TIRR
Foundation, the China Scholarship Council, the John S. Dunn Research
Foundation and the Cullen Foundation.

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11 January 2012

Nanananananana

Liam got his sweet looking Batman suit today. Boy he looks good in it too! This is the SPIO (which stands for Stabilizing Pressure Input Orthosis) that I have been wanting to try out on him for the last year. I'm keeping fingers crossed that insurace will pay for it because by having to go through an orthotist and have them bill insurance/medicaid the cost more than doubled to $450 where as if I bought it outright from SPIO it would have only cost $180. That is what is wrong with insurance and medicaid today...but that's another post.

Anyway.

This vest is so much nicer than the last ones we have trialed. This one has a lycra front that is smooth and form fitting. The back is neoprene and it has a crotch strap keeping it in place. And it goes down low onto his hips for additional stability and input which he sorely needs. Liam's sensory system is all wonky and this vest helps to give him the input he's missing for his core.

The SPIO seems to be made much better than the others we have tried, looks a whole lot better on and Liam was able to wear it all day today with no fussing.

He can easily wear it under his clothes and since it's winter we won't have to worry about him getting hot. The other vests we've used were too thick to wear comfortably next to the skin.

If we could just get Liam stronger in his core it would help him with everything else as well. 



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05 January 2012

And when you laugh too much?

There's no such thing.

But Liam can't catch his breath and he gets the hiccups:

video





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