**A. Fetal Alcohol Syndrome (FAS), a specific dysmorphic phenotype, requires documentation of all of the**



initial developmental, cognitive, and neurobehavioral outcomes, and higher lifetime risk of

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

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

455

The dysmorphic facial appearance of an individual is much less an impact than the complex behaviors, psychopathology and developmental disability caused by alcohol's neurotoxicity. Thus, an individual's level of functioning is affected more by behavioral functioning, intellect, cognitive and communication abilities, executive functioning, temperament, social related‐ ness, emotional regulation, and performance than what his or her face looks like. FAS, the dysmorphic presentation of ARND, is in fact a protective factor for what Ann Streissguth called

Neuroimaging studies suggest that alcohol exposure may be specific rather than global in its teratogenicity, including specific vulnerability in the cerebellum, basal ganglia, and corpus callosum. As well, studies have shown deficits in cognitive functions such as learning and memory, visual-spatial functioning, executive functioning, attention, sequencing, processing and motor control. (Mattson et al 2011) These "functional birth defects" are evidenced by impairment in the brain and central nervous system. Riley and colleagues have shown that functional birth defects are present in children with moderate to heavy prenatal alcohol exposure, even in absence of characteristic (dysmorphic) facial features (Bookstein et al 2001,

It is a critical issue in clinical diagnosis of FASD to understand that the severity of the acquired brain injury is not always correlated with the presence of facial dysmorphology (and FAS facial features commonly change significantly in adolescence and adulthood). Therefore facial features are minimally useful to assess and treat neurocognitive and neurobehavioral deficits associated with prenatal alcohol exposure. (Streissguth, et al., 1991; Steinhausen, et al., 1993, Nowick Brown et al 2011, Kodituwakku et al 2011, O'Malley 2011, Rich & O'Malley 2012).

The first 30 to 40 years of research in FASD has been driven by animal teratology and the pursuit of minute changes in facial dysmorphology as biological markers for the level of prenatal alcohol exposure. Nevertheless, it is becoming quite clear that it is the central nervous system brain dysfunction that is the kernel of the problem and the guide to diagnostic understanding and management. It is not the face that tells the clinician about the underlying brain dysfunction but the complex mixture of developmental disability and psychiatric disorder. FASD, whether dysmorphic FAS or non dysmorphic ARND are developmental psychiatric disorders which, as Susan Rich and Kieran O'Malley describe in their 2012 paper. These conditions can present a neurodevelopmental mixture of mood dysregulation and autonomic arousal with language and social skills deficits, cognitive and executive decision

As far back as 1990, child neuropsychologist Jo Nanson in Saskatoon, Canada, described 6 cases of FAS with autism. As well, the interest in prenatal risk factors contributing to autism has been pursued by a number of authors and this potential aetiological link was published in 1991 by International autism researcher Cathy Lord and colleagues. More recently, since

making dysfunctions and multisensory functional and perceptual deficits

**2.1. The link between FASD and autism or Asperger's disorder**

psychiatric co-morbidities and substance use disorders.

secondary disabilities of FASD ( Streissguth et al 1996).

Riley and McGee, 2005, Coles et al 2011).

**Table 1.** Characteristic Diagnostic Features of FAS (dysmorphic) and ARND ( non dysmorphc)

Among both phenotypes, FAS is the less common condition, accounting for only 20-25% of the affected infants and children exposed to all levels of alcohol exposure. By comparison, nondysmorphic ARND is the more common clinical presentation of affected infants and children, accounting for 75 to 80% of affected infants exposed to all levels of alcohol in pregnancy. While maternal alcohol use is the leading known preventable cause of mental retardation and birth defects, only 20-25% of patients with either dysmorphic FAS or nondysmorphic ARND have a total IQ below 70. In other words, 75 to 80% of patients with FASD are estimated to have a developmental disability or other CNS impairment (acquired brain injury) but are not mentally retarded (Streissguth et al., 1996; Mukarjee et al., 2006). Hence FASD (FAS and ARND) are NOT mental retardation conditions, but are complex neurodevelopmental disorders with initial developmental, cognitive, and neurobehavioral outcomes, and higher lifetime risk of psychiatric co-morbidities and substance use disorders.

• none or not all pathognomonic dysmorphic facial features are present;

B. Clinically significant brain abnormalities observable through imaging.

1. cognitive or developmental deficits or discrepancies

**Table 1.** Characteristic Diagnostic Features of FAS (dysmorphic) and ARND ( non dysmorphc)

A. Head circumference (OFC) at or below the 10th percentile adjusted for age and sex.

• Central Nervous System (CNS) abnormalities:

454 Recent Advances in Autism Spectrum Disorders - Volume I

circumstances, as evidenced by:

5. social skills

2011, O'Malley & Mukarjee 2010, CDC 2011,HHS)

below the mean for standardized testing) or

in at least three of the following domains:

2. executive functioning deficits 3. motor functioning delays

problems, memory deficits, etc.)

4. problems with attention or hyperactivity

issues;

limits.

I. Structural:

• no evidence of growth delay, low birth weight, decelerating weight over time, nor other height and weight

II. Neurological problems not due to a postnatal insult or fever, or other soft neurological signs outside normal

developmental delay in younger children) with performance below the 3rd percentile (2 standard deviations

B. Functional deficits below the 16th percentile (1 standard deviation below the mean for standardized testing)

6. other clinically relevant neurodevelopmental issues (i.e., sensory problems, pragmatic language

(Jones & Smith 1973, 1975, Stratton et al 1996, Chudney et al 2005, BMA 2007, O'Malley 2008, Novick Brown et al

Among both phenotypes, FAS is the less common condition, accounting for only 20-25% of the affected infants and children exposed to all levels of alcohol exposure. By comparison, nondysmorphic ARND is the more common clinical presentation of affected infants and children, accounting for 75 to 80% of affected infants exposed to all levels of alcohol in pregnancy. While maternal alcohol use is the leading known preventable cause of mental retardation and birth defects, only 20-25% of patients with either dysmorphic FAS or nondysmorphic ARND have a total IQ below 70. In other words, 75 to 80% of patients with FASD are estimated to have a developmental disability or other CNS impairment (acquired brain injury) but are not mentally retarded (Streissguth et al., 1996; Mukarjee et al., 2006). Hence FASD (FAS and ARND) are NOT mental retardation conditions, but are complex neurodevelopmental disorders with

III. Functional Performance substantially below that expected for an individual's age, schooling, or

A. Global cognitive or intellectual deficits representing multiple domains of deficit (or significant

The dysmorphic facial appearance of an individual is much less an impact than the complex behaviors, psychopathology and developmental disability caused by alcohol's neurotoxicity. Thus, an individual's level of functioning is affected more by behavioral functioning, intellect, cognitive and communication abilities, executive functioning, temperament, social related‐ ness, emotional regulation, and performance than what his or her face looks like. FAS, the dysmorphic presentation of ARND, is in fact a protective factor for what Ann Streissguth called secondary disabilities of FASD ( Streissguth et al 1996).

Neuroimaging studies suggest that alcohol exposure may be specific rather than global in its teratogenicity, including specific vulnerability in the cerebellum, basal ganglia, and corpus callosum. As well, studies have shown deficits in cognitive functions such as learning and memory, visual-spatial functioning, executive functioning, attention, sequencing, processing and motor control. (Mattson et al 2011) These "functional birth defects" are evidenced by impairment in the brain and central nervous system. Riley and colleagues have shown that functional birth defects are present in children with moderate to heavy prenatal alcohol exposure, even in absence of characteristic (dysmorphic) facial features (Bookstein et al 2001, Riley and McGee, 2005, Coles et al 2011).

It is a critical issue in clinical diagnosis of FASD to understand that the severity of the acquired brain injury is not always correlated with the presence of facial dysmorphology (and FAS facial features commonly change significantly in adolescence and adulthood). Therefore facial features are minimally useful to assess and treat neurocognitive and neurobehavioral deficits associated with prenatal alcohol exposure. (Streissguth, et al., 1991; Steinhausen, et al., 1993, Nowick Brown et al 2011, Kodituwakku et al 2011, O'Malley 2011, Rich & O'Malley 2012).

The first 30 to 40 years of research in FASD has been driven by animal teratology and the pursuit of minute changes in facial dysmorphology as biological markers for the level of prenatal alcohol exposure. Nevertheless, it is becoming quite clear that it is the central nervous system brain dysfunction that is the kernel of the problem and the guide to diagnostic understanding and management. It is not the face that tells the clinician about the underlying brain dysfunction but the complex mixture of developmental disability and psychiatric disorder. FASD, whether dysmorphic FAS or non dysmorphic ARND are developmental psychiatric disorders which, as Susan Rich and Kieran O'Malley describe in their 2012 paper. These conditions can present a neurodevelopmental mixture of mood dysregulation and autonomic arousal with language and social skills deficits, cognitive and executive decision making dysfunctions and multisensory functional and perceptual deficits

#### **2.1. The link between FASD and autism or Asperger's disorder**

As far back as 1990, child neuropsychologist Jo Nanson in Saskatoon, Canada, described 6 cases of FAS with autism. As well, the interest in prenatal risk factors contributing to autism has been pursued by a number of authors and this potential aetiological link was published in 1991 by International autism researcher Cathy Lord and colleagues. More recently, since 2009-2010, adult psychiatrist in London, Raja Mukarjee, has painstakingly clinically analysed the clinical presentation of Autistic Spectrum Disorder in patients with FASD.

disconnectedness, lack of social cognition and awareness, impulsivity, and inability to understand another person's cognitions or feelings (alexithymia). (Bookstein et al 2001).

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

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

457

The underlying organic brain dysfunction at a cellular, neurotransmitter and structural level related to prenatal alcohol exposure sometimes shares significant congruence with ongoing neuroscience research in Autism Spectrum Disorder and Asperger's Disorder, and awaits

There is also accumulating research which highlights the biological roots of fundamental functional problems in FASD which relate to sustained impact on working memory, (Congdon

**1.** The psychological deficit in the child must be present before the onset of the disorder and

**e.** the emphathizing-systematizing or ' extreme male brain' theory ( Hobson 1989,

**2.4. Clinical presentations of Aspergers disorder or autism spectrum disorder with FASD**

This is the arena where the divergence between the classic presentations of Autism Spectrum Disorder and Aspergers Disorder are seen, and offer a way to untangle the different aetiolog‐

FASD begin at birth and can be seen in infancy. The Mental Health Classification system, Zero to three (DC 0-3R, 2005) has a diagnostic category of Regulatory Disorders which aptly describes the immediate clinical presentations of Dysmorphic FAS or non dysmorphic ARND. It is the category of Regulatory Disorder, underresponsive type which is the harbinger of autism Spectrum Disorder or Aspergers Disorder diagnoses in early child hood.So the classic time presentation of Autism Spectrum Disorder or Aspergers Disorder is different in the FASD

Russell 1997, Baren Cohen et al 2000, Pennington 2009)

**2.3. Neuropsychological framework of understanding ASD and Aspergers and its**

collaborative work between the two academic fields.

**2.** Be pervasive among individuals with the disorder.

**relationship to patients with FASD**

so very early in development.

**4.** Different psychological theories

**a.** theory of mind theory

**b.** the executive theory

**d.** the emotion theory

ical routes to these syndromes.

population.

**c.** the praxis/imitation theory

**3.** Be specific to autism

et al 2012)

In the international paediatric and child psychiatric field the last 5 years have brought a wealth of clinical case descriptions and case studies indicating the presence of ADHD co-morbidly with PDD or Autistic Spectrum Disorder. Clinicians and researchers such as Professor Jeremy Turk in the UK have commented on as much as a 25-30% co-morbid link between ADHD and PDD/ASD. Furthermore the complexity of diagnostic issues within FASD have been recently illustrated in a 2011 on line book chapter by Natalie Novick Brown, Kieran O'Malley and Ann Streissguth in which the developmental psychiatric presentations of FASD were shown to include sometimes unrecognized Autistic Spectrum Disorder or Asperger's Disorder.

#### **2.2. Aetiological theories postulated for this link**

It is important to place the possible link between prenatal alcohol exposure and Autism spectrum disorder or Asperger's Disorder in a historical context. Environmental agents, diseases and postnatal interventions have had, it is fair to say, a rather mixed and controversial past, as recently pointed out by Cathy Lord, So Hyun K im and Adriana Dimartino in 2011.

Although as far back as 1971 American child psychiatrist Stella Chess's case review of rubella and thalidomide cases implicated these prenatal infectious and medication exposures as aetiological, the series were small. European researchers Gilberg and Gilberg in 1983 have more rigorously identified a cluster of adverse prenatal complications which may contribute to a clinical presentation of Autism Spectrum disorder in early childhood.

However the most studied, but as well the most problematic, was the potential association between MMR vaccine and Autism Spectrum Disorder. It is not the remit of the chapter to completely review this, ultimately, false trail. Nevertheless it offers a salutary lesson in the emotional reactions that possible environmental agents or interventions can elicit to the public at large, but also the medical profession.

Alcohol has been in society for ever and the acknowledgement of prenatal alcohol and its tertatogenic effect is still relatively a new phenomenon. So it is prudent to not 'scaremonger', but scientifically and clinically carefully piece out the veracity of this possible link.

The science of alcohol teratology continues to advance in leaps and bounds and one of the core findings has been the effect of prenatal alcohol on the dynamic balance of the developing neurotransmitters. In parallel with the more focused autism research on the role of serotoni‐ nergic neurotransmitters has been the identified effect of alcohol on the embryological serotoninergic neurotransmitter system. This research branches into the study of the serotonin transporter gene, by groups such as Bonnin et al in 2011, but again parallel work on epigenetics in alcohol has begun to unravel probable trans-generational shifts in genetic transcription through effects on DNA methylation (Haycock 2009).

Another strand of research in alcohol teratogenesis has been identifying brain areas a more sensitive to alcohol damage. Areas such as the corpus callosum, hippocampus, prefrontal cortex, temporal lobe collectively and individually contribute to a clinical presentation of social disconnectedness, lack of social cognition and awareness, impulsivity, and inability to understand another person's cognitions or feelings (alexithymia). (Bookstein et al 2001).

The underlying organic brain dysfunction at a cellular, neurotransmitter and structural level related to prenatal alcohol exposure sometimes shares significant congruence with ongoing neuroscience research in Autism Spectrum Disorder and Asperger's Disorder, and awaits collaborative work between the two academic fields.

There is also accumulating research which highlights the biological roots of fundamental functional problems in FASD which relate to sustained impact on working memory, (Congdon et al 2012)

#### **2.3. Neuropsychological framework of understanding ASD and Aspergers and its relationship to patients with FASD**


2009-2010, adult psychiatrist in London, Raja Mukarjee, has painstakingly clinically analysed

In the international paediatric and child psychiatric field the last 5 years have brought a wealth of clinical case descriptions and case studies indicating the presence of ADHD co-morbidly with PDD or Autistic Spectrum Disorder. Clinicians and researchers such as Professor Jeremy Turk in the UK have commented on as much as a 25-30% co-morbid link between ADHD and PDD/ASD. Furthermore the complexity of diagnostic issues within FASD have been recently illustrated in a 2011 on line book chapter by Natalie Novick Brown, Kieran O'Malley and Ann Streissguth in which the developmental psychiatric presentations of FASD were shown to

include sometimes unrecognized Autistic Spectrum Disorder or Asperger's Disorder.

It is important to place the possible link between prenatal alcohol exposure and Autism spectrum disorder or Asperger's Disorder in a historical context. Environmental agents, diseases and postnatal interventions have had, it is fair to say, a rather mixed and controversial past, as recently pointed out by Cathy Lord, So Hyun K im and Adriana Dimartino in 2011.

Although as far back as 1971 American child psychiatrist Stella Chess's case review of rubella and thalidomide cases implicated these prenatal infectious and medication exposures as aetiological, the series were small. European researchers Gilberg and Gilberg in 1983 have more rigorously identified a cluster of adverse prenatal complications which may contribute

However the most studied, but as well the most problematic, was the potential association between MMR vaccine and Autism Spectrum Disorder. It is not the remit of the chapter to completely review this, ultimately, false trail. Nevertheless it offers a salutary lesson in the emotional reactions that possible environmental agents or interventions can elicit to the public

Alcohol has been in society for ever and the acknowledgement of prenatal alcohol and its tertatogenic effect is still relatively a new phenomenon. So it is prudent to not 'scaremonger',

The science of alcohol teratology continues to advance in leaps and bounds and one of the core findings has been the effect of prenatal alcohol on the dynamic balance of the developing neurotransmitters. In parallel with the more focused autism research on the role of serotoni‐ nergic neurotransmitters has been the identified effect of alcohol on the embryological serotoninergic neurotransmitter system. This research branches into the study of the serotonin transporter gene, by groups such as Bonnin et al in 2011, but again parallel work on epigenetics in alcohol has begun to unravel probable trans-generational shifts in genetic transcription

Another strand of research in alcohol teratogenesis has been identifying brain areas a more sensitive to alcohol damage. Areas such as the corpus callosum, hippocampus, prefrontal cortex, temporal lobe collectively and individually contribute to a clinical presentation of social

but scientifically and clinically carefully piece out the veracity of this possible link.

to a clinical presentation of Autism Spectrum disorder in early childhood.

**2.2. Aetiological theories postulated for this link**

456 Recent Advances in Autism Spectrum Disorders - Volume I

at large, but also the medical profession.

through effects on DNA methylation (Haycock 2009).

the clinical presentation of Autistic Spectrum Disorder in patients with FASD.

	- **a.** theory of mind theory
	- **b.** the executive theory
	- **c.** the praxis/imitation theory
	- **d.** the emotion theory
	- **e.** the emphathizing-systematizing or ' extreme male brain' theory ( Hobson 1989, Russell 1997, Baren Cohen et al 2000, Pennington 2009)

#### **2.4. Clinical presentations of Aspergers disorder or autism spectrum disorder with FASD**

This is the arena where the divergence between the classic presentations of Autism Spectrum Disorder and Aspergers Disorder are seen, and offer a way to untangle the different aetiolog‐ ical routes to these syndromes.

FASD begin at birth and can be seen in infancy. The Mental Health Classification system, Zero to three (DC 0-3R, 2005) has a diagnostic category of Regulatory Disorders which aptly describes the immediate clinical presentations of Dysmorphic FAS or non dysmorphic ARND. It is the category of Regulatory Disorder, underresponsive type which is the harbinger of autism Spectrum Disorder or Aspergers Disorder diagnoses in early child hood.So the classic time presentation of Autism Spectrum Disorder or Aspergers Disorder is different in the FASD population.

The stereotypic movements, flapping, posturing are less commonly part of the FASD presen‐ tation. However they present more commonly a Developmental Co-ordination Disorder which is diagnosed often Dyspraxia in countries such as Ireland.

Little comment is made on the family stress in this complex mix population but a family centred therapeutic approach is the kernel of management and Identity issues have a completely different resonance in an adolescent who is bright, has ARND, Aspergers disorder and is trying to cope with the early loss of a birth mother to cirrhosis of the liver at 36 when her/she is aware that the ARND has its roots in the birth mothers drinking during pregnancy. In Ireland the 3/ 4 generations of families with FASD creates a transgenerational challenge to unraveling disorganized parenting from disconnected parenting due to fundamental social communica‐

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

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

459

Recent international guidelines have included FASD among the environmentally-induced neurodevelopmental disorders. (Sage Handbook of Developmental Disorders, 2011) Such a neurodevelopmental diagnostic framework for children and adolescents with FASD improves outcome and prognosis in many cases, notably for those with persistent aggressive and antisocial behaviors. Neither the dysmorphic, Fetal Alcohol Syndrome (FAS) nor the nondysmorphic,Alcohol Related Neurodevelopmental Disorder (ARND) condition is currently

Therefore Susan Rich and Kieran O'Malley, 2012, have recently proposed an alternative psychiatric formulation based on a neurodevelopmental model. This was suggested in order to improve clinical understanding and treatment of these complex developmental psychiatric patients. Such a paradigm shift would better identify the large numbers of children who fall through the cracks in diagnostic coding, becoming stuck in a revolving door through psychi‐

These complex cognitive and psychiatric deficits often predispose affected individuals to a high degree of sensitivity to medications, increased risk of overmedication, treatment with medication combinations, susceptibility to changes in dosing regimens, and paradoxical

Increasing clinical experience in using a neurodevelopmental formulation (compared to the traditional multi-axial system) to guide the measured, educated use of psychotropics for treatment of FASD can facilitate dramatic improvements in functioning of this challenging

Early and/or multidisciplinary intervention and treatment can prevent or minimize disruptive and risky behaviors, reduce academic failure, improve placement outcomes and reduce chronic involvement in the legal and probation system. ( O'Malley 2011b, Rich & O'Malley

Although nearly every type of Axis I and II disorder in both DSM IV –TR and ICD 10 Classi‐ fications, as well as most disorders from the 0-3 coding manual can be expressed by individuals with effects of prenatal alcohol exposure, there have been efforts to better characterize the common clinical features associated with ARND. While neurodevelopmental deficits may

**3. The domains of alcohol-related neurodevelopmental disorder**

tion disorders. (Cummings et al 2000)

diagnosable as an Axis I disorder.

responses to certain drugs.

population.

2012)

atric hospitals and institutions. (Brown et al 2011).

The essence of the overlapping clinical presentations comes in the expressive and receptive language area. The qualitative impairments in social awareness, social cognition, social communication are not uncommonly very hard to differentiate whether using clinical assessment by an experienced child psychiatrist or psychologist or using standardized instruments such as ADOS among others. In many countries the ambivalence to accept the true prevalence of FASD( ! in 100 live births) leads school systems and physicians to 'hide' many FASD patients under a Autism Spectrum Disorder or Asperger's Disorder diagnosis because of the expediency of receiving school learning disability services. This is slowly changing, pioneered in countries such as Canada and the USA. Now the UK are acknowledg‐ ing that FASD are the current biggest challenge for teaching as these pupils display complex learning disabilities with co –morbid psychiatric disorders for which there is no regular curriculum ( Professor Barry Carpenter UK, 2012).

This chapter will include psychiatric clinical analysis of patients with FASD who present autism spectrum Disorder or Aspergers Disorder features. with formal cognitive testing done and not uncommonly differing autism assessments which have proved equivocal. The comorbid ADHD is a more frequent issue in the FASD population and this has critical importance in both understanding and management. For example a successful medication treatment of pervasive distractibility visual and auditory can have a positive effect on the child's social functioning as he/she can now attend sufficiently to read faces and verbal and non verbal cues.

Medication is a change in the FASD patients who present with Autism spectrum disorder or Aspergers Disorder features. The more commonly accepted efficacy of SSRI does not neces‐ sarily hold true for FASD children or adolescents with and can lead to unmasking a bipolar diathesis, or in older patients contributing to Extra pyramidal symptoms.. This is especially a problem in Ireland which has a high prevalence of Affective Disorder which is quite common in the mothers who drink alcohol during pregnancy and so this genetic vulnerability can be brought forth by too aggressive use of SSRI for that autism or Aspergers Disorder. As well the psychostimulants can lead to an over focus in the FASD/ ASD group with increased persev‐ eration which can become a source of severe rage if challenged. As well the psychostimulants are more likely to run the risk of bringing a schizoid change in the patient. Atypical agents such as risperidone with its differential effect on 5HT receptor can also prove problematic in management of Autism or Aspergers with a prenatal alcohol exposure history. In this case the longer and prolonged use of the medicine can make the clinical situation worse by unmasking an affective instability. (Rich & O'Malley 2012)

Seizure disorders can be related to prenatal alcohol exposure and the effect of alcohol on the GABA ergic system is one hypothesis. (Daniel Bonthius et al 1992, O'Malley and Barr 1998).unexplained explosive episodes, rage attacks in FASD patients with autism Spectrum disorder or Aspergers Disorder may have origins in seizure disorders which are not related to the lower level of cognitive functioning or IQ as is the accepted rule.

Little comment is made on the family stress in this complex mix population but a family centred therapeutic approach is the kernel of management and Identity issues have a completely different resonance in an adolescent who is bright, has ARND, Aspergers disorder and is trying to cope with the early loss of a birth mother to cirrhosis of the liver at 36 when her/she is aware that the ARND has its roots in the birth mothers drinking during pregnancy. In Ireland the 3/ 4 generations of families with FASD creates a transgenerational challenge to unraveling disorganized parenting from disconnected parenting due to fundamental social communica‐ tion disorders. (Cummings et al 2000)

The stereotypic movements, flapping, posturing are less commonly part of the FASD presen‐ tation. However they present more commonly a Developmental Co-ordination Disorder which

The essence of the overlapping clinical presentations comes in the expressive and receptive language area. The qualitative impairments in social awareness, social cognition, social communication are not uncommonly very hard to differentiate whether using clinical assessment by an experienced child psychiatrist or psychologist or using standardized instruments such as ADOS among others. In many countries the ambivalence to accept the true prevalence of FASD( ! in 100 live births) leads school systems and physicians to 'hide' many FASD patients under a Autism Spectrum Disorder or Asperger's Disorder diagnosis because of the expediency of receiving school learning disability services. This is slowly changing, pioneered in countries such as Canada and the USA. Now the UK are acknowledg‐ ing that FASD are the current biggest challenge for teaching as these pupils display complex learning disabilities with co –morbid psychiatric disorders for which there is no regular

This chapter will include psychiatric clinical analysis of patients with FASD who present autism spectrum Disorder or Aspergers Disorder features. with formal cognitive testing done and not uncommonly differing autism assessments which have proved equivocal. The comorbid ADHD is a more frequent issue in the FASD population and this has critical importance in both understanding and management. For example a successful medication treatment of pervasive distractibility visual and auditory can have a positive effect on the child's social functioning as he/she can now attend sufficiently to read faces and verbal and non verbal cues.

Medication is a change in the FASD patients who present with Autism spectrum disorder or Aspergers Disorder features. The more commonly accepted efficacy of SSRI does not neces‐ sarily hold true for FASD children or adolescents with and can lead to unmasking a bipolar diathesis, or in older patients contributing to Extra pyramidal symptoms.. This is especially a problem in Ireland which has a high prevalence of Affective Disorder which is quite common in the mothers who drink alcohol during pregnancy and so this genetic vulnerability can be brought forth by too aggressive use of SSRI for that autism or Aspergers Disorder. As well the psychostimulants can lead to an over focus in the FASD/ ASD group with increased persev‐ eration which can become a source of severe rage if challenged. As well the psychostimulants are more likely to run the risk of bringing a schizoid change in the patient. Atypical agents such as risperidone with its differential effect on 5HT receptor can also prove problematic in management of Autism or Aspergers with a prenatal alcohol exposure history. In this case the longer and prolonged use of the medicine can make the clinical situation worse by unmasking

Seizure disorders can be related to prenatal alcohol exposure and the effect of alcohol on the GABA ergic system is one hypothesis. (Daniel Bonthius et al 1992, O'Malley and Barr 1998).unexplained explosive episodes, rage attacks in FASD patients with autism Spectrum disorder or Aspergers Disorder may have origins in seizure disorders which are not related

to the lower level of cognitive functioning or IQ as is the accepted rule.

is diagnosed often Dyspraxia in countries such as Ireland.

458 Recent Advances in Autism Spectrum Disorders - Volume I

curriculum ( Professor Barry Carpenter UK, 2012).

an affective instability. (Rich & O'Malley 2012)

Recent international guidelines have included FASD among the environmentally-induced neurodevelopmental disorders. (Sage Handbook of Developmental Disorders, 2011) Such a neurodevelopmental diagnostic framework for children and adolescents with FASD improves outcome and prognosis in many cases, notably for those with persistent aggressive and antisocial behaviors. Neither the dysmorphic, Fetal Alcohol Syndrome (FAS) nor the nondysmorphic,Alcohol Related Neurodevelopmental Disorder (ARND) condition is currently diagnosable as an Axis I disorder.

Therefore Susan Rich and Kieran O'Malley, 2012, have recently proposed an alternative psychiatric formulation based on a neurodevelopmental model. This was suggested in order to improve clinical understanding and treatment of these complex developmental psychiatric patients. Such a paradigm shift would better identify the large numbers of children who fall through the cracks in diagnostic coding, becoming stuck in a revolving door through psychi‐ atric hospitals and institutions. (Brown et al 2011).

These complex cognitive and psychiatric deficits often predispose affected individuals to a high degree of sensitivity to medications, increased risk of overmedication, treatment with medication combinations, susceptibility to changes in dosing regimens, and paradoxical responses to certain drugs.

Increasing clinical experience in using a neurodevelopmental formulation (compared to the traditional multi-axial system) to guide the measured, educated use of psychotropics for treatment of FASD can facilitate dramatic improvements in functioning of this challenging population.

Early and/or multidisciplinary intervention and treatment can prevent or minimize disruptive and risky behaviors, reduce academic failure, improve placement outcomes and reduce chronic involvement in the legal and probation system. ( O'Malley 2011b, Rich & O'Malley 2012)
