Has Anyone Tried Hyperbaric Oxygen Treatment For Learning Disabilities

For Dr. Peterson's Full Disretation click hither: Children with Autism doing HBOT past Dr. Powell

S pecific Aims

Eliminating the behaviors associated with children having autism would relieve this land millions of dollars and improve the lives of countless people. This, of course is not a tenable goal, just it is a testament to the financial burden directly related to autism. The Center for Illness Control estimates the lifetime price to intendance for an individual with autism to be 3.2 million dollars. I in 100 children today is diagnosed with autism, with currently no handling for this status. Educating children with autism is existence done through the public schools; however, treating the condition with hyperbaric oxygen therapy is showing positive results.

Medically

When studying peer reviewed inquiry in autism, it is clearly a medical status. A review of electric current literature will support the reason why medically hyperbaric oxygen therapy should be an avenue for treating autism.

Review of the Literature

Encephalon Research–Hypoperfusion

When a typical person focuses on a task or generates spoken language, the encephalon is doing more than piece of work and in that location is an increment perfusion with the blood flow to the brain. This increment in the blood flow to the brain supplies the brain with more oxygen and glucose, giving the cells their needed energy to perform their task. In autistic children, several studies have shown the contrary; these children actually have diminished blood menstruum to begin with, and when their brain is attempting to perform a task, such as generating speech or focusing, their blood flow does not increase giving them the needed oxygen and glucose the cells need. (Fox, 1986) (Muller, 1999) At that place is vasoconstriction instead of vasodilatation in the blood vessels. (Allen, 2003) This has been verified past studies that show an increment in p53 and a decrease in Bcl-2 in the brains of some children with autism. (Araghi-Niknam, 2003) Thus giving evidence for an indication of damage as a event of cognitive hypoxia (impaired oxygen delivery), resulting from the hypoperfusion. This is in correlation with the previously stated outcome of viral overload affecting the myelination procedure as a outcome of the ischemic effects from inflammatory process in which the vessels become inflamed and a downward spiral furnishings takes identify resulting in cerebral hypoperfusion.

Cerebral hypoperfusion is but decreased blood flow to the brain. There have been numerous studies in the medical literature demonstrating hypoperfusion in children with autism. "Bi-temporal hypoperfusion was confirmed in three independent groups of autistic children and provided the first robust evidence for localized dysfunction of the cerebral cortex in school-age children with principal autism." (Boddaert, 2002) With newer upgraded encephalon-imaging cameras, detecting hypoperfusion in children with autism continues to become more defined. Ane way this has been documented is through the utilise of SPECT scans. One study conducted by Dr. James Wilcox in the Section of Psychiatry at Texas Tech University Health Sciences Center showed the hypoperfusion typically worsened with the age of the kid, becoming "quite profound" in older children. The diminished claret flow can be seen with a articulate correlation to many cadre autistic symptoms/behaviors. For instance, when the Thalamus has hypoperfusion the results are repetitive, self-stimulatory, and unusual behaviors. When hypoperfusion is establish in the temporal lobes the results are desire for sameness and social/communication impairments, or in the cingulate gyrus the consequence is manifested in difficulty recognizing familiar faces. Reduction on cerebral blood flow in the amygdale results in social deficits such as the ability to feel emotion and understand other'southward emotions, and response to danger, and anxiety. (Ohnishi, 2000)

In order to look farther into hypoperfusion, specifically in the temporal lobe, Zilbovicius and colleagues (2000) conducted a study using a PET scan. The advancements in PET scans immune the researchers to expect for abnormalities in regional cerebral blood flow (rCBF). The study consisted of twenty-i children with autism and ten non-autistic. Later, twelve more than children with autism were added to the study. The children each had a PET scan and the image was reconstructed into 63 slices. The images were compared with t and Z statistics. The results revealed that the autistic group had meaning hypoperfusion. There was no hypoperfusion in the comparison grouping. Regions with maximal hypoperfusion in the autistic grouping were centered in the left superior temporal gyrus, the right superior temporal gyrus, and in the correct superior temporal sulcus (thought to process the homo voice and coding facial expressions). These areas are involved in auditory processing. The left side generates an understanding of individual words; the right side deals with pitch, melody and sound intensity. When this study was redone on an additional 12 children with autism, the results were inside millimeters of the initial study. They concluded at that place could exist a correlation betwixt the hypoperfusion and the deficits institute in children with autism. The temporal lobe dysfunction is related to sensory abnormalities, thought also to be central to the processing information about the world around us. The right superior temporal sulcus hypoperfusion may reflect the difficulties for the children to respond to voices and/or read faces.

Critchley and colleagues published a written report where they measured for changes in the cerebral claret flow when people with autistic disorder process facial expressions. Although loftier-functioning individuals with autistic disorder have normal to superior range of intelligence; they have abnormalities in social communication and emotional behavior that tends to non improve over time. The difficulty processing facial expressions of individuals with autism may be linked to the deficits in social behavior. The study used a Functional MRI (fMRI) to investigate brain activity in 9 adults with autistic disorder and 9 controls when consciously and unconsciously processing emotional facial expressions. The individuals all met clinical diagnosis for Asperger syndrome or autism using ICD-10. Subjects were shown pictures with unlike facial expressions, they and so rated the emotion. Their enquiry showed significant differences between the subjects with autism and the control group in processing facial expressions. More specifically this would stem from abnormalities in the medial temporal lobe, striatum and insula when processing facial emotions. This correlates with other studies that associate autism with cerebellar abnormalities. The amygdale (part of the encephalon that allows you to feel emotion and sympathise other's emotions), part of the medial temporal lobe, is crucial to learning and representing the motivational meaning of stimuli. Critchley concluded that while these findings give clues to the difficulty for individuals with autism to process facial expressions, it is not clear every bit to the origin of the deficits. (Critchley, 2000)

Similiar to Critchley, Ohnishi and colleagues besides reported reduced cognitive blood flow in people with autism. They addressed the problem of people with autism having impaired performance in communication and social interaction, abnormal response to sensory stimuli, and desire for sameness that is obsessive in nature. They hypothesize that these areas of deficits may be associated with perfusion in the medial prefrontal cortex and anterior cingulated gyrus of the brain. The study consisted of twenty-three children with infantile autism and 20-half-dozen non-autistic mentally retarded children who underwent SPECT scans (single photon emission computed tomography). Just prior to the browse each patient received an intravenous injection that allowed the researcher to examine the brain perfusion. The patients' scores from the Babyhood Autism Rating Scale (CARS) were compared with the areas of perfusion. The researchers discovered that there were decreases in regional cerebral blood flow in the patients with autism versus the non-autistic patients in the bilateral insula, superior temporal gyri, left inferior frontal gyrus, and left middle frontal gyrus. For the patients with autism there were no areas of increase in cerebral blood flow. There was also a positive correlation between the reduction in cerebral claret flow in the hippocampus (the area for short term memory and the area that regulates emotions—including the gyrus which is very sensitive to oxygen impecuniousness) and the amygdale, which is part of the limbic system (almond-shaped clumps of cells deep in the brain, deals with response to danger, anxiety, possible social interaction.) In conclusion, there was a reduction of cerebral blood flow in children with autism compared to the non-autistic population. These areas are related to the deficits found in children with autism, for example the left anterior cingulated gyrus is associated with advice and social interaction deficits. In that location is besides some question as to the correlation with the amygdale and social deficits. People with frontal damage oft show deficits related to the stereotypical and rigid behaviors often constitute in children with autism. These areas of reduced blood menstruation appear to exist direct related to the deficits constitute in people with autism. (Ohnishi, 2000)

Some other study linked the reduction in cerebral blood flow to impairment in the cerebellum that is often found in people with autism. Muller et. al., conducted their study by doing PET scans on high-functioning adults with autism, with the premise that people with autism take deficits in language that according to former studies are straight related to deficits neurologically. With modern technology in brain imaging techniques, researchers can now study autism as a neurobiological disorder. Studies of normal adults show attending tasks activate the cerebellum; even so, studies of patients with autism take shown the opposite. The researchers took five autistic adults and matched their gender matched with v controls. Cerebral claret menstruum was evaluated while subjects, autistic grouping versus command, were at remainder, listening to tones, and listening to, repeating, and generating sentences using PET scans. The cerebral blood flow was evaluated on two elements, peaks and mean changes. They discovered that the subjects with autism showed reduced cerebellar activation during nonverbal auditory perception, suggesting cerebellar anomalies. This however was not related to motor activities, as the deficit was non shown during judgement repetition. The autistic population versus the command group likewise showed reduced activation during acoustic stimulation in the auditory cortex. The autistic group showed bilateral weaker activations in the superior temporal. They also showed an absence of activation in the middle temporal. However, in the left anterior cingulate gyrus (brodmann'due south 24/32) at that place was an increase in activation that was not seen in the control group. They ended that their findings suggest the autistic group may have deficits in language developed in the cerebellum region. The encephalon mapping suggested the dominance for language might be reversed or reduced. This might suggest early on harm to areas of the brain, peculiarly in the cerebellum. (Muller, 1999)

Encephalon Enquiry–Inflammation

In 2005 John Hopkins University conducted a study on neurological atmospheric condition of autism by conducting autopsies on individuals with autism. They addressed the issue of people with autism having deficits in areas of communication, need for sameness, and social dysfunctions. These skills are directly related to specific areas of the brain. The question they sought to answer was, practise those with autism take increased neuroinflammation in areas related to those deficits. They conducted autopsies and evaluated encephalon tissue from eleven people with autism for inflammation and tissue contents. The cerebrospinal fluid was too evaluated. The control group was seven patients with frozen tissue. They besides collected cerebrospinal fluid from tissues of vi living patients with autism. There was testify of neuroinflammation, or inflammation of the encephalon. The results showed chronic neuroinflammation in the patients with autism. Vargas found the common trait of all the patients with autism was a chronic inflammatory procedure affecting both the brain and allowed organization functioning. The cerebellum showed considerable affects. It is not articulate as to how the brain became affected, neurotoxins was ane expanse considered. The researchers expressed they did not feel the inflammation did not occur exclusively during the prenatal development, rather ongoing chronic neuroinflammation involving both microglia and astroglia. (cells dealing with immune organization and neurological tissues) They concluded that there is chronic neuroinflammation in patients with autism. They recommend "therapeutic interventions" dealing with the inflammation as a possible handling for autism. (Vargas, 2005)

Neuroinflammation was as well addressed as a possible result of enlarged activated astroglia. Aschner (1999) "observed swelling of astrocytes is associated with a near 50% decrease in the average capillary lumen equally measured past electron microscopy, which will result in decreased blood flow because the flow of red blood cells is impeded." Helt et al, brings that ane step farther to show the inflammation results in increasing difficulty in the torso's ability to eliminate waste products from the blood system, "hence impairing the cellular activities associated with neural activity and synchronization" (Helt et al 2008), correlating to Simply and Castelli's research. Every bit a outcome, with time, different areas of the encephalon develop the inability to work together (Muller 2007). One time again, Helt stated, "If this inflammation could exist controlled early in life, it might prevent such atypical evolution from taking identify."

Multiple studies have confirmed the neuroinflammation of children with autism. The inflammation in the brain causes edema, which increases the area betwixt the cells, and therefore, could increase the amount of fluid inside the encephalon cells. Two studies confirmed this through a functional MRI (fMRI) (Hendry, 2006). The question with children affected by autism may not be if they demonstrate neuroinflammation, simply why they have the inflammation.

Zerrate et al., addressed the result of why the neuroinflammation by researching the link between the inflammation, behavioral abnormalities and Terbutaline, a preterm labor drug. The researchers hypothesized a correlation between prenatal drugs or chemical exposure could be a cause of autism. The study consisted of giving pregnant rats Terbutaline on selected days. Afterwards the pups were built-in, they were analyzed for behavior. Later they were anesthetized and the brains removed. The brains were and then studied. The results demonstrated increased hyperactivity in the rats exposed to Terbutaline. There was also neuroinflammation. The most critical times of exposure were the second to third trimester of human brain evolution. They concluded a chemical exposure could touch the growing fetus in behavioral effect and neuroinflammation. This many contribute to the increment in the incidents of autism (Zerrate, 2007).

Herbert and Anderson (2008) advise viruses or heavy metals infiltrating the body during early development as possible crusade for neuroinflammation. The body's disability to eliminate the virus overload or heavy metals from the torso may stimulate an oxidative stress response which may lead to neuroinflammation, leading to deficits with brain synchronization. These early on immunological insults to the brain may thus be core to the deficits seen in autism.

Brain Research—Synchronization

Some more resent research is taking the brain research a footstep further by looking at how the brain of the autistic kid works in synchronization. Only, et al. (2004) looked specifically at the brain's synchronization during a sentence comprehension task. They knew that high-functioning individuals with autism frequently display enhanced cognitive functioning with high vocabulary, yet they show a deficit in processing verbal instructions. The researchers hypothesized, "autistic participants may rely more than on an enhanced word-processing ability (which would be indicated by more than-than-normal activation in Wernicke'south expanse), and rely less on integrating processes that bring the words of a sentence together into an integrated syntactic and semantic structure (indicated by less-than-normal activation in Broca's surface area.)" (Just, 2004) The researchers conducted the report with seventeen loftier-functioning autistic patients and seventeen normal participants. They were each given fMRI while asked questions that required sentence comprehension tasks. The participants were asked to press a push button on either their correct or left hand with the correct response to the question. And so the data was analyzed looking specifically at the left inferior frontal gyrus (LIFG) (Broca's area) and the left superior and centre temporal gyrus (LSTG) (Wernicke'south surface area) and their synchronization. They discovered the autistic patients had a lower degree of synchronization between LIFG and the LSTG. The autistics showed less activation in the left inferior frontal gyrus versus the control group, however, they showed more activation in the left posterior superior temporal gyrus. The researchers concluded that the reduction in synchronization may give explanation for the deficits with auditory comprehension. The possible reason for this may exist the autistic brain puts more emphasis on the individual words and details, with difficulty in higher-level brainchild, instead of comprehending the entire passage. The lack of synchronization may likewise business relationship for social deficits in with the ability to integrate different types of information at abstract levels such as facial expressions, personal intent, and pragmatics (Just, 2004).

Some other study conducted by Castelli, et at., intergraded synchronization with a reduction in cerebral blood flow. Again the research team looked at the functional deficits of a person with autism and compared it to the bodily diagnostic deficits happening in the brain. They used a comparison study with ten adults diagnosed with autism and ten people in the control group made up of students and staff recruited from a university. The participants were shown twelve different cursory animations, four dissimilar animations from three different types. Later viewing, the subjects were questioned about what was happening in the animation. Their descriptions were coded in regards to "intentionality," "appropriateness," and "length." Each bailiwick underwent twelve scans, both PET and MRI, on the aforementioned twenty-four hours. The results were analyzed using software from the Wellcome Department of Cognitive Neurology in London, United Kingdom. The results demonstrated a directly comparison on the 2 groups there was a significant reduction in blood flow velocity in the autism subjects in the basal temporal area, superior temporal sulcus, and the medial prefrontal area. The extrastriate regions (brodmann's 18/19) activated at the same rate; nonetheless, they were not interacting appropriately with the mentalizing network that showed a reduction. They concluded that people with autism do have dumb brain part with reduction in cerebral blood flow and lack of connectivity, especially evident when subject is mentalizing. Ane area of possible origin is the Amygdala (Castelli, 2002).

The pathophysiology of children with autism appears to include a number of unlike brain abnormalities. However, the area that is most oft referred to as the site of the well-nigh abnormality is the cerebellum. The cerebellum damage shows consistent expanse for inflammation and too cell damage. 1 cell in particular is the Purkinje cell. Not only do multiple studies show a reduction in the Purkinje cell, but also Fatemi and colleagues have shown not only a reduction in the number of Purkinje neurons, but besides a reduction in size (Fatemi, 2001). Chronic, ongoing procedure of neuroinflammation is a likely source for the reduction of the Purkinje Cells. Based on the research of Vargas and colleagues the findings of immune responses in the cerebellum were closely associated with degenerating Purkinje Cells, granule cells, and axons. In correlation to thimerosal, a side-effect of ethyl-mercury poisoning is reduction in the number of Purkinje Cells.

In summary equally a human relationship to hyperbaric oxygen therapy

Brain deficits in the area of hypoperfusion/decreased cerebral blood flow, reduction of the Purkinje cells, inflammation, and lack of synchronization is common research in the surface area of autism. These deficiencies are clearly linked to the deficits establish in people with autism. Interestingly, neurological effects of mercury on the brain are in the amygdale, hippocampus, basal ganglia, cerebral cortex, damages Purkinje and granule cells in the cerebellum, paralleling the damage plant in the autistic encephalon.

The neurological abnormalities manifest as deficits in cerebral blood menstruation, hypoperfusion, neuroinflammation, and lack of brain synchronization. This is important to empathize in order to begin to find ways to care for people with autism, and sympathise the theory behind the handling. This is reflective in the treatment of hyperbaric oxygen therapy. When a person receives hyperbaric oxygen therapy the blood flow in the encephalon is increased, and hypoxia and inflammation are reduced. Hence, information technology is reasonable to recognize how hyperbaric oxygen therapy may decrease neurological deficits and reduce symptoms of autism.

Benefits from hyperbaric oxygen therapy may not be limited to the child's early years. In a study by Guy (2007) called "Reversal of neurological defects in a mouse model of Rett syndrome" he demonstrated reversing symptoms associated to Rett'due south Syndrome was shown through biological treatment. The researchers activated MeCP2 in adult mice afflicted with Rett's Syndrome. The results were phenotypic reversal of the syndrome. Guy et al. demonstrated lacking neurons have the ability to be repaired into machismo, contrary to popular belief of the damage being permanent after the "critical period."

No affair the cause of the neuroinflammation the furnishings can be devastating. However, hyperbaric oxygen therapy may be one answer to addressing the neurological deficits in autism to exist treatable.