Vision Issues &
Cortical Vision Impairment

Chapter 7 of the HBOT Manual
As with all indications for HBOT, there is a lack of documentation which shows proof as needed by the Medical Profession.  We will include what we have and add more as it is available.   We are also providing you with testimonials which are considered anecdotal but which will help you in deciding if HBOT is for you.




Now He's Blind?

The following study showed results for CVI:

Dr. Maurine Packard, MD
Divisions of Child Development and Pediatric Neurology
NY Presbyterian Hospital
Box 579, 525 East 68th Street
New York, NY 10021
voice mail 212/746-3393; Fax 212/746-8880

Presented at the University of Graz 18th November 2000

Our study was designed as a randomized, delayed entry trial of the effects of HBOT on children ages 1 to 5 years with moderate to severe CP. Enrollment criteria were 1) age between 1 and 5 years; 2) moderate to severe CP; 3) no evidence of brain malformation; 4) developmental delay of at least 33% in one area; 5) no active seizures for the previous 6 months. The protocol consisted of 40 one-hour sessions HBOT at 1.5 ATA. The sessions were scheduled twice a day, five days a week for four weeks. We did not design a double-blind study, in which some children would receive placebo treatments, for several reasons. First, this was a pilot study to see if there was any evidence of benefit for these children. Second we purposefully enrolled children of various ages and disability levels to evaluate the efficacy of HBOT in a range of affected children. Third, as time in the chamber is very expensive, we wanted as much information about treatment effects as possible. Finally, it seemed unethical to have parents devote so much time and energy to a potentially ineffective treatment.

The study population included 26 children, ages 15 months to 5 years, with cerebral palsy secondary to prenatal insults, premature birth, birth asphyxia, and post-natal hemorrhage. The subjects were enrolled at a rate of 4 per month and matched roughly to age and severity. The average age at enrollment was 30 months. The average motor age was 7.5 months; the average cognitive and language ages were both 12 months. Nine had cortical visual impairments.

After the initial intake the children were randomly assigned to receive HBOT (immediate group) or in 6 months (delayed group). The delayed group served as an untreated control group.

Intake assessments included a neuro-developmental assessment, Bayley II (cognitive assessment), Preschool Language Scale (language assessment), the Peabody Motor Scales (an assessment of gross and fine motor skills), and Pediatric Evaluation of Disabilities Inventory (PEDI), a parental report of specific skill in mobility, self-care, and social interactions. Assessments were conducted at four time points: T1 - at enrollment; T2 - after the immediate group received treatment; T3 - prior to the delayed group's HBOT, 5 months after enrollment; and T4 - after the delayed group's treatments. Two physical therapists that were blind to group status administered the Peabody and the parents completed the PEDI at all four time points. Child psychologists blinded to group status performed the Bayley II and PLS at T1 and T3.

Eleven of the 12 children in the immediate group completed the 40 HBOT sessions. The twelfth child developed complex febrile seizures and was dropped from the study. Twelve of 14 delayed children received a full course of treatment. Two subjects developed seizures and could not participate. Assessments from each time point were available on 9 subjects from the immediate treatment group and from 11 children in the delayed treatment group.

The only side effect of treatment was barotrauma to the middle ear. Nine children and 7 parents required ventilation tube placement or myringotomies.

The parents kept weekly diaries during the treatments. Over the month of treatments, 83% of parents noted a marked improvement in mobility; 43% saw a marked increase in attention and 39% reported a marked increase in language skills. Overall, there was some mobility improvement in 21 of 23 children (91%), in attention in 18 of 23 subjects (78%), in language in 20 out of 23 (87%) and in play in 12 of 23 subjects (52%). One family saw no improvement and six families saw minimal improvement, a total of 30%. Five families (22%) reported major gains in skills and 11 families (48%) claimed modest gains.

Four of the 9 children (44%) with cortical visual impairment, including two infants with no functional vision, had improvement in their vision noted by the families, vision therapists and ophthalmologists.

There was a significant difference (p<0.05) in the improvement of scores on the mobility sub-domains of the PEDI for the time period T2 minus T1 in favor of the immediately treated group. For the period T4 minus T3, there was a trend favoring the recently treated delayed group (p<0.058). For the social function sub-domain of the PEDI, there was a trend favoring the more recently treated group 2.

The two groups were compared on changes in their Peabody scores for T2 minus T1 and T4 minus T3 and for changes in the Bayley II and PLS scores for T3 minus T1. There was no statistical difference in the change scores on any of the blinded assessments.

There are several reasons why our blinded assessments did not show a significant difference while parental reports and observations during therapy saw gains. First, our sample size was quite small and only very dramatic changes would be detected. Second, not all the children were cooperative and happy during their evaluations; we had a student, blind to the group status, review the videotapes of the PT sessions and rate the child's behavior. There was a strong correlation between the child's mood and score; happy kids did better. Third, the instruments we chose as assessment tools are insensitive to the changes that were reported by the parents and observed by the unblinded staff.

The improvements in motor function did not translate into immediate functional gains. Most development tools available required motor dexterity and expressive language skills, areas specifically affected by CP. A better, more sensitive evaluation would involve a skilled professional observing the child at home or in school over a several-hour period.

Our conclusion is that, for some children with moderate to severe CP, there is evidence that HBOT improves motor skills, attention, language, and play. For some, an increase in vision was noted. These are not miraculous changes. These children all still have CP, but there are substantial improvements.

In follow-up interviews over 6 months, it was found that the changes in spasticity were most likely to diminish over time, but the improvement in attention, language and play remained. This increase in attention is particularly important for children must be aware of their environment in order to learn. This represents a direct impact on cognitive functioning. The main differences between HBOT and traditional therapies are the rapid gains over time and the impact on cognitive skills which, in general, are not improved by PT, OT and speech therapies. Whether these changes are the direct result of increased levels of oxygen or the intensive contact with the parent or adult in the chamber or another combination of factors should be the focus of further study.

Dr. Packard also presented remarkable video evidence of the changes seen in four children.

This paper is for private study and not for publication.




By Bill Sardi, reporter at large for FOCUS

For the first time eye researchers are reporting a breakthrough treatment for retinitis pigmentosa with the use of hyperbaric oxygen therapy. Researchers in Italy employed daily hyperbaric oxygen at 2.2 atmospheres
of pressure among 24 RP patients for two years. The electroretinogram readings of RP patients undergoing hyperbaric oxygen treatment improved from 4.86 at the beginning of the study to 14.4 at the end of the study. RP patients who did not undergo oxygen therapy experienced diminished electroretinograms, beginning with an average of 4.92 decreasing to 2.97. Hyperbaric oxygen therapy may rescue retinal photoreceptors (Investigative Ophthalmology 38; 5713 Abstract #3296, 1997). This report provides encouraging news to RP patients since there is no proven treatment for RP save for vitamin A therapy which only slows down progressive loss of vision as measured by an electroretinogram and does not improve the ERG.

K.K. Jain, author of The Textbook of Hyperbaric Medicine, indicates the retina has the highest rate of oxygen consumption of any organ in the body. That hyperbaric oxygen treatment is helpful in cases of RP is an
anomaly because it has been shown to cause severe constriction (narrowing) of retinal blood vessels. The hallmark of RP is poor retinal circulation. The constriction of the retinal blood vessels however is offset by the greatly increased oxygen-carrying capacity of the blood during treatment (oxygen saturation increases by 23 percent).

What is hyperbaric oxygen therapy?

Hyperbaric oxygen chambers are located in hundreds of locations in the United States and other sites throughout the world. These chambers are often used to treat deep sea divers who have experienced rapid reduction of air pressure from rising to the water surface too quickly and who subsequently experience decompression sickness (also called "the bends").  Hyperbaric oxygen applies this essential gas at pressures many times greater than normal atmospheric pressure at sea level. It is also a useful treatment for gas gangrene, radiation damage, osteomyelitis, carbon monoxide poisoning, anaerobic infections and for immune suppressed individuals.

Humans breathe air that is 21 percent oxygen. Hyperbaric oxygen involves 100 percent oxygen administered at pressures two or three times normal. This increases the amount of oxygen the blood caries to body tissues which in turn enhances tissue repair.

Hyperbaric oxygen treatment costs $100+ for each treatment. RP patients would need to check with their health insurance plan to determine coverage for treatment. Eye physicians are likely to be unfamiliar with this type of therapy though some retinal specialists may have experience with hyperbaric oxygen.

Hyperbaric oxygen treatment improves contrast sensitivity (ability to see shades of grey) when administered to healthy volunteers. Even though patients with non-retinal eye disorders have experienced constriction of
retinal blood vessels following hyperbaric oxygen treatment, when there is a lack of oxygen supply to the retina narrowing of retinal blood vessels does not occur. (Undersea & Hyperbaric Medicine 21; 387-90, 1994)

History of hyperbaric oxygen treatment and retinitis pigmentosa

The medical literature reveals that hyperbaric oxygen treatment has been tried on cases of retinitis pigmentosa as early as 1965. (New England Journal of Medicine 281; 25-30, 1969) A 1987 report in the Journal of
French Ophthalmology indicates hyperbaric oxygen treatment improved the visual acuity of a patient with retinitis pigmentosa and macular edema. (Journal French Ophthalmology 10: 381-86, 1987)

Hyperbaric oxygen therapy and the optic nerve

Hyperbaric oxygen treatment has been used as a rescue remedy for optic nerve damage caused by radiation treatment for brain tumors. (Ophthalmology 93; 1083-88, 1986; Journal Clinical Neuro-ophthalmology
113; 98-101, 1993)

Hyperbaric oxygen improved vision among individuals who experienced a sudden loss of vision due to diminished blood supply to the optic nerve. Oxygen therapy must be administered early following onset of the event before shrinkage of the optic nerve occurs. (Arh Hig Rada Tokaikol 45; 19-24, 1994)

Multiple sclerosis patients undergoing 20 hyperbaric oxygen treatments experienced temporary improvement of their symptoms including visual symptoms. (New England Journal Medicine 308; 181-86, 1983)

Recently 100 percent oxygen delivered at 2 times atmospheric pressure did not produce a significant improvement in visual acuity or peripheral vision among patients suffering from a condition known as non-arterial anterior ischemic optic neuropathy. (American Journal Ophthalmology 122; 535-41, 1996)

Hyperbaric oxygen therapy and glaucoma

Among glaucoma patients, hyperbaric oxygen has been shown to expand peripheral vision, an effect which lasted for 3 months. (Acta Ophthalmologica 71; 315-19, 1993)

The fluid pressure in the eye of humans and animals decreases as atmospheric pressure is raised in a hyperbaric chamber. (Investigative Ophthalmology 19; 43-48, 1980)

K.K. Jain, author of Textbook of Hyperbaric Medicine, reports that hyperbaric oxygen has been used to successfully treat cases of glaucoma. Twenty or more 90-minute treatments at 2 atmospheres of pressure
expanded the visual field among all glaucoma subjects tested. There was no change in eye fluid pressure.

Hyperbaric oxygen therapy and retinal artery and vein occlusion

Hyperbaric oxygen treatment combined with a blood-vessel widening drug (vasodilator) has been shown to improve visual function among individuals experiencing retinal artery occlusion. (European Journal Ophthalmology 3; 89-94, 1993)

Hyperbaric oxygen treatment has been successfully used to improve vision among patients with retinal swelling (macular edema) and retinal vein occlusion. (Survey of Ophthalmology 39; 347-66, 1995)

Hyperbaric oxygen treatment has been administered successfully to patients with central retinal swelling (macular edema) resulting from retinal vein occlusion. Among 12 patients who were treated, 10 experienced visual improvement, with median visual acuity improving from 20/100 to 20/25. The hyperbaric oxygen treatment is believed to constrict retinal capillaries and thus decrease leakage of fluid that causes edema. (Ophthalmologica 210; 168-170, 1996)

Possible ocular side effects of hyperbaric oxygen therapy

It has been known that healthy persons can breathe oxygen at 3 times normal atmospheric pressure for 3 hours without any ocular side effects, but during the fourth hour some begin to experience a narrowing of their
visual field.

One reported side effect of hyperbaric oxygen treatment is the development of myopia (nearsightedness). (Journal Hyperbaric Medicine 1; 69-73, 1987) Myopia was first reported in 1978 among 18 of 26 patients undergoing hyperbaric oxygen treatment at 4 atmospheres of pressure. (Transactions American Ophthalmology Society 76; 118-24, 1976) Note: Italian doctors only used 2.2 atmospheres of pressure in their successful treatment of RP with hyperbaric oxygen.

Dogs exposed to 3 atmospheres of pressure at 100 percent oxygen developed retinal problems and a reduction in their electro-retinograms. Narrowing of the visual field and impairment of central vision has been
recorded among humans undergoing hyperbaric oxygen treatment at 3 atmospheres of pressure for more than 4 hours. (Science 151; 466-68, 1966)

Captain Frank K. Butler, Jr. of the U.S. Navy reviewed the ocular effects of hyperbaric oxygen treatment in a recent issue of Review of Ophthalmology. Hyperbaric oxygen may induce myopia (nearsightedness) at the rate of one quarter diopter change in eyeglass prescription per week among patients receiving daily hyperbaric oxygen treatment. The myopia reverses slowly over a course of many weeks. Cataracts have been reported to occur among patients undergoing a prolonged course of daily hyperbaric oxygen treatment which may not be reversible following cessation of treatment, particularly among adults of advanced age. (Survey of Ophthalmology 39; 347-66, 1995) K.K. Jain indicates cataracts may occur among patients undergoing hyperbaric oxygen treatment but that these were seldom observed when less than 200 treatments were administered.

K.K. Jain reports that the most useful role of hyperbaric oxygen in eye care is the relief of blood vessel constriction in central retinal artery occlusion with a success rate as high as 60 percent. Hyperbaric oxygen does not appear to have a useful role in the treatment of diabetic retinopathy. K.K. Jain states "With the pressure and duration of exposures used in clinical practice, ocular complications are not a problem... Hyperbaric oxygen appears to be a safe treatment from the ocular point of view." Confirming its safety, hyperbaric oxygen treatment has been applied in cases of multiple sclerosis with optic neuritis without loss of vision or narrowing of the visual field. Most of the studies reporting adverse effects from hyperbaric oxygen therapy administered oxygen at greater pressure than is clinically used in everyday practice. An extensive discussion on the use of hyperbaric oxygen for eye conditions is included in K.K. Jain's Textbook of
Hyperbaric Medicine, 2nd edition, 1996 Hogrefe & Huber Publishers, Seattle.

Non-ocular side effects of hyperbaric oxygen treatment include oxygen convulsions, sinus blockage, confinement anxiety and inability to equalize middle ear pressure, though these side effects are uncommon.

How to prepare for hyperbaric oxygen treatment

K.K. Jain, author of the Textbook of Hyperbaric Medicine, suggests the use of oral antioxidants during therapy to counter possible side effects such as cataracts in elderly subjects or transient myopia. Jain suggests the use of magnesium (250-400 mg.) and vitamin E (400 units) daily starting two days prior to hyperbaric oxygen treatment to prevent undesirable side effects. High doses of vitamin C may be counter-productive, particularly when consumed without other antioxidants.

Other useful oral antioxidants which may be consumed prior to and during hyperbaric oxygen treatment are alpha lipoic acid, vitamin B12, lutein, beta carotene, lycopene, selenium, bioflavonoids (bilberry) and coenzyme Q10. Iron should be avoided. Ultraviolet blue-violet blocking sun lenses should be worn outdoors following oxygen therapy.

Hyperbaric oxygen treatment has been shown to adversely affect the electroretinograms (ERGs) of rodents fed a diet deficient in vitamin E and selenium. But rodents fed vitamin E alone or vitamin E plus selenium showed no decreases in their ERGs after 15 weeks of hyperbaric oxygen treatment. (Free Radical Biology & Medicine 6; 505-12, 1989)

Now He's Blind?

Discover; 6/1/1999; SUSSMAN, SHARRON

What did Mr. Leonard's back have to do with his eyesight?

When Mr. Leonard was admitted to the hospital, he couldn't meet my eyes. He wasn't shy--he simply couldn't raise his head. His spine was curved so far forward that when he sat, all I could see of him was the top of his head.

Ankylosing spondylitis, the condition that had brought him to this state, sometimes leaves its victims unable to eat or speak normally. In these patients, the stiffly flexed spine pins the chin and lower jaw firmly against the breastbone. The condition, a kind of arthritis that primarily affects the spine and sacroiliac joints, starts insidiously in young adulthood, and the pain is usually mild. But when the wave of inflammation has passed, the joints stiffen permanently, and the ligaments calcify and turn to bone. The once flexible spine becomes, in effect, a single bone from skull to pelvis.

If the condition is diagnosed early, the patient can do exercises to keep the spine upright. Exercises can't keep the joints from stiffening, but they can keep the spine from curving forward severely.

Mr. Leonard's stoop hadn't been diagnosed until his mid-forties, when a sharp-eyed internist had spotted the strangely segmented "bamboo" spine typical of ankylosing spondylitis on a chest X-ray. Mr. Leonard's forward curve was fixed at about 40 degrees beyond the upper limit of normal. It was far too late to alter the deformity with exercises or even with bracing. Still, Mr. Leonard was doing well. He was married, worked as a draftsman, and hiked on weekends. Active treatment had not been necessary.

A rear-end collision a year ago had changed all that. The impact thrust his brittle spine forward, fracturing several vertebrae. Despite attempts to brace the fractures, the forward curve in his spine became much worse.

Now he was being admitted to the spine center at the University of Minnesota Hospital where I was doing my residency in orthopedic surgery. My professor, John Feingold, planned to cut into bone at the base of his neck. By removing a wedge of spinal bone, we could swing Mr. Leonard's neck and head into an upright position. To heal solidly, his spine would have to be held securely in this position for two or three months.

As chief resident, I had to examine Mr. Leonard and prepare him for his operation the next morning. I needed to apply the halo that would hold his head in place after the operation. This device, a metal ring encircling the head just above the eyebrows, is fastened to the skull with pins. The halo is attached to an upper-body brace, a "halo vest."

We washed his hair, and I selected, prepped, and numbed four spots on his scalp and screwed in the pins through holes in the halo. With good purchase in the bone, I used a torque screwdriver on each pin to ensure the correct pressure.

When Mr. Leonard was brought to the operating room the next day, he was seated at the operating table, his forehead and halo resting comfortably on pillows. His neck and upper back were prepped and draped for surgery. He was sedated but alert enough to tell us if we hit a nerve.

Feingold injected a local anesthetic in the skin along the midline of the base of the neck. With a single stroke of the scalpel, he opened an eight-inch incision. Then he injected local anesthetic into the periosteum, the soft tissue directly adjacent to the bone, and peeled it away. The junior resident and I held back skin and muscle layers as he carefully nipped away bone until the pale, tough, glistening sheath around the spinal cord could be seen.

Removing the wedge of bone, while simple in concept, was dangerous in execution. If the bone-cutting instrument strayed too close to the spinal cord, it might damage nerve tissue. There was also the risk of injuring arteries that run up to the brain.

The anesthesiologist checked monitors and fiddled with the IV lines, making sure that Mr. Leonard was drowsy but rousable. After about an hour of chipping and probing, Feingold decided that enough bone had been removed. "He'll need to be a bit deeper now, Jack," he told the anesthesiologist. "This is going to stimulate him."

He grasped the halo through the sterile drapes and firmly tipped Mr. Leonard's head upright. A slight cracking sound and a muffled murmur of protest were heard from under the drape. The surgeon carefully inspected the line where the bony defect he had created was now closed.

"How is he doing, Jack? Do a neuro check." The surgeon held the halo firmly while the anesthesiologist asked Mr. Leonard to move his hands and feet. We rapidly sewed up the incision, slapped a sterile dressing on the wound, and removed the drapes. The orthopedic technician then slipped a pink plastic vest over Mr. Leonard's shoulders and attached the halo to it with bars and clamps.

Mr. Leonard was awake and looking dazed. The circulating nurse slipped a hospital gown on him. Then, as we supported him, he stood up and walked slowly over to the gurney for his ride to the recovery room.

Shortly after six the next morning, we stood at his bed.

"How are you feeling this morning, sir?" Feingold asked.

We watched carefully as Mr. Leonard regarded his surgeon and cleared his throat. "Not too shabby," he said. "That's a fierce neck ache, but the pain shots help."

"Can you wiggle your toes for me?" Feingold asked. He briefly checked the patient's grip, foot and ankle movement, and sensation over face, neck, and limbs. All appeared to be in order; Mr. Leonard seemed to have emerged intact. Feingold told him he'd be away lecturing over the next few days but that "my associate"--meaning me--would watch over his recuperation.

After rounds the team dispersed--Feingold to the airport, and the junior resident, intern, and medical student to the orthopedic clinic. I remained at the nurses' station, leafing through charts. Suddenly Angela, one of the nurses, came up to me and put her hand on my shoulder. "Have you talked to Mr. Leonard?" she asked. "He says there's been something wrong with his eyes since surgery."

"Vision problem?" I repeated stupidly, prickles of dread rising along the back of my neck. "We were just in there."

Angela's calm voice grew even calmer. "He wasn't very clear about it, actually," she said. "Just that things look funny and they have since he was in the recovery room."

I was already halfway across the corridor, trying to think of what might be wrong. It didn't make sense--I had just watched him talking and making eye contact with Feingold. His eyes had moved in synchrony. His face was symmetrical; his speech was not slurred. I mentally ticked off evidence that the cranial nerves that controlled all these functions were intact, not stretched or injured by the dramatic repositioning of his neck.

Mr. Leonard was resting on his pillows, eyes closed. When I entered the room, he opened them and looked right at me. They looked normal, if a bit puzzled.

"Mr. Leonard, your nurse tells me you're having trouble seeing things," I began. "Can you tell me about it?"

"I can't really describe it, Doctor," he said.

"Is your vision blurred?" I asked.

"I don't think so," he said doubtfully. His forehead above the halo wrinkled unhappily.

"I think I'd better examine you," I told him. I needed to start somewhere, even though my ophthalmology skills were definitely rusty.

"Follow my finger with your eyes," I instructed, holding up an index finger to test the function of the muscles that moved the eyes and the nerves that controlled them.

"Your what?" he responded.

At that moment the hair on my scalp nearly stood on end. "I'll be right back," I said.

Less than an hour later, I had at least part of the answer. An ophthalmologist, a neurosurgeon, and a neuro-ophthalmologist rapidly answered my call and examined Mr. Leonard. The problem wasn't in his eyes. Instead, the part of the brain that processes input from the eyes had been injured, so everything "looked funny."

Mr. Leonard could see, but he couldn't understand or recognize what he was seeing. He had suffered a stroke in the visual cortex, which lies close to the base of the brain. The most likely culprit was a problem in the arteries that run through canals in the neck vertebrae to reach the back of the brain. But what happened? Had they kinked when we straightened Mr. Leonard's neck? Had a spike of bone squeezed an artery shut? Should we loosen his halo and flex his neck to relieve compression of the artery?

My consultants agreed that it was important to examine brain circulation. If there was a blockage, it needed to be cleared. After an urgent telephone call to the radiologist, we moved Mr. Leonard to the angiography suite.

His arteriogram, which traced blood flow in the brain, showed a normal pattern. The cut into the vertebra had changed the curve of his spine, but it had not distorted blood flow. There was no hint of lumpy plaques on the vessel walls, so a clot was unlikely. An artery had probably squeezed shut briefly, depriving brain tissue of oxygen and nutrients long enough to do damage. But how much damage? Was it permanent?

Dead neurons cannot be revived, but the injured neurons surrounding a patch of dead ones can sometimes recover. Increasing the supply of oxygen and nutrients, decreasing metabolism and its demands, suppressing inflammation with strong medications--all may have a role in the early treatment of brain injury. A trauma hospital across town had a hyperbaric chamber, which provides higher-than-atmospheric pressures and is typically used to treat decompression illness in divers. The chief of surgery there directed research projects testing its effectiveness for other conditions, including some types of stroke and brain injury. After conferring with him, our neurosurgeon recommended that we send Mr. Leonard over by ambulance and "dive" him on 100 percent oxygen.

Three hours after Mr. Leonard's second 60-minute hyperbaric oxygen treatment, he became less confused about what he was seeing. His vision rapidly returned to its previous level. When he was discharged a few days later, his vision was normal. He probably would have recovered anyway, as many patients with transient brain injuries do. Hyperbaric oxygen has not panned out as a standard treatment for this kind of problem.

Twelve weeks later, X-rays showed that Mr. Leonard's bone had healed nicely. Feingold said it was time to remove the halo. I rounded up a screwdriver and wrench and went to the exam room. Mr. Leonard looked straight at me as I entered. "It's nice to see you," he said, smiling.

I unscrewed the halo pins from his skull and taped dressings over the small wounds. That day he left wearing a plastic neck brace for added support, but within a few weeks his healed bone needed no further protection. Later, I heard Mr. Leonard had resumed all his former activities. His spine was now in a better position than before the accident. His ordeal, with all its risks, had been worth it.

Doctor on Call

Sharron Sussman is an orthopedic surgeon in Berkeley, California. She likes helping patients recover from injuries, she says, and "you get to use really neat instruments and tools." In this photo, taken last July, she is inserting a pin to stabilize a wrist fracture.

The cases described in Vital Signs are based on real patients. Some details have been changed to protect their privacy.

COPYRIGHT 1999 Discover

Eyesight to the blind. (hyperbaric therapy for radiation-induced optic neuropathy)

Medical Update; 4/1/1989


Vision loss resulting from a potent radiation treatment can now be prevented and even reversed, say ophthalmologists at the University of Florida (UF) Eye Center. The blinding disorder, known as "radiation-induced optic neuropathy," is a rare but recognized risk of radiation therapy for brain tumors.

The radiation, designed to shrink tumors inside the head targeted by external beams, occasionally damages blood vessels supplying the optic nerve that enables the brain to register visual impulses. The answer, says UF ophthalmologists Dr. John Guy, is to expose the blind patient to high-pressure oxygen in a hyperbaric chamber, a pressurized, submarine-like tank that made the entertainment news a few years ago when singer Michael Jackson began using one as a preventive measure against aging. Although most physicians consider this usage to be mere quackery, the machine itself is anything but useless, having proven its effectiveness against decompression sickness (occurring whenever scuba divers encounter "the bends"), carbon monoxide poisoning, anemia, and skin graft rejection, among other ailments.

Vision can start to fade, says Guy, either while a patient is still receiving therapy, or afterwards. In fact, he says, blindness may not develop for several months or even years after treatment has ceased. This is why, he says, "the earlier a patient's vision loss is diagnosed, the greater their chances are that hyperbaric therapy will help them." Although quite rare ("We treat about one patient a year at the University of Florida," Guy says), radiation-induced blindness can still be emotionally devastating to people already distraught from their battle against cancer.

Hyperbaric therapy, Guy says, "has been shown to reverse vision loss within two weeks of sight loss, as well as permanently stop the progression of the blinding disorder." Guy first began hyperbaric therapy in 1983 and has treated five patients since. Of that number, two experienced total restoration of vision and a third patient's vision loss was nipped in the bud before total blindness occurred. Saturating the patient's body with three atmospheres of oxygen pressure--the equivalent of being 60 feet below sea level--for two-and-a-half hours a day over a two-week period, Guy says, allows the blood to deliver the extra oxygen directly to the affected area. As a result, vision is either partially or completely restored.

Guy is a pioneer in this form of therapy: "There previously was no treatment for cancer patients who lost their vision as a result of radiation therapy," he says. "Although radiation therapy might cure their tumors, there was no hope to prevent blindness if they developed optic neuropathy after the treatment." Guy adds, "Although radiation-induced blindness is very uncommon, cancer patients having to undergo radiation therapy to the brain can feel more comfortable knowing there is a treatment available if the adverse effect occurs."

COPYRIGHT 1989 Benjamin Franklin Literary & Medical Society, Inc.

Rambam Hospital's hyperbaric chamber helps man regain use of eye

Jerusalem Post; 11/5/2001; JUDY SIEGEL

Headline: Rambam Hospital's hyperbaric chamber helps man regain use of eye
Edition; Daily
Section: News
Page: 04

Monday, November 5, 2001 -- A man who was blind in one eye regained his sight after unusual treatment in the hyperbaric chamber operated by Rambam Hospital's ophthalmology department.

A few days ago, the man, 54, who immigrated from Russia a decade ago, was unable to see with his left eye. He was diagnosed as having a blood clot that blocked the central artery of the retina.

Binyamin Miller, head of the department in the Haifa hospital, said such a blockage prevents the supply of blood to the retina and in most cases causes blindness. "Tests on monkeys a few years ago showed that if the retina is deprived of oxygen for 100 minutes, the blindness is irreversible," he said.

The usual treatment is to lower the pressure inside the eye and expand the blood vessels immediately. In some of these cases, sight returns partially. Rambam ophthalmologists are among the first in the world to start treating the problem by putting the patient into a hyperbaric chamber with high-pressure oxygen.

The chamber is also used to treat divers suffering from "the bends" and victims of carbon monoxide poisoning.

So far, 40 people with this problem have been treated by Rambam doctors using high-pressure oxygen, and most enjoyed improved, but not perfect, sight.

"This last case was unusual, as the patient suffered from complete blindness in one eye and regained his sight fully after treatment in the chamber," Miller said.

Keywords: Rambam Hospital. Optics. Medicine.

Copyright 2001 Jerusalem Post. All Rights Reserved

TESTIMONIALS:  Following are testimonials from emails and from forums or support groups of parents talking about the results they are getting from HBOT.  The email addresses are removed to protect their privacy but you may see an occasional link to a child's web page which they do not mind sharing with you.  

Sent: Tuesday, October 12, 2004 4:45 AM
   Subject: [Corticalvisionimpairments] Amazing update for Zachary.....

   Hey guys! Just an update from us in Charleston!!  I am so excited to share this
news with everyone that I can not contain myself!  Today was session 11 of HBOT and
you will not believe my amazing son!!! He is smiling and laughing!!!  He smiled and
laughed at his nana and mamaw through the entire session.  He has never smiled in his
14 months of life and guess what, during session 4 of HBOT, he grinned!  This is such
a HUGE answer to prayers. I have dreamed of seeing him smiling since before he was
born. Praise the Lord for this amazing accomplishment for my little man!!! He is so
beautiful smiling with those bright eyes!

   Daddy got here tonight and was so excited to see the pictures. I was so excited
to show him that I had to carry the digital camera to the gate so that he could see
them immediately. LOL.  When he got home, Zachary grinned at him and he saw him
smiling big after that. WOW!!

   We are all getting more sleep and into a better routine. A couple of other
changes I have seen in Zachary is his face does not seem as swollen, he is opening
his mouth for his pacifier and food bites, he is going to bed MUCH better at night
and sleeping alot more peaceful, and he eye sight seems to have improved tons. He is
tracking his mobile and will look to a person when being spoken to.

   He has not had any seizures all weekend or today. Although he is having a few of
the infantile spasms, they are just that, a few. We will sort that out when we get
back home and get an appt with the neurologist and EEG clinic.

   I am attaching a few pictures of the smiley boy. I apologize that they are
blurry. Nana was so excited that she snapped the camera so fast that it did not have
time to focus!!  The one picture is of him laughing, you can see all of his teeth!
Thank you so much for you prayers and thoughts for us!! This is just SOOO amazing and
I wish we had done this sooner for our son!!!

   (p.s. for those other parents considering this for your child, PLEASE do it!!!)

   Cam, Nikki and the amazing Zachary

We did HBOT with Zachary at 14 months old. He was able to trach toys again
and seemed to not have CVI at all. However, he did lose his vision again but
I truely believe that was due to the infantile spasms and seizures. We are
finally seizure free and hopefully, can try some more for him. He had
infantile spasms for one year. It is very pricey but also very worth it.
Zachary also began smiling nad laughing with HBOT.
Yes I would recomend HBOT to any parent with a child who has CVI. 
Cayden is 13 months old she did her first 40 sessions of HBOT at 8
months old and her 2nd 40 sessions 2 months later at 9 months...she is
currently doing another round of HBOT but this time we are doing 1 per
day instead of 2 so we are taking 8 weeks to complete this round of date she has had 92 sessions of HBOT.....before begining HBOT
Cayden could only see light...she now looks at thing(she is not yet
tracking objects but I am sure she will be able to do that)...she is
looking at objects and she looks towards people when they walk by
her...she has looked at her hands several times....there is a journal
of Caydens HBO progress on her website
There are also some pics of her....though I need to update it with
pics of her in her little room and using her light box.

Good luck to you with your decission.  But YES I would definently do
Hi. My name is Diana and my daughter is Abigail (3 yrs). We did 50
treatments of HBOT total in 2004 and the biggest improvement I saw
was also with her vision. Her eyes all but stopped crossing and she
seemed to focus much better on things. It's good to hear you had
the same results. We are planning on another 50 hopefully this
My son Jeromy also had infantile spasms, resolved around 15 months.  He also has spastic quad CP, G-tube, and CVI, but his epilepsy is now controlled and he has been seizure free for almost 2 years (yay!).  When he was having the IS, his vision was pretty poor, but it has improved significantly with seizure control.  I think it improved further when we did 40 HBOT treatments last summer.  Jeromy is now 3, and still has CVI, but he tracks objects, recognizes faces, looks to locate the source of a sound, and smiles when I smile at him even if I make no noise.  Our biggest problem right now is distance vision (questionable) and visual attention; he can't focus on one thing for very long.  But we are a LONG way from where we were, so I'd say don't give up hope that Ryan will see better in the future.
My son Jason did 23 sessions of HBOT Nov-Dec 2004. He had a brain bleed at 5 weeks (lost 90% of his brain), hydro (resolved), Infantile Spasms (resolved w/Vigabatrin), LGS (myoclonics and abscence, controlled with Depakene and Keppra), and has spastic quad CP. He will be 2 on Feb 1, and cannot hold his head up, roll over etc. He is a happy little guy, very responsive and full of smiles. His visual dx is cortically blind. His last opthamologist and functional vision assessment done in Sep 2004 re-confirmed this dx.

Prior to HBOT, his eyes were constantly roaming and twitching (nystgmus). Sometimes they would respond to light, at other times not, and his pupils were always small.

About 2 weeks into HBOT, we noticed his eyes weren't roaming as much, and his pupils seemed bigger. About two weeks after HBOT, we started to get consistent visual responses and occaisional tracking.
If I hold a bright toy to the left of his face (Jason always positions his head to the right) and say "Jason, look", he now turns his head and his eyes fix on the toy and he smiles. This is new and very exciting! I occaisionally see him tracking me as I walk past him - at first I didn't think anything of it, just coincidental eye roaming, but now I believe he is tracking me at times.

He has a long way to go vision-wise, but this is the first time since his bleed that we've seen any consistent visual function.

Aside from the vision, I would say he has slightly improved in motor function as well, and the host of many that work with him all feel there has been changes for the better in general. In addition, his reflux which has always been a pain, seems to be gone. We haven't discontinued his Zantac yet, but once we run out of the current vat
we'll see how he does without it.

All due to HBOT? I can't say 100% for sure, but since we've been doing everything we can for his vision for what seems like forever with no results, I think it has helped him significantly.

We are ecstatic as vision is so important in development, so we hope that his improvements will continue and it will start to transfer into cognitive and motor skills. Jason is currently rated at 6-9 months cognitively, physically he's very delayed due to the CP, but he can hold and mouth a toy, kicks both legs wildly, and will use both hands (spastically though) when in his "Little Room".

All in all, we will definately be doing HBOT again, probably in the spring.

Take care everyone,
Sharon, mom to Jason, soon to be 2
I have been reading the posts for a while, and am finally getting around to our introduction! My son Jeromy is 3, he is a twin born at 33 weeks. He had a Grade IV interventricular hemmorrage shortly after birth, infantile
spasms at 5 months, now has spastic quad CP, G-tube, CVI, and epilepsy. He has been seizure free since May '03 on one seizure med, Felbatol. When he had the IS his vision was pretty poor; he would look at lights and things that were yellow, but didn't track or focus well. Now, after seizure control and 40 sessions of HBOT his vision is much improved. Jeromy can focus on and recognize faces, he tracks well horizontally and okay
vertically, he will look at an object / person if we ask him to more than 50% of the time.
Hi, my name is Meghan and I have 3-year old twin boys. One is developing normally, but Jeromy has severe spastic quad CP, G-tube, CVI, and epilepsy (although he has not had a seizure for about 18 months (yeah!)). Jeromy cannot sit, stand, roll, talk or eat. He is very social, and seems to understand some things we say, but his cognitive level is unknown.

In terms of his vision, he is certainly not blind. He does track horizontally and some vertically, watches and recognizes faces, and attempts to play with objects he sees. However, his vision is inconsistant, and with his motor limitations we are struggling to find a way for him to communicate. Right now we are introducing
Boardmaker pictures, and trying to teach more/all done and yes/no. We have to rely on eye gaze at this point, because his motor control is so unreliable. Of course his vision isn't reliable either, but we have to try something!

We have seen improvement in his vision in the past two years-first, when we achieved seizure control, and second, after doing 40 sessions of HBOT. I'm hoping it will continue to improve.
We are currently on our 3rd round of 40 treatments...we did 40 in February another 40 in April now we are doing another 40(but this time we are only doing once a day instead of twice/day)

If you check out Cayden's website you can see a journal which has the things I noticed since begining HBO....
Before starting HBO Cayden could not put her hands in her mouth, she just could not coordinate that....she first put her hands in her  mouth during her second week of the end of that week she also (while sleeping in my arms) put her hands together, she was holding one fist with the other hand.....after during the 3rd week of HBO I noticed she was awake alot more often, only napping during treatments, so 1 hour naps twice a day....this is from a child who 3 weeks prior to that was sleeping 3 hours at a time waking to
breastfeed then back to sleep....or crying....that is another thing that we noticed, she is not as fussy, she used to (prior to HBO) cry all the time, we could NEVER put her down on the floor or she would scream and not stop crying until picked up and even picking her up many times did not work...and if she was in a position and she was not crying we did not dare move her or she would start screaming crying again...since doing HBO she is so much less fussy and we can change her positions with out her screaming crying about it....also
during her first round of HBO....she laughs and is just better natured than before her first round of HBO....she smiles much more often.....the 3rd or 4th week it seemed she was trying to use her sight...but I was never really sure if I was imagining it or if she was really looking towards things.....she would look towards things
and then look away....she continued looking towards objects and then looking away even after her first round was over(during our break in March).....during her second round of HBO I noticed more improvement in her sight as she continued looking at objects for a few seconds and then turning away....she is not yet really tracking but I have noticed a big improvement in her vision...she actually looks towards  things and she has tracked her rattle from midline to the left not all the way to the left but maybe about halfway....she has done this a few times and it is very exciting but of course it is hard to get her to do it again when we "want" her    She uses her arms more...she will hold herself up for a few seconds while on her tummy on the floor, if we put her hands under her....she can grasp a toy now and put it in her mouth(we have worked alot at this)....she does not grab for the toy but once put in her hand she can hold on to it...though she does drop it

Check out her website you can see some pics of her and the weekly journal with her progress....
Hi all!
We just had another eye doctor appt yesterday to check my sons  progress with hyperbaric treatments.  Here are the changes we have  seen:  (4/05/05 is just prior to starting hyperbaric treatments.  We 
started the first Monday of May.)
OD+4.75  +4.25
OD +2.75
OD +2.5
OD +2.25  +1.75
Visual Acuity w/out glasses
20/60  20/50
20/60  20/50
20/50   20/50
The 2 readings under visual acuity account for 2 eyes (one for each  reading).  Our eye doctor is so amazed that she is going to go meet  with the hyperbaric doctors we see.  :)
Hope that helps some.  Let me know if you have any questions.  Again,  I keep all of this updated here:

Join the
by Going to their
to see testimonials from parents of children with CVI