 saw “medications are poisons with positive side effects” can be useful. So is “start low and go slow but don’t forget to go” if there are no positive effects and side effects.|
|5. Use behavioral data, rating scales, measures of drug side effects to monitor treatment response. Many behavioral monitoring systems can be adapted to incorporate dose changes, serum drug levels, improvement on psychiatric rating scales into graphic data representations.|
|6. Serum drug levels can be very useful for patients with no response to high doses or severe side effects at low doses; monitor drug-drug interactions and adapting treatments. Free drug fractions measurements can be useful for valproic acid; 10-11 epoxide levels for carbamazepine. Serum drug and metabolite levels and can provide clues about CYT P450 polymorphisms|
|7. In psychopharmacology remember that more is not always better and a rush to polypharmacy may complicate rather than simplify treatment.|
|8. If you find yourself in a quandary about too many drugs, carefully review each, why they were added, what side effects they might have that complicates the clinical presentation, and carefully reduce, if possible beginning with the first ineffective drug and decrease slowly. An increase in target behaviors may not represent a relapse, if possible wait 1-2 weeks before increasing the old drug or jumping to new one.|
|9. Maintenance treatments are critical for many chronic mental disorders, but maintenance doses may be lower than those required for initial responses. Many increases in challenging behaviors are state related and may not require long term, high dose medication management. Reductions should also “start with small decrements and go slow”. Transient withdrawal states are not uncommon- they resemble extinction surges noted by behavioral therapists when reinforcers are removed.|
|10. Define your comfort zone: when you feel outside it or things don’t make sense, consult. Many IDD syndromes have associated co-occurring metabolic and neurological conditions. Always remember akithisia and the long list of non antipsychotic drugs and conditions that resemble it.|
The field of IDD and dual diagnosis requires that the clinician maintain a good working knowledge of ongoing research in the behavioral and developmental neurosciences and psychopharmacology. As more data become available on behavioral phenotypes, epigenetics, and behavioral pharmacology, the clinician will be required to synthesize this new data with existing behavioral and mental health practices. The old approaches relying upon behavior/psychiatric disorder, nature/environment versus nurture/genetic risk, organic/functional disorders will need to be revised. These changes will bring us to conclude:
Brain behavioral relationships are too complex to be conceptualized in terms of single anatomical sites or neurotransmitters. Treating based on suspected neurotransmitter abnormalities are woefully reductionist and may lead to unnecessary polypharmacy.
Challenging behaviors and psychiatric disorders are heterogeneous phenomena that cannot be fully captured by a traditional behavioral analysis or psychiatric diagnosis. We will need to adapt our thinking to ongoing work on subtyping challenging behaviors and endophenotypes of primary psychiatric disorders. We will need to sharpen our diagnostic skills to meet this challenge and adapt our treatment planning to match this new knowledge.
Alternative treatments such as transcranial magnetic stimulation, deep brain stimulation and models of neuropharmacology that focus on intracellular mechanisms and alterations in gene regulation are on the horizon. This shift will require us to understand the basic neurobiology of developmental disorders; how it differs from neuro-typical patients, and what special adjustments we will need to make to accommodate these differences (35, 45).