Saturday, December 27, 2008

Stem Cells For Parkinson's

By Amy Price PhD

Brain picture
Can Parkinson's patients benefit for stem cell therapy? The answer is likely that in the future this will be possible. Right now stem cells for orthopedic applications are a working reality and cardiac
applications are showing great success.

It was interesting to see a company with customer testimonials claiming success for Parkinson's . What happens is they are injecting stem cells intravenously and claiming these cell are migrating to the brain to "fix" Parkinson's. There are big problems with this...some cells migrate but the number of cells that would actually make it to the brain are fewer than finding a friend in a 50,000 seat foot ball stadium, the rest of the cells go the the lungs and then are reabsorbed by the body and filtered out through the liver and excreted by body wastes. Patients are paying thousands of dollars and travel expenses for cells they will end up flushing.

Think about it this way. If cultured cells could just fix things intravenously why would leukemia
patients even need bone marrow transplants?
With Parkinson's the underlying cell structure in the brain has been compromised and unless that is restructured new cells will be taken over like ants on a chocolate cake. For stem cells to work treatment needs to be targeted and care needs to be given as to how to best treat the underlying problem.

So why are some Parkinson's "patients" saying it could be working for them?
First of all Parkinson's is a dopamine deficiency issue. Anytime we do something
that brings pleasure or excitement, dopamine is circulated. For a short period of time patient's actually feel better. This principle is biological not psychosomatic. Plus the cells have some anti inflammatory properties so this benefit is felt as a temporary relief from pain.

Just after Thanksgiving a family member ran over our cat in full view of three small children. Having done some veterinary work and some first aid I could see the cat was not long for this world. She was bleeding from her mouth and her lungs were filling with blood and yet I held her in my arms and my son and I drove to the vet in hopes that someone bigger and smarter could do something...they couldn't. I guess I would do the same for a person I cared about and so would a lot of people. This makes us vulnerable in spite of knowledge so even when a celebrity claims to be healed it may not be the whole story. About the Parkinson's stem cells.... no fMRI or electrical studies of before and after treatments are shown and a search on PubMed turned up nothing.

This is in stark contrast to stemcell company scientists who publish research results and actual case studies to show where and how treatment is progressing. One question to ask when you are considering a new medical treatment is do the people I am dealing with offer any other options in case of candidates that are not suitable for the procedure?

What can you do right now until stem cells catch up with the ability to treat
brain disorders? There are meds, deep brain stimulation and brain training
options that can all help. The love and care we surround people with also makes
maximum use of the dopamine available and can enhance the quality of life for a
loved one with Parkinson's.....keep posted as soon as we see safe viable
treatment it will be posted here!



Monday, December 8, 2008

Fibromyalgia Pain and Cognition


By Amy Price PhD
Photo courtesy of (Earthopod, 2009 )depicting pain areas in fibromyalgia.
Fibromyalgia (FMS) comes from three words, the Latin term for fibrous tissue (fibro) and the Greek ones for muscle (myo) and pain (algia). Another way of saying this is muscle knots tied by painful ropes. This condition is not amenable to the medical model so clinicians fell back on the old standby “It’s all in your head” implying the problem is generated by emotional instability rather than specific biological origins.


Fibromyalgia was tagged a syndrome (Fibromyalgia, com, 2008). Patients got mad. They refused to be stonewalled by ignorance or marginalized. Instead they formed strong lobby groups and started campaigning for funding and action (Fibromyalgia network, 2008). This resulted in research getting funded, better treatment options and social change. (CRISP lists 695 NIH funded projects since 2000)


Researchers are finding that FMS could be a disorder of the central processing system resulting in neuroendocrinal and neurotransmitter dysregulation (Bennett, 2008). The FMS patient experiences pain amplification because their pain sensors are slow to recognize pain but the pain they feel spreads across a wider area, lasts longer and is more severe than in a person without FMS ( Staud et al, 2008). Increasingly scientific studies demonstrate physiological abnormalities in the FMS patient including increased levels of substance P in the spinal cord (Helle et al ,1998), low levels of blood flow to the thalamus region of the brain (Kwiatek et, 2000), HPA axis hypo function (McBeth et al, 2007) low levels of serotonin and tryptophan plus abnormalities in cytokine function (Crofford, 1998). Abnormalities like these spell pain. This leads to losses in sleep quality, cognition and coordination, and to increased drug use susceptibility.


New research strengthened by the advent of physical evidence such as SPECT, PET, FMRI and QEEG is confirming fibromyalgia is a biological problem that may cause psychological distress rather than a psychosomatic hysteria pioneered by women as appears to be insinuated by Mcdermid et al, (2008)

New hope may come for some FMS sufferers in the discovery of the brain’s ability to regenerate dendrites a process known as neuroplasticity (Toates, 2006). It is possible that targeted brain and body training may alleviate the severity of chronic pain and cognitive dysfunction associated with FMS (Leurding et al, 2008)


Leurding et al (2008) demonstrates that in fibromyalgia both white and grey brain matter is compromised. Brain imaging studies in FMS patients point to alterations in regional cerebral blood flow (Mountz et al., 1995), in cerebral processing of sensory and nociceptive stimuli (Gracely et al., 2002; Cook et al., 2004) also in dopamine response to pain (Wood et al., 2007). Leurding (ibid) used these imaging studies as a foundation for neuropsychological tests to show that the changed state of brain matter leads to “brain fog” rather than psycho-social maladaption, drug induced confusion, or loss of sleep as primary factors.


Patients offered cognitive rehabilitation tools may improve mental function when these tools are offered before significant white and grey matter dysfunction appears. Neuroplasticity can still be of benefit after damage occurs but progress is slower (Saczynski, 2004)
Brain areas responsible for proprioception damaged in fibromyalgia may be modified by body awareness training according to a pilot study carried out by (Kendall et al, 2000). Targeted body awareness physiotherapy programs led to patient improvement in pain levels and functional capacity even when patients were retested eighteen months after treatment (Kendall et al 2000).
Kendall et al (2000) were dismissive of positive effects realized by stress reduction, hypnosis or neurofeedback training but other researchers such as Meuler et al, 2001 found these treatments were beneficial. FMS is not one size fits all (Bennett, 2006).


A trial of cognitive rehabilitation synergised with neurofeedback and cognitive rehabilitation is underway to determine how combining passive and active therapy can multiply positive effects. Participants will be tested at timely increments and their ongoing level of progress studied.


Another option is to decrease pain to restore function. This is where regenerative medicine can help with therapies like adult stem cell treatment and prolotherapy. Another option is a treatment called IMS where overly sensitized nerve points are reset using a medical system similar to acupuncture.



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