Prozac & Vision Problems in DS

DS symptoms include a myriad of vision issues: strabismus, nygastimus, esotropia, refraction errors. Jett had nystagmus (really bad ocular flutter--like that guy in the movie The Crying Game). He was cured through TCM: accupressure, herbal teas etc. Western medicine says it's incurable.

On Prozac, I didn't see a sudden difference in Jett except that his crossing eyes had slowly cleared up, which I did attribute to Prozac, but had forgotten just how bad his eyes were. I had taken it for granted. But, once I took Jett off Prozac for 2 weeks, I saw just how much Prozac was helping him.

Off Prozac his eyes were crossing so much that he had to turn his head all over the place to try to see better. At times, his eyes were as bad as a googly-eyed doll! His left eye went inward a lot and the right eye... I'm not quite sure.

Perhaps because of the vision issues, I couldn't leave him to play independently anymore because he would find a sock or some string to wave in front of his face and go, "Eeeeeeeeeeeeee," until I redirected him. This may be because he was trying to self stimulate his vision in order to try to correct. (See post Some TV is Good for Our Kids!) This stimming behavior would happen within five minutes of setting him on the floor to play.

His vision is much too important for me to mess with.... Back on Prozac for only 3 days, he can play independently again because the stimming is gone and his eyes are much better--not completely gone, but hopefully will clear up again sooner than later.

These eye issues can lead to amblyopia. Amblyopia is where the brain turns off the vision to one eye and depth perception is lost.

Many individuals with DS have to do the "Step-step" on stairs rather than alternating feet on the steps. You need depth perception. Jett's been crawling on the stairs great since his eyes were fixed--we just took down his stairs to have our sofa back for company (his stairs were made out of sofa cushions), but I can't imagine him trying to walk them with poor vision!

It is hard to learn, have coordination, alternate you feet on the steps, if you can not see.

Can you imagine trying to read with the vision issues our kids have?

The following study abstract detail the severity of the vision problems.

GOAL: Improved vision to improve learning.

Wikipedia: Amblyopia is a developmental problem in the brain, not an organic problem in the eye (although organic problems can give rise to amblyopia which continue to exist after the organic problem has resolved).^[4] The part of the brain receiving images from the affected eye is not stimulated properly and develops abnormally

Amblyopia and visual acuity in children with Down's syndrome.

Tsiaras WG, Pueschel S, Keller C, Curran R, Giesswein S.

Department of Ophthalmology, Rhode Island Hospital/Brown University School of Medicine, Providence, RI 02903, USA.Abstract

BACKGROUND/AIMS: Amblyopia in people with Down's syndrome has not been well investigated. This study was designed to determine the prevalence and associated conditions of amblyopia in a group of home reared children with Down's syndrome.

METHODS: All children in the study group underwent an evaluation of visual acuity. In addition, previous ophthalmological records were reviewed, and a subgroup of children was examined. For the purposes of this study, amblyopia was defined quantitatively as a difference of two Snellen acuity lines between eyes or if unilateral central steady maintained (CSM) vision and a clear fixation preference was observed. A high refractive error was defined as a spherical equivalent more than 3 dioptres and astigmatism more than 1.75 dioptres. Anisometropia was defined as a difference of at least 1.5 dioptres of sphere and/or 1.0 dioptre of cylinder between eyes. 68 children with Down's syndrome between the ages of 5 and 19 years were enrolled in the final study group.

RESULTS: Amblyopia was observed in 15 (22%) of 68 patients. An additional 16 (24%) patients had bilateral vision less than 20/50. Strabismus, high refractive errors, and anisometropia were the conditions most commonly associated with decreased vision and amblyopia

CONCLUSION: This study suggests that the prevalence of amblyopia is higher than previously reported. Fully 46% of these children with Down's syndrome had evidence of substantial visual deficits. These patients may be at higher risk for visual impairment and should be carefully examined for ophthalmological problems.

Visual acuity and accommodation in infants and young children with Down's syndrome.

by J M Woodhouse, V H Pakeman, K J Saunders, M Parker, W I Fraser, S Lobo, P Sastry

Accommodation and visual acuity were measured in 53 children with Down's syndrome aged between 12 weeks and 57 months. Results were compared with data for 136 control (typically developing) children aged between 4 weeks and 48 months. Whereas the control children accommodated accurately on near targets, accommodation was defective in 92% of the children with Down's syndrome, and there was no change in accommodative ability with age. On the other hand, visual acuity lay within normal limits for the younger children. Children over the age of 2 years showed a below-normal visual acuity, which is not explained either by refractive error or by the effect of poor accommodation. The data suggest a sudden change in the rate of development of visual acuity which may be associated with physiological changes in the visual cortex. Previously reported defects of accommodation and visual acuity in older children and adults with Down's syndrome are confirmed by our findings in infants and young children.

Visual acuity in infants and children with Down syndrome.

by M L Courage, R J Adams, S Reyno, P G Kwa

The authors used the Teller acuity cards to assess the visual acuity of 51 infants and children with Down syndrome aged between two months and 18 years. The success rate and test times were comparable to those reported for normally developing children. Even those DS subjects in the study who were free of ocular disorders and/or who were wearing optical correction during testing showed significantly poorer visual acuity than individuals without Down syndrome. The development of visual acuity in infants and children with Down syndrome lags behind that of age-matched peers without Down syndrome, especially after the age of six months. These findings are discussed in terms of the neurological and optical factors that might account for the deficits in visual acuity that were observed

Is the selective serotonin reuptake inhibitor fluoxetine (Prozac) a fountain of youth?

Elizabeth M Quinlan​‌

Evaluation of: Maya Vetencourt JF, Sale A, Viegi A et al.: The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science 320, 385–288 (2008). The potential for synaptic strength to be regulated by experience is high early in postnatal life, and declines thereafter. The constraint of synaptic plasticity in the adult visual system is thought to underlie the resistance to therapy for the treatment of amblyopia. However, a recent report by Maya Vetencourt et al. demonstrates that systemic administration of the popular antidepressant fluoxetine reactivates synaptic plasticity in the visual system of adult rats, and enables the recovery of function in an eye chronically deprived of vision. Fluoxetine administration stimulated a decrease in basal levels of extracellular GABA, an increase in the level of BDNF and the return of long-term potentiation in slices of visual cortex. The ability to reactivate robust synaptic plasticity in the adult mammalian visual system has clear therapeutic potential for the treatment of amblyopia in adults.

The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex

1. José Fernando Maya Vetencourt1,*, Alessandro Sale1,Alessandro Viegi1,
2. Laura Baroncelli1, Roberto De Pasquale1, Olivia F. O'Leary3, Eero Castrén3 and Lamberto Maffei1,2² Institute of Neuroscience, Consiglio Nazionale delle Recerche, Via Moruzzi 1, I-56100 Pisa, Italy.
3. ³ Neuroscience Centre, University of Helsinki, 00014 Helsinki, Finland.
4. * To whom correspondence should be addressed. E-mail: jf.maya@in.cnr.it

Abstract

We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.

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Improve Your Child's Vision

According to Donald J. Getz, O.D., up to 75 to 80 percent of what a child learns is through what he sees. Since our children with Down syndrome often have vision problems such as poor eye tracking, central vision or visual perceptual issues -- it needs to be fixed this so that our children's ability to receive information is maximized! Fortunately, there are many fun and easy games you can play to improve your child's vision while increasing his chances to learn.

Since eyes are controlled by muscles, they must be exercised like any other muscle to perform and function at optimal levels. Eye tracking exercises not only flex those muscles, but can also improve eyesight by helping the eye maintain proper focus, which is the capability of tracking objects between near and far points and in everyday tasks.

If your child is over four months old and sometimes crosses his eyes or has a lazy eye, (when one eye turns inward or outward during tracking,) you may want to consider eye exercises. If his eyes aren't addressed, this not only limits visual input needed for learning but it can also effect hand-eye coordination needed for learning how to write or participate in sports.

Jett's poor central vision was the first thing we addressed and conquered. (If your child looks at you from the "top" of his eyes or tilts his head a lot when watching TV or in pictures, that's a tip off that the central vision is poor.) And he has an inward turning eye that we've been working on for quite some time. His Neurodevelopmentalist, Kay Ness, has given us very helpful exercises tailored to his needs. I haven't shared them all here since they are specific to his issues, but have included these exercises that help with tracking. We are seeing improvement. The more I work on it, the more it helps. I feel it's an issue I should have focused more on earlier. You know how it is, there are so many issues, it's difficult to know what to prioritize!

While Jett's Developmental Vision Ophthalmologist (DVO) gave us some great eye exercises to do, she also gave us a prescription for glasses. But we aren't getting them at this young age (2 1/2). Kay assures us that the visual system is very plastic and changeable. Giving your child appropriate stimulation opportunities for normal function is a better choice over resorting to artificial means of vision enhancement. It is best to try to achieve normal vision and convergence (the ability of the eyes to work together) before looking to artificial means of glasses or surgical intervention. By treating the root cause of the problems rather than treating the symptoms, sensory dysfunction can be improved and often resolved with appropriate stimulation.

After only two months of vision therapy, Jett's depth perception has already improved. He can see objects in space much better and has an easier time going down the stairs and walking through doorways where there are floor changes. Jett's DVO was very pleased with his progress.

Have fun with these exercises that address eye tracking skills! Jett loves all his therapy.

Activities for visual stimulation

Watch the Airplane!

This exercise works great with children and infants when you use something exciting to look at like a toy that lights up or moves. I use a small toy airplane that lights up on top of a tube (that was originally filled with candy) which my mother bought from Walgreens for $5 

Have them stand or sit comfortably and then take the toy and place it near, but not on, the tip of their nose. Then gradually move the object away from their nose until you're about arms length from their nose. Try to get them to keep focusing on the toy the entire time.  

Next, bring the toy back toward their nose. By repeating this exercise about 20 times, you can exercise the eye to maintain focus and improve tracking ability.  

Follow the Light!

Using a flashlight, stand in a dark room with your child. This game is fun and will also help the eyes track in varying degrees of darkness. The point of this type of exercise is to help the eyes follow and track moving objects. For example, you can slowly move the flashlight beam around the room or focus on various objects. 
Go up, down, left, right and diagonally. Your child will then take his flashlight and follow your flashlight as it moves around the room. 

Look out for the Ball!

Another great way to exercise the eyes and improve tracking speed is to hang a tennis or ping-pong ball from a string tacked to the ceiling. Hold the ball and pull it away from your child. Watching the ball, your child to track its movement and get out of the way without moving his feet. This exercise helps increase the speed at which their eyes can track objects and offers additional benefits for speed and coordination as well.

Air Writing! 

Move a brightly colored object slowly across your child's visual field, approximately 12 inches from the face. Make an "H" in the air to see if he can move his eyes up and down and left and right. Make an "X" in the air to see if he can track diagonally. Be sure to go in each direction and watch the eyes.

Bat the Ball! 

Suspend a beach ball from the ceiling or door frame with a strong string or rope. Have your child bat it back and forth and left and right while watching the ball. Try the same with a balloon.

Alphabet Antics! 

Write the letters of the alphabet in a random pattern on a large poster board with a bright marker. Have your child use a pointer (broom handle or yard stick) to touch letters to spell words or go in alphabetical order.

Skewer the Beads! 

Give your child 10 brightly colored beads in a small bowl. Hold a wooden skewer with ends dulled and move it slowly around while your child tries to locate it with his eyes and put a bead on the skewer.

Find it! 

Practice mazes, word finds and hidden pictures to improve visual perceptual skills. 

Caution 

If your child has balance or equilibrium issues, make sure that he is in a secure seated position when doing these exericses. People prone to seizures should use caution and consult a physician before starting an eye exercise program. These exercises are not intended to be a substitute for professional services such as vision therapy or occupational therapy. 

More exercises

This website has fun online eye exercises for children old enough to follow simple directions: eyecanlearn.com

Supplements for Eye Health

Zeaxanthin  Jett takes 4mg twice a day.
Vitamin C  Jett takes this, in large doses, three times a day.
Bilberry an herb that supports eye health. Jett doesn't take this at the moment.
Vitamin A Jett takes a dose that is larger than the daily recommendation.
Lutein is another supplement that's good for the eyes but it's not good for the DS population. When Jett took it, (for only 3 days) he was very whiney and crabby and acted very uncomfortable. 

Sources

Eye-tracking-in-children

Eye exercises for tracking problems perception

http://www.preventive-health-guide.com/lutein.html

http://www.livestrong.com/article/299038-eye-tracking-in-children/#ixzz1IkQ5cGX1, 

http://www.livestrong.com/article/29304-eye-tracking-exercise/#ixzz1IkPUatue

http://www.livestrong.com/article/267040-eye-exercises-for-tracking-problems-perception/#ixzz1IkQjxyuh

Optometrists Network: Vision and Reading

"Pediatrics"; Joint Statement: Learning Disabilities, Dyslexia and Vision; American Academy of Pediatrics, et al; July 2009

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Prozac Cures Lazy Eye!

Scroll to bolded text.

By Jonah Lehrer
July 6, 2008

PROZAC IS ONE of the most successful drugs of all time. Since its introduction as an antidepressant more than 20 years ago, Prozac has been prescribed to more than 54 million people around the world, and prevented untold amounts of suffering.
But the success of Prozac hasn't simply transformed the treatment of depression: it has also transformed the science of depression. For decades, researchers struggled to identify the underlying cause of depression, and patients were forced to endure a series of ineffective treatments. But then came Prozac. Like many other antidepressants, Prozac increases the brain's supply of serotonin, a neurotransmitter. The drug's effectiveness inspired an elegant theory, known as the chemical hypothesis: Sadness is simply a lack of chemical happiness. The little blue pills cheer us up because they give the brain what it has been missing.

There's only one problem with this theory of depression: it's almost certainly wrong, or at the very least woefully incomplete. Experiments have since shown that lowering people's serotonin levels does not make them depressed, nor does it worsen their symptoms if they are already depressed.

In recent years, scientists have developed a novel theory of what falters in the depressed brain. Instead of seeing the disease as the result of a chemical imbalance, these researchers argue that the brain's cells are shrinking and dying. This theory has gained momentum in the past few months, with the publication of several high profile scientific papers. The effectiveness of Prozac, these scientists say, has little to do with the amount of serotonin in the brain. Rather, the drug works because it helps heal our neurons, allowing them to grow and thrive again.

In this sense, Prozac is simply a bottled version of other activities that have a similar effect, such as physical exercise. They aren't happy pills, but healing pills.

These discoveries are causing scientists to fundamentally reimagine depression. While the mental illness is often defined in terms of its emotional symptoms - this led a generation of researchers to search for the chemicals, like serotonin, that might trigger such distorted moods - researchers are now focusing on more systematic changes in the depressed brain.

"The best way to think about depression is as a mild neurodegenerative disorder," says Ronald Duman, a professor of psychiatry and pharmacology at Yale. "Your brain cells atrophy, just like in other diseases [such as Alzheimer's and Parkinson's]. The only difference with depression is that it's reversible. The brain can recover."

Given the prevalence of depression - more than 16 percent of people will suffer from a major depressive episode at some point in their lives - a more accurate scientific understanding of the disease is of immense value. In fact, this research is already being used to develop more effective treatments for the mental illness, some of which are currently in clinical trials.

The progress exemplifies an important feature of modern medicine, which is the transition from a symptom-based understanding of a disease - depression is an illness of unrelenting sadness - to a more detailed biological understanding, in which the disease is categorized and treated based on its specific anatomical underpinnings.

In the 19th century, the "fever" was a common medical illness. Of course, doctors now realize that a fever is merely a common symptom of many different diseases, from the flu to leukemia.
Likewise, when Richard Nixon declared a "War on Cancer" in 1971, scientists largely defined cancer in terms of its most tangible characteristic: uncontrolled growth leading to a tumor. As a result, every cancer was treated with the same blunt tools. Over time, of course, scientists have discovered that cancer is not a single disease with a single biological cause. Breast cancer, for instance, can be triggered by a wide variety of genes and environmental risk factors. Because doctors can look beyond the superficial similarities of the symptoms - all tumors are not created equal - they are able to tailor their treatments to the specific disease.

Neuroscience is only beginning to catch up. Thanks to a variety of new experimental tools, such as brain scanners and DNA microarrays, researchers are now refining their understanding of mental illness. In many instances, this means recategorizing disorders, (like DS as a neurobiological disorder) so that patients are no longer diagnosed solely in terms of their most obvious symptoms.
"We used to think there was only one kind of anemia," says Arturas Petronis, a scientist at the University of Toronto who investigates the underlying causes of schizophrenia. "But now we know there are at least 15 different kinds. We'll likely learn the same thing about many mental illnesses."
. . .
One of the first cracks in the chemical hypothesis of depression came from a phenomenon known as the "Prozac lag." Antidepressants increase the amount of serotonin in the brain within hours, but the beneficial effects are not usually felt for weeks.

This led neuroscientists to wonder if something besides serotonin might be responsible. Duman, for instance, began to study a class of proteins known as trophic factors, which help neurons grow and survive. Trophe is Greek for nourishment; what sunlight and water do for trees, trophic factors do for brain cells. Numerous studies had shown that chronic stress damages the brain by suppressing the release of trophic factors. In a series of influential papers published earlier this decade, Duman demonstrated that the same destructive hallmark is seen in depression, so that our neurons are deprived of what they need.

"The mental illness occurs when these stress mechanisms in the brain spiral out of control," he says.

Once that happens, the brain begins to shut itself down, suppressing all but the most essential upkeep. Not only do neurons stop growing, but the brain seems to stop creating new cells. A 2003 study, led by Columbia University neuroscientist Rene Hen, found that when the birth of new brain cells was blocked with low doses of radiation in "depressed" rats, antidepressants stopped working.

A recent study by Italian researchers, published in the journal Science, helps to reveal another mechanism by which antidepressants reverse the damage of depression. The scientists were interested in seeing if fluoxetine, the active ingredient of Prozac, could increase the potential of brain cells in the adult rat. They studied animals with severe cases of "lazy eye," a condition characterized by poor vision in one eye due to underdevelopment of the visual cortex. The scientists showed that fluoxetine gave brain cells the ability to take on new roles and form new connections, which erased the symptoms of the disorder. (Jett had nystagmus, which is an eye flutter and occasional eye crossing. Although western medicine says that nystagmus is incurable, his nystagmus is gone [maybe from acupressure and Traditional Chinese Medicine?]. He also had occasional eye crossing which rarely occurs now on Prozac.)

"The drug appears to make brain cells quite young," says Jose Vettencourt, a lead author. The scientists are currently repeating the experiment with humans, raising the possibility that fluoxetine will soon be used to treat lazy eye and related conditions.

"Even five years ago, this would have seemed like a very strange idea," Vettencourt says.
Duman's lab has demonstrated, in a paper published earlier this year, that physical exercise seems to stimulate the same regenerative pathways. Mice given access to running wheels not only showed reduced anxiety and stress, but also increased levels of the same trophic factors activated by antidepressants. When the activity of these trophic factors was blocked, the benefits of exercise disappeared. The mice stayed stressed, even when they were allowed to run on their wheel.

It is jarring to think of depression in terms of atrophied brain cells, rather than an altered emotional state. It is called "depression," after all. Yet these scientists argue that the name conceals the fundamental nature of the illness, in which the building blocks of the brain - neurons - start to crumble. This leads, over time, to the shrinking of certain brain structures, like the hippocampus, which the brain needs to function normally.

In fact, many scientists are now paying increased attention to the frequently neglected symptoms of people suffering from depression, which include problems with learning and memory and sensory deficits for smell and taste. (Common problems in autism and DS. Young autistic children are often treated with SSRI's to reestablish these pathways). Other researchers are studying the ways in which depression interferes with basic bodily processes, such as sleeping, sex drive, and weight control. Like the paralyzing sadness, which remains the most obvious manifestation of the mental illness, these symptoms are also byproducts of a brain that's literally withering away.
"Depression is caused by problems with the most fundamental thing the brain does, which is process information," says Eero Castren, a neuroscientist at the University of Helsinki. "It's much more than just an inability to experience pleasure."

This new scientific understanding of depression also offers a new way to think about the role of drugs in recovery. While antidepressants help brain cells recover their vigor and form new connections, Castren says that patients must still work to cement these connections in place, perhaps with therapy. He compares antidepressants with anabolic steroids, which increase muscle mass only when subjects also go to the gym.
"If you just sit on your couch, then steroids aren't going to be very effective," he says. "Antidepressants are the same way: if you want the drug to work for you, then you have to work for the drug."
Jonah Lehrer is an editor at large at Seed magazine and the author of "Proust Was a Neuroscientist." He is a regular contributor to Ideas.
© Copyright 2008 Globe Newspaper Company.

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