HyperMED - Cerebral Palsy, Autism, Behavioral
difficulties
“My son was born 12-weeks premature eventually diagnosed with cerebral palsy. At age 8, Daniel has never been able to walk independently without crutches. Botox injections provided temporary relief eventually wearing off.
After 20 HBOT sessions he can now walk in excess of 20-minutes unassisted, he can now sit upright without falling over, and is capable of feeding himself more independently.” J Cameron
Case Study - 8 year old boy with Cerebral Palsy
Master DC. aged 8 suffers cerebral palsy with diplegia. His mother states that she suffered late pregnancy complications, preeclampsia resulting with Daniel being delivered 12-weeks premature.
Diagnosis of cerebral palsy was not given until after 12-months of age where he had been observed to be behind the normal development milestones. Daniel has received corrective hip surgery and a course of several botox injections without sustained improvement.
MRI investigation prior to commencing HBOT revealed subtle T2 hyperintensity in the deep white matter adjacent to the posterior aspects of the atria of both lateral ventricles. This is consistent with developmental ‘terminal’ zones, which are commonly seen persisting into the first and second decades. The inferior periatrial white matter appears mildly attenuated bilaterally with slight prominence of the atria of both ventricles. This can be seen as a sequel to periventricular leukomalacia related to prematurity. In addition, fluid signal intensity throughout the mastoid air cells bilaterally consistent with mastoid air cell inflammatory disease. Mild degree of mucosal thickening is present within the anterior ethmoid air cells and both maxillary antra.
After an initial problem associated with the noise during the compressive phase of the chamber procedure, Daniel settled extremely well. His mother has kept a diary record of his progress and after an initial 12 90-minute sessions reported the following :
“Daniel is now standing upright when attempting to walk with his crutches. Before therapy he was unable to walk independently more than a few steps at a time. Even with his crutches he would tend to lean forward completely supporting his weight over his crutches. He is now able to walk with his heels down. Before commencing HBOT he only ever walked on his toes or some times on the toes and ball of his foot.
Daniel is normally very weak in his trunk and tends to lean to one side when sitting for any period of time. When sitting in the car, he tended to fall over from side to side. Since starting HBOT he is now able to sit more upright. Previously he would lean backwards when seated on the toilet seat, now he sitting upright without requiring support.
Daniel’s walking with his crutches has also become a lot quicker. Daniel dresses himself in the mornings even though it is a big effort for him to do, but this is also becoming a lot quicker and less dramatic task for him to do.
At the age of 6-years, Daniel became a bed wetter, since commencing HBOT Daniel is now only having an accident at night approximately once per fortnight. Before treatment he used to wet his bed at least once per night.”
After 18 90-minute chamber sessions the parents reported that Daniel is now walking in excess of 18-minutes without the use of crutches. Before commencing HBOT treatments he was completely incapable of this accomplishment. Parents report that his 'walking has become a lot smoother, his legs are not as stiff and he is no longer walking like a ‘robot’. Daniel is now capable to lift his legs high enough to get himself into the car'.
His grandparents also reported that they have observed he is now capable of using his hand and fingers with greater dexterity. Daniel had difficulty with upper limb dexterity easily fatiguing when attempting to feed himself using a spoon and bowel. He is now capable of independently finishing his meal from a bowel. According to his grandparents’, this ‘activity has improved considerably’.
Daniel continues with the early stages of his HBOT and therapy. Click for more
patient Testimonials.
HYPERMED
Medical Update
Cerebral Palsy and related disorders
Cerebral palsy and numerous forms of childhood related disorders could affect us all regardless of race, religion, or community standing. How we deal with the associated problems and how well the child and general family copes are often very dependent upon our own attitudes as parents.
Many parents do not cope with a child with disability. Many simply avoid the issue and expect the community to provide and do the work for them. Others take opportunity to explore the options, considering the potential benefits that can be gained in an attempt to improve the quality and existence of their child. Some programs and courses simply is a waste of both time and money and some can be potentially harmful to the child.
This information is approached with empathy. For this reason I have attempted to give a clear and rationale approach regarding the treatment of cerebral palsy and related disorders with the use of Hyperbaric Medicine. At the conclusion of this section are a list of websites and links for further resource and information.
Cerebral palsy affects one in every 400 children and until recently the condition was assumed to be permanent, with no treatment benefits other than supportive palliative care. In fact, this condition is reported to affect up to 750,000 patients in the USA.
Recent studies and case history presentations of brain injured children from countries including Russia, China, Brazil, England and the United States of America have demonstrated dramatic changes and improvements after receiving Hyperbaric Oxygenation, even when administered many years after the initial damage.
In ‘Hyperbaric Oxygen Therapy for cerebral palsy children’ by Philip James MB ChB, DIH, PhD, FFOM, Wolfson Hyperbaric Medicine Unit (1999), The University of Dundee, Ninewells Medical School, Dundee DD1 9SY, Dr James states that hyperbaric conditions are required to significantly increase the delivery of oxygen into damaged tissues. When tissue is damaged the blood supply within the tissue is also damaged, and consequently too little oxygen may be available for effective recovery to take place.
James contends that Hyperbaric Medicine is not taught in most medical schools, and is often dismissed by traditional and orthodox medical doctors as "alternative" medicine. James states that in fact it is the drugs that are alternative. More is known about oxygen, its benefits and the problems associated with deficiency states compared with the problems associated with most pharmaceutical drugs.
There is no more important intervention than to give sufficient oxygen to correct a tissue deficiency, but unfortunately oxygen is mainly restricted to hospital usage and restricted to levels that only restore ‘normal’ levels in the blood rather than adopting a medicinal therapy. James states that considerable medical evidence demonstrates that additional oxygen provided in a hyperbaric environment may assist numerous forms of neurologic and brain related dysfunction including children and adults suffering cerebral palsy.
The following is extracted from literature available from Dr Philip James MB ChB, DIH, PhD, FFOM, Wolfson Hyperbaric Medicine Unit, The University of Dundee, Ninewells Medical School, Dundee DD1 9SY.
How can Hyperbaric Medicine help Cerebral Palsy?
Hyperbaric Medicine is a method of safely delivering high doses of oxygen to the patient by breathing 100% O2 through a mask or hood while inside a pressurised air chamber.
The pressure inside the chamber causes the increased oxygen breathed to be dissolved at greater levels in the blood. The net effect of HBOT provides an additional 15-20 fold increase in tissue oxygenation. This significantly accelerates the rate of healing, stabilisation and repair of damaged and severely impaired tissue structures due to inadequate blood flow.
Approximately 20-30% of the body’s consumption of oxygen occurs within 3-5% of the body mass – the brain and spinal cord structures. These structures are extremely sensitive to oxygen, which can result in dramatic effects with a deficiency state or benefits gained through Hyperbaric Therapy (Jain 1995).
When does the damage occur?
Ultrasonic scanning of the brain has shown that in most children the events which cause the development of cerebral palsy (CP) occur at the time of birth (Pape 1979), although it may be many months before evidence and signs of spasticity develop (Dubowitz 1985).
Where does the damage occur?
The areas affected in CP are in the middle of the hemispheres of the brain and one side or both sides may be involved. The critical area is the internal capsule structures (the area in the middle of the brain) where 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 fibres activate the muscles of the legs and arms.
Why does the damage occur?
Cerebral hypoxia is defined as oxygen depravation to the brain and its structures. Oxygen is vital, and oxygen deficiency, regardless of the cause, starts a vicious cycle of destructive pathological changes in the brain tissue. This cycle, unless interrupted, continues with progressive disabling consequences.
Cerebral edema is a frequent finding in many disorders of the CNS (Central Nervous System including brain and spinal cord structures). Cerebral edema can be directly influenced by numerous factors including heart related conditions, obstructive circulatory conditions including thrombosis and atherosclerosis and toxic effects.
Other conditions influencing cerebral edema include infectious processes, vitamin deficiency, and trauma due to direct head impact and neck injury including birth trauma. Other pregnancy related disorders that have been shown to produce foetal hypoxia include maternal diabetes, heart disease, eclampsia, and placental hypoxia, cord strangulation and trauma of neurovascular structures during the birthing process.
Brain and upper spinal cord edema and hypoxia is life threatening, due to the rise in intracranial pressure. Edema and hypoxia can further aggravate any potential neurological deficits of numerous conditions and may trigger destructive demylination and vascular effects.
Could Hyperbaric Medicine help nervous system damage in newborns?
The development of the myelin sheaths, which form the white of white matter by covering the nerve fibres normally begins at about two weeks before term. The process begins in the spinal cord and proceeds towards the newest areas of the brain to develop - the frontal lobes of the hemispheres, being complete by about the age of 2.
The blood vessels of the brain undergo dramatic changes in the last 2 weeks in utero in preparation for birth. If a child is born prematurely the brain may not be able to deal with the period of oxygen deficiency during delivery - in the change from placental to lung oxygen transfer. As a result there is development of edema and as a consequence oxygen deficiency (hypoxia) in the mid brain. This mechanism can be directly influenced through Hyperbaric Oxygenation.
The damage prevents the migration of the oligodendrocytes which form myelin forward from the brain stem and so the white matter does not develop correctly. The extent to which this process can be ameliorated depends on the degree of damage - in the most severely affected children this area of the brain undergoes cystic degeneration.
'After HBO there was a sharp increase in tracer uptake in areas showing hypometabolism on the pre-HBO study...Reduced spasticity, improved ambulation and speech, and cessation of drooling were noted.'
'Hyperbaric oxygen (HBO) efficiently increases the diffusional driving force for oxygen, thereby increasing tissue oxygen availability. This overcomes ischemia/hypoxia and so reduces cerebral edema, restores integrity to the blood/brain barrier and cell membranes, neutralizes toxic amines, promotes phagocytosis, scavenges free radicals, stimulates angiogenesis, and reactivates idling neurons.'
How can damage be measured?
SPECT (Single Photon Emission Computed Tomography) scanning has ushered in a new age of neurological investigation with patients who have developed disorders of the brain and related function. SPECT has the ability to image the pathophysiological blood flow throughout the brain. Numerous articles on this topic are readily available through Internet sources.
Click for patient testimonial:
SPECT study before and after HBOT
SPECT provides a radioisotope contrast when performed in conjunction with Hyperbaric Oxygenation therapy. The enhanced tracer uptake into the damaged parts of the brain confirms primary ischemia (restricted blood flow) which is overcome by the direct increased hyperoxia vasoconstrictive effects of HBOT driven into the passive damaged vascular beds with subsequent activation of idling, non functional nerve cells (Jain 1995).
SPECT scans, together with Hyperbaric Medicine are currently being used with numerous forms of complex neurovascular deficits including stroke victims, multiple sclerosis, supra nuclear palsy, near drowning, chronic carbon monoxide poisoning, closed head injury, numerous brain and spinal cord related neuropathies and degenerative motor neuron disorders.
Hyperbaric Oxygenation and repeat SPECT scans help identify viable non-functional brain tissue, which has the potential to respond to the stimulatory and reparative effects of repetitive HBOT. In many neurological disorders this potential has been realized with actual increased brain blood flow on the final SPECT scans and reduction of hyperintensity changes on MRI (Magnetic Resonance Imaging) (James 1999).
What causes paralysis and spasticity to develop?
When the controlling nerve cells in the brain and spinal cord structures are disconnected the signals to the arms and legs cannot pass and the ability to move is altered or even lost.
Eventually, because the nerve cells in the spinal cord are separated from the control of the brain, they send an excess of signals to the muscles, causing the uncontrolled contractions known as spasticity. The areas carrying the nerve fibres to the legs are the closest to the ventricles of the brain where the blood supply is poorest, consequently the legs are most commonly affected (Takashima 1978). This is commonly termed diplegia, to indicate that the problem is in the brain, and distinguish it from paraplegia where the damage is in the spinal cord.
Why is spasticity delayed?
This is a crucial question not adequately explained. Children who develop spasticity often appear to develop normally for several months and then gradually and progressively lose function. Because in many children there is voluntary movement for a time after birth, the connections must still be intact. Why are they then lost, allowing spasticity to develop? The answer almost certainly is due to the failure of the coverings of the nerve fibres, known as myelin sheaths to develop. This evidence has been confirmed with MRI investigations. (Dubowitz 1985)
Myelin sheaths envelop the nerve fibres in order to increase the speed of impulse transmission. Myelination normally begins about a month before birth and progresses to completion by the age of two. If there is tissue swelling in the mid-brain, the delicate cells that form myelin die, and the nerve fibres, left exposed slowly deteriorate, with the ultimate development of spasticity.
What may be possible?
Loss of function in the brain can be either due to tissue swelling, which is reversible, or tissue destruction, which is not. The recoverable areas can be identified by SPECT, which reflects the metabolism of the brain directly related to oxygen availability. By giving oxygen at high dosages under hyperbaric conditions, areas that are not dead but dysfunctional or often termed ‘sleeping’ can be awakened.
The potential for recovery in the adult brain is much less than in children who are still growing. Primal cells may be present in children and capable of regeneration. Whatever factors stimulate these precursor cells, there can be no doubt that high levels of oxygen are necessary for brain cell growth and repair. No one currently knows how much repair either a child or the adult brains are capable of when conditions are optimised including the use of Hyperbaric Oxygenation.
How can Cerebral Palsy children be helped?
Clearly the appropriate time to use oxygen based therapy is at the start of a disease process and not after a delay of months or years. Unfortunately, most complex neurovascular conditions do not commence therapy until years after insult, when secondary degenerative effects are well developed. Nevertheless, a course of oxygen therapy sessions at increased pressure has been repeatedly demonstrated to resolve tissue swelling and hypoxic effects even after the lapse of years.
HBOT works by constricting blood vessels and interrupting the vicious cycle where oxygen lack leads to tissue swelling, which then leads to further oxygen deficiency. Although formal studies have yet to be undertaken of children with cerebral palsy, there is every reason to believe that exactly the same effect that is seen in stroke patients can occur. Also, in children the brain is still developing and therefore the prospects for improvement are very much greater than in adults. Recovery of brain damage resulting from cardiac surgery in children has been documented using X-ray scanning.
Will Oxygen Therapy ‘cure’ Cerebral Palsy?
Probably not. There are extreme and varying cases that come under the label of cerebral palsy. Structural problems may be either congenital or developmental, and genetic related factors obviously influence the outcome. However, it is reasonable to assume that the inclusion of Hyperbaric Oxygenation may be an excellent pro-active measure that will enhance not only the rehabilitation of the child, but in many children, dramatically change the clinical presentation.
Hyperbaric Medicine is not claimed to be as a ‘cure’, it is simply a way of ensuring the most complete and dynamic recovery possible. It is recommended as an adjunctive measure, in conjunction with other forms of medical directed therapy, exercise programs and conductive education programs.
Are there any dangers or risks?
The initial sessions usually require the patient to adapt to the pressure exerted on the ears, the effects of which are similar to those experienced in an aircraft when descending. Careful medical supervision and advice can easily overcome this simple problem. Some parents raise concerns regarding oxygen toxicity and any possible negative effects. Extensive Hyperbaric testing including children with cerebral palsy and epilepsy disorders have demonstrated that HBOT performed at a pressure 1.5-1.75 ATA is considered safe, without complication and treatment effective.
Are there any formal studies?
Formal studies are now being conducted in the USA and Canada, subsequent to a recent ‘pilot study’ performed at the McGill University. The McGill study is available through Internet sources.
The small McGill pilot study was limited to include 25 subjects comprising 10 girls and 15 boys. The mean age was 5.6 years, with the age participants ranging from 3.1 to 8.2 years. The children selected for the study all had established functional diagnosis of ‘spastic diplegia’. All subjects received a small allocation of Hyperbaric Oxygen Therapy limited to 20 one-hour chamber sessions administered at a pressure of 1.75 atmospheres. The same medical physician, physical and occupational therapist evaluated subjects at both established pre and post treatment intervals. Participant children underwent two post treatment evaluations, the first within two weeks post treatment and the second at a three-month post treatment period.
The pre and post treatment evaluations consisted of the following elements: an evaluation of gross motor function using the Gross Motor Function Measure (GMFM); an evaluation of fine motor function using the Jebsen Test for hand function; an evaluation of spasticity using the modified Ashworth Scale (evaluation completed by both the physical therapist and the physician); and an evaluation of reflexes. Subsequently, the parents were contacted by telephone to respond to a therapist directed questionnaire. All measures were compared pre and post treatment using the Wilcox on matched pairs signed rank test for non parametric measures at levels of p<0.05 and p<0.01.
The results demonstrated that the improvement in Gross Motor Function was significant. Improvements recorded including crawling, sitting, kneeling, rolling, standing, walking, running and jumping. The Jebsen Test for fine motor function was also significant for card turning, lifting objects, and stacking checkers. Spasticity was decreased in the hip adductors, hamstrings and ankle plantar flexors (p<0.01) and significantly reduced in the quadriceps. Reflexes including patellar tendon and achilles tendon previously hypertonic were found to be significantly reduced. The parental interactive questionnaire confirmed improvements, identifying numerous clinical gains.
The pilot McGill study clearly demonstrates that Hyperbaric Medicine is effective in the management and treatment of cerebral palsy, improving motor function and reducing spasticity in children with spastic diplegia. The limited study (small sample size, no control group, minimal number of treatments) demonstrates that further research is definitely required to ascertain the potential of this treatment for children with cerebral palsy.
University of Texas Galveston, USA
Research recently performed under the direction of Dr Kevin Barrett, M.D., F.A.C.P. Dr Barrett is Professor of Hyperbaric Medicine and has co-authored with Kevan P, Corson C, Jon T, and Mader MD.
A pilot study investigating the effects of HBOT with paediatric cerebral palsy. The objective of the study was to determine if 1.5 ATA hyperbaric oxygen therapy can ameliorate the neurologic deficits associated with paediatric cerebral palsy.
Background: Numerous anecdotal reports attest to the amelioration of neurologic deficits in a variety of chronic cerebral insults including cerebral palsy. Improvement is attributed to the metabolic up-regulation through improved local cerebral blood flow in a residual chronic ischemic penumbra.
Methods: Five children, average age 41.8 months, were treated with 1.5 ATA hyperbaric oxygen therapy (HBOT) for a total of sixty treatments administered for one hour daily, five days per week. A modified test of gross motor and fine motor function (GMFM-m) and a modified Ashworth Spasticity Scale were employed before and after hyperbaric therapy.
One patient with cortical blindness was assessed with visual evoked potentials before and after HBOT. One patient dropped out of the study before completion. Information was obtained on only four patients.
Results: Modest decreases in spasticity and improvements in the modified GMFM scores for all patients completing the study. Cortical visual evoked potentials, which were absent before therapy in one patient were measurable after HBOT.
Conclusion: Hyperbaric oxygen therapy effected improvements in tests of gross motor and fine motor function and decreased spasticity as measured by the modified Ashworth spasticity score in patients with chronic cerebral palsy. Functional reorganization in the visual cortex is suggested by the reappearance of visual evoked potentials.
Hyperbaric Oxygenation for children with spastic diplegic cerebral palsy - a pilot project
'Effects of hyperbaric oxygen therapy on children with spastic diplegic cerebral palsy: a pilot project'. Undersea Hyper Med 1999 Winter;26(4):235-42. Underwater and Hyperbaric Med. 15 (2000) 232. Montgomery D, Goldberg J, Amar M, Lacroix V, Lecomte J, Lambert J, Vanasse M.
Hyperbaric oxygen (HBOT) therapy for children with cerebral palsy (CP) is not new. Research documenting the effects in this population has been anecdotal. We evaluated the effects of HBO2 therapy for 25 children (X = 5.6 +/- 1.6 yr) with a functional diagnosis of spastic diplegic CP.
Pre- and post-HBOT evaluations consisted of the following measures: gross motor function measure (GMFM), fine motor function (Jebsen test for hand function), spasticity (modified Ashworth scale), video analysis, and parental questionnaire.
The protocol for HBO2 therapy was 20 treatments of 95% oxygen at 1.75 atm abs for 60 min. The Wilcoxon matched-pairs signed-rank test for non-parametric measures was used to compare pre- and post-treatment data. 'Results showed improved gross motor function in three of the five items in the GMFM test, improved fine motor function in three of the six hand tests, reduced spasticity in three of four muscle groups when assessed by a physician specializing in CP, and improvements for four of nine questions posed to parents'.
Hyperbaric Medicine and Epilepsy
Proceedings of the 11th International Congress on Hyperbaric Medicine : 'Treatment of Children's Epilepsy by Hyperbaric Oxygenation: Analysis of 100 Cases' ; Wong Qibiao, Wang Hon~un, Chen Linzheng, Zhao Cuiyun from the Hyperbaric Oxygen Treatment Center, Zhujinag Hospital.
In order to find an effective anticonvulsant treatment for children, the researchers began a treatment using Hyperbaric Oxygen in 1987. The group included 100 patients including 72 males and 21 females with ages ranging from 4 days to 14 years. In 23 patients there was no known cause for their epilepsy. The others had established medical etiology including : cerebral lesion due to birth injury and trauma in 55 patients, encephalitis in 14 children, high fever in 2 children, anoxic cerebropathy in 4 children, brain tumour in 1 child, cerebrovascular malformation in 1 child. Intelligence was impaired in 61 of the 100 children.
The types of seizures included : grand mal seizures in 32 children, psychomotor in 12 children, petit mal in 10 children, focal in 44 children, autonomic symptoms in 2 children.
Hyperbaric Oxygenation was performed with 100% oxygen at a pressure between 1.7-2.0 atm, with patients treated daily for a period of 80-minutes. An initial course was for a period of between 15-30 days. Some patients had therefore been treated 35-45 times.
The clinical results demonstrated varied improvements, many of them significant. Seizures were greatly diminished, an observation which was confirmed with follow up EEG investigation. 43% of the children no longer required any anticonvulsant medication and in a number of patients the amount of medication needed was moderately decreased.
Post treatment evaluation revealed that 82% of the patients demonstrated improved cognitive function including intelligence, personality, and mentalities. 51% children were recorded to have improved study capability. 14% of patients were recorded to have had no change after being treated 30 times. 76% of the patients were observed for the following 3-year period. 40 of the children had been completely free of anticonvulsants during this period. Three children had one or two slight attacks every year. 25 children required a reduced dosage of anticonvulsants, with seizures reported to have diminished. In 11 children the levels of seizure episodes did not change with Hyperbaric Therapy.
The researchers concluded that 'children suffering birth trauma as the cause for seizures demonstrated the most improvement with Hyperbaric Oxygenation as evidenced by improved cerebral circulation and reduction of cerebral edema. HBOT promoted the energy metabolism of cerebral cells, improving recovery of epileptic foci.'
Epilepsy often impairs the patient’s intelligence. HBOT was demonstrated not only to control and reduce the attacks of epilepsy, but also to assist in preventing the occurrence of intelligence impairment. It was concluded that most patients require between 2-3 years of periodic HBOT. In infants who do not have high fever or respiratory inflammation, it was recommended that HBOT treatment begin within several days after birth related trauma.
Autism and Attention Deficit Disorder (ADD) - Another possible causative effect : Mycoplasma
Recent publication (27-03-00) by Prof. Garth Nicolson
gnicimm@ix.netcom.com, President & Chief Scientific Officer, The Institute for Molecular Medicine California USA, have established a new study working with paediatricians who have patients with Autism and/or Attention Deficit Disorder to determine a causal connection between the signs and symptoms suffered by these patients and chronic infections caused by Mycoplasmas or other chronic infectious pathogens.
Mycoplasmas are microscopic micro-organisms similar to bacteria but without a rigid cell wall, and the pathogenic forms of these micro-organisms can penetrate into cells and enter the Central Nervous System (refer to section on Chronic Illness). Mycoplasmas and related opportunistic infections have been recently isolated as a causative influence including Chronic Fatigue Syndrome, Fibromyalgia Syndrome, Gulf War Illness, Rheumatoid Arthritis and other complex autoimmune diseases where they cause system-wide or systemic infections that invade virtually every tissue in the body and can compromise the immune system, permitting opportunistic infections by viruses, bacteria, fungi and yeast. The signs and symptoms of patients with multiple chronic infections can be quite complex, and each patient tends to have their own unique set of problems.
Nicoloson (2000) has recently correlated the incidence of these and other infectious agents with Autistic children indicating a high incidence of systemic mycoplasmal infections. Similarly, in children with ADD, Nicolson has again identified 'an alarming rate of Mycoplasmal infections approaching one-half of cases'.
In addition to their association with Autism and ADD, systemic mycoplasmal infections can cause chronic fatigue, reoccurring fevers, night sweats, joint and muscle pains, stomach upsets and cramps, diarrhoea, breathing problems, sleep disturbances, sinus congestion/pain, headaches, skin rashes, kidney pain, dizziness, nausea, short term memory loss, vision problems, such as light sensitivity, blurred vision, hair loss, urination problems, eye pain, heart and thyroid problems and in extreme cases autoimmune-like disorders, abnormal allergic responses, peculiar neurological symptoms, heart abnormalities, respiratory ailments, gastric discomforts ranging from ulcers to irritable bowel syndrome, and in extreme instances encephalitis and/or meningitis.
Mycoplasmal infections can start as respiratory infections or post-vaccination illnesses that cause a flu-like illness that progresses to a systemic condition.
Nicolson recommends clinical investigation with treatment including cyclic antibiotics and immune stimulation and dietary supplements. Unfortunately, most children are too young to take strong antibiotics, with the exception of azithromycin, which has been shown to paediatric safe. Children over the age of 7 can take low-dose doxycycline or low-dose Biaxin. Children with Autism and ADD and confirmed diagnosis of systemic mycoplasmal infections have been successfully treated for these conditions with antibiotics, immune support, and dietary supplements with vitamins and minerals.
The International Institute for Molecular Medicine is currently researching the effects of mycoplasma and childhood developmental disorders including Autism and ADD.
Conclusion -
All patients with closed head involvement (including chronic brain dysfunction) suffering neurological deficits due to hypometabolism, confirmed with pre/post SPECT/MRI HBOT studies, are recommended to commence Hyperbaric Oxygenation at 1.5 – 2.0 ATA (Jain 1995) -
The response of HBOT requires an initial intensive oxygen saturation effect. Usually 40-60 and even up to 80 HBOT sessions are considered as an introduction. HBOT should be maintained whilst demonstrable improvements are noted by both patient and physician. Sessions are carried out daily -
The benefits of HBOT are dependent upon the size of the penumbra zone (recoverable neurons) and the extent of initial neuronal damage done during the original insult or trauma. This should be measured by investigative MRI and SPECT -
Spasticity appears to be consistently reduced, mobility and ambulation improved and speech and cognitive behaviour improved in most cases with Hyperbaric Oxygenation. Improvement is thought to relate directly to the possible revascularization of ischemic zones and the reactivation of idling neurons. (Jain 1995). Clinical emphasis also provides direct support that deals with the mechanisms associated with joint dysfunction, spasticity, abnormal alignment and subsequent postural and spinal problems -
HBOT should be instituted early in the rehabilitative process. Those treated with HBOT within the initial 6-12 months of developmental cerebral palsy with spasticity have greater chances of recovery -
HBOT at 1.8 ATA is safe and well tolerated by impaired neurological patients including cerebral palsy children -
Response to HBOT may not be observed in the initial sessions. Oxygen saturation effects vary from patient to patient. Some case studies report in excess of 100-200 chamber sessions before impact of the oxygenation process was observed clinically -
Fixed neurological deficits persisting for years after closed head injury are not a contraindication to HBOT management. Neubauer and End (1980) and Holbach (1977) have demonstrated improvement with stroke and other brain injured patients more than five years after the initial stroke or trauma onset. Neubauer (1996) and Steenblock recorded significant improvement with patients who suffered closed head injury including stroke, more than 15 years from injury -
SPECT and MRI investigations are essential measures to identify potentially viable neuronal cells and regions of the brain that can be influenced with HBOT. HBOT programs cannot be instigated without this current information
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