HyperMED - Multiple Sclerosis

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Hyperbaric Medicine has been used as an excellent adjunctive measure in the treatment and management of patients with severe debilitating neurological conditions including multiple sclerosis (MS). It has been recorded that MS affects about 100-150 per 100,000 of the population in western countries. The disease process underlying the disease has been shown by magnetic resonance imaging (MRI) to be present in 2% of the population in whom the disease is not manifest. Recent reports indicate that more than 10,000 Americans are newly diagnosed each year. Other studies indicate that there are even greater numbers than these (Neubauer 1998).

Whilst multiple sclerosis is not considered fatal, it can severely cripple and dramatically alter the existence and quality of life of the sufferer. Disabilities of mobility and motion, speech, vision, bladder and bowel control are common to all MS sufferers.

Hyperbaric Medicine has been clearly documented as an important and effective weapon in the battle against this crippling disease. It has been shown to control and stabilize the effects of MS and in numerous cases hold the disease process from further progression (Neubauer 1998). However, HBOT and its effects vary from patient to patient and of course the commencement of HBOT in relation to the onset of the disease is also a significant variable.

What is Multiple Sclerosis

Multiple sclerosis is a condition where the nerve fibers in the brain and spinal cord gradually lose their protective covering, which is made of a fatty substance called ‘myelin’. Nerve impulses are basically electrical impulses, so myelin covers and insulates a nerve in the same way insulation covers an electrical wire. MS varies from patient to patient: even a so-called mild demyelinating lesion in the cord will result in 20% damage of axons (Putnam and Alexander 1947).

A nerve that is covered with full thickness myelin conducts impulses more rapidly and effectively than a nerve with reduced thickness myelin. When the nerve loses its myelin, signals do not travel through the nerve properly, becoming interrupted and irregular. This leads to altered and dysfunctional messages being conveyed to the region that the nerve is supplying, with altered and abnormal impulses being conveyed back through the nervous system to the brain.

As a result of the demyelination process, MS results in hardened, scarred patches called ‘plaques’, which develop in the affected areas of the brain and throughout the spinal cord. Symptoms associated with MS vary from patient to patient and from time to time in the same patient, depending upon where these plaques occur and how extensive they are.

Plaques are not the only mechanism that occurs in the multiple sclerosis patient producing clinical symptoms. ‘MS also causes swelling and edema which leads to a reduction of effective oxygen being delivered to the nerve tissues, resulting in a variety of widespread symptoms’. In many patients these ‘disturbed areas’ may heal spontaneously without plaque formation. Because of the spontaneous remissions, a firm evaluation of the patient’s condition is difficult and diagnosis is usually reserved for at least a 2-year period (Neubauer 1998).

Women tend to suffer from MS more often than men. Research confirms that people most likely to develop and suffer MS are those in a colder climate. The disease has also been shown to occur more commonly among the relatives of patients who have MS. However, there is no clear identified hereditary pattern.

Multiple sclerosis begins slowly, usually in young adulthood, and continues progressively deteriorates over adult life. Initial symptoms are numbness and/or abnormal sensations in the arms and legs and or on one side of the face. Other early symptoms include slight disturbances such as double vision and partial blindness, muscle weakness and dizziness. Later in the course of the disease blurred vision, loss of muscle control, partial and or complete paralysis, abnormal reflexes, slurred speech, loss or irregular control of both bladder and bowel function occur.

Multiple sclerosis causes a number of secondary problems, including inflammation of the membranes covering the brain and spinal cord. This leads to significant problems of exciting nerves from the spinal cord and cranial nerves from the brain. Advanced MS effects all regions of the body dependent upon intact central nervous system function and control. Partial total lack of function and control is the outworking of this progressive disease process.

Multiple sclerosis occurs in one of two patterns. The first pattern is known as ‘relapsing remitting’ type. This type of MS is the most common form of presentation. During a relapse, the disease is active and the nerves are damaged. As a result, new symptoms may appear or existing symptoms may worsen. The relapse usually only lasts for a few days or may continue for several months. In a remission, the disease process is usually quiet, but symptoms are still present because of the damage previously done to the nerve cells. The damage may improve, but does not entirely disappear. After each relapse the patient progressively loses more and more ground, with greater residual disability (Neubauer 1998).

The second pattern of MS is known as ‘chronic and progressive’ pattern. This type of pattern is experienced in about 18% of all MS patients. In this pattern, there is a gradual worsening of symptoms over many years, without relapses or remissions. Symptoms may fluctuate, but in general advance steadily with a continuing worsening prognosis.

People with MS sometimes experience impairments in their thinking ability. They are sometimes subject to mood swings and other emotional difficulties. They may feel angry, frightened, worried or beyond hope. Denial – a state where the patient attempts to ignore the disease is common. The patient may think, with some justification, that revealing his or her degree of anger or fear might be more than family or close friends can accept. On the other hand, family members are frequently desperate for advice on how to best assist the patient. In fact, because of the anxiety of both patients and their families, few other diseases have been the subject of such a variety of treatments.

The causes of Multiple Sclerosis

No one is yet sure of what causes multiple sclerosis. The autoimmune hypothesis is the most common explanation for the mechanisms of MS. However, Jain (1995) reports that despite extensive diagnostic and clinical efforts, no specific antigen has been identified. Many detailed and involved studies in animal models have not identified the ‘key’ other than to document the outworking and effects. In fact, Bradley (1984) identified the process of MS in normal patients with the use of MRI (Magnetic Resonance Imaging). Bailey (1953), demonstrated demyelination in the aging spinal cord, which is inevitable with advancing age.

James (1982) described the ‘microembolism concept’ which causes focal demyelination, originally observed in professional divers. Although ‘embolism is generally considered to be synonymous with occlusion and infarction, microemboli have been demonstrated to disturb the blood brain barrier in transit, with significant breakdown in the supporting veins'. This has been identified as the perivenous syndrome (Zulch and Tzonos 1965).

'Essentially, fat particles may become lodged within the blood vessels of the brain, creating a blockage in the circulation.  This lack of circulation causes swelling (edema), which in turn causes neurovascular lesions to form. The edema reduces the oxygen transport mechanism and the inflammation increases oxygen demand - hence hypoxia and fatigue’.

Another clinical observation includes the fact that the late lesions associated with fat embolism are indistinguishable from the acute lesions associated with MS (Scheinker 1943, Courville 1959, Sevitt 1962, Lumsden 1970, James 1982). 'A microembolism mechanism may explain the abrupt onset of symptoms, sites affected and the blood brain dysfunction' (Jain 1995).

Jain reports that 'focal edema is a significant factor in the mechanism of MS', emphasizing the importance of adjunctive oxygen. Further, Jain states that regardless of the cause of the multiple areas of sclerosis, it is established beyond dispute that the lesions of the disease are 'perivenous and involve a disturbance of the essential blood brain barrier'. Fog (1950) and Oppenheimer (1978) have confirmed the perivenularity of lesions of the spinal cord.

Pozzilli (1988) provided evidence of 'blood brain barrier disturbances' with multiple sclerosis. Recent advances including Magnetic Resonance Imaging (MRI) injected with contrast gadolinium; isotopic scanning and SPECT (Single Photon Emission Computed Tomography) confirm blood brain barrier involvement with positive changes when treated with Hyperbaric Oxygenation. 

Jain reports that although these investigative procedures cannot identify the exact cause of blood brain barrier disturbance, evidence does support the fact that edema is a major factor, with symptom correlation. Sukoff and Ragatz (1982) correlated the 'effectiveness of HBOT in the reduction of global cerebral edema'.

‘Blood brain barrier stability is essential for the management of MS. The most critical factor in barrier restoration and tissue repair in the central nervous system is not arterial oxygen tension, but tissue oxygen availability' (Jain 1995).

Others believe an environmental factor is at work.  This approach believes that circulating toxins such as mercury contribute to inducing MS. Consequently, numerous MS patients have been replacing their mercury amalgam dental fillings with fillings made of other materials, such as porcelain, composite or gold, to halt the progression of symptoms. Some people do have adverse responses to certain dental materials, including silver, tin, zinc, mercury, and copper. But the idea that such fillings can cause or aggravate MS is still open to question.  

Hyperbaric Medicine and Multiple Sclerosis

Drug therapies for multiple sclerosis can cause significant side effects, which may feel worse than the discomforts they are designed to relieve. A number of different drugs are used in MS therapy, including interferon and various steroids. These drugs not only cause a wide variety of side effects, but are also extremely expensive.  The average cost of managing an MS patient in the USA with drug therapies is reported to be more than US$25,000 per year (Neubauer 1988).

Hyperbaric Medicine is currently the only treatment that offers the MS patient some form of relief from the clinical symptoms without serious side effects. Unlike most of the other therapies, it is the only drug-like treatment that has been shown to work on a continuing basis. In addition, HBOT has been the therapy used on the largest number of patients for the longest period of time, which means that it is the therapy with the longest period of follow-up results.  

How does Oxygen help Multiple Sclerosis patients?

Dr Phillip James MB ChB, DIH, PhD, FFOM, Wolfson Hyperbaric Medicine Unit (1999), University of Dundee, Scotland to hbo-list@lists.best.com in response to over 1.2 million chamber sessions performed during the past 13 years specifically for MS patients.

‘Multiple sclerosis is a disease which is characterised by multiple areas of leakage from the blood vessels in the brain and spinal cord causing symptoms. Treatment should be instituted when the first area is affected, but this is not yet an objective in neurology. Vessels in the nervous system are engineered to form a barrier - the blood-brain barrier - to prevent the leakage of large molecules such as proteins because their escape causes inflammation’ (James 1999).

The blood vessels involved in MS are actually veins and the leakage causes inflammation in the surrounding areas. This is usually in the white matter, which contains vulnerable cells, which form the myelin sheaths. As the damage progresses the sheaths are removed and the fibres are destroyed causing disability. Further progression is characterised by loss of the structure of the tissue and healing by scarring - sclerosis. Once the sclerosis has formed, recovery of the normal architecture is not possible. The key to the successful management of the established disease is to give the normal recovery mechanisms the best environment to repair the tissue before scarring takes place.

'The object of giving a concentrated dose of Oxygen is to restore the level of Oxygen in the affected area to normal and interrupt the progression to scar formation. Oxygen is necessary, not only for all metabolism, but also for the regulation of many aspects of blood vessel and blood cell function. The blood-brain barrier requires energy and oxygen to maintain its integrity. Giving more Oxygen in fact constricts the diameter of blood vessels and yet paradoxically improves the transport of Oxygen to the tissues. Oxygen also modulates the behaviour of white blood cells and the inner lining of the vessels'. 

Trials of oxygen therapy in MS patients have shown benefit especially in bladder function and balance but, because neurologists have wanted to avoid the possibility of spontaneous improvement - which is of course oxygen dependent - they have chosen to study patients who have advanced disability.

Most trials have used patients with disease duration typically in excess of two years. The only trials in the history of multiple sclerosis, which matched pairs of patients and then randomly allocated them to either treated or control groups, demonstrated unequivocal evidence of benefit. (p< 0.0001). 'Because the blood vessel barrier may not repair completely, many patients need to continue oxygen therapy on a regular basis. This is also the reason for the need to continue with beta interferon injections, which also acts by stabilizing the blood-brain barrier’. (Fischer BH et al. 'Hyperbaric oxygen in the treatment of multiple sclerosis; a randomised placebo-controlled double-blind trial'. New England Journal of Medicine 1983;308:181-186).  

Clinical Studies

Waksman (1983) states that there are four important mechanisms in the MS destructive process that may be affected by the use of HBOT:

• inflammation involving vascular damage and edema, together with cellular infiltration that is primarily perivascular and mononuclear

• destruction of the surrounding supporting myelin nerve sheath and other surrounding tissue structures

• proliferation of scarring after progression of tissue damage

• decreased nerve conduction due to edema, demylination and progressive scar formation

Boschetty and Cernoch (1970), in a trial of 26 patients, used HBOT provided for two 30 minute sessions per day at 2 ATA for between 10-20 days. Improvement of limited duration was recorded in 15 patients. Neubauer (1978) whilst treating a patient with osteomyelitis who was also suffering MS, observed significant neurological improvements in the MS symptoms. 

The Neubauer-Gottlieb theory proposes that 'multiple sclerosis is caused by lack of vital Oxygen into essential central nervous system structures'. This theory has been strongly supported by continued research showing that HBOT, which overcomes a lack of oxygen, is an effective treatment method in not only MS but also numerous clinical conditions dependent upon adequate oxygen tensions within the tissue structures.

In 1983, New England Journal of Medicine published a report on ‘Hyperbaric Oxygen Treatment of Multiple Sclerosis a Randomised, Placebo Controlled, Double Blind Study.’ Neubauer reports that the wording of the report, which ‘came after almost a year of extensive analysis, revision and review, was deliberately cautious’.  But the message was clear, it did offer a good measure of hope :  “… these preliminary results (on HBOT) suggest a positive, though transient effect of Hyperbaric Oxygen on advanced Multiple Sclerosis warranting further study”. 

The trial was conducted between 1980 and 1982 by Drs Fischer, Marks and Reich at the New York University Medical Centre. 40 patients with chronic MS were divided randomly into two groups.  The experimental group received pure oxygen and the control group received a mixture of 10 per cent oxygen and 90 per cent nitrogen.  Both groups were treated at a pressure of 2.0 atmospheres absolute (ATA), however, it was recorded that an effective pressure of only 1.4 ATA was achieved due to leakage from the masks. Sessions were scheduled for 90-minutes daily, for a total of 20 exposures.

The investigators discovered that '12 of the 17 patients (70%) who received HBOT observed clinical symptoms improve, including mobility, fatigability, and balance and bladder function. Those patients with a less severe form of the disease had a more favourable and long lasting response'. This reinforces emphasis upon early diagnosis and aggressive intervention with Hyperbaric Medicine.

In contrast only one out of 20 in the placebo group showed improvement. Three of the 20 patients in this group dropped out of the study before it was completed, but in the control group of patients who inhaled the equivalent of room air under pressure, just one in 20 (5%) improved. After one year of follow-up, deterioration was found in only two of the patients (12%) who had received pure oxygen, compared with 11 patients (55%) in the control group.

Barnes and co-workers publishing in the Journal of Neurology, Neurosurgery and Psychiatry demonstrated a 'remarkable slowing of cerebellar function (coordination) deterioration in their report of 120 MS patients', one year following Hyperbaric Medicine treatments.

Pallotta (1986) followed 22 patients with MS for eight years. All received an initial course of 20 chamber sessions and 11 of the patients were treated thereafter with two exposures every 20 days. The 'frequency of relapses decreased dramatically in the prolonged treatment group', whereas they gradually increased in the group which received only initial treatments.

Webster (1989) in a 2-year study of 128 patients with chronic progressive and stable MS reported the 'positive effects on bladder function' (urodynamic studies) with continuing HBOT. All patients received an initial course of 20 1-hour sessions with the chamber pressure varied to suit the tolerability of the patient. In 37 chronic progressive patients, deteriorating for one year prior to treatment commencing, 26 who continued treatment for two years were stabilized. The objective of chronic progressive MS patients is to stabilize the disease.

Schumacher (1974) former chair-person of the International Federation of Multiple Sclerosis Societies stated “Far more realistic as an indicator of therapeutic effect than the lessening of symptoms or signs, is the halting of the progression of neurological deficit. The sole criterion of efficacy should be the prevention of the downhill progression or recurrent exacerbation” (Jain 1995). Hyperbaric Oxygenation appears to dynamically influence the outcome of MS patients.

A number of studies have criticised HBOT as a treatment for MS. In reviewing many of these studies, Dr Neubauer believes there were a number of factors that were either not considered or were inappropriate. For example, inadequate HBOT pressures were used, patients were not screened appropriately, or patients with severe and advanced MS, did not receive enough HBOT treatments. It has been established that a number of authors associated with negative reporting and criticism have now established Hyperbaric Medicine Centres in Great Britain, in fact they are specifically treating multiple sclerosis (Jain 1995).

Neubauer (1984), states that more than 10,000 MS patients in over fourteen countries were receiving continuing HBOT for MS. Neubauer states that the 'vast majority of patients (in excess of 70-74%) demonstrated improvement in areas including bowel and bladder control, balance and coordination, muscular spasticity, brain function and memory patterns, and other systemic disorders brought on by the disease process'. 

There was also 'marked absence of deterioration and fewer relapses among patients who participated in a booster hyperbaric program and patients who continued with HBOT on a reduced basis' (Pearlmutter 1998).

In a double blind, placebo controlled 1986 study conducted by Dr T Yamada and colleagues in Japan, it was reported that all MS patients treated with HBOT, even for a short period, showed objective improvement. The investigators concluded that 'long-term HBOT treatment led to an overall significant decrease in the number and intensity of relapses'.

One group that continues to fund research into MS and HBOT is the England based, Action for Research into Multiple Sclerosis (ARMS). The results of one of the initial studies were published in 1989. The two-year study conducted by researchers from the Ninewells Medical School at the University of Dundee in Scotland, involved 128 HBOT treated MS patients who were compared to an equal number of control patients. 70% of the treated MS patients did not deteriorate, had their conditions stabilize or demonstrated variable improvements.

Action for Research into MS (ARMS) has 63 private non-hospital based monoplace chamber facilities throughout England and Scotland. A detailed study involving over 703 patients receiving treatment over 10 years has been observed.