**4. A neurodevelopmenatal approach to management**

### **4.1. General diagnostic problems**

Although psychiatrists and mental health professionals treat patients with FASD, there is presently no consistent way within DSM-IV TR to code for either the dysmorphic phenotype (Fetal Alcohol Syndrome, FAS) or the non-dysmorphic condition (Alcohol-related Neurode‐ velopmental Disorder, ARND). Therefore, treatment of affected individuals is inadequate due to lack of diagnostic clarity, and lack of scientifically tested or accepted psychiatric treatment protocols. FAS, the leading non-hereditary cause of mental retardation and preventable birth defects, is buried in Appendix G of the DSM-IV TR as a congenital malformation (760.71) and the ICD-10 includes Fetus and newborn affected by maternal use of alcohol (P04.3) but excludes FAS (Q86.0) (DSM IV-TR, 2000). (Nowick Brown et al 2011, O'Malley 2011b, Rich & O'Malley 2012).

At the current time because there is no appropriate DSM-IV TR or ICD 10 diagnostic frame‐ work, most psychiatrists and mental health professionals attempt to apply inadequate Axis I diagnoses which are often poorly suited to the clinical understanding of this population. This results in individuals being given a laundry list of psychiatric diagnoses, from ADHD, autism, pervasive developmental disorder and bipolar disorder, to conduct disorder, reactive attach‐ ment disorder, personality disorders, and oppositional defiant disorder.

In a large study of secondary disabilities in 415 persons with ARND [FAS or Fetal Alcohol Effect (FAE)], a majority (94%) had a history of co-occurring mental health problems. Among both adults and children, attention deficits were the most frequently reported problems (61%) reported whereas in adults alone, depression was most frequently reported (52%) (Stratton et al., 1996). A smaller study has shown that the proportion of subjects with a history of psychi‐ atric disorders (74%) was greater than expected from the general population, including alcohol or drug abuse (60%), major depressive disorder (44%), avoidant personality disorder (29%). Researchers have shown a link between ADHD symptoms and FASD over the past several years, indicating an acquired (non-genetic) etiology for a subtype of children with ADHD. Infants and toddlers with FASD can present with Regulatory Disorder Type I, II, or III (DC Zero to 3, 2005). Autistic behaviors have been noted in both younger children as well as school age children prenatally exposed to alcohol (Streissguth et al, 1996; Streissguth & O'Malley, 2000, Mukarjee et al 2012).

You could build a case that nearly all disorders developing during childhood listed in the DSM IV-TR may be induced by exposure to alcohol in utero. Co-morbidities of FASD include other behavioral, mood, anxiety, and conduct problems. The link between ADHD and FASD is finding more universal acceptance and the link between autism and Aspergers disorder and FASD will not be far behind. (O'Malley 2011a).The lifetime prevalence of mental health or psychiatric disorders in individuals with FASD is as high as 90% (Streissguth et al 1996, HHS, 2000), highlighting the importance of correct diagnosis and clinical management. Accurate, informed diagnosis is critical in psychiatry to avoid over-medication or inappropriate treat‐ ment, leading to worsening of symptoms and poor outcomes.

The current standard of care or "treatment as usual" for individuals with FASD is inadequate due to lack of diagnostic clarity, lack of accepted psychiatric treatment protocols, and further complicated by the presence of Alcohol Related Birth Defects (ARBD) which are multisystem organ involvement (i.e., seizure disorders; renal, eye, cardiac, g.i. problems and skeletal).

Early accurate diagnosis and intervention may be effective in preventing the development of secondary disabilities (i.e., academic or school failure, conduct disorders and antisocial behaviours leading to legal problems, sexually inappropriate behaviours, lack of steady employment and housing).

### **4.2. The utilization of a neurodevelopmental formulation**

need restraint because of his reactivity to the environment. He had not responded to high doses of SSRIs (which produced increased suicidality thoughts), and atypical, especially risperidone which made him more affectively unmanageable. When he was assessed in the community his clear history of sensory reactivity to tactile, olfactory, gustatory, visual and auditory stimuli was unraveled as was his history of significant prenatal alcohol exposure. Which had been ignored in previous assessments. A combined multi-modal approach addressing his sensory reactivity combined with low dose buspirione was much more effective and he did not need psychiatric hospitalization. As well he did not present any facial features as adult or as a young child. He had been labeled as having unusual paranoid features but these were really his correct sensitivity to what he perceived as a hostile challenging environment. His adoptive parents recounted many stories of his oversensitivity to noise, light,fabrics food when he was

Although psychiatrists and mental health professionals treat patients with FASD, there is presently no consistent way within DSM-IV TR to code for either the dysmorphic phenotype (Fetal Alcohol Syndrome, FAS) or the non-dysmorphic condition (Alcohol-related Neurode‐ velopmental Disorder, ARND). Therefore, treatment of affected individuals is inadequate due to lack of diagnostic clarity, and lack of scientifically tested or accepted psychiatric treatment protocols. FAS, the leading non-hereditary cause of mental retardation and preventable birth defects, is buried in Appendix G of the DSM-IV TR as a congenital malformation (760.71) and the ICD-10 includes Fetus and newborn affected by maternal use of alcohol (P04.3) but excludes FAS (Q86.0) (DSM IV-TR, 2000). (Nowick Brown et al 2011, O'Malley 2011b, Rich & O'Malley

At the current time because there is no appropriate DSM-IV TR or ICD 10 diagnostic frame‐ work, most psychiatrists and mental health professionals attempt to apply inadequate Axis I diagnoses which are often poorly suited to the clinical understanding of this population. This results in individuals being given a laundry list of psychiatric diagnoses, from ADHD, autism, pervasive developmental disorder and bipolar disorder, to conduct disorder, reactive attach‐

In a large study of secondary disabilities in 415 persons with ARND [FAS or Fetal Alcohol Effect (FAE)], a majority (94%) had a history of co-occurring mental health problems. Among both adults and children, attention deficits were the most frequently reported problems (61%) reported whereas in adults alone, depression was most frequently reported (52%) (Stratton et al., 1996). A smaller study has shown that the proportion of subjects with a history of psychi‐ atric disorders (74%) was greater than expected from the general population, including alcohol or drug abuse (60%), major depressive disorder (44%), avoidant personality disorder (29%). Researchers have shown a link between ADHD symptoms and FASD over the past several years, indicating an acquired (non-genetic) etiology for a subtype of children with ADHD.

ment disorder, personality disorders, and oppositional defiant disorder.

growing op and just saw him as 'over fussy'.

464 Recent Advances in Autism Spectrum Disorders - Volume I

**4.1. General diagnostic problems**

2012).

**4. A neurodevelopmenatal approach to management**

The utilization of a neurodevelopmental formulation can guide the development of effective multiisystem and multimodal intervention strategies, including appropriate psychopharma‐ cologic management (O'Malley 2008).


The interaction of the childhood experience on the expressed FASD phenotype cannot be overlooked. Therefore, the neurodevelopmental biological vulnerability profile of FASD during infancy, toddlerhood, childhood, and adolescence predisposes an individual to adverse psychological outcomes resulting from early institutionalization, parental loss, physical/ emotional/sexual abuse, neglect, and other forms of trauma(Cummings et al 2000,Elias et al 2011, Rich & O'Malley 2012).

tions of FAS and ARND (Fitzgerald M, 2010). Clinicians using a neurodevelopmental approach

Clinical Implications of a Link between Fetal Alcohol Spectrum Disorders (FASD) and Autism or Asperger's…

http://dx.doi.org/10.5772/54924

467

Multi-modal treatment can improve the developmental, social, academic, and mental health trajectory of these children (O'Malley 2008, Nowick Brown et al 2011). Brain organization and function is affected in many individuals with FASD/ARND and can be enhanced by appro‐

As with Autistic Spectrum Disorders, FASD diagnosis and treatment involves early interven‐ tion with a multimodal team approach (genetics, developmental pediatrics, psychologists, psychiatrists, PT/OT, speech, special education) (O'Malley 2008, 2011b, Kodituwakku et al

A capacity for consequential thinking is a key requirement for "decisional capacity." This is an expectation for adolescents or young adults in the school, work legal system, who have been involved in antisocial and/or violent acts. Unfortunately, due to the neurocognitive deficits associated with ARND, these individuals are often mentally and emotionally discon‐ nected from the consequences of their actions, misread social cues, are easily frustrated and provoked, and are unable to navigate logical decision making. So called 'high functioning 'autistic patients fit this neurocognitive profile and have the added challenge of unexpected response to medication because of unrecognized brain damage (Coles et al 2009, Kodituwakku

Clinical experience has shown that proper medication combined with comprehensive, early intervention services will improve their neurodevelopmental and psychiatric outcomes. To that end, psychotropic medication can be viewed as an integral part of multi-modal manage‐ ment program for dysmorphic and non-dysmorphic ARND (FAS Diagnosis, 2005; Byrne

No National Institute of Mental Health (NIMH), NICE (UK), or industry-sponsored studies exist on the safety and efficacy of medication in children, adolescents, or adults with FASD,

There is literature on the pharmacological management of ADHD, Autism, Fragile X, aggres‐ sion and addictive disorders (Hagerman 1999, Lee et al 2001, Glancy et al 2002 a, b, Vocci et al 2005, Turk 2012), which is often mis-extrapolated to apply to individuals with FASD. Since there is no definitive diagnosis in the current DSM-IV TR for FASD outside of 760.71 (which is embedded in the ICD-9 codes in the Appendices under both "FAS" and "toxic exposure to alcohol in utero"), no impetus exists for large scale clinical trials in psychiatric and mental health research. Such controlled clinical studies are needed to determine "best practices," or even smaller studies to determine safety and efficacy, or to gain FDA or NICE guideline approval for use of the medications in this unique neurodevelopmental psychiatric patient

**4.4. The specific use of medication in FASD with or without autistic features**

*4.4.1. Off — Label or off license use of psychopharmaceuticals in patients with FASD*

so this continues to be a barrier to measured and safe treatment for all individuals.

will have more success in understanding and treatment of FASD.

priate multi-modal treatment strategies.

et al 2011, Hosenbucus et al 2012).

2008, Coles 2009; Novick Brown, et al., 2011).

2011).


*A neurodevelopmental formulation provides the best option for clinical understanding of these types of FASD complex cases, but*

*especially if autistic features are the presentation, and the patient has borderline or low intellectual function or a marked split ( 12-15*

*points) between verbal and performance I.Q. (O'Malley 2008, Chapter 1)*

#### **4.3. The practical utility of a neurodevelopmental approach**

The challenges in the treatment of FASD currently relate to their clinical presentations having an array of apparent psychiatric co-morbidity, and a general lack of diagnostic clarity. In practice in both North America and Ireland/ UK clinicians who recognize the clinical signifi‐ cance of FAS or ARND, are given a number of psychiatric diagnoses (ADHD, Autism, Aspergers disorder, intermittent explosive disorder, conduct disorder, mood disorder, etc.). It is becoming increasingly evident that early onset dysregulation, social communication and forensic issues are presenting complex mixtures of biological and environmental vulnerabili‐ ties which display developmentally changing clinical presentations. The autistic presentation coupled with ADHD symptoms and intermittent unexplained explosive episodes is particu‐ larly perplexing and hard to manage. Thus, given that both conditions are common presenta‐ tions of FAS and ARND (Fitzgerald M, 2010). Clinicians using a neurodevelopmental approach will have more success in understanding and treatment of FASD.

psychological outcomes resulting from early institutionalization, parental loss, physical/ emotional/sexual abuse, neglect, and other forms of trauma(Cummings et al 2000,Elias et al

**3.** 3.The implications of FASD on development, behavior, academic and adaptive function‐ ing over the life span can be best understood in the context of the interaction of social and familial factors with an individual's neurodevelopmental deficits. Early institutionaliza‐ tion, neglect, abuse, and family violence may engender different nosological (diagnostic) presentations in this patient population, depending on the quality and degree of under‐ lying neurodevelopmental impairment. So co-occurring diagnosis of Reactive Attachment Disorder or Post Traumatic Stress Disorder, Developmental Trauma Disorder are quite appropriate and herald the psychiatric and care complexities of the patient. It is therefore of vital importance that care must be taken to tease out symptoms based on acquired developmental versus social history in order to develop a holistic, appropriate under‐ standing of the interplay between brain-based and environmental (post-natal) origins of

**4.** Deficits in emotional regulation and mood, implicit ability to comprehend the nuances of social situations, auditory or visual information processing, functional working memory, and/or other executive functions put individuals at risk for further psychopathology in the face of environmental stressors. These neurodevelopmental (CNS) and psychiatric sequellae persist through the life course and may progress to worsening conditions with devastating outcomes and poor prognosis (Streissguth and O'Malley, 2000, Rich &

*A neurodevelopmental formulation provides the best option for clinical understanding of these types of FASD complex cases, but*

*especially if autistic features are the presentation, and the patient has borderline or low intellectual function or a marked split ( 12-15*

The challenges in the treatment of FASD currently relate to their clinical presentations having an array of apparent psychiatric co-morbidity, and a general lack of diagnostic clarity. In practice in both North America and Ireland/ UK clinicians who recognize the clinical signifi‐ cance of FAS or ARND, are given a number of psychiatric diagnoses (ADHD, Autism, Aspergers disorder, intermittent explosive disorder, conduct disorder, mood disorder, etc.). It is becoming increasingly evident that early onset dysregulation, social communication and forensic issues are presenting complex mixtures of biological and environmental vulnerabili‐ ties which display developmentally changing clinical presentations. The autistic presentation coupled with ADHD symptoms and intermittent unexplained explosive episodes is particu‐ larly perplexing and hard to manage. Thus, given that both conditions are common presenta‐

2011, Rich & O'Malley 2012).

466 Recent Advances in Autism Spectrum Disorders - Volume I

psychopathology.

O'Malley 2012).

*points) between verbal and performance I.Q. (O'Malley 2008, Chapter 1)*

**4.3. The practical utility of a neurodevelopmental approach**

Multi-modal treatment can improve the developmental, social, academic, and mental health trajectory of these children (O'Malley 2008, Nowick Brown et al 2011). Brain organization and function is affected in many individuals with FASD/ARND and can be enhanced by appro‐ priate multi-modal treatment strategies.

As with Autistic Spectrum Disorders, FASD diagnosis and treatment involves early interven‐ tion with a multimodal team approach (genetics, developmental pediatrics, psychologists, psychiatrists, PT/OT, speech, special education) (O'Malley 2008, 2011b, Kodituwakku et al 2011).

A capacity for consequential thinking is a key requirement for "decisional capacity." This is an expectation for adolescents or young adults in the school, work legal system, who have been involved in antisocial and/or violent acts. Unfortunately, due to the neurocognitive deficits associated with ARND, these individuals are often mentally and emotionally discon‐ nected from the consequences of their actions, misread social cues, are easily frustrated and provoked, and are unable to navigate logical decision making. So called 'high functioning 'autistic patients fit this neurocognitive profile and have the added challenge of unexpected response to medication because of unrecognized brain damage (Coles et al 2009, Kodituwakku et al 2011, Hosenbucus et al 2012).

#### **4.4. The specific use of medication in FASD with or without autistic features**

Clinical experience has shown that proper medication combined with comprehensive, early intervention services will improve their neurodevelopmental and psychiatric outcomes. To that end, psychotropic medication can be viewed as an integral part of multi-modal manage‐ ment program for dysmorphic and non-dysmorphic ARND (FAS Diagnosis, 2005; Byrne 2008, Coles 2009; Novick Brown, et al., 2011).

#### *4.4.1. Off — Label or off license use of psychopharmaceuticals in patients with FASD*

No National Institute of Mental Health (NIMH), NICE (UK), or industry-sponsored studies exist on the safety and efficacy of medication in children, adolescents, or adults with FASD, so this continues to be a barrier to measured and safe treatment for all individuals.

There is literature on the pharmacological management of ADHD, Autism, Fragile X, aggres‐ sion and addictive disorders (Hagerman 1999, Lee et al 2001, Glancy et al 2002 a, b, Vocci et al 2005, Turk 2012), which is often mis-extrapolated to apply to individuals with FASD. Since there is no definitive diagnosis in the current DSM-IV TR for FASD outside of 760.71 (which is embedded in the ICD-9 codes in the Appendices under both "FAS" and "toxic exposure to alcohol in utero"), no impetus exists for large scale clinical trials in psychiatric and mental health research. Such controlled clinical studies are needed to determine "best practices," or even smaller studies to determine safety and efficacy, or to gain FDA or NICE guideline approval for use of the medications in this unique neurodevelopmental psychiatric patient population (Turk 2009). Presently, there currently are no FDA, AACAP, APA guidelines for medication usage in adolescents or young adults with FASD who present with neuropsychi‐ atric disorders. Therefore, all medications are used "off label" or 'off license' in this population.

*4.4.3. Psychopharmacological targeting of neurodevelopmental deficits to improve current function and*

Clinical Implications of a Link between Fetal Alcohol Spectrum Disorders (FASD) and Autism or Asperger's…

http://dx.doi.org/10.5772/54924

469

It is well recognized that patients with acquired brain injury respond differently to medications

International clinical experience with this population indicates that individuals with alcoholinduced brain damage (FAS and ARND) often respond to medications similarly to those with

A prudent therapeutic approach in this group of patients is to streamline the numbers of medications the person is taking in order to reduce drug-drug interactions and prevent complications from over-medication (Stratton et al, 1996; O'Malley & Storoz 2003; Byrne

Medications need to be started at low doses and increased slowly – with the goal of maximizing efficacy and minimizing side effects to the sensitive/vulnerable central nervous system. This can be achieved more often than not by simplifying the medication regimen, reducing the drug-drug interactions, and providing targeted therapy combined with medication manage‐

Psychotropic agents do improve brain organization and function (i.e., "neuron glue") and y can facilitate cognitive processes by dampening the spontaneous or random firing of mislaid pathways in the brain. As well, psychotropic medications may improve mood, behavior, and performance in individuals with FASD by altering the physiology of the "injured brain" structure and function. Among these medications are the atypical antipsychotics, such as risperdal, ziprazidone, aripiprizole, and olanzapine. Uses of lamotrigine, carbamazepine, valproic acid, lyrica, frisium have also been anecdotally helpful in patients with generalised anxiety, aggressively, impulsivity, and mood dysregulation. We believe that correctly chosen, appropriately managed medications can have a positive effect on cognitive functioning and

The principles guiding use of medications in the organically compromised brain (targeted medications, lower doses, and gradual increases in dosing) combined with psychotherapy and comprehensive community supports, psychiatrists can improve the complex neurodevelop‐

Medications may have positive or negative outcomes as patients with FASD are more sensitive

**i.** For example, selective serotonin reuptake inhibitors (SSRI's) such as fluoxetine,

due to augmentation of a pre-existing, organically-driven impulsivity.

paroxetine, or citalopram, used not infrequently in Autism, may be more likely to precipitate agitation, activation, or suicidality in these brain- damaged adolescents

decision making. (Hosenbus et al 2012, O'Malley 2010, Turk 2012).

*4.4.4. General principles regarding medication usage in FASD*

mental issues in these individuals.

to the CNS effects of medications.

*general prognosis*

2008; O'Malley 2008).

ment.

than individuals with no brain injury.

other types of acquired or traumatic brain injury.

#### *4.4.2. Caution in use of medication in ARND*

While research is scarce in patients with FASD, this population may be even more vulnerable than those with brain injury sustained in the postnatal period, childhood, adolescence, or adulthood. Individuals with FASD, whether FAS or ARND, have had fetal whole-body exposure during prenatal development, leading to the potential for unrecognized Alcohol Related Birth Defects ( ARBD) in a number of organ systems (kidney, heart, liver/g.i. system, eye, immune system, neurological) (Stratton et al 1996). These underlying problems with physical organs and structures may lead to unanticipated side effects to even low doses of medication.

#### For example

	- **•** differential or paradoxical medication response ;
	- **•** prenatal alcohol-induced neurochemical or structural CNS changes (i.e., acquired brain injury);
	- **•** complications related to multisystem organ involvement (absorption, metabolic or elimination problems related to kidney, gastro-intestinal or liver problems related to ARBD);
	- **•** an increased incidence of seizure disorders in this population (i.e., lower seizure thresh hold);
	- **•** overall greater risk of side effects from multiple drug combinations, higher doses of medications, and sensitivity to psychopharmaceuticals.

#### *4.4.3. Psychopharmacological targeting of neurodevelopmental deficits to improve current function and general prognosis*

population (Turk 2009). Presently, there currently are no FDA, AACAP, APA guidelines for medication usage in adolescents or young adults with FASD who present with neuropsychi‐ atric disorders. Therefore, all medications are used "off label" or 'off license' in this population.

While research is scarce in patients with FASD, this population may be even more vulnerable than those with brain injury sustained in the postnatal period, childhood, adolescence, or adulthood. Individuals with FASD, whether FAS or ARND, have had fetal whole-body exposure during prenatal development, leading to the potential for unrecognized Alcohol Related Birth Defects ( ARBD) in a number of organ systems (kidney, heart, liver/g.i. system, eye, immune system, neurological) (Stratton et al 1996). These underlying problems with physical organs and structures may lead to unanticipated side effects to even low doses of

**i.** cardiac problems such as conduction anomalies, structural defects, and pathologic murmurs may be linked with adverse events with stimulant medications.

**ii.** Overt seizure disorders and irritability of the brain (associated with random and

**iii.** Other medical complications associated with alcohol-related birth defects (ARBD)

**iv.** Therefore, caution in use of medications should be given due to the unique vulner‐

(O'Malley & Barr 1998, Hagerman 1999,Bonthius et al 2001

need to be considered prior to beginning medication.

**•** differential or paradoxical medication response ;

triggered electrical discharges) may be present due to neuro-anatomical changes in the ARND brain. Therefore, safety issues related to decreased seizure threshold for certain medications should be considered prior to treatment of this population.

ability of these patients for severe and catastrophic side effects of certain medications

**•** prenatal alcohol-induced neurochemical or structural CNS changes (i.e., acquired

**•** complications related to multisystem organ involvement (absorption, metabolic or elimination problems related to kidney, gastro-intestinal or liver problems related

**•** an increased incidence of seizure disorders in this population (i.e., lower seizure

**•** overall greater risk of side effects from multiple drug combinations, higher doses

of medications, and sensitivity to psychopharmaceuticals.

*4.4.2. Caution in use of medication in ARND*

468 Recent Advances in Autism Spectrum Disorders - Volume I

medication.

For example

due to:

brain injury);

to ARBD);

thresh hold);

It is well recognized that patients with acquired brain injury respond differently to medications than individuals with no brain injury.

International clinical experience with this population indicates that individuals with alcoholinduced brain damage (FAS and ARND) often respond to medications similarly to those with other types of acquired or traumatic brain injury.

A prudent therapeutic approach in this group of patients is to streamline the numbers of medications the person is taking in order to reduce drug-drug interactions and prevent complications from over-medication (Stratton et al, 1996; O'Malley & Storoz 2003; Byrne 2008; O'Malley 2008).

Medications need to be started at low doses and increased slowly – with the goal of maximizing efficacy and minimizing side effects to the sensitive/vulnerable central nervous system. This can be achieved more often than not by simplifying the medication regimen, reducing the drug-drug interactions, and providing targeted therapy combined with medication manage‐ ment.

Psychotropic agents do improve brain organization and function (i.e., "neuron glue") and y can facilitate cognitive processes by dampening the spontaneous or random firing of mislaid pathways in the brain. As well, psychotropic medications may improve mood, behavior, and performance in individuals with FASD by altering the physiology of the "injured brain" structure and function. Among these medications are the atypical antipsychotics, such as risperdal, ziprazidone, aripiprizole, and olanzapine. Uses of lamotrigine, carbamazepine, valproic acid, lyrica, frisium have also been anecdotally helpful in patients with generalised anxiety, aggressively, impulsivity, and mood dysregulation. We believe that correctly chosen, appropriately managed medications can have a positive effect on cognitive functioning and decision making. (Hosenbus et al 2012, O'Malley 2010, Turk 2012).

#### *4.4.4. General principles regarding medication usage in FASD*

The principles guiding use of medications in the organically compromised brain (targeted medications, lower doses, and gradual increases in dosing) combined with psychotherapy and comprehensive community supports, psychiatrists can improve the complex neurodevelop‐ mental issues in these individuals.

Medications may have positive or negative outcomes as patients with FASD are more sensitive to the CNS effects of medications.

**i.** For example, selective serotonin reuptake inhibitors (SSRI's) such as fluoxetine, paroxetine, or citalopram, used not infrequently in Autism, may be more likely to precipitate agitation, activation, or suicidality in these brain- damaged adolescents due to augmentation of a pre-existing, organically-driven impulsivity.

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 fluoxetine have proven anecdotally beneficial for some patients

**5. Discussion**

(DSM 5 Symposium 2012).

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

Clinical Implications of a Link between Fetal Alcohol Spectrum Disorders (FASD) and Autism or Asperger's…

http://dx.doi.org/10.5772/54924

471

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

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

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

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

probably rank next to ADHD as the commonest clinical phenotype of FASD.

brain hypothesis will then inform management at many levels.

could dramatically improve our understanding of brain function.

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

#### *4.4.5. The future for medication use in FASD including those with common presentations of ADHD, mood disorders and/or autism*

