**5. Discussion**

At the same time, given that individuals with FASD may have deficiencies and/or differences in neurotransmitter systems such as serotonin and dopamine, low doses of sertraline and

**ii.** Adolescents and young adults with ARND and co-occurring seizure disorders have

*4.4.5. The future for medication use in FASD including those with common presentations of ADHD,*

**i.** Obviously multicenter, randomized controlled clinical trials (ideally international) are needed in this vulnerable and clinically complex population. (Turk 2009)

**ii.** There is a need for scientific testing and evaluation of new clinical instruments which

**iii.** It is long recognized that the use of multiple psychotropic medications is a risk for

cation interactions, but no data was given or studies forthcoming.

toxicity and acute confusional state, even in absence of underlying neurocognitive problems. The mechanism of multidrug interaction leading to toxicity relates to individual drugs competing for absorption through the liver cytochrome P450 2D6 enzyme system. In turn, certain medication blood levels increase (i.e., paroxetine is well known to increase blood levels of other psychotropic medications). In a recent lecture at the First European Conference on FASD in Rolduc, Holland (Nov 3rd to 5th 2010), Ken Warren, Acting Director of NIAAA, mentioned concern about medi‐

combine cognitive, language, and behavioral response as the 'gold standard' for assessing medication efficacy and safety in patients with FASD. Currently there are no validated clinical instruments to evaluate the developmental, cognitive, language and behavioral response of a patient with FAS or ARND to psychotropic medication. There is a non-specific neuropsychiatric rating scale, but most drug rating scales (with the exception of those used in Alzheimer's disorder) evaluate clinical symptoms related to psychiatric disorder (i.e., Connor's Questionnaire, Beck Depression

a prenatally kindled organic brain dysfunction as a result of alcohol-induced damage to the corpus callosum, cerebellum or hippocampus. There is anecdotal clinical evidence that antiepileptics (i.e., carbamazepine, valproic acid, lamotrigine, neuro‐ ntion) can be effective in preventing this kindling effect. The prenatal effects of alcohol can also result in a change in the balance of the developing neurotransmitters. Animal research has shown that prenatal alcohol can induce decrease in inhibitory neuro‐ transmitter GABA in the hippocampus, and this neurochemical imbalance can underpin development of seizures (Hannigan et al 1996, Riley et al 2006). The effects of antiepileptics should be weighed carefully since some medications for seizures may also increase anxiety, affective/mood liability, and reduce learning and cogni‐

fluoxetine have proven anecdotally beneficial for some patients

470 Recent Advances in Autism Spectrum Disorders - Volume I

Inventory, Hamilton Rating Scale, CBCL).

tion.

*mood disorders and/or autism*

This chapter has attempted to highlight the overlapping clinic al presentations of patients with FASD, whether dysmorphic FAS or non –dysmorphic ARND. Autism and Aspergers Disorder probably rank next to ADHD as the commonest clinical phenotype of FASD.

The lack of DSM or ICD Axis I codes for these individuals means that treating psychiatrists do not usually identify either disorder (dysmorphic or nondysmorphic conditions related to prenatal alcohol exposure as aetiological factors to be considered in diagnosis. The organic brain hypothesis will then inform management at many levels.

Nevertheless, the arrival of DSM V will hopefully herald new diagnostic categories which will capture more correctly some of these patients with FASD who show what are deemed ';autistic' features. Two proposed diagnostic categories, Social Communication Disorder and Alcohol Related Neurobiological Disorder are in serious consideration. It is hoped that Alcohol Related Neurodevelopmental Disorder (ARND), already well recognized, will replace the new category it more correctly captures the essence of the developmental psychiatric disorder (DSM 5 Symposium 2012).

Currently the generic "treatment as usual" prevents individuals with FASD from receiving appropriate multisystem and multimodal services, and further results in predictably poor outcomes for affected individuals and ultimately costly consequences for communities.

Brain imaging such as MRI, fMRI or SPECT scans studies may begin to map more specific areas of brain dysfunction related to prenatal alcohol exposure and psychiatric clinical presentation (Riley, et al 2005, Kodituwakku et al 2011, Coles et al 2011). Historically our scientific knowl‐ edge of damaged or diseased brain structure associated with infections such as syphilis, AIDS or lesions associated with cerebrovascular accidents has informed our diagnostic accuracy and informed treatment progress. Therefore it is not unrealistic to expect that correlations between the structural and functional deficits in individuals exposed at certain points during pregnancy could dramatically improve our understanding of brain function.

Finally, the ability to distinguish FASD with an autistic clinical presentation from a geneticallyacquired or non-organic cause of this neurodevelopmental condition. This aetiological knowledge ultimately better describes the pathophysiology and neuropsychiatric phenomen‐ ology of the patient's clinical diagnosis. The neurodevelopmental clinical frame expands the clinician's understanding that the autistic presentation is actually a phenotype form of this specific acquired brain injury, The prenatal alcohol exposure creates a chemical, structural, and even electrical CNS environment that is "hard wired" very different from the other aetiological pathways for autism. The child or adolescent psychiatrist (ideally trained in developmental psychiatry) has a long recognized central role as the "case supervisor" for patients with patients with FASD, and is in the better position to manage the unfolding and clarification of the neurodevelopmental formulation, differential diagnosis, psychiatric comorbidities, and psychopharmacology. Increased understanding of these complex patients through a neurodevelopment formulation, unraveling such issues as the hidden aetiology to the autism presentation will improve holistic clinical outcomes including the appropriate, targeted use of medication by the treating child/adolescent psychiatrists.

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