School-Related Medical Issues Archive 2009
Dr. John L. Digges, MD, MPH, FAAP
Dr. Digges practiced general and behavioral pediatrics in Oklahoma and California for 14 years. From 1998 to 2006, he served as the Forensic (Child Abuse) Pediatrician for Kern County, California; and has had a private practice limited to ADHD consultations for the past ten years. He has been a CME surveyor for the Institute of Medical Quality (CMA) for the past eight years, and currently serves a President of the Kern County Medical Society.
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Could hypothyroidism due to Hashimoto’s Disease be the cause of her learning problems?
My daughter has struggled all her life with many health and learning problems. She is 14 years old and entering high school, but she is now said to be over five grades behind. The school says her cognitive is at a low 85 and there is no help for her. She was just diagnosed with hypothyroidism due to Hashimoto’s Disease. Her TSH was at 449.5 when we found out. Her specialist says that she has been losing her thyroid for all of her school life. Could this condition be the cause of her learning problems?
Shirla Jackson, CA
Hashimoto’s thyroiditis is a condition in which the body makes antibodies which gradually destroy thyroid tissue. Since the thyroid gland produces hormones which help regulate several body functions (including digestion, metabolism and reproduction), destruction of thyroid can produce varied symptoms. Abnormal thyroid function may also trigger preexisting genetic tendencies, and thereby produce new symptoms or make existing symptoms worse.
An elevation in thyroid stimulating hormone (TSH) results from the body’s attempt to get the thyroid to produce more thyroid hormone. If the thyroid is not able to produce adequate amounts of thyroid hormone, the hypothalamus will produce more TSH in a futile attempt to get the thyroid gland to respond. This can result in the markedly elevated TSH your daughter had at the time of diagnosis.
Typical symptoms caused by hypothyroidism include lack of energy, depression, cold intolerance, weight gain, dry skin, constipation, and muscle aches. Difficulties involving concentration, attention, and memory have also been reported. Symptoms such as decreased energy, depression, inattention, reduced concentration and faulty memory could certainly contribute to poor school performance. Replacement of thyroid hormone leads to a reduction in TSH, and generally by the time the TSH has returned to normal, most symptoms will have resolved. However, problems with depression, low energy level and maintaining attention may persist and require specific treatment.
There is also a very rare condition known as Hashimoto’s encephalopathy, which may be caused by inflammation of blood vessels in the central nervous system. This condition can be diagnosed on the basis of impaired cognitive function, clouding of consciousness, elevated serum antithyroid antibody concentrations, and usually abnormal EEG findings.
Whether your daughter’s learning problems were caused by her thyroid condition or were caused by something else (and possibly made worse by her thyroid condition) is best determined by a thorough evaluation including history, physical examination and appropriate testing. A pediatric endocrinologist would generally have the most experience treating Hashimoto’s thyroiditis in children. Consultation with a pediatric neurologist may be helpful in determining whether your daughter meets the diagnostic criteria for Hashimoto’s encephalopathy. After her thyroid functioning has been normalized, it will be important to determine what symptoms persist. Both non-pharmacologic and pharmacologic treatment strategies can then be devised to address those remaining symptoms.
Having an IQ score of 85 within the normal range. Children with normal intelligence can nevertheless struggle in school, and this may result from any of a number of causes. Such causes would include discreet information processing difficulties (learning disability) or other conditions such as Attention Deficit/Hyperactivity Disorder. After her thyroid condition and any other coexisting conditions are treated, it is possible that her academic performance may improve significantly.
Your school should be able to provide you with the help you need to ensure that your daughter gets as much out of her educational experience as she can. We wish you and your daughter well in your attempts to meet the many challenges that confront you.
John L. Digges, MD, PhD, MPH, FAAP
What is the difference between Ritalin and Focalin?
I had heard so many concerning things about Ritalin that I didn’t want my 6 year old son to be on that medicine. His doctor prescribed Focalin XR, and my son has been doing well. I now find out that Ritalin and Focalin are very similar and are made by the same company. What is the difference between them?
Thank you for your question, Allison, as it raises some important issues. Ritalin, which has indeed received some poor press in recent years, is the trade name for the chemical compound d,l – methylphenidate. Ritalin is a mixture of equal parts of the d-isomer and the l-isomer (the d-isomer rotates light to the right, while the l-isomer rotates light to the left) of methylphenidate, which are mirror images of one another. This compound is the active ingredient in other brand name AD/HD preparations, such as Concerta, Metadate, and Daytrana. The differences between these preparations lies in the mechanism used to release the d,l – methylphenidate. Focalin is the name of the preparation which contains only the d-isomer of the methylphenidate mixture (generic name d - methylphenidate). Ritalin and Focalin are trade names owned by Novartis.
Stimulant medications such as methylphenidate have been observed to produce improvement for AD/HD patients in two different domains. First, they help decrease the hyperactivity, and second, they help improve cognitive performance. It turns out that the reduction in hyperactivity is related to the dose or amount of medication in the child’s system. The cognitive improvement, however, generally correlates with the period of time during which the concentration of medication in the body is increasing (the “ramp” or “upslope” portion of the curve produced when the blood level of medication is plotted over time). Consequently, even though Ritalin in tablet form is metabolized over about 4 hours, it is believed to be providing help with cognitive functions for only about the first 2 hours, or the time during which the concentration of the medicine in the blood is increasing. This hypothesis is based upon observations of behavior correlated with the level of medication in the blood.*
* Although the concentration of medicine in the brain and the strength of the bond between the molecule and a specific brain receptor are more crucial than the concentration of medicine in the blood, the presumed activity of the molecule in brain is generally inferred from the concentration of the molecule in blood, as blood concentration levels are much more easily measured.
Both Ritalin and Focalin are available as tablets (immediate release) and capsules (extended release, e.g. Ritalin LA (“long acting”) and Focalin XR (“extended release”)). The tablet preparation dissolves in the stomach and then is absorbed into the bloodstream. Long acting capsules contain small beads of medication, some of which are bare while others have a coating. The bare medication bead dissolves rather rapidly in the stomach, but it takes the gastrointestinal tract about 4 hours to dissolve the coating before the active medication contained in the previously coated bead is released into the blood stream. In Ritalin LA and in Focalin XR, there is an approximately 50:50 proportion of medicine released at the two time periods, so equal amounts of medicine are released about 4 hours apart.
If you have 10 mg of the d,l – methylphenidate compound, you have 5 mg of the l – methylphenidate and 5 mg of the d – methylphenidate. The d – methylphenidate isomer has been identified as the biologically active form, while the l – isomer is thought to be fairly inactive in the body. The initial expectation was that by using only half as much medication (e.g. 5 mg Focalin vs.10 mg Ritalin), the side effects would be reduced by half. Unfortunately, the d – methylphenidate isomer produces both the desirable and the undesirable effects of the medicine. However, an unanticipated outcome was observed in patients who took the Focalin tablet, as the beneficial effects on cognition seemed to last from 4-6 hours. In contrast, the improvement in cognition after taking the Ritalin tablet was generally limited to about 2 hours. Although much remains to be understood about the precise workings of these compounds in the brain, it has been observed that the Focalin (tablet or XR capsule) appears to provide a longer duration of action for cognitive improvement than does the Ritalin (tablet or LA capsule), even when the Focalin dose is one half the Ritalin dose.
As mentioned previously, both Ritalin and Focalin are available in immediate release and timed release forms. Prior to the development of timed release formulations of the d,l – methylphenidate, there were several concerns related to the immediate release preparation. Dosing had to occur three times a day to cover morning, afternoon, and after school periods. However, the downslope portion of the curve may have presented a “gap” in coverage for optimal cognitive improvement, even while the hyperactivity was being reduced.
When the dose of immediate release Ritalin is increased, the duration of action is not increased, but the steepness of the upslope and downslope curves is accentuated. Many children will experience an increase in emotional lability (spontaneous tearfulness or increased irritability and tantrum behavior) as the concentration of medication drops rapidly. Additionally, since the immediate release preparation requires in-school dosing, there is the risk that the child’s right to privacy concerning medical conditions may be compromised.
The long acting preparations help to avoid some of these limitations inherent in the short acting preparations. However, there still may be times when a shorter acting preparation is preferable. For example, the acting preparations taken in the morning are more likely to produce appetite suppression at lunch time. This can usually be addressed by: 1. Having the child eat a well balanced breakfast with sufficient protein, 2. Using a “liquid meal” preparation for lunch if the child cannot eat a regular lunch, 3. Providing a “lunch-like” snack/meal after school, and 4. Being flexible with dinner time, as the child may not be hungry between 5 & 6 PM if they just finished “lunch” at 3 PM. Additionally, I will use the shorter acting preparation when initiating stimulant treatment in a child for whom I have increased concern about their ability to tolerate medication side effects. I would rather expose that child and the family to undesirable side effects for a shorter period than a longer one! Once I am satisfied that the medication is well tolerated, then I can switch the child over to a longer acting preparation.
For some children, the long acting preparation they take covers the school day quite adequately, but the morning hours before school continue to be a “battle ground.” Other children may be “rapid metabolizers,” and the medication may be wearing off before they have time to complete their homework. These children may benefit from the judicious use of shorter acting “booster” doses to tide them over during high-demand periods of time.
I hope this helps clarify for you the differences between Ritalin and Focalin, as well as the differences between immediate release and extended release preparations of these medications. I wish you and your son continued success.
Could a malformed heart and ADHD be related?
We have an 11 year old student in our school who was born with a malformed heart. He has had surgeries requiring heart bypass on three occasions, and is expecting to have a heart transplant sometime in the future. He is physically doing OK now, but he also has been diagnosed with ADHD, is often disruptive in class, and is falling behind in his schoolwork. Could the two conditions be related? Can you offer any thoughts on strategies to improve his learning?
Angie W., San Francisco
My daughter was adopted from Russia at 3 1/2 we know that her first two years were very bad. She was born from a mother who used drugs and alcohol, but she did not have any signs of fetal alcohol syndrome. She does have scars on her body from abuse, one on her head. When we brought her home she was very small and didn'tspeak much. We have been thru counseling to help with the abuse, she had her adenoids removed due to constant infections causing hearing problems, she has seen a Neurologist and hearing specialists, and is now on Vyvanse for ADD. Now fast forward to her turning 9 in January and competing at State level two years in a row ingymnastics.
I still think she is not diagnosed correctly and is not getting the specific help she needs. She is very forgetful, just last night she said, "I have "radish" on my fingers" as she was clearing her plate. We weren't eating radishes. What she was trying to say is that she had "dressing" on her fingers but could not come up with the word and had no idea what a radish was, and that is just one example. She also does things like walk away and leaving the faucet running after washing her hands. She is alwaysforgetting where she puts things. She struggles in school but they have always said "it was because of her first 3 1/2 years knowing another language" and have put her inreading programs. She can read just fine, but can't recall what she just read. Her current doctor said it is ADD, and she is unable to focus, therefor she isn't able to recallthings. But I'm still not convinced because we aren't seeing any improvement in memory or comprehension.
Any ideas on what are we missing and how I help my girl?
Indeed the two conditions could very well be related. Although you did not state his specific heart condition, suffice it to say that studies performed on children born with several forms of complex cyanotic heart disease (e.g. hypoplastic left heart syndrome, total anomalous pulmonary venous return and velocardiofacial/ DiGeorge syndrome) show a marked increase in prevalence of ADHD in these populations (up to 75%!) One possible hypothesis to explain the connection would be that these children have a higher risk of experiencing hypoxemia, which may then injure parts of developing brain during periods of heightened susceptibility to decreased levels of oxygen in the blood. If the injured regions involve the frontostriatal dopaminergic fiber tracts, then it would be possible to produce a constellation of symptoms which could be clinically indistinguishable from the symptoms seen in a child who is believed to have inherited his ADHD from his ADHD parents.
The experience of having had the function of his heart and lungs being assumed by a machine on three separate occasions introduces an additional element of risk for hypoxemic injury. Being born with a significant cardiac abnormality may also cause the child’s experience of life to be far different from that of his peers. This experience, coupled with the knowledge that he will need a heart transplant in order to survive, would likely produce a profoundly different view of the world in terms of such concepts as safety, trust and fairness.
If either parent becomes overprotective of the youngster or overindulges the child, then the child may very well develop additional behavioral problems. Such children often become uncooperative, disobedient, argumentative and irritable. They also tend to develop more somatic complaints.
We might theorize that children with ADHD symptoms caused by some degree of injury to brain may have similar biochemical deficits as do the children who inherited their ADHD. If this were true, then in both instances we would infer that insufficient neurotransmitter concentrations in the synaptic cleft would be contributing to the children’s problems.
There may be the potential for medications used to treat ADHD to have a detrimental effect on a compromised cardiovascular system, therefore, non-pharmacologic strategies may be necessary. Helping a child to stay emotionally connected with the teacher, the subject matter, or both may help to normalize. Using positive behavior supports wherever feasible would also be an important step in improving both his behavior and his academic success in school. These can help with organizational chores, tracking their progress, and appropriate prompting.
The use of medications must be undertaken with utmost caution. Pediatric cardiology consultation would be prudent, which would include ECG and echocardiography. Once cleared by cardiology, the child could be started on a low dose stimulant preparation with very gradual titration of the dose. These children should be monitored simultaneously for reduction in ADHD symptoms and their sequelae and for increases in such side effects as anxiety, irritability, tics and sleep disturbance.
Atomoxetine (Strattera) is a non-stimulant FDA approved treatment for AD/HD, which has no “black-box” warning about sudden cardiac death, but it affects heart rate and blood pressure in a manner that is very similar to the stimulant preparations. Medication management in a child with AD/HD and a significant structural cardiac abnormality is complex, and requires close coordination between patient, family members, cardiac physician(s), general pediatrician and the AD/HD physician. I hope this is helpful for you.
John L. Digges, MD, PhD, FAAP
The above submitted question was answered jointly by Dr. Stivers (clinical psychologist) and Dr. Digges (behavioral pediatrician). It will appear in both the Mental Health and School Related Medical Issues sections of Ask A Specialist for April, 2009.
Thank you for writing. It appears that your daughter is doing far better than are most of the children we see with similar backgrounds. Many of them function well below age level in many areas, have extreme difficulty with interpersonal relationships, and engage in explosive, out-of-control behavior. Evidently your daughter is a resilient individual who had the amazingly good fortune to find a dedicated parent with the skills and persistence to consistently provide a supportive and enriching environment. You should be very proud of her and we hope that you also take pride in your role in supporting her success.
Despite having overcome the odds for someone with her early history and having developed areas of competence, such as gymnastics, your daughter still seems to struggle to master some of the skills she needs. Your concern is that her ADD* diagnosis is insufficient to explain her current problems. We concur. Even though “she did not have any signs of fetal alcohol syndrome,” we cannot conclude that she was unaffected by prenatal exposure to alcohol. Recent literature suggests that alcohol exposure needs to occur sometime between day 21 and day 24 of development (i.e. before mother knows she is pregnant) in order for the classic facial features of fetal alcohol syndrome to be manifested. The implication of this research is that we now realize that children can be exposed to large amounts of alcohol over an extended portion of their fetal development, and still “look normal.” Unfortunately, their brains may have suffered significant damage as a result of the neurotoxic effects of alcohol. Children whose brains have been injured by prenatal exposure to alcohol but who appear normal can be diagnosed with ARND or alcohol related neurodevelopmental disorder.
An additional risk factor for her stems from the potential negative impact on the development of her brain as a result of the abuse to which she was subjected. Recent literature in this field indicates that the essential processes of synaptogenesis (brain growth) and synaptic “pruning” (trimming back of unused pathways) can be impaired by limitations in the quality or number of unconditionally supportive relationships with caring adults in the early years of development.
As you might suspect, children with ARND and a history of abuse often have sustained significant injury to broad regions of the brain, so they may experience a wide range of consequences. These can include a negative impact on:
- executive functioning (mental control over attention, thinking, and behavior)
- learning and memory (assimilating, storing, and retrieving information)
- language (understanding language and/or self-expression)
- visual processing (includes pattern recognition, visual discrimination)
- sensory processing and modulation (tendency to over- or under-react to sensations such as touch or sound and experience chronic discomfort)
- motor development (fine, gross motor coordination, visual-motor integration)
- social development (social insight and skills for developing relationships)
- higher-order reasoning, abstract thinking, and problem-solving
Your daughter appears to have challenges in the first area, executive functioning. Executive functions include the abilities to resist distractions and focus on what we need to do, organize and keep track of materials, find effective strategies to accomplish tasks, and develop and follow through on plans. Difficulties with executive functioning are highly characteristic of AD/HD. The absent-minded behaviors you described, such as forgetting to turn water off and where she put things, are part of her your daughter’s AD/HD. Have these behaviors improved since she started taking medication? Children with AD/HD typically have trouble focusing on what they’re doing unless extremely interested in the activity itself or in being with the individuals who are performing the activity. Gymnastics may qualify, but not the water running in the sink. The brains of children with AD/HD tend to function best when they are participating in an activity with which they are emotionally connected (novel, related to interests….). It is very likely that her AD/HD also contributes to her lack of reading comprehension (she decodes the words automatically but doesn’t pay continuous attention to content), although there may be other factors involved.
Interventions can help improve the functioning of children with AD/HD. These interventions generally consist of environmental modifications and instruction to increase critical skills. “To-do” lists and visual charts or checklists for daily routines can help remind her to follow steps in the proper sequence, even though they may “slip her mind.” Labeling where things go with words and/or pictures may also be helpful. To the extent possible, making mundane activites appear novel or connecting boring tasks with desirable rewards may help to establish the emotional connection which is believed to contribute to normalizing the brain function of children with AD/HD.
Your daughter may remain “absent-minded,” but it will be less disruptive to the flow of her day. Often, especially as they progress to higher grades in school, students with AD/HD also need ongoing help with study skills, organization of time and materials, and project planning. You and the staff at her school can collaborate to support her organizational, planning, and study skills.
Your letter also suggested that your daughter may have some challenges in the area of verbal learning and memory. The radish-dressing word substitution incident indicates that she may sometimes have word-finding problems based on inefficient storage (mental organization) and/or retrieval of verbal material. Many of us experience word-finding problems at times and it can be quite frustrating. From your letter, it is unclear to us how significant a problem this poses in her life. Does it occur every 10 minutes or once or twice a week? Does she seem distressed about it? Is it interfering with her learning in school or social interactions?
There are several strategies for helping children successfully manage word retrieval difficulties. You may wish to consult with the staff at your daughter’s school, especially the speech and language therapist. For further suggestions about executive functioning and word retrieval, google: “CHADD” and “All Kinds of Minds.”
Overall, AD/HD appears to be an accurate diagnosis for your daughter in that it describes several of the difficulties that significantly impact her functioning. However, you are probably correct in pointing out that it does not encompass all of the areas in which she experiences difficulty. The diagnoses of ARND (alcohol related neurodevelopmental disorder) and mixed neurodevelopmental disorder may also be appropriate. Post Traumatic Stress Disorder (PTSD) is seen in some children with a history of abuse, but we do not have enough history to know whether this may have applied to your daughter.
Medically, the use of pharmaceuticals can often help normalize abnormal brain physiology. The goal is to achieve an acceptable balance between symptom resolution and side effects, and this delicate balance can best be obtained by working closely with her physician.
Educationally, no matter what her medical diagnoses, interventions may be warranted in areas where she is having difficulty acquiring the skills she needs. It is not clear from your letter how severe her difficulties are with word retrieval or reading comprehension. Do these difficulties interfere significantly with learning, resulting in below grade level skills? If so, and if it has not already been done, you may request that the school district conduct a psychoeducational assessment. This should result in a more thorough understanding of her learning strengths and weaknesses and lead to either formal or informal plans to remediate any identified learning or language weaknesses.
We hope this information is helpful. Thank you for writing, and we wish you and your daughter continued success.
Marji Stivers, PhD, Clinical Psychologist
John L. Digges, MD, PhD, Behavioral Pediatrician
*ADD or ADD without hyperactivity were terms that were replaced in the 1994 DSM IV (Diagnostic and Statistical Manual, 4 th Edition) with “AD/HD Predominantly Inattentive Type.” We suspect from your letter that this is your daughter’s diagnosis. Children with this subtype often respond to lower potency and lower doses of stimulant preparations than do children with hyperactivity.
Does the Diagnostic Center have information about the affects of parental meth addiction?
My name is Jean Fetterhoff. I am the Superintendent/Principal of Kings River-Hardwick Elementary School in Hanford. We have a Kindergarten child living with his adoptive parents whose natural mother was a meth addict before he was born. He experiences periodic uncontrollable angry outbursts that we’d like to learn more about. Does the Diagnostic Center have information about the affects of parental meth addiction or some websites you can recommend that would give us insights into beneficial ways of dealing with this child? We’d like to learn all we can.
Thank you in advance for any help you can give us.
Our current knowledge concerning the impact of prenatal methamphetamine exposure on developing infants is incomplete. The studies conducted generally fall within one of two categories: studies on non-human animal species and studies tracking outcomes in human infants whose mothers used methamphetamine during their pregnancy. All of these studies have limitations in terms of our ability to generalize from their results to make accurate predictions in the case of a particular child.
Studies on rats exposed to methamphetamine prenatally have found an increase in retinal defects, cleft palate, and rib deformities; reduced growth rates, and delays in motor development. Prenatal methamphetamine exposure in rats has been found to be toxic to nerves which depend on serotonin to pass messages from one neuron to the next. The toxic effects on these neurons were found to be responsible for impairments in learning, deficits in behavior and increases in motor activity level. One study involved rats exposed to methamphetamine in what would be equivalent to “early” and “late” third trimester in humans. Both groups showed increases in their startle response to auditory stimuli and impairments in performance on a complex maze task. The effects appeared to be long lasting and to involve both cognitive and arousal functions.
Studies on humans are limited due to imprecise knowledge of the dose, purity, and timing of the exposures and the fact that often there are other potentially neurotoxic drugs which the mother has also taken. Notwithstanding these limitations, it is known that methamphetamine produces vasoconstriction in the uteroplacental system, which reduces blood flow and may result in inadequate oxygen and nutrient delivery to developing tissues, including brain. Methamphetamine using mothers will often have suppressed appetites, so that their nutrient intake is reduced and the fetal nutrient supply may be further compromised. Not surprisingly, reduced fetal growth and reduction in head size (and by extension brain size) have been consistently found in infants prenatally exposed to methamphetamine. In addition, studies have found that rates of placental abruption and premature delivery are increased in pregnancies during which the mother took methamphetamine. Studies on humans have also found an increased incidence of cleft lip, cleft palate, and cardiac anomalies.
A longitudinal study in Sweden showed that the infants who were prenatally exposed to higher doses of methamphetamine for longer periods of time had more severe problems with aggression and social adjustment at 8 years of age. By the time they reached ages 14-15 years, their performance in math, language and sports were all impaired compared to their classmates. It is difficult to discern the exact contribution of the prenatal methamphetamine exposure to their poorer performance, as they also were exposed to the increased stress associated with maternal alcohol abuse and they experienced more foster care placements.
A magnetic resonance spectroscopy study reported in 2001 found that total creatine was increased in the corpus striatum region of the brain in children exposed to methamphetamine in utero, which suggests that these children have an abnormality in energy metabolism involving their brains. A 2003 study showed prenatal methamphetamine exposure was associated with growth restriction in term babies, while a 2006 study showed that infants exposed to methamphetamine in utero were 3.5 times more likely to be small for gestational age than were the unexposed infants. Neonates with intrauterine methamphetamine exposure are reported to have increased tone, sleep through feedings, have a diminished suck reflex, appear more agitated, and have difficulty with self-regulation, especially during times of stress.
The take home message is that intrauterine methamphetamine exposure places the developing brain at risk to injury, but the precise nature of the injury and the functional implications will be determined by a complex interaction between multiple environmental and genetic factors. The more nurturing and supportive the home environment, the more likely the child’s brain will be able to create alternate pathways to replace those which may have been damaged by the methamphetamine exposure. A thorough neurodevelopmental exam might identify patterns of symptoms which lend themselves to specific therapeutic interventions. A thorough psychoeducational evaluation will help delineate both the strengths and weaknesses of this particular child, and should provide the foundation for an intervention strategy tailored to help create an educational environment which will optimize his potential for learning.
John L. Digges, MD, PhD, FAAP
His mother has gone off the deep end and doesn’t want him to take medicine anymore.
I live in Kansas City, Mo. I am the grandmother. My son and his 10 year old son live with us. He has been diagnosed with adhd and was taking 27 mg Concerta. His mother has gone off the deep end and doesn’t want him to take medicine anymore. Her idea to solve this is "beat his ass". My son and I went to the parent-teacher conference this past Thursday and we took his medical records and he is not doing very well at all in school. Since he has been diagnosed with ADHD they are trying everything they can in class to help him. At the rate he is going he probably will not pass the 5th grade. I am deeply concerned about him because when he was taking the medicine he was doing very well.
Do you have any suggestions on what we can do?
Your son’s 10 year old son has been diagnosed with ADHD and experienced a reduction in symptoms on Concerta 27 mg. His mother has discontinued her son’s treatment with Concerta, choosing instead to “beat his ass.” Your grandson is apparently struggling in school currently, and you are asking for suggestions on how you can help him.
I would explore answers to the following questions:
- What is mother’s understanding of her child’s diagnosis of ADHD?
- What is the nature of the current relationship between mother and father and what is the quality of the communication occurring between the two?
- What does mother believe regarding optimal treatment for a child with ADHD who is struggling academically? Does she see any role for medications in the treatment of ADHD? Does she have reservations concerning the particular medicine prescribed for her son?
- Has mother been diagnosed with ADHD? Does she have any other children or family members who have been diagnosed with ADHD?
Non-pharmacologic treatments can be very helpful for children with ADHD, and pursuing them is certainly reasonable. To “beat his ass” however, would not constitute optimal non-pharmacologic management, and may place mother at risk of losing custody if abuse (either physical or emotional) has occurred. For those children who do not respond optimally to evidence based non-pharmacologic interventions, a trial of medication is an appropriate choice. If the child did indeed respond well to Concerta 27mg, then the question arises as to why mother decided to discontinue therapy with Concerta.
The goal in using medications to treat children with ADHD is to compensate for an insufficient concentration of neurotransmitter in the space between adjacent neurons in specific regions of the brain. Increasing the neurotransmitter concentration in that space should allow the impulse to be transmitted from one neuron to the next, and should thereby enable his brain to function more like the brains of his classmates who do not have ADHD.
Concerta is the brand name of a product which uses a racemic mixture of d,l-methylphenidate in an OROS tablet. Approximately 22% of the medication is applied as a coating to the outside of the tablet. After ingestion, this coating begins to dissolve in the gastrointestinal tract and enter the bloodstream, generally being well absorbed within about 30-45 minutes. Following this period, another 26% of the total dose is gradually squeezed out through a laser-drilled hole in one end of the non-soluble tablet over about the next three to four hours, resulting in its being absorbed into the bloodstream. The second medication chamber within the tablet contains about 52% of the total dose; that is, it is twice as concentrated as the medication in the first chamber. This more concentrated medication is also delivered out of the tablet and absorbed over a period of about three to four hours.
The reason for doubling the concentration in the second chamber is to provide as long and smooth of an ascending portion of the pharmacokinetic curve as is possible. Cognitive improvement is generally optimal during the time that the concentration of medication in the system is continuing to rise (“upslope”), while decreases in hyperactivity are usually associated with the quantity of medicine absorbed (“plateau”). Depending upon a number of variables, the medication may be expected to give good results with improved cognition for between 6 and 9 hours and also provide a significant decrease in non-goal-directed motor activity excess for an additional one to three hours more for most children.
Abruptly discontinuing Concerta 27 mg would not be expected to cause withdrawal symptoms. Unless your grandson demonstrated unusual sensitivity to Concerta on his previous trial (headaches and abdominal pain), he would be expected to tolerate restarting at the 27 mg dose. If he did experience side effects, then his dose could be decreased to 18 mg for a week or so, and then titrated to 27 mg as needed.
Attending to mother’s questions and reservations about the diagnosis and treatment of ADHD in her son should be a first step towards identifying a “common ground” where both parents’ concerns are addressed and the child receives the help he needs and deserves. A supportive relationship with a physician knowledgeable about ADHD and willing to act as a resource for the parents and the child is a cornerstone of successful collaboration in the treatment of this chronic condition. Recent literature on resiliency suggests that having one or more adults who are unconditionally supportive of the ADHD child may be instrumental in determining that child’s ultimate degree of success. Your role can be to help provide that support for your grandson and thereby assist both him and his parents through this difficult period.
Dr. John Digges
Stressful occurrences and hormonal changes associated with puberty can certainly complicate the treatment of a child with ADHD.
I have a daughter. We took her off of the 40mg of Strattera during August and September because she had become angry, defiant, and completely unable (or unwilling) to follow through on even the simplest requests. She was also "starving" all the time. She wanted to eat more than me (214 lbs).
My other half has doubts about ADHD in general, believing that medicine and therapy should fix the symptoms 99% all the time. So we tapered off and stopped. I contend that the onset of puberty, changes in weight and other factors (6th grade is scary) make it necessary to sometimes adjust medication and parenting tactics.
Without the medicine, the behavior problems continued. In addition, she lost, forgot to turn in, or didn't finish nearly all of her schoolwork. So she re-started a lower dosage the beginning of October and is now at 40mg again. Defiance has decreased, fewer tantrums, better focus. But she is often lethargic. We see her doctor again on the 29th to discuss adding a stimulant or increasing her dosage of Strattera.
Twila L. Stephens
You raise a number of important questions. First, ADHD is best viewed as a chronic medical condition, analogous to asthma or diabetes. We are not currently able to “cure” any of these conditions, but we are able to offer treatments designed to help normalize the underlying pathophysiology and thereby reduce symptoms and suffering.
In ADHD, a basic problem is the inability of certain neural pathways in the brain to transmit electrical impulses from one neuron to another. This inability results in deficits in portions of the brain which control self-regulatory skills and “executive functions.” There are two commonly used methods for increasing the neurotransmitter concentration in the space between two adjacent neurons and allowing the electrical impulse to be passed along normally. One of these mechanisms involves having a child establish an emotional connection with a subject or individual, while the other entails the use of medications.
ADHD children who are bored (not emotionally engaged) experience a reduction in the flow of blood, oxygen and nutrients to regions of the brain which are responsible for reasoning, problem solving, and integrating past lessons learned with decisions about the potential consequences of an action about to be taken. They also experience an unpleasant feeling state (sometimes called dysphoria), which they can resolve by establishing an emotional connection with someone or something. One way to view their behaviors is as their best effort to reduce the unpleasant or dysphoric feeling state (rather than as willful disobedience).
Medications such as stimulants and atomoxetine (Strattera) can also be used to increase the concentration of neurotransmitter available in the space between adjacent neurons. Strattera tends to take longer to produce an optimal response in children than do members of the stimulant class, so I often use the summertime to gradually titrate the dose from about 0.5 mg/kg to a range of about 1.2-1.4 mg/kg, unless optimal results are noted at a lower level.
Appetite suppression is common with stimulants, but not so much with atomoxetine. However, some children with ADHD turn to eating as a way of experiencing pleasurable feelings on a reliable basis; because they may have difficulty finding pleasure in academic achievement, social relations, sports, or creative endeavors. Successful treatment of the ADHD symptoms may allow the child to experience more success in both academic and social domains, and thereby reduce their need to turn to food as a way of experiencing pleasure.
Stressful occurrences and hormonal changes associated with puberty can certainly complicate the treatment of a child with ADHD. Addressing those changes directly will generally be more beneficial then adjusting medication doses or changing medicines.
ADHD medicines generally are initiated at a low dose and then gradually increased until either excellent symptom control is achieved or the child develops unacceptable side effects. Some children will not respond sufficiently even at the highest FDA approved dosage for a particular medication. It then falls upon the physician to discuss the advantages and disadvantages of “off-label” dosing versus trying a different medication. Strattera effects one of the neurotransmitters (norepinephrine) selectively, while stimulants generally impact dopamine more than norepinephrine. It may be hypothesized that within the universe of ADHD children, there are some that have more of a norepinephrine deficit than a dopamine deficit, and these children would be expected to perform better on Strattera than on stimulants. Some children may require help with both norepinephrine and dopamine, and a combination of atomoxetine and a stimulant may be a reasonable choice for those patients. You as parents and your physician are faced with integrating all of the available information and applying it to the demands presented by your child in their environment. The challenge is daunting, but the rewards can be enormous; and life altering for both the patient and the patient’s family.