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Hyperbaric oxygen offers hope after brain injury.

FORT LAUDERDALE, FLA. -- They come in after a near drowning, near hanging, umbilical cord strangulation, cardiac arrest, or carbon monoxide poisoning. They have anoxic ischemic encephalopathy, and their families are seeking the hope offered by hyperbaric oxygen against an otherwise dismal prognosis, according to a presentation at a symposium on hyperbaric oxygen therapy.

Prolonged and difficult labor, surgical mishaps, anesthetic reactions or complications, and severe traumatic injuries are other leading reasons these patients come to the Ocean Hyperbaric Neurologic Center, sponsor of the symposium.

"Anoxic ischemic encephalopathy, as you all know, most of the time becomes a catastrophic event. These are the patients who carry the biggest burden and the biggest price," said Dr. George Daviglus, an associate neurologist at the center in Fort Lauderdale, Fla.

Even minimal oxygen deprivation can cause anoxic ischemic encephalopathy (AIE), Dr. Daviglus said. "Brain injury secondary to severe hypoxia--in almost all cases--causes irreparable damage to a group of neurons. In a very short time, brain necrosis occurs."

Neurologic deficits can occur within minutes, or in as long as 4 hours. A coma caused by AIE is "undoubtedly the most severe" type, Dr. Daviglus said. "Outcome is usually pretty dismal if the Glasgow score goes below six." These patients have virtually no chance of recovery if their coma lasts 3 months or more, he added.

Hyperbaric oxygen therapy (HBOT) can return function to the ischemic penumbra, a region of idle neurons surrounding damaged tissues, Dr. Daviglus said. "The neurons are receiving enough oxygen to be alive, but they are not functional."

HBOT stimulates angiogenesis, promotes neuronal plasticity, restores cell membrane integrity, reinstates the blood-brain barrier, promotes scavenging of free radicals, and increases the concentration of adult stem cells, Dr. Daviglus said. "Despite their hopeless prognoses expressed by their treating physicians, there are varying degrees of clinical improvement" with HBOT, Dr. Daviglus said. Clinical improvements correlate with increased perfusion and metabolism with the reactivation of the idle neurons, he added. The ultimate long-term prognosis depends on the size and location of insult, volume of surrounding dormant neurons, and plasticity of sensory and motor neurons.

HBOT is only one component of therapy provided by the Ocean Hyperbaric Neurologic Center. "Hyperbaric oxygen is not a panacea, but an old and hardly used therapy that offers a new dimension to neuro-rehabilitation in conjunction with physical therapy, occupational therapy, speech therapy, acupuncture, nutrition, and biofeedback," Dr. Daviglus said.

HBOT success stories include a 32-year-old man who had attempted suicide by hanging 9 years earlier and a 32-year-old man in a semicomatose state for 13 years from carbon monoxide poisoning.

The patient with AIE from near hanging presented apallic and severely anoxic with a Glasgow coma score of 3. He showed marked improvements after 150 sessions of HBOT, evidenced by changes between baseline and posttreatment SPECT scans. His Glasgow score improved to 7 and the patient demonstrated increased alertness, motor capabilities, and nutritional intake. "He was able to squeeze his mother's hands."

Before referral for hyperbaric oxygen therapy, the patient with AIE from carbon monoxide poisoning had received "all kinds of therapy at different levels in his community." He had "dramatic results" after 500 HBOT sessions, and was able to return to society. "We have many cases where the patients return to society.

"We need to continue with our clinical research at all levels in order to prove to the payers and reimbursement agencies the significant savings over a long term with our approach to the brain-injured patient," Dr. Daviglus said.


Miami Bureau
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Title Annotation:Neurology
Author:McNamara, Damian
Publication:Internal Medicine News
Geographic Code:1USA
Date:Nov 1, 2006
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