Cerebral Palsy and Regenerative Medicine ©

By David Steenblock, M.S., D.O.

"The obstacle is the path." Zen Proverb


Overview

Cerebral palsy is a disorder caused by damage to the brain during pregnancy, delivery or shortly after birth. It is often accompanied by seizures, hearing loss, difficulty speaking, blindness, lack of co-ordination and/or mental retardation. About 25 percent of cases come from a prenatal cause such as anemia, improper nutrition, viruses, x-rays or premature delivery. About 40 percent are caused by a lack of oxygen (hypoxia), and the remaining causes are unknown.

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In an unpublished manuscript, Dr. Philip James describes tissue hypoxia: "The areas affected in CP are in the middle of the hemispheres of the brain and one side or both sides may be involved. These critical areas, called the internal capsules, are where the fibres from the controlling nerve cells in the grey matter of the brain pass down on their way to the spinal cord. In the spinal cord, they interconnect with the nerve cells whose fibers activate the muscles of the legs and arms...When any event causes lack of oxygen, the blood vessels leak, the tissues become swollen and there may even be leakage of blood. The increased water content, termed edema, reduces the transport of oxygen."

Brain hypoperfusion in cerebral palsy has been demonstrated by two SPECT studies (Lee et al, 1998 and Yamada et al. 1995).

Hypoxia and Brain Injury

Without sufficient oxygen and nutrients, brain cells are injured and killed.

In discussing the causes and treatment for cerebral palsy, several terms will keep reappearing, such as mitochondria, oxyradical damage and apoptosis. The mitochondria produce energy in the form of ATP (adenosine triphosphate) for cell function. The cell carries on all of its work, including waste removal, metabolism, immune defense, protein synthesis, etc. with the energy produced by the mitochondria. In the process of creating ATP, the mitochondria also produce “oxyradicals”. These molecules have unpaired outer electrons and will break up the bonds of other molecules so the outer electron will be paired. These other molecules may be working efficiently together for the good of the cell and tissue. However, when they are disrupted by oxyradicals, the work stops and the cells become less efficient. This becomes a chain reaction of one molecule after another breaking the bonds of functioning “married” molecules. An excess of oxyradicals causes injury to the mitochondria. Less ATP is produced, and the cell has less energy for waste removal, immune function, protein synthesis and survival. If enough injury occurs, the mitochondria will signal a cascade of events that leads to the death of the cell (apoptosis – programmed cell death). Antioxidants protect the mitochondria from oxyradical damage by variety of methods, including bonding with the unpaired electron.

The Mitochondria and ATP

A reduction in blood circulation (ischemia) causes disruption in the energy producing mitochondria of the neurons. This disruption promotes free radicals such as hydrogen peroxide that can cause injury to the mitochondria and neuron.

The lack of oxygen also stimulates the release of excitatory neurotransmitters such as glutamate and aspartate that open the cell membranes to an influx of sodium. The struggling mitochondria, still deficient in oxygen and now accumulating free radical damage have to work harder to provide energy (ATP) so that the cell to pump out the sodium.

The cell injury also invites an inflammatory immune response that increases the release of hydrogen peroxide, cell damage and swelling. As the mitochondria become depleted in energy, they trigger programmed cell death and calcium entry. The calcium triggers the release of proteases which begin to devour the cell proteins. The cell breaks up into smaller fragments so that phagocytes can then ingest the remains. This is the cascade of events that can result from the lack of cerebral blood flow and oxygen. The causes of this ischemia/hypoxia scenario can include traumatic brain injury and blood vessel break or blockage, chemical toxicity, nutritional deficiencies, atherosclerosis, infection, allergies, and hypoglycemia (a deficit of glucose has similar effects on neurons as oxygen deficit), as well as emotional stress. All of these factors promote an excess of glutamate and glutamate is toxic to neural stem cells.

Maximum repair and regeneration for cerebral palsy patients should therefore include:

  1. The treatment of any infections, chemical toxicities, heavy metal poisoning, etc.
  2. The promotion of neural stem cell growth to replace dead and injured neurons.
  3. Oxygen therapies to reduce ischemia/hypoxia.
  4. Neuroprotective diet and therapies that include antioxidants to protect new neurons from excitotoxins and oxyradicals.
  5. An endogenous stem cell/stress reduction program that continues to promote repair and regeneration as a lifetime program in Wellness.

A. Preliminary Therapies

For maximum healing and regeneration, factors that are toxic to stem cells and new neurons should be minimized. These include:

  1. Infections and inflammatory sites throughout the system.
  2. Heavy metals (lead, cadmium, mercury, arsenic, etc) are toxic to new neurons and should be reduced through oral or I.V. chelation to the point where no excess heavy metals can be identified after a DMSA challenge test.
  3. Leaky gut syndrome and bacterial overgrowth in the gut (gut dysbiosis) should be treated to prevent toxins from bacteria, viruses and fungi from entering the body and destroying new neurons.
  4. Cortisone, steroids, glutamate (MSG), and alcohol (read labels of medications) are toxic to new neurons and should be eliminated as much as possible.


B. Umbilical Cord-Derived Stem Cell Therapy

Bone marrow transplants that include stem cells have been used successfully since 1968 and are now used to treat patients diagnosed with leukemia, aplastic anemia, lymphomas such as Hodgkin's disease, multiple myeloma, immune deficiency disorders and some solid tumors such as breast and ovarian cancer. About 7,000 patients nationwide receive bone marrow transplants each year. However this amounts to only 30 percent of those needing this procedure, since a suitable bone marrow donor cannot be found for the remaining 70% (www.bmtnews.org). There is therefore great interest in shifting to the use of purified CD34+ stem cells since comparable results are obtained but without significant Graft versus Host complications. (Handgretinger, 2001).

Embryonic stem cells are capable of unlimited self-renewal and have the ability to give rise to all tissue types in the body. The use of human embryonic stem cells for tissue and cell therapies is under intense research but is clouded by the moral and ethical issues involved with the destruction of human embryos to obtain the cells. In addition, embryonic stem cell lines in the United States may have reduced viability and many of these stem cell lines have been exposed to mouse “feeder” cells and are no longer purely human stem cell lines.

Cord blood, like bone marrow, is enriched with CD 34+ stem cells, capable of self-renewal and differentiation into various cell lineages, including immune and haematopoietic progenitors. Unlike bone marrow transplants, cord blood is easier and less expensive to obtain. Umbilical cord cells have been demonstrated to function equally to, if not better than bone marrow derived stem cells for reconstitution of the haematopoietic system. Recent studies have demonstrated that umbilical cord derived stem cells, like bone marrow and embryonic stem cells, are multipotent and capable of differentiating into non-blood cell types, such as neurons (Rogers, 2003). Umbilical cord stem cells used in place of embryonic stem cells should soon become widespread both in research and clinical applications.

There have been over 1,000 successful transplants in the U.S. (and over 3,000 transplants worldwide) using cord blood since 1988. The various disorders treated include leukemia (Wadhwa, 2002), solid tumors: breast cancer (Paquette, 2000), prostate cancer, ovarian cancer; aplastic anemia (Meagher, 2002), Fanconi’s anemia (Croop, 2001), immune disorders, storage diseases (Meagher, 2002), and bone marrow reconstruction after cancer irradiation (Stevens, 2002). There are additional animal and test tube studies demonstrating the potential for heart cell regeneration in heart disease (Kao, 2001), T-lymphocyte transplantations to fight specific infections (Sun, 1999), gene insertion therapy (Meagher, 2002) and therapies for brain disorders and injuries (Chen, 2001, Ende, 2001).

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