Children and adolescents affected by prenatal exposure to alcohol who have brain damage that is manifested in functional impairments of neurocognition, self-regulation, and adaptive functioning may most appropriately be diagnosed with neurobehavioral disorder associated with prenatal exposure. This Special Article outlines clinical implications and guidelines for pediatric medical home clinicians to identify, diagnose, and refer children regarding neurobehavioral disorder associated with prenatal exposure. Emphasis is given to reported or observable behaviors that can be identified as part of care in
pediatric medical homes, differential diagnosis, and potential comorbidities. In addition, brief guidance is provided on the management of affected children in the pediatric medical home. Finally, suggestions are given for obtaining prenatal history of in utero exposure to alcohol for the pediatric patient.
Psychiatric concerns about the consequences of prenatal alcohol exposureBARRY STANLEY 2 fasd
Psychiatric concerns about the consequences of prenatal alcohol exposure
I have omitted the references in these papers. They can be downloaded.
In 2014 the US National Institute of Mental Health (NIMH) announced it was going to divert research funding from abstract psychiatry to the neurobiological roots of disease.
This has resulted in identification of the abnormal brain functions relating to the behavioral diagnoses of the DSM5. These brain disfunctions are not the cause of DSM5 mental illnesses: they are the true pathology of those mental illnesses. The question is- what is the cause of those brain disfunctions?
Psychiatry has never explored the role of prenatal alcohol, or preconceptual alcohol in the etiology of mental illnesses.
This is in spite of anecdotal, behavioral, epidemiological, neurological and epigenetic correlations.
Meanwhile mental illness, addictions and suicides continue unabated, in spite of huge expenditures.
The day will come when the genes that control individual aspects of brain function will be identified. Changes in gene expression will be related to clinical presentations, such as those in the DSM5: the generation at which those changes occurred will be determined.
The agent that caused those changes, with other environmental factors, will be identified.
Then we will understand to what degree alcohol has determined the nature of mental illness.
The utility of psychotropic drugs on patients with fetal alcohol spectrum dis...BARRY STANLEY 2 fasd
ABSTRACT
BACKGROUND: Treatment of the complications arising from Prenatal Alcohol Exposure (PAE) has largely been focused on psychosocial and environmental approaches. Research on the
use of medications, especially psychotropic medications, has lagged behind.
OBJECTIVES: This systematic review sought to investigate psychotropic medication related findings and outcomes in those diagnosed with Fetal Alcohol Spectrum Disorder (FASD).
METHODS: Comprehensive searches were conducted in seven major databases (Medline/
PubMed, Scopus, Web of Knowledge, Embase, PsycINFO, Cochrane Library, and
PsycARTICLES) up to February 2017. Key search terms with synonyms were mapped on these databases. There were no timeline restrictions and no grey literature searches. Two reviewers
independently assessed 25 studies that met the inclusion criteria. Most studies were reviews of treatment and retrospective case series.
RESULTS: Two crossover randomized trials were reported, and the findings were not amenable to meta-analysis. Several conditions (depression, agitation, seizures, and outburst) combined with the most frequent presentation, ADHD, to represent the rationale for prescribing psychotropic medications. Second-generation antipsychotics were found to improve social skills, but the paucity of data limited the extent of clinical guidance necessary for the field.
CONCLUSIONS: The systematic review showed that there are some clinical evidence displaying
the validity of psychopharmacological interventions in people with FASD, which varies across the spectrum of disease severity, age, and gender. There is a need for more clinical evidencebased studies in addition to clinical expert opinions to substantiate an optimal ground for individualized management of FASD.
The study protocol for this review was registered in PROSPERO with registration number
CRD42016045703
Fetal Alcohol Spectrum Disorder (FASD) and Sexually Inappropriate Behaviors: ...BARRY STANLEY 2 fasd
ABSTRACT
Affecting millions of individuals in North America, Fetal Alcohol Spectrum Disorder (FASD) is characterized by impairments in cognitive, social, and adaptive functioning. The presence and severity of these symptoms vary widely by individual, as such typical mental health screening, assessment, and diagnostic processes often fail to accurately identify FASD. A consequence of diagnostic difficulties is that individuals with FASD often go untreated or receive ineffective treatment services. It is common for some individuals with FASD to struggle to comprehend interpersonal cues and non-verbal behaviors of others,
understand normative social boundaries, control one’s impulses, and find socially appropriate ways to express sexual desires.
When adequate treatment services are not provided, individuals with FASD may become inadvertently involved in the legal system for crimes including sexual misconduct. Individuals with FASD who become involved in the criminal justice system often have more difficulty obtaining benefit
it from services provided compared to those without FASD and maybe at greater risk for recidivism. This is especially the case when interventions, services, and supports fail to take into account the short and long-term deficits caused by prenatal alcohol exposure. To serve as a guide for criminal justice and forensic mental health professionals,
This article provides background information on FASD, explores the role of FASD symptoms in sexually inappropriate behaviors discusses screening and assessment considerations, identifies potential treatment and intervention options, and makes recommendations for future research. Finally, example cases are provided to assist the reader in understanding how FASD influences the individual who engages in inappropriate sexual behaviors. These examples provide detailed descriptions of the various areas of functioning affected by FASD and how this can result in different kinds of inappropriate sexual behaviors
resulting in involvement in both the mental health and criminal justice systems.
Twin study confirms virtually identical prenatal alcohol exposures can lead t...BARRY STANLEY 2 fasd
Abstract
Background: Risk of fetal alcohol spectrum disorder (FASD) is not based solely on the timing and level of prenatal alcohol exposure (PAE). The effects of teratogens can be modified by genetic differences in fetal susceptibility and resistance. This is best illustrated in twins.
Objective: To compare the prevalence and magnitude of pairwise discordance in FASD diagnoses across
monozygotic twins, dizygotic twins, full-siblings, and half-siblings sharing a common birth mother.
Methods: Data from the Fetal Alcohol Syndrome Diagnostic & Prevention Network clinical database was used. Sibling pairs were matched on age and PAE, raised together, and diagnosed by the same University of Washington interdisciplinary team using the FASD 4-Digit Code. This design sought to assess and
isolate the role of genetics on fetal vulnerability/resistance to the teratogenic effects of PAE by eliminating
or minimizing pairwise discordance in PAE and other prenatal/postnatal risk factors.
Results: As genetic relatedness between siblings decreased from 100% to 50% to 50% to 25% across the four groups (9 monozygotic, 39 dizygotic, 27 full-sibling and 9 half-sibling pairs, respectively), the prevalence of pairwise discordance in FASD diagnoses increased from 0% to 44% to 59% to 78%. Despite virtually identical PAE, 4 pairs of dizygotic twins had FASD diagnoses at opposite ends of the fetal alcohol spectrum—Partial Fetal Alcohol Syndrome versus Neurobehavioral Disorder/Alcohol-Exposed.
Conclusion: Despite virtually identical PAE, fetuses can experience vastly different FASD outcomes.
Thus, to protect all fetuses, especially the most genetically vulnerable, the only safe amount to drink is none at all.
Psychiatric concerns about the consequences of prenatal alcohol exposureBARRY STANLEY 2 fasd
Psychiatric concerns about the consequences of prenatal alcohol exposure
I have omitted the references in these papers. They can be downloaded.
In 2014 the US National Institute of Mental Health (NIMH) announced it was going to divert research funding from abstract psychiatry to the neurobiological roots of disease.
This has resulted in identification of the abnormal brain functions relating to the behavioral diagnoses of the DSM5. These brain disfunctions are not the cause of DSM5 mental illnesses: they are the true pathology of those mental illnesses. The question is- what is the cause of those brain disfunctions?
Psychiatry has never explored the role of prenatal alcohol, or preconceptual alcohol in the etiology of mental illnesses.
This is in spite of anecdotal, behavioral, epidemiological, neurological and epigenetic correlations.
Meanwhile mental illness, addictions and suicides continue unabated, in spite of huge expenditures.
The day will come when the genes that control individual aspects of brain function will be identified. Changes in gene expression will be related to clinical presentations, such as those in the DSM5: the generation at which those changes occurred will be determined.
The agent that caused those changes, with other environmental factors, will be identified.
Then we will understand to what degree alcohol has determined the nature of mental illness.
The utility of psychotropic drugs on patients with fetal alcohol spectrum dis...BARRY STANLEY 2 fasd
ABSTRACT
BACKGROUND: Treatment of the complications arising from Prenatal Alcohol Exposure (PAE) has largely been focused on psychosocial and environmental approaches. Research on the
use of medications, especially psychotropic medications, has lagged behind.
OBJECTIVES: This systematic review sought to investigate psychotropic medication related findings and outcomes in those diagnosed with Fetal Alcohol Spectrum Disorder (FASD).
METHODS: Comprehensive searches were conducted in seven major databases (Medline/
PubMed, Scopus, Web of Knowledge, Embase, PsycINFO, Cochrane Library, and
PsycARTICLES) up to February 2017. Key search terms with synonyms were mapped on these databases. There were no timeline restrictions and no grey literature searches. Two reviewers
independently assessed 25 studies that met the inclusion criteria. Most studies were reviews of treatment and retrospective case series.
RESULTS: Two crossover randomized trials were reported, and the findings were not amenable to meta-analysis. Several conditions (depression, agitation, seizures, and outburst) combined with the most frequent presentation, ADHD, to represent the rationale for prescribing psychotropic medications. Second-generation antipsychotics were found to improve social skills, but the paucity of data limited the extent of clinical guidance necessary for the field.
CONCLUSIONS: The systematic review showed that there are some clinical evidence displaying
the validity of psychopharmacological interventions in people with FASD, which varies across the spectrum of disease severity, age, and gender. There is a need for more clinical evidencebased studies in addition to clinical expert opinions to substantiate an optimal ground for individualized management of FASD.
The study protocol for this review was registered in PROSPERO with registration number
CRD42016045703
Fetal Alcohol Spectrum Disorder (FASD) and Sexually Inappropriate Behaviors: ...BARRY STANLEY 2 fasd
ABSTRACT
Affecting millions of individuals in North America, Fetal Alcohol Spectrum Disorder (FASD) is characterized by impairments in cognitive, social, and adaptive functioning. The presence and severity of these symptoms vary widely by individual, as such typical mental health screening, assessment, and diagnostic processes often fail to accurately identify FASD. A consequence of diagnostic difficulties is that individuals with FASD often go untreated or receive ineffective treatment services. It is common for some individuals with FASD to struggle to comprehend interpersonal cues and non-verbal behaviors of others,
understand normative social boundaries, control one’s impulses, and find socially appropriate ways to express sexual desires.
When adequate treatment services are not provided, individuals with FASD may become inadvertently involved in the legal system for crimes including sexual misconduct. Individuals with FASD who become involved in the criminal justice system often have more difficulty obtaining benefit
it from services provided compared to those without FASD and maybe at greater risk for recidivism. This is especially the case when interventions, services, and supports fail to take into account the short and long-term deficits caused by prenatal alcohol exposure. To serve as a guide for criminal justice and forensic mental health professionals,
This article provides background information on FASD, explores the role of FASD symptoms in sexually inappropriate behaviors discusses screening and assessment considerations, identifies potential treatment and intervention options, and makes recommendations for future research. Finally, example cases are provided to assist the reader in understanding how FASD influences the individual who engages in inappropriate sexual behaviors. These examples provide detailed descriptions of the various areas of functioning affected by FASD and how this can result in different kinds of inappropriate sexual behaviors
resulting in involvement in both the mental health and criminal justice systems.
Twin study confirms virtually identical prenatal alcohol exposures can lead t...BARRY STANLEY 2 fasd
Abstract
Background: Risk of fetal alcohol spectrum disorder (FASD) is not based solely on the timing and level of prenatal alcohol exposure (PAE). The effects of teratogens can be modified by genetic differences in fetal susceptibility and resistance. This is best illustrated in twins.
Objective: To compare the prevalence and magnitude of pairwise discordance in FASD diagnoses across
monozygotic twins, dizygotic twins, full-siblings, and half-siblings sharing a common birth mother.
Methods: Data from the Fetal Alcohol Syndrome Diagnostic & Prevention Network clinical database was used. Sibling pairs were matched on age and PAE, raised together, and diagnosed by the same University of Washington interdisciplinary team using the FASD 4-Digit Code. This design sought to assess and
isolate the role of genetics on fetal vulnerability/resistance to the teratogenic effects of PAE by eliminating
or minimizing pairwise discordance in PAE and other prenatal/postnatal risk factors.
Results: As genetic relatedness between siblings decreased from 100% to 50% to 50% to 25% across the four groups (9 monozygotic, 39 dizygotic, 27 full-sibling and 9 half-sibling pairs, respectively), the prevalence of pairwise discordance in FASD diagnoses increased from 0% to 44% to 59% to 78%. Despite virtually identical PAE, 4 pairs of dizygotic twins had FASD diagnoses at opposite ends of the fetal alcohol spectrum—Partial Fetal Alcohol Syndrome versus Neurobehavioral Disorder/Alcohol-Exposed.
Conclusion: Despite virtually identical PAE, fetuses can experience vastly different FASD outcomes.
Thus, to protect all fetuses, especially the most genetically vulnerable, the only safe amount to drink is none at all.
Twin study confirms virtually identical prenatal alcohol exposures can lead t...BARRY STANLEY 2 fasd
Abstract
Background: Risk of fetal alcohol spectrum disorder (FASD) is not based solely on the timing and level of prenatal alcohol exposure (PAE). The effects of teratogens can be modified by genetic differences in fetal susceptibility and resistance. This is best illustrated in twins.
Objective: To compare the prevalence and magnitude of pairwise discordance in FASD diagnoses across
monozygotic twins, dizygotic twins, full-siblings, and half-siblings sharing a common birth mother.
Methods: Data from the Fetal Alcohol Syndrome Diagnostic & Prevention Network clinical database was used. Sibling pairs were matched on age and PAE, raised together, and diagnosed by the same University of Washington interdisciplinary team using the FASD 4-Digit Code. This design sought to assess and
isolate the role of genetics on fetal vulnerability/resistance to the teratogenic effects of PAE by eliminating or minimizing pairwise discordance in PAE and other prenatal/postnatal risk factors.
Results: As genetic relatedness between siblings decreased from 100% to 50% to 50% to 25% across the four groups (9 monozygotic, 39 dizygotic, 27 full-sibling and 9 half-sibling pairs, respectively), the prevalence of pairwise discordance in FASD diagnoses increased from 0% to 44% to 59% to 78%. Despite virtually identical PAE, 4 pairs of dizygotic twins had FASD diagnoses at opposite ends of the fetal alcohol spectrum—Partial Fetal Alcohol Syndrome versus Neurobehavioral Disorder/Alcohol-Exposed.
Conclusion: Despite virtually identical PAE, fetuses can experience vastly different FASD outcomes.
Thus, to protect all fetuses, especially the most genetically vulnerable, the only safe amount to drink is none at all.
Article fetal alcohol spectrum disorder and firesetting behaviors a guide for...BARRY STANLEY 2 fasd
"Fetal Alcohol Spectrum Disorder and Fire setting Behaviors:
A Guide for Criminal Justice, Fire, and Forensic Professionals"
setting fires can be a problem for those with FASD.
IMO it is a means of escaping the chaos of "boredom" by those who have a sensory disability that relates to fire.
Challenges in accurately assessing prenatal alcohol exposure inBARRY STANLEY 2 fasd
Comment on the paper - Challenges in accurately assessing prenatal alcohol exposure in a study of Fetal Alcohol Spectrum Disorder in a youth detention center.
A systematic review of prevention interventions to reduce prenatal alcohol ex...BARRY STANLEY 2 fasd
Fetal alcohol spectrum disorder (FASD) is a preventable, lifelong neurodevelopmental disorder caused by prenatal alcohol
exposure. FASD negatively impacts individual Indigenous communities around the world. Although many prevention
interventions have been developed and implemented, they have not been adequately evaluated. This systematic review updates
the evidence for the effectiveness of FASD prevention interventions in Indigenous/Aboriginal populations internationally, and in specific populations in North America and New Zealand, and offers recommendations for future work.
Conclusions reached from my involvement with the Canadian criminal justice system. 2011.
amd- 2021
References of papers published by Dr Mansfield Mela, and others regarding FASD, PAE, Mental Health, and the Justice System.
Dr Mela is one of the very few Forensic Psychiatrists who understands and advocates for those with FASD.
Summary of activities related to FASD at the Ron Joyce Children's Health Centre, Hamilton, ON, Canada presented at: FASD - Achieving New Heights Together in Burlington, ON, Canada on March 22, 2019.
Fetal alcohol spectrum disorders: an overview from the glia perspectiveBARRY STANLEY 2 fasd
Abstract
Alcohol consumption during pregnancy can produce a variety of central nervous system (CNS) abnormalities in the offspring resulting in a broad spectrum of cognitive and behavioral impairments that constitute the most severe and long-lasting effects observed in fetal alcohol spectrum disorders (FASD). Alcohol-induced abnormalities in glial cells have been suspected of contributing to the adverse effects of alcohol on the developing brain for several years, although much research still needs to be done to causally link the effects of alcohol on specific brain structures and behavior to alterations in glial cell development and function. Damage to radial glia due to prenatal alcohol exposure may underlie observations of abnormal neuronal and glial migration in humans with Fetal Alcohol Syndrome (FAS), as well as primate and rodent models of FAS. A reduction in cell number and altered
development has been reported for several glial cell types in animal models of FAS. In utero alcohol exposure can cause microencephaly when alcohol exposure occurs during the brain growth spurt a period characterized by rapid astrocyte proliferation and maturation; since astrocytes are the most abundant cells in the brain, microenchephaly may be caused by reduced astrocyte proliferation or survival, as observed in in vitro and in vivo studies. Delayed oligodendrocyte development and increased oligodendrocyte precursor apoptosis has also been reported in experimental models of FASD,
which may be linked to altered myelination/white matter integrity found in FASD children. Children with FAS exhibit hypoplasia of the corpus callosum and anterior commissure, two areas requiring guidance from glial cells and proper maturation of oligodendrocytes. Finally, developmental alcohol exposure disrupts microglial function and induces microglial apoptosis; given the role of microglia in synaptic pruning during brain development, the effects of alcohol on microglia may be involved in the abnormal brain plasticity reported in FASD. The consequences of prenatal alcohol exposure on glial
cells, including radial glia and other transient glial structures present in the developing brain, astrocytes, oligodendrocytes and their precursors, and microglia contributes to abnormal neuronal development, reduced neuron survival and disrupted brain architecture and connectivity. This review highlights the CNS structural abnormalities caused by in utero alcohol exposure and outlines which abnormalities are likely mediated by alcohol effects on glial cell development and function.
Keywords: astrocyte, microglia, oligodendrocyte, fetal alcohol syndrome, fetal alcohol spectrum disorder.
Abstract: Fetal alcohol spectrum disorder (FASD) is a significant public health issue in Australia that is poorly diagnosed, chronic and costly.
FASD is a diffuse acquired brain injury secondary to prenatal alcohol exposure. The prevalence rate of FASD among the general population in Australia is currently unknown; however, an Australian study in a selected high-risk population reported some of the highest rates of FASD in the world. A common misconception among clinicians is that a child must have ‘the face’ of FASD to have the disorder. This is incorrect. The three
sentinel facial features only occur in the minority of individuals with FASD. FASD should be considered as a ‘whole body’ disorder as increased susceptibility to chronic health problems suggests suboptimal in utero environments places the individual at risk of later disease. Clinicians are reluctant to consider FASD as a possible diagnosis because of the concern of inducing stigma; however, this concern is neither supported by the
evidence nor patient stories. The Australian Guide to the Diagnosis of FASD is now available to assist health professionals in providing timely and accurate diagnoses, which can lead to improved outcomes via evidence-based intervention and is an important first step in future prevention.
Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): ...BARRY STANLEY 2 fasd
Neurobehavioral Disorder Associated with Prenatal Alcohol
Exposure (ND-PAE): Proposed DSM-5 Diagnosis
Julie A. Kable1,Mary J. O’Connor2, Heather Carmichael Olson3, Blair Paley2, Sarah N. Mattson4, Sally M. Anderson5, Edward P. Riley.
Abstract Over the past 40 years, a significant body of
animal and human research has documented the teratogenic
effects of prenatal alcohol exposure (PAE). Neurobehavioral
Disorder associated with PAE is proposed as a new
clarifying term, intended to encompass the neurodevelopmental
and mental health symptoms associated with PAE.
Defining this disorder is a necessary step to adequately
characterize these symptoms and allow clinical assessment
not possible using existing physically-based diagnostic
schemes. Without appropriate diagnostic guidelines,
affected individuals are frequently misdiagnosed and treated
inappropriately (often to their considerable detriment)
by mental health, educational, and criminal justice systems.
Three core areas of deficits identified from the available
research, including neurocognitive, self-regulation, and
adaptive functioning impairments, are discussed and
information regarding associated features and disorders,
prevalence, course, familial patterns, differential diagnosis,
and treatment of the proposed disorder are also provided.
The impact of traumatic childhood experiences on cognitive and behavioural fu...BARRY STANLEY 2 fasd
Early diagnosis and interventions can help to prevent or reduce secondary conditions
associated with FASD: early diagnosis is associated with fewer adverse and more positive life outcomes in individuals with FASD (Streissguth et al., 2011) and emerging data on interventions are showing a similar effect (Carmichael-Olson & Montague, 2011). Interventions generally include pharmacological, behavioural and educational treatments, and many of these have shown promising results, but much more data are required in order to inform and develop theoretical foundations, methods and outcomes (Chandrasena, Mukherjee, & Turk, 2009; Mukherjee, Cook, Fleming, & Norgate, 2016). Moreover, risk factors such as abuse and neglect have received little attention within the FASD literature, leaving a risk that these factors are confounding results and conclusions.
This thesis was proposed in a collaboration between the National FASD Clinic and the University of Salford in order to develop the limited understanding of the expected presentation and development of children with exposure to both prenatal alcohol and postnatal trauma, with the long-term aim of improving interventions in this population.
Response to the five Danish papers. Submitted but not accepted for publicationBARRY STANLEY 2 fasd
In 2012 the British Journal of Obstetrics and Gynaecology publish five papers from the Danish Lifestyle During Pregnancy Study Group. These publications received a great deal or world wide media coverage. The emphasis of most of this coverage was in support of drinking low to moderate amounts of alcohol during pregnancy.
Over a period of approximately six months I corresponded with the editor of the BJOG to have a letter of response published in the journal. Although I modified my letter as was requested it was not published.
Barry Stanley
Twin study confirms virtually identical prenatal alcohol exposures can lead t...BARRY STANLEY 2 fasd
Abstract
Background: Risk of fetal alcohol spectrum disorder (FASD) is not based solely on the timing and level of prenatal alcohol exposure (PAE). The effects of teratogens can be modified by genetic differences in fetal susceptibility and resistance. This is best illustrated in twins.
Objective: To compare the prevalence and magnitude of pairwise discordance in FASD diagnoses across
monozygotic twins, dizygotic twins, full-siblings, and half-siblings sharing a common birth mother.
Methods: Data from the Fetal Alcohol Syndrome Diagnostic & Prevention Network clinical database was used. Sibling pairs were matched on age and PAE, raised together, and diagnosed by the same University of Washington interdisciplinary team using the FASD 4-Digit Code. This design sought to assess and
isolate the role of genetics on fetal vulnerability/resistance to the teratogenic effects of PAE by eliminating or minimizing pairwise discordance in PAE and other prenatal/postnatal risk factors.
Results: As genetic relatedness between siblings decreased from 100% to 50% to 50% to 25% across the four groups (9 monozygotic, 39 dizygotic, 27 full-sibling and 9 half-sibling pairs, respectively), the prevalence of pairwise discordance in FASD diagnoses increased from 0% to 44% to 59% to 78%. Despite virtually identical PAE, 4 pairs of dizygotic twins had FASD diagnoses at opposite ends of the fetal alcohol spectrum—Partial Fetal Alcohol Syndrome versus Neurobehavioral Disorder/Alcohol-Exposed.
Conclusion: Despite virtually identical PAE, fetuses can experience vastly different FASD outcomes.
Thus, to protect all fetuses, especially the most genetically vulnerable, the only safe amount to drink is none at all.
Article fetal alcohol spectrum disorder and firesetting behaviors a guide for...BARRY STANLEY 2 fasd
"Fetal Alcohol Spectrum Disorder and Fire setting Behaviors:
A Guide for Criminal Justice, Fire, and Forensic Professionals"
setting fires can be a problem for those with FASD.
IMO it is a means of escaping the chaos of "boredom" by those who have a sensory disability that relates to fire.
Challenges in accurately assessing prenatal alcohol exposure inBARRY STANLEY 2 fasd
Comment on the paper - Challenges in accurately assessing prenatal alcohol exposure in a study of Fetal Alcohol Spectrum Disorder in a youth detention center.
A systematic review of prevention interventions to reduce prenatal alcohol ex...BARRY STANLEY 2 fasd
Fetal alcohol spectrum disorder (FASD) is a preventable, lifelong neurodevelopmental disorder caused by prenatal alcohol
exposure. FASD negatively impacts individual Indigenous communities around the world. Although many prevention
interventions have been developed and implemented, they have not been adequately evaluated. This systematic review updates
the evidence for the effectiveness of FASD prevention interventions in Indigenous/Aboriginal populations internationally, and in specific populations in North America and New Zealand, and offers recommendations for future work.
Conclusions reached from my involvement with the Canadian criminal justice system. 2011.
amd- 2021
References of papers published by Dr Mansfield Mela, and others regarding FASD, PAE, Mental Health, and the Justice System.
Dr Mela is one of the very few Forensic Psychiatrists who understands and advocates for those with FASD.
Summary of activities related to FASD at the Ron Joyce Children's Health Centre, Hamilton, ON, Canada presented at: FASD - Achieving New Heights Together in Burlington, ON, Canada on March 22, 2019.
Fetal alcohol spectrum disorders: an overview from the glia perspectiveBARRY STANLEY 2 fasd
Abstract
Alcohol consumption during pregnancy can produce a variety of central nervous system (CNS) abnormalities in the offspring resulting in a broad spectrum of cognitive and behavioral impairments that constitute the most severe and long-lasting effects observed in fetal alcohol spectrum disorders (FASD). Alcohol-induced abnormalities in glial cells have been suspected of contributing to the adverse effects of alcohol on the developing brain for several years, although much research still needs to be done to causally link the effects of alcohol on specific brain structures and behavior to alterations in glial cell development and function. Damage to radial glia due to prenatal alcohol exposure may underlie observations of abnormal neuronal and glial migration in humans with Fetal Alcohol Syndrome (FAS), as well as primate and rodent models of FAS. A reduction in cell number and altered
development has been reported for several glial cell types in animal models of FAS. In utero alcohol exposure can cause microencephaly when alcohol exposure occurs during the brain growth spurt a period characterized by rapid astrocyte proliferation and maturation; since astrocytes are the most abundant cells in the brain, microenchephaly may be caused by reduced astrocyte proliferation or survival, as observed in in vitro and in vivo studies. Delayed oligodendrocyte development and increased oligodendrocyte precursor apoptosis has also been reported in experimental models of FASD,
which may be linked to altered myelination/white matter integrity found in FASD children. Children with FAS exhibit hypoplasia of the corpus callosum and anterior commissure, two areas requiring guidance from glial cells and proper maturation of oligodendrocytes. Finally, developmental alcohol exposure disrupts microglial function and induces microglial apoptosis; given the role of microglia in synaptic pruning during brain development, the effects of alcohol on microglia may be involved in the abnormal brain plasticity reported in FASD. The consequences of prenatal alcohol exposure on glial
cells, including radial glia and other transient glial structures present in the developing brain, astrocytes, oligodendrocytes and their precursors, and microglia contributes to abnormal neuronal development, reduced neuron survival and disrupted brain architecture and connectivity. This review highlights the CNS structural abnormalities caused by in utero alcohol exposure and outlines which abnormalities are likely mediated by alcohol effects on glial cell development and function.
Keywords: astrocyte, microglia, oligodendrocyte, fetal alcohol syndrome, fetal alcohol spectrum disorder.
Abstract: Fetal alcohol spectrum disorder (FASD) is a significant public health issue in Australia that is poorly diagnosed, chronic and costly.
FASD is a diffuse acquired brain injury secondary to prenatal alcohol exposure. The prevalence rate of FASD among the general population in Australia is currently unknown; however, an Australian study in a selected high-risk population reported some of the highest rates of FASD in the world. A common misconception among clinicians is that a child must have ‘the face’ of FASD to have the disorder. This is incorrect. The three
sentinel facial features only occur in the minority of individuals with FASD. FASD should be considered as a ‘whole body’ disorder as increased susceptibility to chronic health problems suggests suboptimal in utero environments places the individual at risk of later disease. Clinicians are reluctant to consider FASD as a possible diagnosis because of the concern of inducing stigma; however, this concern is neither supported by the
evidence nor patient stories. The Australian Guide to the Diagnosis of FASD is now available to assist health professionals in providing timely and accurate diagnoses, which can lead to improved outcomes via evidence-based intervention and is an important first step in future prevention.
Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): ...BARRY STANLEY 2 fasd
Neurobehavioral Disorder Associated with Prenatal Alcohol
Exposure (ND-PAE): Proposed DSM-5 Diagnosis
Julie A. Kable1,Mary J. O’Connor2, Heather Carmichael Olson3, Blair Paley2, Sarah N. Mattson4, Sally M. Anderson5, Edward P. Riley.
Abstract Over the past 40 years, a significant body of
animal and human research has documented the teratogenic
effects of prenatal alcohol exposure (PAE). Neurobehavioral
Disorder associated with PAE is proposed as a new
clarifying term, intended to encompass the neurodevelopmental
and mental health symptoms associated with PAE.
Defining this disorder is a necessary step to adequately
characterize these symptoms and allow clinical assessment
not possible using existing physically-based diagnostic
schemes. Without appropriate diagnostic guidelines,
affected individuals are frequently misdiagnosed and treated
inappropriately (often to their considerable detriment)
by mental health, educational, and criminal justice systems.
Three core areas of deficits identified from the available
research, including neurocognitive, self-regulation, and
adaptive functioning impairments, are discussed and
information regarding associated features and disorders,
prevalence, course, familial patterns, differential diagnosis,
and treatment of the proposed disorder are also provided.
The impact of traumatic childhood experiences on cognitive and behavioural fu...BARRY STANLEY 2 fasd
Early diagnosis and interventions can help to prevent or reduce secondary conditions
associated with FASD: early diagnosis is associated with fewer adverse and more positive life outcomes in individuals with FASD (Streissguth et al., 2011) and emerging data on interventions are showing a similar effect (Carmichael-Olson & Montague, 2011). Interventions generally include pharmacological, behavioural and educational treatments, and many of these have shown promising results, but much more data are required in order to inform and develop theoretical foundations, methods and outcomes (Chandrasena, Mukherjee, & Turk, 2009; Mukherjee, Cook, Fleming, & Norgate, 2016). Moreover, risk factors such as abuse and neglect have received little attention within the FASD literature, leaving a risk that these factors are confounding results and conclusions.
This thesis was proposed in a collaboration between the National FASD Clinic and the University of Salford in order to develop the limited understanding of the expected presentation and development of children with exposure to both prenatal alcohol and postnatal trauma, with the long-term aim of improving interventions in this population.
Response to the five Danish papers. Submitted but not accepted for publicationBARRY STANLEY 2 fasd
In 2012 the British Journal of Obstetrics and Gynaecology publish five papers from the Danish Lifestyle During Pregnancy Study Group. These publications received a great deal or world wide media coverage. The emphasis of most of this coverage was in support of drinking low to moderate amounts of alcohol during pregnancy.
Over a period of approximately six months I corresponded with the editor of the BJOG to have a letter of response published in the journal. Although I modified my letter as was requested it was not published.
Barry Stanley
Paper presented at-
Beyond Diagnosis: Interventions for Individuals Living with
Fetal Alcohol Spectrum Disorder. St. Michael’s Hospital,
Toronto. September, 2005.
Seminar1240 www.thelancet.com Vol 387 March 19, 2016.docxtcarolyn
Seminar
1240 www.thelancet.com Vol 387 March 19, 2016
Attention defi cit hyperactivity disorder
Anita Thapar, Miriam Cooper
Attention defi cit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a prevalence
of 1·4–3·0%. It is more common in boys than girls. Comorbidity with childhood-onset neurodevelopmental
disorders and psychiatric disorders is substantial. ADHD is highly heritable and multifactorial; multiple genes and
non-inherited factors contribute to the disorder. Prenatal and perinatal factors have been implicated as risks, but
defi nite causes remain unknown. Most guidelines recommend a stepwise approach to treatment, beginning with
non-drug interventions and then moving to pharmacological treatment in those most severely aff ected. Randomised
controlled trials show short-term benefi ts of stimulant medication and atomoxetine. Meta-analyses of blinded trials
of non-drug treatments have not yet proven the effi cacy of such interventions. Longitudinal studies of ADHD show
heightened risk of multiple mental health and social diffi culties as well as premature mortality in adult life.
Introduction
Attention defi cit hyperactivity disorder (ADHD) is a
childhood-onset neurodevelopmental disorder char ac-
terised by developmentally inappropriate and impairing
inattention, motor hyperactivity, and impulsivity, with
diffi culties often continuing into adulthood. In this
Seminar, we aim to update and inform early career
clinicians on issues relevant to clinical practice and
discuss some controversies and misunderstandings.
Defi nitions of ADHD
ADHD is a diagnostic category in the American
Psychiatric Association’s Diagnostic and Statistical
Manual of Mental Disorders 4th edition (DSM-IV)1 and
the more recent DSM-5.2 The broadly equivalent
diagnosis used predominantly in Europe is hyperkinetic
disorder, which is defi ned in WHO’s International
Classifi cation of Diseases (10th edition; ICD-10).3 This
defi nition captures a more severely aff ected group of
individuals, since reported prevalence of hyperkinetic
disorder is lower than that of DSM-IV ADHD, even
within the same population.4 Key diagnostic criteria are
listed in the panel. DSM-5 has longer symptom
descriptors than those used in DSM-IV; these descriptors
also capture how symptoms can manifest in older
adolescents and adults. DSM-IV distinguished between
inattentive, hyperactive–impulsive, and combined sub-
types of ADHD; a diagnosis of the combined subtype
required the presence of symptoms across the domains
of inattention and hyperactivity–impulsivity. However,
ADHD subtypes are not stable across time,5 and DSM-5
has de-emphasised their distinctions. ICD-10 does not
distinguish subtypes; symptoms need to be present from
the three separate domains of inattention, hyperactivity,
and impulsivity for a diagnosis of hyperkinetic disorder.
The diagnosis of ADHD or hyperkinetic disorder also
requires the pre.
Written in response to Misattributions and Potential Consequences: The Case of Child Mental Health Problems and Fetal Alcohol Spectrum Disorders. John D. McLennon. Canadian Journal of Psychiatry. Vol 60, No 12, December 2015.
Not published: too many words and references
In his fourth and concluding lecture of the IMMH Conference in San Antonio, 2014, Dr. Cady reviews the statistics, epidemiology, biological nature and pharmacologic treatment of ADHD. The first part of the presentation was absolutely conventional allopathic psychiatry, inclusive of brain imaging.
The second part of the presentation considered: "If we are thinking about biological, psychological, and behavioral interventions for a 'psychiatric' patient, shouldn't we be considering the TWO biological levels?" The most normal biological level that "biologically trained psychiatrists" consider is medications and medication effectiveness. However, sometimes even the most vigorous, precise, and heroic efforts do not work. The potential confound it the underlying physiological, hormonal, nutrient, antioxidant, PUFA-rich state associated with optimal health and well being.
In the final analysis, shouldn't we make sure that we have BOTH of these biological foundations right?
We hope that you enjoy this provocative slide presentation.
In the broader list of cognitive concerns, neuropsychological testing has shown that attentional impairment may have a specific burden in Fibromyalgia Syndrome (FMS).
Preliminary observations have reported a subset of FMS patient screened for attention disorders fulfilling the actual diagnosis of ADHD, a neurodevelopmental disorder characterized by
developmentally inadequate levels of inattention, hyperactivity and impulsivity that might persist in adulthood. Yet, no study to date has systematically examined the history and the specific
contribution of ADHD to FMS in terms of clinical impact and related specific disabilities.
In this study, 106 individuals with a FMS diagnosis based on the 2010 criteria of the American College of Rheumatology have been assessed for (a) the presence of ADHD; (b) the burden of
disability caused by ADHD versus FMS; (c) the presence of other psychiatric disorders. Results indicated that ADHD was present in 24.5% of FMS individuals, it was associated with higher FMS symptoms severity and a greater functional impairment, particularly in the work/school domain.
Moreover, patients with both FMS and ADHD had higher frequency of substance use disorders than those with FMS only (38.5% versus 3.8%) and mainly opioids. Overall, results suggest that ADHD can increase burden adding specific disability in work and social activities, and it is associated with
a trend for the excessive use of opioid painkillers. Detection of neurodevelopmental and actual symptoms of ADHD is highly recommended especially in patient prone to increase the dose of antipain medication.
Similar to Neurobehavioral disorder associated with prenatal alcohol exposure (20)
The Nomenclature of the Consequences of Prenatal Alcohol Exposure: PAE, and t...BARRY STANLEY 2 fasd
An historical account of the nomenclature relating to the effects of alcohol on the developing fetus.
The significance of facial features; the dose/threshold question; epigenetics, transgenerational consequences, and adult health issues, are raised.
The inadequacy of the present nomenclature is detailed
Effects of Hyperbaric Oxygen Therapy on Brain Perfusion, Cognition and Behavi...BARRY STANLEY 2 fasd
Abstract
A 15-year-old girl diagnosed with FASD underwent 100 courses of hyperbasic oxygen therapy (HBOT). Prior to HBOT, single motion emission compute tomographic begin imaging (SPECT)
revealed areas of hypo-perfusion bilaterally in the orbitofrontal region, temporal lobes and right dorsolateral—frontal, as well the medial aspect of the left cerebellum. Following two sets of HBOT treatments (60 plus 40), over 6 months, there was improvement in perfusion to the left cerebellum as well as the right frontal lobe. This was paralleled by improvement in immediate cognitive tests and an increase in functional brain volume. A follow-up 18 months after HBOT showed sustained
improvement in attention with no need for methylphenidate, as well as in math skills and writing.
This year as a priority of Proof Alliance’s legislative platform, major legislation that requires all children entering foster care be screened for prenatal exposure to alcohol in Minnesota was passed and signed into law. It is believed Minnesota is the first state in the nation to pass this legislation.
Four year follow-up of a randomized controlled trial of choline for neurodeve...BARRY STANLEY 2 fasd
Abstract
Background
Despite the high prevalence of fetal alcohol spectrum disorder (FASD), there are few interventions targeting its core neurocognitive and behavioral deficits. FASD is often conceptualized as static and permanent, but interventions that capitalize on brain plasticity and critical developmental windows are emerging. We present a long-term follow-up study evaluating the neurodevelopmental effects of choline supplementation in children with FASD 4 years after an initial efficacy trial
Abstract
This presentation includes a brief review of research into boredom, normal brain resting state and corresponding default mode[s].
The possible equivalence to the brain activity of those with FASD in relation to “being bored” is explored, with reference to brain anatomy and function.
Actual FASD clinical cases are presented to illustrate what individuals with FASD mean by “boredom”: describing the role of perseveration as a relief process.
Finally, the manner in which these processes are misinterpreted is explored, with implications for Psychiatry and the Justice System.
Association Between Prenatal Exposure to Alcohol and Tobacco and Neonatal Bra...BARRY STANLEY 2 fasd
IMPORTANCE Research to date has not determined a safe level of alcohol or tobacco use during pregnancy. Electroencephalography (EEG) is a noninvasive measure of cortical function that has previously been used to examine effects of in utero exposures and associations with
neurodevelopment.
OBJECTIVE To examine the association of prenatal exposure to alcohol (PAE) and tobacco smoking (PTE) with brain activity in newborns.
CONCLUSIONS AND RELEVANCE These findings suggest that even low levels of PAE or PTE are
associated with changes in offspring brain development.
Submitted to –
National Institute for Health and Care Excellence Fetal alcohol spectrum disorder
Consultation on draft quality standard – deadline for comments 5pm on 03/04/20
Clinical course and risk factors for mortality of adult inpatients with covid...BARRY STANLEY 2 fasd
Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help
clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale
for a strategy of isolation of infected patients and optimal antiviral interventions in the future.
Outcomes of Online Mindfulness-Based Cognitive Therapy for Patients With Residual Depressive SymptomsA Randomized Clinical Trial
Zindel V. Segal, PhD1; Sona Dimidjian, PhD2; Arne Beck, PhD3; et alJennifer M. Boggs, PhD3; Rachel Vanderkruik, MA2; Christina A. Metcalf, MA2; Robert Gallop, PhD4; Jennifer N. Felder, PhD5; Joseph Levy, BA2
Author Affiliations
JAMA Psychiatry. Published online January 29, 2020. doi:10.1001/jamapsychiatry.2019.4693
Significance for fasd
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
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Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Neurobehavioral disorder associated with prenatal alcohol exposure
1. Go to:
Pediatrics. Author manuscript; available in PMC 2017 Oct 1.
Published in final edited form as:
Pediatrics. 2016 Oct; 138(4): e20151553.
doi: 10.1542/peds.2015-1553
PMCID: PMC5477054
NIHMSID: NIHMS860403
PMID: 27677572
Neurobehavioral Disorder Associated With Prenatal Alcohol Exposure
Joseph F. Hagan, Jr, MD, FAAP, Tatiana Balachova, PhD, Jacquelyn Bertrand, PhD, Ira Chasnoff, MD, FAAP,
Elizabeth Dang, MPH, Daniel Fernandez-Baca, MA, Julie Kable, PhD, Barry Kosofsky, MD, PhD,
Yasmin N. Senturias, MD, FAAP, Natasha Singh, MPA, Mark Sloane, DO, Carol Weitzman, MD, FAAP, and
Jennifer Zubler, MD, FAAP , on behalf of Neurobehavioral Disorder Associated With Prenatal Alcohol Exposure
Workgroup, American Academy of Pediatrics
University of Vermont College of Medicine, Burlington, Vermont
University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Centers for Disease Control and Prevention, Atlanta, Georgia
Children’s Research Triangle, Chicago, Illinois
University of Florida, Gainesville, Florida
Emory University, Atlanta, Georgia
Weill Cornell Medical College, New York, New York
University of North Carolina, Chapel Hill, North Carolina
Western Michigan University, Portage, Michigan
Yale Medical School, New Haven, Connecticut
Address correspondence to: Joseph F. Hagan Jr, MD, FAAP, 128 Lakeside Ave, Suite 115, Burlington, VT 05401-4936. jhagan@aap.net
Copyright notice
The publisher's final edited version of this article is available free at Pediatrics
See other articles in PMC that cite the published article.
Abstract
Children and adolescents affected by prenatal exposure to alcohol who have brain damage that is
manifested in functional impairments of neurocognition, self-regulation, and adaptive functioning may
most appropriately be diagnosed with neurobehavioral disorder associated with prenatal exposure. This
Special Article outlines clinical implications and guidelines for pediatric medical home clinicians to
identify, diagnose, and refer children regarding neurobehavioral disorder associated with prenatal
exposure. Emphasis is given to reported or observable behaviors that can be identified as part of care in
pediatric medical homes, differential diagnosis, and potential comorbidities. In addition, brief guidance
is provided on the management of affected children in the pediatric medical home. Finally, suggestions
are given for obtaining prenatal history of in utero exposure to alcohol for the pediatric patient.
Neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE) is a newly proposed
mental health diagnosis associated with the teratogenic effects of in utero exposure to alcohol. This
behavioral and mental health diagnosis is under the umbrella of fetal alcohol spectrum disorders
(FASDs), which also includes fetal alcohol syndrome (FAS), partial FAS (pFAS), and alcohol-related
birth defects; additional information is available at the American Academy of Pediatrics (AAP) Web
a b c d
c e f g
h c i j
c
a
b
c
d
e
f
g
h
i
j
1
2. Go to:
site (http://www.aap.org/fasd). ND-PAE was introduced into the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM-5) of the American Psychiatric Association in 2013 as a
“Condition for Further Study,” as well as a specified condition under “Other Specified
Neurodevelopmental Disorder” (International Classification of Diseases, Ninth Revision code 315.8,
International Classification of Diseases, 10th Revision code F88). The intent of this new diagnostic
designation is to better capture the behavioral and mental health effects of in utero exposure to alcohol
of individuals with and without the physical dysmorphia associated with prenatal alcohol exposure, in
contrast to the term alcohol-related neurodevelopmental disorder, which applies only to individuals
with neurobehavioral effects in the absence of physical dysmorphia effects. This report outlines the
clinical manifestations of ND-PAE that are most salient for the pediatric medical home, including
identification of children in need of evaluation, diagnosis, comorbid or differential diagnosis, referral,
and management. Although they do not represent AAP policy, specific suggestions are provided for
assessment of maternal use of alcohol during pregnancy at routine pediatric visits.
The most recent national data from the Centers for Disease Control and Prevention (CDC) indicate that
alcohol consumption during pregnancy is not a rare event, with 10.2% of pregnant women reporting
that they consumed alcohol in the past 30 days and 3.1% reporting binge drinking in the past 30 days.
Furthermore, approximately half of pregnancies are unplanned, and a woman might not know she is
pregnant until the sixth week of gestation or beyond, a period when she might still be consuming
alcohol and causing damage. Thus, many pregnancies are alcohol-exposed and represent a population
of children at risk for FASDs, especially ND-PAE. Recent studies including active, expert clinical
assessment of school-aged children report estimates that ~2% to 5% of children in the United States
have an FASD. Review of medical records indicates that most of these children are not identified
or diagnosed.
Criteria for ND-PAE are based on extensive brain imaging and animal model studies of adverse effects
of prenatal alcohol exposure despite the absence of physical features (ie, dysmorphia and growth
restriction). In fact, only ~25% of children affected by in utero exposure to alcohol exhibit
physical features. In 2011, under the auspices of the Interagency Coordinating Committee on Fetal
Alcohol Spectrum Disorders, the National Institute on Alcohol Abuse and Alcoholism and the CDC
convened a panel of experts to evaluate the research on FASDs not associated with the typical physical
features. (Information on these proceedings can be found at http://www.niaaa.nih.gov/about-niaaa/our-
work/ICCFASD/proceedings/2011.) In their consensus statement, 3 major areas of impairment were
identified: neurocognition, self-regulation, and adaptive functioning. These areas of deficit, along with
evidence of in utero exposure to alcohol, formed the basis of the ND-PAE diagnostic criteria.
CLINICAL FEATURES OF ND-PAE
Diagnosis of ND-PAE is appropriate if a child presents with impairment in neurocognition, impaired
self-regulation, 2 impairments of adaptive functioning, and a history of more than minimal exposure to
alcohol in utero (Table 1), as long as the disorder is not better explained by other factors (eg, genetic or
teratogenic syndrome). Although these broad domains overlap with other disorders of childhood,
specific deficits within them are indicative of ND-PAE. As with any developmental condition,
impairments in these domains present differently as a child matures. To aid identification of patients
with ND-PAE across development, age-specific traits in the framework for the continuous and
comprehensive developmental screening included in The Bright Futures Guidelines, fourth edition, are
presented in Fig 1A, Fig 1B, and Fig 1C.
1
2
3,4
5
6
7–10
11
3,12–14
15
3,13
16
6. A. More than minimal exposure to alcohol during gestation, including prior to pregnancy
recognition. Confirmation of gestational exposure to alcohol may be obtained from maternal self-
report of alcohol use in pregnancy, medical or other records, or clinical observation.
B. Impaired neurocognitive functioning as manifested by one or more of the following:
1. Impairment in global intellectual performance (i.e., IQ of 70 or below, or a standard score
of 70 or below on a comprehensive developmental assessment).
2. Impairment in executive functioning (e.g., poor planning and organization; inflexibility:
difficulty with behavioral inhibition).
3. Impairment in learning (e.g., lower academic achievement than expected for intellectual
level; specific learning disability).
4. Memory impairment (e.g., problems remembering information learned recently; repeatedly
making the same mistakes; difficulty remembering lengthy verbal instructions).
5. Impairment in visual–spatial reasoning (e.g., disorganized or poorly planned drawings or
constructions; problems differentiating left from right).
C. Impaired self-regulation as manifested by one or more of the following:
1. Impairment in mood or behavioral regulation (e.g., mood lability; negative affect or
irritability; frequent behavioral outbursts).
2. Attention deficit (e.g., difficulty shifting attention; difficulty sustaining mental effort).
3. Impairment in impulse control (e.g., difficulty waiting turn; difficulty complying with
rules).
D. Impairment in adaptive functioning as manifested by two or more of the following, one of which
must be (1) or (2):
1. Communication deficit (e.g., delayed acquisition of language; difficulty understanding
spoken language).
2. Impairment in social communication and interaction (e.g., overly friendly with strangers;
difficulty reading social cues; difficulty understanding social consequences).
3. Impairment in daily living skills (e.g., delayed toileting, feeding, or bathing; difficulty
managing daily schedule).
4. Impairment in motor skills (e.g., poor fine motor development; delayed attainment of gross
motor milestones or ongoing deficits in gross motor function; deficits in coordination and
balance).
E. Onset of the disorder (symptoms in Criteria B, C, and D) occurs in childhood.
F. The disturbance causes clinically significant distress or impairment in social, academic,
occupational, or other important areas of functioning.
G. The disorder is not better explained by the direct physiologic effects associated with postnatal use
of a substance (e.g., a medication, alcohol or other drugs), a general medical condition (e.g.,
traumatic brain injury, delirium, dementia), another known teratogen (e.g., fetal hydantoin
syndrome), a genetic condition (e.g., Williams syndrome, Down syndrome, Cornelia de Lange
syndrome), or environmental neglect.
Open in a separate window
Reprinted with permission of the American Psychiatric Association.
Impairment in Neurocognition
Criteria for neurocognitive impairment include evidence of 1 of the following: global impairment,
executive dysfunction, deficits in learning, memory problems, or trouble with visual–spatial reasoning.
These criteria may be assessed by standardized testing, clinical observation, or, more often, clinical
history. To ensure the integrity of the diagnostic criteria for ND-PAE, findings based on clinical
observation or history are best if based on specific examples of impairment and documented in the
7. medical record.
For global deficits, comprehensive standardized testing results are the gold standard. This might
require referral for testing or coordination with school psychologists. However, for diagnosis it is
important to recognize that not all affected children perform in the range of intellectual disability.
Clinical research has found that 86% of individuals with any of the FASDs have an IQ in the low
average or borderline ranges. The important point is that the child under consideration is functioning
below what would be expected relative to his or her peers.
Even if global delay or impairment is not present, specific deficits can indicate neurocognitive
impairment consistent with ND-PAE. Impairment in executive function often presents as poor planning
skills, inflexibility, or difficulty with behavior inhibition. Impaired learning or specific learning
disabilities often manifest in the areas of math, visual–spatial reasoning, or abstract academic material.
Finally, memory problems might be seen as problems remembering recently learned materials or
repeatedly making the same mistake. These particular types of learning and memory problems often
lead caregivers and educators to mistakenly assume the child is being defiant or willfully disobeying
rather than having genuine difficulty, the “can’t vs won’t” error.
Self-Regulation
Impaired self-regulation might include difficulty regulating mood or behavior, attention deficits, or
poor impulse control. Early signs of mood and behavior regulation problems might include sleep
problems or severe reactions to discomfort for infants and extended tantrums for toddlers. For
older children, increased incidence of externalizing behaviors and severe reactions to stress are most
common. However, increased levels of anxiety and depression have been documented.
Attention problems are often associated with prenatal alcohol exposure. Children with ND-PAE can
have particular difficulty shifting attention, resulting in behavior problems. Poor impulse control is an
additional impairment. These difficulties in all areas of self-regulation are particularly challenging
for the entire family of a child with ND-PAE. The sleep problems and mood lability with frequent
behavior outbursts, typically caused by frustration with task shifting, are often the presenting
complaints to a pediatrician.
Adaptive Functioning
Adaptive functioning is the ability to acquire daily skills for personal and social sufficiency.
Impairment in adaptive functioning can occur in communication, social communication and
interaction, daily living skills, or motor skills for very young children. Adaptive functioning is an area
of special concern of children with ND-PAE because these impairments are pervasive across domains
and situations as children age. Therefore, meeting this criterion requires impairment across 2 domains
of adaptive functioning. Although most language milestones (eg, babbling, first words, and syntax) are
acquired on schedule, individuals with ND-PAE might exhibit communication problems such as
difficulty in understanding figurative language (eg, understanding idioms, jokes, or sarcasm) and social
communication conventions (eg, how to effectively enter a conversation). Socially, they can be
overly friendly with strangers, be at high risk of bullying, have difficulty learning social rules through
experience (eg, how to join a group on the playground), or be highly susceptible to manipulation by
others. Because of attention and memory problems, a child with ND-PAE might initially learn daily
skills such as hygiene or house rules, yet maintaining those skills and organizing daily activities present
a challenge. Finally, motor skills can be impaired at the fine motor level (eg, poor writing skills)
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or gross motor level (eg, poor coordination or balance).
In Utero Exposure to Alcohol
Unlike FAS, which can be diagnosed when information about history of prenatal alcohol exposure is
unavailable, diagnosing other conditions along the continuum of FASDs, including ND-PAE, requires a
confirmed history of in utero exposure. There are clear and strong research human and animal data
documenting adverse neurodevelopmental outcomes from moderate to heavy levels of prenatal
exposure to alcohol and adverse reproductive (eg, prematurity) effects from even very low exposure
levels. Linking adverse neurodevelopmental outcomes to in utero exposure at these lower levels
remains a challenge but can be revealed with more sensitive testing. Despite clear evidence for the
association between prenatal exposure to alcohol and the wide profile of strengths and weaknesses that
might be observed across children with ND-PAE, the specificity of the profile is not yet known.
Therefore, the criterion of more than minimal gestational exposure is required for the ND-PAE
diagnosis. More than minimal exposure is defined as maternal consumption of ≥13 drinks per month
during pregnancy (ie, any 30-day period of pregnancy). The “More than minimal” criterion is not
intended to denote a threshold for safe consumption of alcohol during pregnancy. It is simply an
acknowledgment of ongoing controversy about low levels of exposure and an attempt make sure the
diagnosis was not overused because the base rate of drinking any alcohol among women of
childbearing years is relatively high.
Suggestions for obtaining a prenatal history of alcohol exposure are presented in the Appendix.
The primary care pediatrician needs to be aware that there is no known level of alcohol use during
pregnancy that has been established as safe. The US surgeon general still advises that women who are
pregnant, or are considering pregnancy, should abstain from consuming alcohol. Primary care
pediatricians will want to provide this important health message to their adolescent patients and
mothers-to-be and obtain information on prenatal exposure to alcohol for all patients.
DIFFERENTIAL AND COMORBID DIAGNOSES
As would be expected, symptoms associated with the diagnostic criteria of ND-PAE may be observed
in children with other disabilities. The diagnosis must be applied with care and based on all available
information, especially prenatal exposure history. It is important to keep in mind that the specific
constellation of impairments and unique manifestations of the criteria are most relevant for recognition
and diagnosis rather that the general symptom domains. Specifying co-occurring disorders can provide
the most complete picture of the child’s strengths and weaknesses to determine treatment or referral
course. Differential diagnoses of ND-PAE can be particularly challenging because the disorder
does not always present the same way in all children because of differences in timing and amount of
prenatal alcohol exposure and difference in genetic predispositions or postnatal environment.
Table 2 presents key differences between ND-PAE and several neurobehavioral conditions. The
severity of presentation and the constellation of characteristics vary greatly from child to
child. In a sample of children with FASDs, comorbid mental health conditions included (in
descending order) mental retardation (ie, intellectual disability), sleep abnormalities, reactive
attachment disorder, anxiety, posttraumatic stress disorder, oppositional defiant disorder, language
disorder, learning disability, depression, bipolar disorder, some features of autism, and specific
phobias. Other conditions such as enuresis, encopresis, and eating disorders may be present
depending on the age of the child.
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9. TABLE 2
Differential Diagnosis for ND-PAE
Neurocognitive
Behavioral
Regulation
Adaptive
Functioning
Key Differential
From ND-PAE
ND-PAE (formerly
referred to as
alcohol-related
neurodevelopmental
disorder
Intellectual skills
may be in the
intellectually
deficient range for
some but not most.
Deficits in
executive
functioning skills,
learning, memory,
and visual spatial
reasoning are
common.
Self-regulation
impairments may
take the form of
poor mood or
behavioral
regulation skills,
attention deficits,
and poor impulse
control. They are
best characterized
by arousal
dysfunction
involving slower
gating of
incoming
stimulation and
reduced capacity
to inhibit
attending to
distracting stimuli.
They respond to
simplification of
sensory input
(fewer distracters
and slower
presentation).
Adaptive
functioning skills
often fall below
that of their
overall IQs, and
often there are
declines in their
skills as they
grow older
relative to their
peers. This
decline may
result in the
standard scores
being lower as
they age. They
often have
impairments in
the pragmatic
communication
skills, are
socially
disinhibited, and
have poor motor
skills or
coordination,
with the latter
being a greater
deficit in young
rather than older
children.
Not applicable.
Global
developmental
delay or intellectual
disability
Children with
global
developmental
delay by definition
have impairments
in multiple
domains of
Behavioral
regulation skills
are variable,
depending on the
nature of the
disorder causing
the developmental
Adaptive
functioning skills
are also in the
low or deficient
range and are
generally stable
over the lifetime
Overall
development
or IQ is often
not delayed or
intellectually
impaired in
ND-PAE.
Open in a separate window
ASD, autism spectrum disorder.
FASDs
10. The diagnosis of ND-PAE encompasses the behavioral, developmental, and mental health aspects of
FASDs. Other diagnoses along the spectrum, such as FAS or pFAS, focus on structural and
neurophysiological central nervous system abnormalities (eg, microcephaly or neurologic soft signs).
Physical features such as facial dysmorphia or growth restrictions (either prenatal or postnatal) are
required for FAS and pFAS. Thus, for children with both physical findings and behavioral findings
consistent with ND-PAE, it is appropriate that a comorbid diagnosis of FAS or pFAS also be used.
Intellectual Disability
As mentioned, a majority of children with any of the FASDs score in the low range of normative
intellectual functioning. The history of more than minimal in utero exposure to alcohol will be a
major decision point between children with ND-PAE comorbid with intellectual disability and children
with intellectual disability due to another etiology. However, deficits specific to ND-PAE are
recognized. For example, even with repeated experience and an IQ within normal limits, the memory
and learning impairments of a child with ND-PAE may mean that he or she has difficulty with
previously learned skills, such as finding his or her locker at school on a routine basis despite repeated
instructions and practice or forgetting how to tie his or her shoes, despite previous mastery, and
having to relearn that skill entirely. This is different from regression of emerging skills seen in some
children with autism.
Finally, children with intellectual disability without prenatal alcohol exposure tend to have lowered
functioning across all neurocognitive domains. In contrast, individuals with ND-PAE tend to have
specific difficulty with nonverbal aspects of cognition such as visual–motor skills, learning and
memory for recently learned skills, and executive functioning, resulting in behavioral problems.
Cognitive impairment coupled with behavioral problems should prompt clinicians to consider a
diagnosis of ND-PAE.
Attention Problems
Current research demonstrates differences in manifestations of attention-deficit/hyperactivity disorder
(ADHD) and FASDs. Behaviorally, children with FASDs have higher rates of social behavioral
problems resulting from difficulties in social cognition and emotional processing. They might also be
more likely to have problems dealing with overstimulation than children with simple ADHD. In
contrast, children with ADHD due to etiology not attributable to alcohol have difficulty with focus and
sustained attention. Medication for symptoms of ADHD can result in unexpected outcomes in
children with a history of prenatal alcohol exposure. Stimulant medications are often ineffective
for children with prenatal alcohol exposure. Care should be given to investigate whether in utero
exposure to alcohol contributes to attention problems for any child because treatment and management
plans could differ.
Early Trauma
Children who experience early trauma (including physical events, psychological events, and abuse or
neglect) often display serious behavioral problems, receiving a mental health diagnosis of conduct
disorder, oppositional defiant disorder, anxiety, or depression. Because of overlap between these other
behavioral disorders and ND-PAE, at a general level (especially for the self-regulation component) it is
important for a clinician to consider these as both differential and comorbid diagnoses. Until additional
data are available about the validity and reliability of all childhood behavior disorders, including ND-
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PAE, this will continue to be a tricky diagnostic issue. Furthermore, for some children a history of early
trauma, abuse, neglect, or parental loss will be the only presenting problem because children with
prenatal exposure to alcohol are at higher risk for these negative events. Therefore, it is particularly
important to obtain prenatal exposure history in these situations. Such early trauma has been
shown to drastically worsen the effects of prenatal alcohol exposure and must be taken into account.
Other Conditions
Children with diagnoses of conduct disorder, oppositional defiant disorder, or even posttraumatic stress
disorder (PTSD) are often aggressive without appropriate provocation, whereas children with ND-PAE
might have behavioral outbursts caused by situational frustrations they experience when interacting
with others or by their own neurodevelopmental limitations. Furthermore, children with other early
trauma diagnoses might have inappropriate social interactions but tend to withdraw from others as self-
protection, whereas children with ND-PAE are more likely to be overly friendly, seeking out
companionship and social acceptance, although often in an inappropriate manner.
Foster Care and Adoption
A special issue regarding ND-PAE and early trauma is that among children in the child welfare system
and children adopted internationally. Researchers have found disproportionately high rates of children
with FASDs, including diagnoses without physical features such as ND-PAE, in these
populations. Because these children also often experience early trauma, separation, and poor early
caregiving, they are at elevated risk for a comorbid diagnosis of reactive attachment disorder or PTSD
after abandonment. Obtaining information about, and documenting, possible prenatal exposures
for all who have a current or history of involvement with the child welfare system is prudent clinical
practice. Such information can inform assessments and evaluation at older ages.
Finally, although prenatal alcohol exposure does occur in various contexts and varying levels, the
presence of ongoing alcohol or substance abuse in the home confers additional risk. Families with
substance abuse problems are more likely to suffer from multiple forms of trauma, antisocial behavior,
financial instability, and poverty. These factors can lead to additional comorbid conditions in a child
with ND-PAE.
REFERRAL AND MANAGEMENT
Although providing appropriate diagnoses (including comorbidities) can make a positive impact by
giving families and clinicians a framework for understanding a child’s behavior, it is only a starting
point. Ongoing care is the major role of the pediatric medical home. Although specific and targeted
early interventions have been shown to be most effective, more general special education and support
services also improve outcomes.
Individuals with FASDs, including children without physical stigmata, can experience a host of
physical conditions and secondary disabilities including mental health problems, disrupted school
experiences, trouble with the law, incarceration or confinement, inappropriate sexual behavior, alcohol
or drug problems, dependent living, and problems with employment. In 1 study, only 8% of people
diagnosed with FAS or a related condition did not have problems with independent living or
employment. Even if this finding encompasses some amount of ascertainment bias because it is a
clinical sample, the number of individuals with FASDs who do not achieve independent living is
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61–64
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12. striking and cause for concern. Early diagnosis and treatment of children with FASDs, including ND-
PAE, can reduce the risk of additional disabilities and adverse lifelong consequences. This protective
effect of early diagnosis has been demonstrated in a number of studies. In addition, referral
to other specialist may be warranted (eg, genetics, neurology, cardiology, nephrology).
Medications
The evidence base for pharmacologic treatment in this population is limited, with no
medications indicated specifically for ND-PAE. Studies on human and animal models are inconclusive
at this time, and more data are needed for proper guidance. However, findings from small pilot studies
suggest that ADHD stimulant medication can improve hyperactive symptoms but not attention and
impulsivity. And another small study found that neuroleptics can be more beneficial than
psychostimulants for improving social skills. A poor or adverse clinical response to stimulants (ie,
ineffective clinical response or significant side effects) can occur, and clinicians should plan to adjust
medications as necessary. Such medication failure also might be an indicator to consider a diagnosis
under the umbrella of FASDs.
Behavioral, Mental Health, and Academic Referrals
By definition ND-PAE is a behavioral or mental health diagnosis, and therefore such patients will
benefit from referral to specialties that can address these needs. In addition, academic problems
are a natural sequela of these primary disabilities. An overview of interventions developed specifically
for these children found that effective interventions include explicit teaching techniques, repetitive
presentation, and caregiver instructions about specific strengths and weaknesses associated with
prenatal alcohol exposure. As with many aspects of ND-PAE, additional systematic research is
needed to develop new intervention strategies and to get a clearer picture of the long-term effectiveness
of available programs. However, a sample of currently available evidence-based and
evidence-informed interventions are described in the online Supplemental Information.
It is important to remember that all aspects of the ND-PAE diagnosis (ie, neurocognition, self-
regulation, and adaptive behavior) are developmental processes, and the type of specialty needed might
change across development. For younger children, allied health referrals, such as physical or
occupational therapies, might be most appropriate. Early intervention might focus on general
developmental skills for the infant or preschooler. Occupational therapy is often recommended for fine
motor impairments, sensory integration problems, and emerging self-regulation problems. For older
school-age children, several evidence-based interventions targeting specific skills and adapted for
children with FASDs are available and can be recommended to school-age children. Several of these
interventions are described in the online Supplemental Information. More information on such
interventions is available at the National Organization on Fetal Alcohol Syndrome (www.NOFAS.org).
Older children with ND-PAE might need more traditional mental health services and can begin to
benefit from modified insight-based therapies. Referral to a psychiatrist or psychologist can be
appropriate. Referral for substance abuse evaluation or treatment also might be warranted. For the
medical home provider, however, it is most effective to provide background information on the
strengths and weaknesses of a child with ND-PAE in addition to child specific symptoms when making
such a referral.
Of special note for this population is that many affected children and adolescents do not qualify for
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special education under standard criteria, yet they still need services. This gap must be addressed
at the individual patient or student level. Psychoeducational testing (by school personnel or private
psychologists) might be required for diagnostic confirmation and treatment planning. Creative
solutions and closely engaging with the family, school, and community by the pediatric medical home
can facilitate meaningful results (see the AAP FASD Toolkit at www.aap.org/fasd).
Family Support
Parental education about ND-PAE, and even about FASDs in general, is particularly effective. For
parents there might be fears about stigma or the legal implications of the child’s diagnosis. It is
important that clinicians ask the difficult questions to screen for prenatal alcohol exposure when they
suspect a child might have been prenatally exposed to alcohol.
Caregivers appreciate information about how the behavioral difficulties they experienced with their
child were directly related to their child’s exposure to alcohol in utero. Instruction on the use of
explicit explanations that avoid idioms or other figurative language, the value of routines, and the need
to relearn some skills and obtain repeated instruction is a practical technique. Furthermore, such
instruction provides reassurance and support. It often helps to explain to parents that structural
brain abnormalities and the resulting neurobehavioral manifestations their child has (eg, problems with
poor problem solving and executive dysfunction) might make him or her less responsive to
pharmacotherapy than other children with a developmental disability. The pediatric medical home is an
ideal setting to provide such education and reassurance that the child’s primary care pediatrician will be
available to work with the family to address problems as they arise. It is especially helpful for the
clinician to explain that the vulnerabilities of a child with ND-PAE might not be readily recognizable
by others. For example, the child’s good structural language skills and friendly nature can give a false
impression of competence, and forgetting previously learned material might give a false impression of
a defiant or oppositional disorder. Additionally, the medical home provider caring for the child with
ND-PAE can help explain how the needs of the child change across development and provide
anticipatory care.
SUMMARY AND PEDIATRIC MEDICAL HOME PRACTICE
SUGGESTIONS
The value of the medical home starts at the identification and diagnostic stage and continues through
treatment planning and ongoing care. Although barriers to diagnosis and treatment remain, the AAP
endorses the identification, diagnosis, referral, and management of all children and adolescents with
FASDs, including ND-PAE. The brain damage that is caused by prenatal alcohol exposure is permanent
and irreversible, resulting in impaired neurocognitive functioning regardless of IQ; however,
interventions can improve function.
Although additional taxometric research on ND-PAE is needed, an extensive scientific literature
already provides support for its constellation of symptoms and criteria. Several efforts are under way to
obtain appropriate taxometric data, with results forthcoming (J. Kable, PhD, personal communication,
2015); our understanding may require modification once tested in a sizable cohort of children with
developmental disabilities. Children and adolescents with ND-PAE can reach their full potential with
proper identification, diagnosis, and treatment if clinicians and families work as a team, especially
toward early identification, treatment, and family support. Diagnosis and care of the patient with
ND-PAE provides the child, family, and pediatric clinician with a lens through which to help that child
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reach his or her developmental potential. Specific points to consider are presented in Table 3.
TABLE 3
ND-PAE Points for the Pediatric Medical Home
Universally screen for prenatal alcohol exposure, prenatally, in the newborn period, at the time of adoption,
and for new patients; the diagnosis should be considered throughout childhood (especially at developmental
transitions).
Document the presence and, if possible, the amount of prenatal alcohol exposure in the child’s medical
chart.
Perform frequent developmental screening with early referral to developmental specialist if concerns are
identified.
Identify comorbid diagnoses to effectively manage ND-PAE or, if appropriate, identify as a comorbid
diagnosis.
Treat ND-PAE as a chronic condition in a medical home.
Educate women about the risks of alcohol use during pregnancy and advise them to avoid alcohol
consumption while pregnant or when conception is possible.
Clinical and research evidence clearly indicates that children affected by ND-PAE and their families
face substantial challenges. Although these recommendations do not represent AAP policy, early
recognition in the medical home can capitalize on neural plasticity, early intervention, and ongoing
support systems to maximize the developmental potential of these children. Thus the pediatric medical
home plays a central role in maximizing the developmental outcomes of children with ND-PAE.
Supplementary Material
Supplemental
Click here to view.
Acknowledgments
The authors thank Rachel Daskalov and Joshua Benke for their assistance with preparation and
submission of this article.
FUNDING: Supported by Cooperative Agreement 5U58DD000587, funded by the Centers for Disease
Control and Prevention.
ABBREVIATIONS
(2.6M, pdf)
15. Go to:
AAP American Academy of Pediatrics
ADHD attention-deficit/hyperactivity disorder
CDC Centers for Disease Control and Prevention
DSM-5 Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition
FAS fetal alcohol syndrome
FASDs fetal alcohol spectrum disorders
ND-PAE neurobehavioral disorder associated with prenatal alcohol exposure
pFAS partial fetal alcohol syndrome
PTSD posttraumatic stress disorder
APPENDIX: SUGGESTED SCREENING FOR PRENATAL EXPOSURE TO
ALCOHOL
Maternal self-report remains the major approach for identifying alcohol consumption during
pregnancy, even though women might be reluctant to reveal prenatal alcohol use. More accurate
reports about alcohol use are elicited when screening is conducted in a nonjudgmental and
nonconfrontational manner, respecting confidentiality. Use of alcohol by a mother during
pregnancy should be assessed, avoiding questions that require “yes/no” answers (eg, “Do you drink
alcohol?”). Because of the stigma associated with alcohol use during pregnancy, asking patients about
prepregnancy drinking can improve accuracy of the screening. Questions about alcohol use can be
imbedded in a general conversation about health behaviors during pregnancy (eg, smoking, diet,
current medications). Furthermore, single binge drinking questions have been shown to be effective at
identifying women at risk for alcohol use during pregnancy and are consistent with current CDC and
National Institute on Alcohol Abuse and Alcoholism recommendations.
Based on international work that involved minimal questioning and clinical experience, the ND-PAE
workgroup suggests beginning screening with an introductory statement, such as “I ask all patients
standard health questions to understand factors that may affect health of their child and their
health.” To approach the topic of alcohol and quickly determine whether prenatal exposure
occurred, the following sets of questions are suggested in the newest edition of Bright Futures :
“How often do you drink beer, wine or liquor in your household?” (Continue for any response
other than “never”)
“In the 3 months before you knew you were pregnant, how many times did you have 4 or more
drinks in a day?”
“During the pregnancy, how many times did you have 4 or more drinks in a day?”
If positive responses are given to any of the above questions, the clinician can follow up to determine
frequency and extent of consumption by asking,
“During the pregnancy, on average, how many days per week did you have a drink?”
“During the pregnancy, on a typical day when you had an alcoholic beverage, how many drinks
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did you have?”
Any affirmative answer indicates maternal at-risk drinking; a brief intervention or referral is indicated.
The Bright Futures Guidelines (4th ed) suggests that these questions be asked at the prenatal visit, at an
initial postnatal well visit, for all new patients, based on clinical suspicion, and if a caregiver describes
cognitive or behavioral concerns consistent with ND-PAE criteria. Documentation of findings is very
important because not all criteria for a ND-PAE diagnosis might present in a single visit or might have
emerged at the time of screening. For example, executive function deficits often do not become
apparent until school age, but documentation of prenatal exposure to alcohol would put those deficits in
the proper context.
One concern expressed by some clinicians is that obtaining exposure information will trigger scrutiny
by child welfare agencies. The Child Abuse Prevention and Treatment Act does not require clinicians
to report to Child Protective Services if a child has been prenatally exposed to alcohol. Referral to
Child Protective Services is required if the child has been diagnosed with an FASD in the period
between birth and 3 years. The intent of this referral is to develop safe care and possible treatment
plans if needed, not to initiate punitive actions.
Although discussing prenatal alcohol exposure with patients might be a challenge, and some providers
express discomfort about discussing alcohol use with their patients, it is an important component of
both prenatal and postnatal care and is necessary for diagnosing FASDs.
Footnotes
Disclaimer: The guidelines/recommendations in this article are not American Academy of Pediatrics policy, and
publication herein does not imply endorsement.
This report was prepared and written by the American Academy of Pediatrics Neurobehavioral Disorder–Prenatal
Alcohol Exposed (ND-PAE) Work Group. Each member of the Work Group contributed to the conceptualization and
preparation of this document; Dr Hagan served as chair of the ND-PAE Work Group, planned the preparation of this
report, and participated in drafting the initial manuscript; Drs Balachova, Chasnoff, Kable, Kosofsky, Senturias,
Sloane, Weitzman, and Zubler participated in drafting the initial manuscript and assisted in the multiple conference
calls needed to craft the final manuscript; Dr Bertrand participated in drafting the initial manuscript and obtained
Centers for Disease Control and Prevention approval for the final manuscript; Ms Dang and Ms Singh participated
in drafting the initial manuscript and assisted in the multiple conference calls needed to craft the final manuscript;
Mr Fernandez-Baca assisted in research and served as the Work Group’s technical writer; and all authors
approved the final manuscript as submitted.
The findings and conclusions of this report are solely those of the authors and do not necessarily represent the
official position of the Centers for Disease Control and Prevention.
FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article
to disclose.
POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to
disclose.
COMPANION PAPER: A companion to this article can be found online at
www.pediatrics.org/cgi/doi/10.1542/peds.2016-1999.
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