Parkinson's Disease

The central nervous system is what allows people to walk without worrying about stumbling. It also controls the movement features of the face and aids in many bodily functions that most would take for granted. For people that suffer from Parkinson's disease though, the central nervous system is damaged and many sufferers find that movement capability gradually goes away. Friends and family will begin to look for alternative treatments such as hyperbaric oxygen therapy treatments that will help those that are stricken with this unkind disease. Hyperbaric oxygen therapy can help nervous system disorders like Parkinson's in the area of memory loss and nerve damage.

For memory loss associated with Parkinson's disease, many people feel obligated to focus care on routine medical treatment solely devoted to prescription drug treatments because they were ill advised by non-medical types. Many Parkinson's sufferers are unaware of the state of the art treatments being found through hyperbaric oxygen therapy. Hyperbaric oxygen helps the nervous system by replenishing vital oxygen in pure form to body tissues where Parkinson's disease or stroke has damaged nerve endings. Hyperbaric oxygen therapy is innovative technology that many afflicted with Parkinson's disease had tried and believe is a godsend. Researchers have found that the nerve endings that cause tremors associated with Parkinson's disease responded incredibly well to hyperbaric oxygen treatments. When the patient's nervous system is saturated with pure oxygen, many families have noted that the healing response is tremendous.

Hyperbaric oxygen therapy can be accomplished at home, or at medical treatment facilities around the world. Home treatments are most preferred because they can be done at any time of the day or night. The hyperbaric chamber is comfortable and many activities can be done while the oxygen treatments are being administered. Dozing is allowed during treatments and this in itself is reason to relax and let the healing process begin. In the high-oxygen environment, there is moderate air pressure and nerve endings seem to have no other recourse but to let healing cycle to continue. Immediate results vary with each individual. Many will feel enlightened and euphoric after the first treatment and this is due to the rich oxygen environment. A smile might be the first indication that the therapy is working as promised, or the arms might swing again when the patient walks.

The healing process will be virtually unnoticeable for some patients if they are in the advanced stages of the disease, but with repeated sessions, it is expected that impressive improvements will be seen. Hence, the need for hyperbaric oxygen treatments at home. This timetable is normal when such damage occurs because the central nervous system is a complex matrix of nerve endings. Parkinson's disease causes joints to seize up and become unresponsive. The central nervous system will respond quicker in some patients and slower in others. As the nervous system disorder is introduced to the renewed flux of oxygen many changes will occur to damaged areas of the body. Many people are grateful for this innovative, cutting edge technology.


Hoggard ML, Johnson KE and Shirachi DY.

Chico Hyperbaric Center, Chico, CA 95926 and Department of Physiology and Pharmacology, T.

J. Long School of Pharmacy, University of the Pacific, Stockton, CA 95207, USA.

Parkinson’s Disease (PD) is a chronic neurodegenerative disorder, which is characterized by the loss of dopaminergic neurons whose cell bodies are located in the substantia nigra pars compacta (SNpc) and project to the striatum. The initiation of this neuronal degeneration is not known, however the process of neuronal loss is suggested to occur via apoptosis rather than by necrosis (1). With the onset of the neurodegeneration of these neurons is the associated loss of the neurotransmitter, dopamine (DA), from its nerve endings and its subsequent release in the striatum. The major symptoms which are observed due to the progressive loss in function of the nigro-striatal dopaminergic neurons may be one or more of the following: resting tremor, rigidity, bradykinesia and/or postural instability. The actual clinical manifestation of the disease in any one patient is highly dependent upon the degree of severity of the neuronal loss, age of the patient and the length of time passed between the onset of the symptoms and the time of diagnosis. Early detection is important in order to institute a therapeutic strategy to relieve the symptoms and/or delay the progression of the disease state. The major treatment strategy currently used is to affect the function of DA. Because systemically administered DA does not cross the blood-brain barrier; Levodopa (pro drug) is administered, which is taken up into the brain. Since Levodopa is metabolized both peripherally and centrally to DA by a DOPA decarboxylase, carbidopa an inhibitor of this enzyme is administered in combination with Levodopa to decrease its metabolism peripherally increasing its uptake into the brain. DA agonists and monamine oxidase-B (MAO-B) inhibitors are also administered as a monotherapy or as an adjunct to Levodopa-carbidopa (Sinemet) therapy, depending upon the clinical condition. Taking a very different approach in the treatment of PD, Borromei et al. in 1996 showed that hyperbaric oxygen (HBO) therapy appeared to be effective in ameliorating many of the behavioral and motor deficits observed in PD patients (2). The objective of this study was to determine whether HBO therapy might enhance the effects of an antiparkinson treatment in a PD patient as an adjunct therapeutic modality.

Brief patient history: A 72 year old male was diagnosed with idiopathic PD and placed on Sinemet (10/100) three doses 3 times daily. One year after diagnosis for PD the patient was diagnosed with total occlusion of the right coronary artery. A successful total occlusion angioplasty was performed and he was placed on Lopressor and Lipitor 10 mg daily. There were no complications from this surgical procedure. Eighteen months after being diagnosed as a PD patient he was treated with hyperbaric oxygen (HBO) at 1.9 ATA for 90 min. The patient was treated daily 5 times each week for 5 weeks (25 treatments). During the treatment the patient gradually reduced his dose of Sinemet until he was completely off of this medication between the 3rd and 4th week of HBO treatment. At this point his physician placed him on selegiline 10mg twice daily. Clinical testing: The patient’s voice and speech were evaluated by a speech-language pathologist, and the Jebsen-Taylor hand function test was performed by an occupational therapist prior to and after the end of the HBO therapy. The patient was informed of all aspects of hyperbaric oxygen therapy, including all risks of adverse effects according to the Declaration of Helsinki. The patient also signed an informed consent form detailing the treatment and the rights of the patient.

Voice and speech. There was little change in the overall evaluation of voice and speech after HBO therapy. Communication status changed very little. He appeared to be talking more and his rate was somewhat improved. He still had difficulty projecting his voice. Jebsen-Taylor Hand Function Test. The results of this test are shown in Table 1. In testing the dominant hand there were small increments of improvement after HBO. The total improvement was more than 10%, while the improvement in the non-dominant hand was nearly 32%. During the treatment period, the patient voluntarily reduced his Sinemet doses until he was completely off the drug after 3-4 weeks of HBO therapy, which was an unexpected result. He has continued to remain off of Sinemet therapy. No complications or adverse side effects such as myopia were observed. The long-term exposure of HBO was tolerated well by the patient.

PD is characterized by the loss of dopaminergic neurons of the nigro-striatal pathway. It is not clear how this neuronal degeneration is initiated, but there appears to be a number of potential ways in which this might occur in any one individual, including genetics, disease, drugs or other chemicals, oxidative stress and/or other environmental factors. However, once it is initiated there seems to be agreement that the degenerative process involves apoptosis and not necrosis. The results of this study suggest that HBO might be a possible new modality of treatment for PD because it appeared to be able to replace Sinemet as a therapeutic regimen. The mechanism by which the HBO effect might be occurring may be partly due to an anti-apoptotic effect. It has been shown that HBO increased the expression of Bcl-2 protein, a major anti-apoptotic protein, in treating forebrain cerebral ischemia in gerbils (3). The Bcl-2 protein has also been elevated by repeated HBO treatment in normal gerbils (4). So it is possible that HBO in this study inhibited the apoptotic pathway involved in the progressive neuronal degeneration by stimulating the expression of the Bcl-2 proteins. Other possible HBO effects should not be discounted such as improved oxygen perfusion due to increased extravascular oxygen diffusion and to possible angiogenesis (5). Axonal repair and regeneration and/or synaptogenesis could occur due to increased expression of neurotrophin(s), since HBO has been shown to increase vascular endothelial growth factor (6) and act synergistically with platelet derived growth factor and transforming growth factor-beta (7). The results of this case study agree with much of the results observed in the clinical study by Borromei and his coworkers. It is not clear from their study whether some of their patients were concurrently being treated with anti-parkinson drugs. In our study, HBO replaced the Sinemet therapy and appeared to improve the clinical condition. Thus, results from this case study suggest that HBO therapy might be a potential therapeutic modality in treating patients suffering from PD without causing untoward side effects such as dyskinesia observed in long-term Sinemet therapy. In conclusion, we suggest that HBO therapy might be neuroprotective in nature to the nigrostriatal neurons by acting as an antiapoptotic process. This could stabilize neuronal function, thereby potentially decreasing the progression of the neurodegeneration observed in Parkinson’s Disease.

  1. Thatte U and Dahanukar S. Apoptosis: clinical relevance and pharmacological
    manipulation. Drugs. 1997; 54(4): 511-532.
  2. Borromei A. OTI efficiency in decompensated-complicated Parkinson’s Disease. In: Proceedings of the International Joint Meeting on Hyperbaric and Underwater Medicine. Marroni A, Oriani G and Wattel F, eds. XII International Congress on Hyperbaric Medicine. Milano, Italy. 1996, pp 599-604.
  3. Zhou J-G, Liu J-C and Fang Y-Q. Effect of hyperbaric oxygen on the expression of proteins Bcl-2 and Bax in the gerbil hippocampus CA1 following forebrain ischemia reperfusion. Chin J Appl Physiol. 2000; 16(4): 298-301.
  4. Wada K, Miyazawa T, Nomura N, Yano A, Tsuzuki N, Nawashiro H and Shima K. Mn- SOD and Bcl-2 expression after repeated hyperbaric oxygen. Acta Neurochir. 2000 (Suppl) 76: 285-290.
  5. Marx RE. Radiation injury to tissue. In: Kindwall EP, (Ed) Hyperbaric Medicine Practice. Best Publishing Co. Flagstaff, AZ. 1995:450-455.
  6. Sheikh AY, Gibson JJ, Rollins MD, Hopf HW, Hussain Z and Hunt TK. Effect of hyperoxia on vascular growth factor levels in a wound model. Arch Surg. 2000; 135(11): 1293-97.
  7. Zhao LL, Davidson JD, Wee SC, Roth SI and Mustoe TA. Effect of hyperbaric oxygen and growth factors on rabbit ear ischemic ulcers. Arch Surg. 1994; 129(10): 1043-9.
Table 1. Jebsen-Taylor Hand Function Test.
Clinical Testing : Time (in sec)Pre-HBOPost-HBOPre-HBOPost-HBO
Dominant HandNon Dominant Hand
Card Turning7684
Manipulating Small Objects1111117
Simulated Feeding11101212
Stacking Small Objects85138
Lifting Large Light Objects111096
Lifting Large Heavy Objects8675

Hyperbaric oxygenation in the complex treatment of Parkinson disease

[Article in Russian]

Neretin Via, Lobov MA, Kotov SV, Cheskidova GF, Molchanova GS.

Hyperbaric oxygenation (HBO) was used for the treatment of 64 patients suffering from parkinsonism of different etiology. HBO sessions were provided daily, 8-12 per course, the treatment pressure amounted to 1.3-2 atm exposure to 40-60 minutes. The beneficial effect was marked in 55 patients. The results of the treatment turned out better in vascular parkinsonism, in patients under 65 years, with a disease standing of 1-5 years. The akineticorigid syndrome regressed to a greater degree, whereas in trembling hyperkinesis, HBO turned out to be less potent.

Publication Types: Case Reports

PMID: 2618228 [PubMed - indexed for MEDLINE]