Treatment Philosophy

When problems are psychiatric, treatment is psychiatric and behavioral.

When problems are both psychiatric and neurological, treatment is both neuropsychiatric and neurobehavioral.

As explained by David Riedel, M.D., Board Certified Child and Adolescent Psychiatrist, Facility Medical Director:

What we would like to see a child achieve at Meridell is to learn to control their own life. When they get here, their life has gotten out of control. And the more out of control it is, the more control they then turn over to others: to educational institutions, to psychiatric institutions, to legal institutions. Our job here is to have each child become again the hero of his or her own destiny and in control of their own life.

When children get here, they invariably recreate the kind of dysfunctional patterns they had in different systems before they got here. I think that we really excel at being a collaborative team, and constantly evaluating ways in which we can withstand the unstable and dysfunctional dynamics that children bring in here. Instead of punishing children for recreating their dysfunctional patterns, we work to understand their patterns of thinking and behavior. And we help them correct their behaviors by the way we react to them: in a more functional way than the previous systems might have.

We get a lot of parents who tour Meridell before they make a decision about placing their children here. And quite often their feedback is: this place just feels good; this place seems like my child could get better here.

As explained by Larry Fisher, Ph.D., UHS Neurobehavioral Systems Corporate Director of Pediatric Neuropsychology:

Heres a behavioral issue: A toddler may misbehave by testing your limits or reaching for something after you’ve told him not to touch it. This is purposeful misbehavior. Parents respond by setting limits and giving consequences.

Heres a related biological issue: A toddler is upset, moody, throwing toys, trying to kick the dog. This is irritable behavior. Irritable behavior is usually a biological issue: dirty diaper, sleepy, hungry, new tooth, fever. Parents understand that you cannot punish away irritability. Children would only get more irritable; they cant help it. Parents understand that to fix irritability you must find and fix the cause (e.g., change the diaper, give a nap, feed the child, fix the tooth, or treat the illness).

With children and teens at Meridell, we recognize that purposeful misbehavior is very different from irritable behavior. There are different underlying causes for these different kinds of behavior. Therefore treatment is very different. Our Neurobehavioral Units are designed for irritable children, where we try to find and fix the cause of that irritability. We do not try to punish away irritability. We use a softer form of discipline on these units, which is less confrontational. Short temper can be a very difficult problem for a family to deal with; we train our staff to manage it safely and to stabilize it effectively. We find out what is causing the irritability or temper outbursts, and we fix it.

To find the cause we do psychiatric interviewing, psychological testing, neuropsychological testing, and brain electrical testing. We try to avoid mere sedation and instead target medication to treat the underlying problem. In addition to medications, we use intensive therapies, including individual psychotherapy, group therapy, family therapy, behavioral therapy, recreational therapy and milieu therapy. We specialize in the hard-to-treat child or adolescent who may be irritable, impulsive, or explosive. With this unique population we have been very successful, not in every case, but in the vast majority of cases.

As explained by Daniel Matthews, M.D., Neuropsychiatrist, UHS Neurobehavioral Systems Corporate Director of Neuropsychiatry:

All emotion is processed in the limbic brain: from elation to rage. (For more information, please Google Limbic System). With patients at Meridell, we understand that the biology of the brains limbic system, the emotion brain, underlies anger and aggression. For example: a patient has a history of being impulsive and explosive. Diagnoses may include bipolar and ADHD. For ADHD, doctors prescribe a stimulant medication, perhaps Ritalin, Adderall or Concerta. Most patients respond favorably; they become more focused. Some patients respond unfavorably: they go into outer orbit. Why?

If the limbic brain is not stable, medications such as stimulants will irritate it. ADHD may be a correct diagnosis. Stimulant medication is indicated for patients with ADHD. But if the patients limbic brain is not stable, then the patient will over-react to a stimulant. What do we do?

We evaluate the limbic brain. At Meridell, this neurophysiological evaluation is a Cognitrace Study or Quantitative EEG with Evoked Potential (QEEG). Our Pediatric Neurologist reviews and assesses neuro-electrical responses in the limbic brain. If a patients limbic brain response is not stable, meaning two or more standard deviations from a normal limbic response, then we know that we are dealing with a neurological problem or a brain problem. This verifies what many parents tell us: Something else must be going on.

At this point, we know the specific medical, neurological problem. We now know what medications are needed and at what dosage. Just as importantly, we know what medications are not helpful.

As a patients limbic brain becomes more stable with correct medication, the patient becomes more behaviorally functional. For example, with limbic instability, we may see teeth clenched, fists tight, irritability on the brink of anger and aggression. After stabilizing the limbic brain, we see a calmer, more functional response. And that is because the patient becomes biologically capable of responding functionally.

As explained by Daniel Matthews, M.D., Neuropsychiatrist, UHS Neurobehavioral Systems Corporate Director of Neuropsychiatry:

Dear Colleague,

The clinical information below is provided in response to multiple requests from physicians treating children and adolescents who have undergone Neuropsychiatric diagnostics and treatment at either the Meridell Center near Austin, or another of our UHS neuropsychiatric programs. These patients would typically have had significant findings on the Neurophysiology exam according to the evaluating Pediatric Neurologist. The corresponding Neuropsychiatric medication recommendations and rationale follow. References are attached.

Rationale for the Use of Amantadine in the Treatment of Frontal Lobe Dysfunction

Inadequate frontal lobe function is demonstrated clinically as deficient impulse control, poor concentration, problems with working memory, weakness in executive cognition, and/or emotional dyscontrol. This dysfunction can result from traumatic brain injury, toxic or anoxic insults, or genetic abnormalities. The above described deficiencies, often labeled as a Dysexecutive Syndrome, are resultant from inadequate dopaminergic (primarily D-4) receptor function in conjunction with related increase in NMDA glutamate receptor activity. This is either a result of a neurometabolic “cascade effect” that occurs secondary to injury or insult, or is due to a genetic aberrancy of expression in the D-4 receptor.

Traditionally, in psychiatry, this Dysexecutive Syndrome has been addressed with alpha-adrenergic agonists (clonidine or guanfacine) which actually decrease norepinephrine activity frontally by occupying receptor binding sites with an inactive compound. This is sort of like putting a governor on the accelerator to compensate for the problem of “bad brakes” (e.g.; inadequate dopamine) frontally. This treatment concept was introduced by Bob Hunt about 25 years ago and has been relatively successful.

Alternatively, and frequently more effectively, one can use Amantadine 100 mg BID or TID (approximately 6-8 hours apart) to directly address the dopaminergic deficiency by agonistically increasing dopaminergic activity in the anterior cingulate gyrus, orbitofrontal and/or other affected ventromedial prefrontal structures. This agonistic effect occurs primarily at the D-4 receptor sites with only minimal effect at D-1 and D-2 receptor sites. Amantadine has an added beneficial effect as a moderate NMDA glutamate receptor antagonist. Since the above described clinical picture of deficient impulse control, poor concentration, problems with memory, and/or emotional dyscontrol are seen in a hyperglutamatergic state; restoring the D-4 to NMDA glutamate balance is beneficial in positively impacting the Dysexecutive Syndrome.

If Amantadine is used, one needs to be aware of the following facts:

1. Maximum benefit is usually achieved in the range of 200-300 mg per day. Little further benefit is seen beyond this dosage range.

2. In approximately 25% of individuals, the beneficial effect is lost between 4-6 weeks. This is thought to be due to “receptor exhaustion”. This problem, and the corrective intervention for it, were discovered during its use (as Symmetrel) in the treatment of ParkinsonĂ­s. The corrective action is to suspend administration for 48 hours and then reinstitute it at the previously effective dose. If this phenomenon occurs, it will reoccur at the same intervals, thus requiring repeating this procedure at the same interval as it first occurred. In our experience, this is best managed by planning the suspension for the closest Sat. and Sun. after week 4, 5, or 6 (whichever was the time of effect loss).

3. If Amantadine alone does not provide sufficient benefit, then Clonidine can be added since they have no drug/drug interaction and its actions are at norepinephrine receptors.

4. If the patient has had (or currently has) tics, then Amantadine may cause a reoccurrence or increase of tics due to its action at D-1 and D-2 receptors. If this occurs, then discontinuation is necessary, and the tics should resolve.

Please see the attached reference list for further information and/or feel free to call or e-mail me at any time regarding questions about Amantadine or any of the other medications that were prescribed to your patient while under our care.

Collegially yours,

Daniel T. Matthews, M.D.

Corporate Director of Neuropsychiatric Services

(800) 272-4641

Email: [email protected]

AMANTADINE REFERENCES

Draus, M.F. & Maki, P.M. (1997). The combined use of Amantadine and l-dopa/carbidopa in the treatment of chronic brain injury. Brain Injury, 11(6), 455-460.

Horrigan, J.P. & Barnhill, J. (2002, Winter). Amantadine for psychostimulant-resistant attention-deficit/hyperactivity disorder in boys (Abstract). Paper presented at the annual meeting of the American Neuropsychiatric Association. J. Neuropsychiatry Clin Neurosci 14(1), 105.

Karli, D.C., Burke, D.T., Kim, J.J., Calvanio, R., Fitzpatrick, M., Temple, D., et al., (1999). Effects of dopaminergic combination therapy for frontal lobe dysfunction in traumatic brain injury rehabilitation. Brain Injury, 13(1), 63-68.

Karus, M.F., Smith, G.S., Butters, M., Donnell, A.J., Dixon, E., & Yilong, et al., (2005). Effects of the dopaminergic agent and NMDA receptor antagonist Amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: A study using positron emission tomography (PET), Brain Injury, 19(7), 471-489.

Kraus, M.F. & Maki, P.M. (1997). Effect of Amantadine hydrochloride on symptoms of frontal lobe dysfunction in brain injury: Case studies and review. J. Neuropsychiatry Clin Neurosci 9(2), 222-230.

Lyketsos, C.G., Rosenblatt, A., & Rabins, P., (2004). Forgotten Frontal Lobe Syndrome or “Executive Dysfunction Syndrome”. Psychosomatics, 45(3), 247-255.

Meythaler, J. M., Brunner, R.C., Johnson, A., & Novack, T.A. (2002). Amantadine to improve neurorecovery in traumatic brain injury-Associated Diffuse Axonal Injury: A pilot Double-blind randomized trial. J. Head Trauma Rehabil, 17(4), 300-313.

Thomas, T. C., Grandy, D.K., Gerhardt, G.A., & Glaser, P.EA., 2008. Decreased Dopamine D4 Receptor Expression Increases Extracellular Glutamate and Alters Its Regulation in Mouse Striatum. Neuropsychopharmacology, 1-10.

Williams, S. E. (2007). Amantadine treatment following traumatic brain injury in children. Brain Injury, 21(9), 885-889.

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