A recent study has changed my thinking about ADHD, and I hope it changes the way that all children with ADHD are evaluated and treated. And that parents are treated. Parents deserve better understanding and support than they traditionally get. Dr. Andrea Chronis and her team at the University of Maryland make a compelling argument that whenever children have ADHD, getting help for their parents should be thoughtfully undertaken.

ADHD tends to run in families. In the Maryland ADHD Program study of 214 children, the parents of children with ADHD were 24 times more likely to have ADHD themselves than were parents of children without ADHD. These results were published in the December 2003 Journal of the American Academy of Child and Adolescent Psychiatry. As is often the case, many kids in the study also had Oppositional Defiant Disorder (ODD) or Conduct Disorder (CD) in addition to their ADHD. Their parents had higher rates of depression and other psychological problems, including alcohol and other types of substance abuse.

Is this genetic? Or might it result from the increased stress of dealing with ADHD? Both are probably true to some extent. Significantly, all treatments for ADHD tend to be less effective when the parents have their own psychological issues. It makes sense that parent with ADHD might be less able to make needed environmental changes. Even medications, however, are less effective when the parents. problems are untreated. This has important implications.

Whether or not parents have symptoms of their own, they are likely to be under great stress. Dealing with a child with ADHD can be exhausting, frustrating, and embarrassing (as well as creative, energizing, and delightful). Listening to parents and offering practical support should start at the beginning of an ADHD evaluation and continue through the course of treatment. The treatment plan should be developed with this in mind.

‘Medications alone are not sufficient to treat ADHD,’ Dr. Chronis emphasized when we spoke about her study. ‘We need to look beyond the child to recognize and treat the parents’ issues,’ for their own sakes and for the sakes of the children. Dr. Chronis is the director of the Maryland ADHD Program.

When treating obesity in children, I know that success is most likely if the whole family eats healthier and spends more time being active . even if only one child is obese. It makes deep sense to me that family changes would also have the greatest impact in ADHD, even if parents don.t have psychological issues. If parents do have ADHD or are depressed, it makes sense that success in the children would be extremely difficult without helping everyone.

I hope I never look at a child with ADHD in isolation again.

Related concepts:

Hearing loss, Conductive hearing loss, Sensorineural hearing loss

Introduction to deafness:

In that first golden moment when you gazed at your baby in the delivery room, he was already beginning an amazing journey of learning. And how do children learn? They take in the world by using their five senses. The sight of your face, the feel of your touch, the taste of your milk, the scent of your unique aroma, and the sound of your voice combine to teach your child about the world.
Some children enter the world in silence.
We now know that hearing loss can significantly impair the ability to learn — not just learning to speak but also to walk, to read, to write, to do well in school and to get along well with others.
The sooner hearing loss is detected and addressed; the better children will do overall.

What is deafness?

In a healthy ear, sound waves enter the ear canal and vibrate the eardrum at the end of the canal. The eardrum transmits the sound waves across the three tiny bones of the middle ear into the inner ear, where the information is converted to electrical impulses that travel along nerves to the brain, allowing us to hear.
There are two main types of hearing loss.
In conductive hearing loss, children have a problem transmitting sound waves through the outer ear, through the eardrum, or through the tiny bones of the middle ear.
In sensorineural hearing loss, the problem is with converting sound waves to electrical impulses, or in transmitting this electrical sound information along the auditory nerves to the brain.
Either conductive or sensorineural hearing loss may be present at birth, or may be acquired along the way. Hearing loss may be mild, complete, or somewhere in between.

Who gets deafness?

Usually severe sensorineural hearing loss in childhood is genetic (it runs in families – even if this child is the first). Sometimes, however, sensorineural hearing loss is a result of other problems, such as a rubella or CMV infection during pregnancy or meningitis infections later on.
Each year about 20,000 children in the United States are born with permanent hearing loss. Often this isn’t discovered until the children are 3 years old and their language is noticeably delayed.
But these 20,000 children with congenital hearing loss are only the tip of the iceberg. In April 1998, the Journal of the American Medical Association reported a staggering 7 million children in the United States with hearing loss significant enough to impair the ability to learn. Most of these children have temporary hearing loss, but even though the hearing loss is temporary, the impact can last a lifetime.
The most common cause for temporary hearing loss is the fluid in the middle ear space associated with ear infections. Whenever a child has an ear infection, germ-containing fluid enters the middle ear space from the back of the nose or throat. The eardrum can’t vibrate freely, resulting in a 15 to 40 decibel hearing loss.

What are the symptoms of deafness?

Hearing loss may be suspected in children who don’t startle to loud sounds or don’t turn to look for the source of sounds. Babies who don’t seem to notice you until they see you may have some form of hearing loss.
Speech development in babies with hearing loss may be unusual. They will often focus on gargling, vibrating noises that they can feel. Speech delay at any point suggests hearing loss as a possibility.
Language development during the first few years of life is nothing short of amazing! A child is born unable to understand any words, and yet is speaking in complete sentences within a few years. During this flowering of development, there are certain critical windows when different sounds are learned. For instance, someone who reaches 8 to 10 months of age without hearing Chinese will lose the ability to distinguish between some of the vocal sounds of that language.
Sometimes the language you miss out on hearing is your own! The most common age for temporary hearing loss is during that same precious time when the miracle of language development is unfolding.

Is deafness contagious?

Not directly.

How long does deafness last?

Some hearing loss is permanent. The most common form of hearing loss is quite brief – but casts a long shadow. On average, fluid lingers for 3 weeks following an ear infection, but it can remain for months at a time. Usually, 12 weeks of fluid is considered the cut-off for concern. However, some investigators have been able to detect long-term language delays (noticeable 9 years after the fact) in children who had 8 or more weeks of fluid between 6 and 12 months of age.

How is deafness diagnosed?

Without a newborn hearing test, the average age at which congenital deafness is diagnosed is 2 years old! Children whose deafness is treated in the first months of life gain critical time and perform far better on developmental tests than those whose diagnosis is delayed. It’s no surprise that the National Institutes of Health and the American Academy of Pediatrics both recommend that all babies have their hearing tested, preferably before they first leave the hospital.

How is deafness treated?

The treatment of hearing loss depends on the cause.
Temporary conductive hearing loss is often treated by properly managing the ear infections. For other types of hearing loss, treatment might involve reconstructive surgery, hearing aids, or cochlear implants (replacement inner ears). Sign language may become important to learn for the child – and for friends and family.

How can deafness be prevented?

All too often, hearing loss cannot be prevented. However, preventing congenital infections, preventing ear infections, preventing meningitis, and preventing hearing damage from exposure to loud noises can all help to preserve hearing.

Related A-to-Z Information:

Attention Deficit Hyperactivity Disorder (ADHD), Cataracts, Chickenpox (Varicella), Cleft Lip and Palate, CMV (Cytomegalovirus), Colorblindness, Depression, Ear Infection, Encephalitis, Glaucoma, Meningitis, Rubella (German measles), Streptococcus (Strep)

Back in 1995, a man died tragically when he was only 42 years old. The official diagnosis was liver failure from alcoholic cirrhosis. No autopsy was done. The body was cremated. No clues remained. End of story. Or was it?

The July 7, 2001 issue of The Lancet chronicles a story of deductive reasoning, genetic medicine, and international cooperation. A physician relative of the deceased kept wondering if the death might have been not due to alcohol but instead from a rare genetic disorder.

The only remaining clue was tiny bits of his skin left in an old electric shaver. These were sent to Semmelweis University in Budapest, Hungary. The genes were analyzed by means of polymerase chain reaction (PCR) amplification in the US.

The result?

The unfortunate man was found to have undiagnosed Wilson disease. This rare genetic condition causes the relentless build-up of copper in the liver, leading to liver failure and brain damage. Effective treatments are available, but Wilson disease is fatal if untreated.

The family learned that alcoholic cirrhosis was not the cause of death. They also learned that his two children (and his father) are carriers of the rare recessive condition. What powerful information was gleaned from nearly-forgotten traces of DNA in that old electric shaver!

If you save a precious lock of your child’s hair, or those tiny baby teeth, or the remnants of her umbilical cord, your memento may prove to have more than just sentimental value as we move through the 21st century.

Pediatric News (33(8):2, 1999), has reported on a significant new  study coming out of Finland.

Up until now, the relationship between cow’s milk and type 1 diabetes has been controversial. This is the first carefully designed, controlled prospective study, and it shows a dramatic reduction in diabetes in high-risk children who avoided cow’s milk products for the first 6-8 months of life.

If there is type 1 diabetes in the immediate family, I would recommend avoiding cow’s milk-based formulas.

It’ll take awhile for scientists to sort out the details, but the early word is — yes, cow protein can trigger diabetes in those who are genetically susceptible.

Dr. Greene’s Answer:

The dazzling experience of color begins when light strikes a canvas of tightly-packed nerve cells in the back of the eye. These rods and cones, as they are commonly called, fire a storm of nerve impulses in response to the light, which then travel down the optic nerve to the visual centers of the brain. The rods are the “black-and-white” receptors; they photograph the ever-changing patterns of light and darkness that are before our eyes. The cones are responsible for the wonder of color vision.

We humans are all born colorblind! The cones don’t begin functioning until a baby is about 4 months old. At that time the baby undergoes a gradual transformation that is as remarkable as the scene in the Wizard of Oz when Dorothy leaves the black-and-white world of Kansas for the brilliant colors of Oz. About one out of 40,000 babies never develops cones, seeing only in black-and-white throughout life. This is called achromatopsia, or rod-monochromatic colorblindness.

There are many other versions of colorblindness, but by far the most common is red-green colorblindness, which affects as many as one out of 25 people. These people either do not have red cones (protanopia) or green cones (deuteranopia). They are unable to distinguish between green and red, but with their remaining two types of cones are able to see all of the other colors. The absence of blue cones is extremely rare.

Colorblindness is usually tested for at children’s four-year physicals. The doctor asks them to identify a red and a green line on the eye chart. If any question remains, more precise visual testing can determine the exact nature of the problem.

Colorblindness is almost always a hereditary condition. Red-green colorblindness is a recessive condition passed on the X chromosome. Only one healthy color vision gene is necessary to provide color vision. Since boys have only one X chromosome, it is much easier for them to be colorblind. If their mothers are carriers (having one normal X chromosome and one colorblind X chromosome), the sons have a 50% chance of having the condition. Red-green colorblindness occurs in about 8 per cent of American males. These men cannot pass the condition on to their sons (since they give their sons a Y, not an X, chromosome), but they will pass the gene to their daughters.

All girls whose fathers are colorblind will at least carry the gene for colorblindness. In order for a girl to actually be red-green colorblind, she must have a mother who is a carrier AND a father who is colorblind. This happens in only about 0.64 percent of American girls (although these numbers vary considerably in other population groups).

Dr. Greene’s Answer:

Wendy, the rash you describe sounds like keratosis pilaris, a common mild condition in which the backs of the upper arms look rather like dried out, plucked chicken flesh. If this is the case, half of your son’s children are likely to have the same future in store for them (unless your grandchildren’s mom also has it, in which case about 3/4 of the grandkids will). Keratosis pilaris is hereditary. Wendy, this is yet another way that you are linked to your son.

The characteristic rash is caused by firm little plugs forming in the hair follicles. The plugs themselves are made of bits of keratin, the main protein found in the outermost protective layer of skin (thus the name keratosis). These plugged follicles give the skin a raised, stippled appearance — usually called goosebumps. The bumps are usually skin color or slightly pinker, and do not itch. The rash is often not noticeable to others, except on close inspection.

Classically the condition appears in early childhood, often around the age of two or three. Since the rash is associated with and worsened by dryness of the skin, most people experience a clear-cut seasonal variation — generally worse in the winter. Although the rash changes in intensity from time to time, the baseline usually stays the same until middle adolescence, when it begins to improve. Adults who still have keratosis pilaris often experience further improvement during the middle decades. The average age when spontaneous improvement is first noted is sixteen (British Medical Journal, June 1994).

Although keratosis pilaris is hereditary, the rash is more common in those with eczema, dry skin, or vitamin A deficiency (or a number of more esoteric skin conditions). The most common spot on the body for keratosis pilaris is the backs of the upper arms (92% of affected people have it there). Next most common is the thighs (59%) (British Medical Journal, June 1994). It can also occur on the face, buttocks, and eyebrows.

Since the rash is often neither unattractive nor bothersome, treatment is entirely optional. The simplest treatment is to keep the skin moist with the frequent use of moisturizers, particularly just after the skin has become wet. Increasing the humidity in the sleeping quarters has also been shown to improve the rash (Clinical Pediatric Dermatology, Saunders 1993). Gentle exfoliation with a body scrub, loofah sponge, pumice sponge, or even a washcloth, can help loosen the plugs.

Also be sure that you and your son get adequate amounts of vitamin A in your diet, and perhaps from a vitamin supplement. Don’t overdo it on the supplements, however, since it is possible to overdose on vitamin A.

If further treatment is desired, your doctor can discuss adding an acid (urea, lactic, glycolic, alpha-hydroxy, or salicylic acid) to a moisturizer. This combination can be quite effective. You might have to experiment to find the optimum concentration of acid for you and your son (often different), to decrease the keratosis without irritating the skin. Ureacin is a strong, urea-containing moisturizer that often works quite well, and comes in different strengths.

The same manufacturers also make Lazer Creme, a gentle, natural moisturizer formulated for keratosis, and containing both vitamins A and E. (On the opposite extreme, chemotherapeutic agents used to treat cancer have as one of their few slightly positive side effects that they improve or eliminate keratosis pilaris — obviously not worth it as a treatment).

I like the idea, though, of using topical retinoic acid (Retin-A). This common medication used for the treatment of acne (and of wrinkles) should combine the benefits of both vitamin A and a gentle acid. I haven’t been able to locate a research study supporting its use, but we do know that the rash contains receptors to retinoic acid (Dermatologica, 1986) and that oral retinoic acid works (Cutis, April 1980) — although usually the risks outweigh the benefits of oral use.

Whether you choose to try some of these treatments or do nothing at all, when you and your son gently rub your hands over the backs of each other’s arms you can feel your connectedness. Your DNA, the distillation of who you are, is linked to his — a connectedness that links both of you to past and future generations of your family. Your life continues on in him, just as you carry your parents forward into this generation. Perhaps the keratosis pilaris will remind you to notice this connectedness even in situations where the link itself is invisible.

Dr. Greene’s Answer:

Keratosis pilaris is a common mild condition in which the backs of the upper arms look rather like dried out, plucked chicken flesh. Sometimes it is referred to as KP or follicular keratosis.  Keratosis pilaris is hereditary.

The characteristic rash is caused by firm little plugs forming in the hair follicles. The plugs themselves are made of bits of keratin, the main protein found in the outermost protective layer of skin (thus the name keratosis). These plugged follicles give the skin a raised, stippled appearance — usually called goosebumps. The bumps are usually skin color or slightly pinker, and do not itch. The rash is often not noticeable to others, except on close inspection.

Classically, the condition appears in early childhood, often around the age of two or three. Since the rash is associated with and worsened by dryness of the skin, most people experience a clear-cut seasonal variation — generally worse in the winter. Although the rash changes in intensity from time to time, the baseline usually stays the same until middle adolescence, when it begins to improve. Adults who still have keratosis pilaris often experience further improvement during the middle decades. The average age when spontaneous improvement is first noted is sixteen (British Journal of Dermatology, June 1994).

Although keratosis pilaris is hereditary, the rash is more common in those with eczema, dry skin, or vitamin A deficiency (or a number of more esoteric skin conditions). The most common spot on the body for keratosis pilaris is the backs of the upper arms (92% of affected people have it there). Next most common is the thighs (59%) (British Journal of Dermatology, June 1994). It can also occur on the face, buttocks, and eyebrows.