Autism is a neurodevelopmental illness that affects as many as one out of every 166 children in the United States and is characterized by deficits in social interaction, communication difficulties, and restrictive and repetitive behaviors.
Children from all socioeconomic and ethnic backgrounds are affected. Prior to the 1990s, autism was thought to be a rare illness, affecting around one in every 2,500 children. However, the frequency of autism spectrum disorders climbed 556% between 1991 and 1997, according to the US Department of Developmental Services.
Autism is currently more common than childhood cancer, cerebral palsy, Down syndrome, spina bifida, or cystic fibrosis. Furthermore, autism is encountered all over the world, and the worldwide incidence is increasing at a rate of 3.8% per year. Autism is an illness that is still poorly understood, but recent clinical research is beginning to shine a light on a few of its mysteries.
Overview of hyperbaric oxygen therapy
Hyperbaric oxygen therapy (HBOT) has been used successfully in several cerebral hypoperfusion syndromes, including cerebral palsy, fetal alcohol syndrome, closed head injury, and stroke.
HBOT can compensate for decreased blood flow by boosting the oxygen content of plasma and body tissues and, in some cases, can even correct oxygen levels in ischemic tissue. In addition, animal studies have demonstrated that HBOT has potent anti-inflammatory effects as well as a reduction in oxidative stress. Furthermore, new research suggests that HBOT mobilizes stem cells from human bone marrow, which may promote recovery in neurodegenerative illnesses. Based on these findings, it is predicted that HBOT will alleviate symptoms in autistic people. A retrospective case series is offered to support this theory.
Hyperbaric oxygen therapy (HBOT) involves inhaling 100% oxygen at greater than one atmosphere absolute (1 ATA) in a pressurized chamber. HBOT has been used successfully in humans at varying pressures to treat a range of conditions.
Many clinical applications of HBOT (over 2.0 ATA) include the treatment of decompression sickness, arterial gas embolism, carbon monoxide poisoning, amyotrophic lateral sclerosis, and complex regional pain syndrome.
However, HBOT has been used with therapeutic success at lower pressures (1.4 ATA or less) in disorders such as fetal alcohol syndrome and ischemic brain injury. In a prospective trial of 168 patients with closed head trauma, HBOT at 1.5 ATA resulted in a significant reduction in mortality (32% versus 17%).
HBOT has been shown to increase the oxygen content of plasma and body tissues and can even normalize oxygen levels in ischemic tissue. In fact, the amount of oxygen delivered by HBOT at 3.0 ATA and 100% oxygen is able to keep tissue viable even without oxygen input from circulating hemoglobin. HBOT has been shown in rat models to minimize the effects of hypoxia and ischemia on the newborn brain. Human studies show that HBOT causes modest vasoconstriction, which reduces blood flow while increasing oxygen delivery and levels in target organs. HBOT can reduce edema in ischemic tissue, including the brain, by producing modest vasoconstriction, resulting in lower intracranial pressure.
How can hyperbaric oxygen therapy improve symptoms in autistic children?
Autism is a neurodegenerative illness characterized by cerebral hypoperfusion, neuroinflammation, and elevated oxidative stress, according to multiple studies. HBOT aids in the treatment of hypoperfusion, has anti-inflammatory properties, and decreases oxidative stress. HBOT also mobilizes stem cells from human bone marrow. As a result, HBOT will alleviate autism symptoms.
Improving cerebral hypoperfusion in autism
Several studies have found that reduced blood flow to the temporal regions and other brain areas correlates with many clinical findings associated with autism, such as repetitive, self-stimulatory, and stereotypical behaviours, as well as impairments in communication, sensory perception, and social interaction. Furthermore, a correlation between decreased IQ and hypoperfusion of the temporal and frontal lobes has been described in autistics.
The cause of this decreased blood flow is unknown, however it could be a result of changes in cerebral artery resistance. When the metabolic rate and functionality of local brain tissue rises, cerebral blood flow increases. However, in autistic children, this response may be reversed.
Inflammation is a known source of decreased blood flow, and various inflammatory disorders, including lupus, Sjogren’s syndrome, Behcet’s illness, viral encephalitis, and acute Kawasaki disease, have been linked to cerebral hypoperfusion.
Zones of the autistic brain affected by decreased blood flow and symptom correlations
Cerebral hypoperfusion may contribute to some of the more peculiar aspects of autism behavior. Reduced blood flow to the thalamus has been linked to autistic clinical characteristics such as repetitive, self-stimulatory, and odd behaviors, as well as resistance to changes in routine and surroundings.
Temporal lobe hypoperfusion has also been linked to higher autism symptom profile scores, including “obsessive desire for sameness” and “impairments in communication and social interaction”. Another study on “high functioning” autistics found that blood flow to the temporal lobe and amygdala was reduced, which was associated with clinical abnormalities in understanding facial expressions and emotions. A recent research of autistics found decreased blood flow to the “fusiform face area”, which is responsible for identifying familiar faces.
Many of the clinical findings associated with autism, such as self-stimulatory activities and difficulties in speech, sensory perception, and social interaction, have been linked to hypoperfusion of the temporal and other brain regions. This decreased blood flow could be caused by neuroinflammation. More research on the impact of inflammation on blood flow in the autistic brain is needed, particularly in the temporal lobes, where hypoperfusion is widespread. Whatever the origin of the hypoperfusion, it is possible that the increased oxygen delivery to the brain achieved by HBOT will alleviate some of the symptoms seen in autistic children.
M-HBOT and cerebral hypoperfusion
The oxygen delivered by HBOT can restore hypoxia induced by hypoperfusion in brain tissues. Hypoxia is caused by cerebral hypoperfusion, which induces electrical failure in brain cells. Worsening hypoxia finally leads to ion pump failure, which then leads to cell death. Idling cells are those that have electrical failure but retain ion pump ability. They are alive but nonfunctional.
Although HBOT reduces cerebral blood flow by vasoconstriction, it also increases cerebral oxygen tension and may accelerate brain recovery from ischemia. In one case report, 80 sessions of 1.5 ATA HBOT enhanced oxygenation to the ischemic penumbra on SPECT scans and dramatically restored cognitive and motor function in a patient with an ischemic brain injury caused by a near-drowning experience 12 years earlier.
HBOT has been shown to be clinically useful in various cerebral hypoperfusion conditions, such as lupus and traumatic midbrain syndrome, and may be beneficial in acute ischemic stroke and acute myocardial infarction.
Furthermore, HBOT has been utilized in a number of trials on children with cerebral palsy (CP). On SPECT scans, some children with CP caused by prenatal asphyxia exhibit localized regions of cerebral hypoperfusion. One study performed in Canada on children with Cerebral Palsy reported significant clinical improvements after 20 sessions of HBOT at 95% oxygen and 1.3 ATA.
Heuser et al. used lower pressure HBOT at 1.3 ATA on a four-year-old autistic boy and showed “dramatic improvement in behaviour, including memory and cognitive functioning” after just 10 sessions. Moreover, the child’s cerebral hypoperfusion improved as evaluated by pre- and post-HBOT SPECT scans. These case reports are noteworthy because they show that HBOT can improve clinical outcomes in several “irreversible” and persistent neurological disorders.
Number of treatments required
It is unknown how many HBOT sessions are required to produce complete clinical improvements from cerebral hypoperfusion or ischemia. In one research that combined SPECT with HBOT, an average of 70 sessions were required to demonstrate a substantial improvement in cerebral blood oxygenation and metabolism in patients with chronic neurological illnesses such as cerebral palsy, stroke, and traumatic brain injury. It is worth noting that the pace of increase in cerebral blood oxygenation was greater during the final 35 sessions compared to the first 35. Furthermore, data from certain HBOT researchers show that younger patients improve faster than older patients. As a result, elderly individuals may require more treatments.
What other benefits does M-HBOT provide in the treatment of Autism Spectrum Disorder?
Reducing neuroinflammation
Several studies have shown that HBOT can decrease both neuroinflammation and gastrointestinal inflammation in autistic children, potentially leading to improvements in symptoms.
The effect of HBOT on oxidative stress
Multiple studies have shown neutral effects on oxidative stress with M-HBOT (Mild Hyperbaric Oxygen Therapy) use. In fact in a study called “The effect of mild-pressure hyperbaric therapy (mHBOT) on fatigue and oxidative stress” the authors concluded that mHBOT is helpful in reducing oxidative stress and improving fatigue while posing minimal risks.
Several studies demonstrate that HBOT lowers oxidative stress. Furthermore, oxidative stress appears to be less of a concern at pressures under 2.0 ATA, which are often used clinically.
Improving stem cell mobilization in autism
HBOT was recently proven to mobilize stem/progenitor cells from human bone marrow. The number of colony-forming cells increased almost 2-fold, indicating a rise in the amount of CD34+ cells. This finding has relevance since many people believe that autism and hypoxic brain damage are permanent diseases. However, current evidence indicates that even long-standing brain diseases may be somewhat curable.
Recently, stem cells have been isolated in the adult brain. This leads to the possibility of neuropoiesis, or regrowth, of certain brain cells. A possible scenario for inducing brain repair through the use of existing mature brain stem cells has been described and is dependent on an intact vascular supply and adequate oxygen, both of which can be enhanced by HBOT.
Hyperbaric oxygen therapy may improve symptoms in autistic children
There is a strong possibility that HBOT could play an important role in improving brain disorders associated with hypoxia, hypoperfusion, inflammation, and fusion disorders. It was also hypothesized that low pressure HBOT would help autism, a disease in which cerebral hypoperfusion is a key component.
Recent research suggests that low pressure hyperbaric treatment at 1.3 ATA with less than 100% supplied oxygen may improve symptoms in several disorders related with cerebral hypoperfusion. One research, for example, revealed that hyperbaric therapy at 1.3 ATA pressurised with ambient air improved clinical outcomes in certain children with cerebral palsy, a disorder associated with decreased cerebral blood flow.
Lastly, one case report indicated ‘‘striking improvement’’ in a 4-year-old child with autism after using hyperbaric therapy for 10 sessions at 1.3 ATA and room air. The child also had improvement of cerebral hypoperfusion as measured by pre- and post-HBOT SPECT scans. Based upon these findings, it was hypothesized that low pressure HBOT would improve symptoms of autism. A retrospective case series was examined to evaluate this hypothesis.
Sources:
[1] Hyperbaric oxygen treatment in autism spectrum disorders[2] Hyperbaric oxygen therapy may improve symptoms in autistic children[3] Therapeutic use of hyperbaric oxygen therapy for children with autism spectrum disorderCredits:
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