Brain Radiation Necrosis
- Hyperbaric Oxygenation in the treatment and management of Brain Radiation effects
Case Study - 19-year old male - Glioblastoma; brain radiation necrosis
No. 1 MRI: PRIOR to surgery, chemo and radiation
No. 2 MRI: AFTER surgery, chemo and radiation: pre-HBO
BEFORE Hyperbaric Oxygenation – MRI revealed a brain mass measuring 7.5cm/4.2cm/6.0cm (MRI image on the above right)
AFTER 170 hours -HBOT – MRI revealed the mass reduction now measuring 5.5cm/3.2cm/4.2cm
MRI performed after conventional oncology including surgery, chemotherapy and radiation unfortunately revealed an aggressive increase in tumor size. The parents were informed nothing further could be done!
During 2002 this young man started to complain of headaches and numbness down his right arm. Medical review including a CT Scan showed a brain tumour. He was sent straight to hospital and a diagnosis of 'Glioblastoma' was made confirmed on biopsy. He was operated on and the family informed that they were able to remove a certain portion of the tumour. He was then treated with chemotherapy and we were told that the tumour had shrunk dramatically.
An additional 6-weeks of radiation therapy with follow up MRI confirmed that the tumour had not only grown back but in fact had increased dramatically and described as extremely aggressive! Further chemotherapy had NO effect.
The family were informed that nothing further could be done and told to take their son home!
Desperate to find anything that would give their son some relief from his headaches, neck pain and his epileptic seizures; they approach us for possible application of Hyperbaric Oxygenation. We reviewed his condition and recommended HBOT combined with continuing medical strategies and supportive immune stimulating approaches.
After 70-hours of Hyperbaric Oxygenation; the mother reports:
- ‘Tremendous improvement has been made; he continues to improve - thank God!’
- ‘He has regained his energy, is having less seizures, less headaches, has a stronger appetite and overall is feeling stronger every day.’
We would like to thank Dr. Hooper from Melbourne Hyperbaric and the Spinal Rehab Group for all his help in making our son’s treatment possible.
After 170-hours of HBOT combined medical management we recommended an additional MRI to re-establish the base line of the tumor size. The results are outstanding!
- Pre HBOT – MRI revealed a brain mass measuring 7.5cm/4.2cm/6.0cm
- After 170-HBOT – MRI revealed the mass reduction now measuring 5.5cm/3.2cm/4.2cm
Unfortunately the issue of continuing financial burden confronts all patients whose conditions are ineligible under Australian Medicare provision. The parents ultimately decided to cease his HBOT and medical recommendations at our facility due to the expense.
We lost contact with the family but were eventually informed that after an extended time period; the tumour had re-grown; his condition deteriorated and he slipped into a coma and unfortunately - died.
I am of the opinion that provision for continued Hyperbaric Oxygenation may have not just improved his quality of life; but possibly altered the outcome of this young man. The requirement for HBOT is early in the disease process and not as a last resort!
Hyperbaric Oxygenation is NOT recommended as a cure; but should be recommended as part of an integrated clinical approach that monitors the course of the condition with appropriate clinical investigations and is tailored to the treatment requirements of that individual.
Approximately 35,000 new cases of intracranial tumors are diagnosed in the United States each year, of which 15,000 are primary brain tumors. Radiation therapy can be primary or adjunctive for the treatment of these brain tumors, and for conditions such as arterio-venous malformations.
Radiation induced necrosis can be divided into focal necrosis, and diffuse white matter injury. Both injuries are believed to result from increased tissue pressure from edema, vascular injury leading to infarction, damage to endothelial cells, and fibrinoid necrosis of small arteries and arterioles. Damage to oligodendroglial supporting cells with demyelination, reactive gliosis, and coagulation necrosis also may occur.
Brain radiation necrosis is often considered a late finding; often appearing within 3-months but in many cases up to several years after treatment is completed. Approximately 3-9% of patients irradiated for brain tumors develop clinically detectable focal radiation necrosis. The breakdown of white matter may induce marked edema and mass effect. Clinicians may incorrectly suspect tumor recurrence; embarking on another round of radiation with ultimate consequences. Diffuse white matter injury develops in at least 40% of patients irradiated for intracranial neoplasms following large volume or whole brain.
Decreased intellectual functioning has been observed in adults after cranial irradiation. All post radiation patients who have suffered cognitive decline should be investigated for the effects of radiation necrosis. Certain cognitive functions such as memory may be more susceptible to decline than others, and may prevent patients from returning to their premorbid occupation. Clinical features range from mild lassitude or personality change to incapacitating dementia. Some patients with cerebral atrophy may have gait disturbance and urinary incontinence similar to the syndrome of normal pressure hydrocephalus. The nervous system of the child has many sites vulnerable to radiation damage.
The diagnosis of radiation necrosis may be difficult to confirm. MRI may show a contrast-enhancing mass with extensive white matter alterations and hyperintensity of the periventricular white matter. Cerebral cortical atrophy is manifest as enlarged cerebral sulci and ventricular dilatation.
Many patients with radiographic changes have no symptoms, but in those who do, the degree of impairment correlates approximately with the severity of the MRI appearance. Many patients have a mixture of tumor and radiation necrosis, and a biopsy may be necessary to distinguish. Neither symptoms nor radiographic findings clearly distinguish radiation necrosis from tumor.
Emerging techniques involving PET scan and SPECT studies have been useful in differentiating differentiate radionecrosis from recurrent tumor. There may also be a role for MRI spectroscopy.
The benefit of Hyperbaric Oxygen Therapy for radiation-induced bone and soft tissue damage has been extensively reported in osteoradionecrosis, cystitis, proctitis, and other soft tissues. HBOT raises the tissue pO2 creating a steep oxygen gradient, which initiates cellular and vascular repair mechanisms.
Wound healing requires oxygen delivery to the injured tissues. Radiation damaged tissue has lost blood supply and is oxygen deprived (hypoxia). Chronic radiation complications result from scarring and narrowing of the blood vessels within the area that received radiation. Hyperbaric Oxygen Therapy provides a better healing environment and leads to the growth of new blood vessels in a process called re-vascularization. It also fights infection by direct bacteriocidal effects.
Extensive trials are being conducted and in particular the University of Cincinnati and at Duke University . Both have instituted comprehensive, multidisciplinary approaches with ongoing clinical and imaging assessments. The "teams" include radiation oncology, neurosurgery, neurology and hyperbaric medicine. The participants in the Duke protocol are followed with periodic neuropsychological testing as well.
There is mounting evidence that HBOT can be of significant value in the treatment of brain radiation necrosis in fact: it appears that HBOT is the only treatment potentially capable of reversing brain radiation necrosis.
In addition; we recommend that individuals review Internet sources including PubMed, MedScape, etc. for publications regarding Brain Radiation Necrosis and Hyperbaric Oxygen Therapy.
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