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SCHOOL-BASED CLASSIFICATION OF INTE
SCHOOL-BASED CLASSIFICATION OF INTERNALIZING DISORDERS
Public Law 108-446, Individuals with Disabilities Education Improvement Act (IDEA; 2004) is the third reauthorization of the Education for all I Iandicapped Children Act of 1975 (PL 94-142, 1975). IDEA includes definitions for the different disabilities that can be identified to entitle individuals for services, including the development of an individualized education program (EP) and the oppor-tunity to receive an education in the least restrictive environment (LRE). Emo-tional Disturbance (In) is the category used to identify individuals with internalizing disorders such as depression and anxiety. The definition for ED is quite different from (he 16M diagnostic categories. There are three main parts to the criteria for the classi (ion of El). First, the !vhavior must occur for a long time, to a severe degree, and adversely impact the child's school functioning. Second, the behavior must fall into one of the following five categories: (1) inability to learn that can't be accounted by factors such as intellectual, sensory, or health factors; (2) inability to build interpersonal relationships with peers and teachers; (3) inappropriate behaviors or feelings under normal circumstances; (4) a general, pervasive mood of depression or unhappiness; or (5) a tendency to develop physical symptoms or fears associated with personal or school prob-lems. Finally, the term ED does not apply to children who are socially mal-adjusted unless it is determined they also have an emotional disturbance. Although vague, it is relatively clear that mood disorders and anxiety disorders qualify for services under numbers 4 and 5 in the ED definition. There is no mention of etiological considerations, so internalizing disorders secondary to brain dysfunction would qualify a child for services under IDEA.
MIXED ANXIETY-DEPRESSION
It has been argued that Major Depression and Generalized Anxiety Disorder are closely associated in children, sometimes referred to as mixed anxiety-depression, and may be variations of the same disorder (Cannon & Weems, 2006; Clark & Watson, 1991; Moffitt et al., 2007). Andrade and colleagues (2003) found major depression to be comorbid with GAD in ten countries from North America, Latin America, Europe, and Asia. Further, during the developmental period, anxiety and depression in children follows a hetero-typic course, that is, sometimes changing symptomatic patterns between anxiety and depression (Caspi, Elder, & Bern, 1988; Ferdinand, Dieleman, Ormel oz Verhulst, 2007). The issue of comorbidity has particular relevance because there is consideration being given to including Major Depression and GAD in the same diagnostic category in upcoming revisions of the DSM. It should be noted that Kessler et al. (2008) argue, based on a longitudinal, prospective study of comorbidity, that their finding of different risk factors for GAD and Major Depression suggests these two disorders are not mani-festations of the same underlying factor. Despite this finding, the majority of published studies provide convincing evidence for the association between major depression and anxiety.
TRIPARTITE MODEL OF INTERNALIZING DISORDERS
The tripartite model of anxiety and depression has been provided as a framework for interpreting the high comorbidity and heterotypic nature of these two internalizing disorders (Chorpita, Plummer, & Moffitt, 2000; Clark & Watson, 1991). The model posits that the primary feature shared by anxiety and depression is negative affect. It is further hypothesized that physiological hyperarousal is associated with anxiety and low positive affect is related to depression. Subsequent studies have shown physiological hyperarousal to be positively related to panic disorder and negatively related to generalized anxiety disorder (Brown, Chorpita, Barlow, 1998; Chorpita et al., 2000). However, Greaves_Lord and colleagues (2007) have argued, based on physi-ological measurement data that it is an oversimplification to say that physiological hyperarousal is specific to anxiety and not to depression. What appears to be clear from the literature is that negative affectivity undergirds both anxiety and depression. The research on the neural basis of negative affectivity (discussed below) is therefore particularly relevant to neuropsychological understanding of internalizing disorders.
DEVELOPMENTAL PSYCHOPATHOLOGY Applying neuropsychological methodologies to school-aged children and adolescents requires attention to developmental features of internalizing disorders. In very general terms the emergence of an internalizing disorder can be traced to the interaction of a physiological and biological vulnerability (diathesis) and the introduction of environmental stress, known as the diathe-sis-stress model (Charney & Manji, 2004; Earnheart et al., 2007; Miller, 1998). Studies indicate that the organization of the developing child may be affected by pervasive anxiety that is out of context or extreme reactions to neutral threats (Pathak & Perry, 2006). For example, parent modeling of affective responses inconsistent to the situation can produce a diathesis during critical early developmental periods. In regard to depression, the model was extended to identify cognitive diatheses, that is, a pattern of negative cognitions, and was called the cognitive diathesis-stress model (Hilsman & Garber, 1995). This notion of the development of internalizing disorders, that there is a predisposition toward psychopathology that is activated by stressful events, is c useful framework on which to link the burgeoning literature base on the develop-mental psychopathology of internalizing disorders.
BRAIN SYSTEMS AND INTERNALIZING DISORDERS
As indicated above, children with brain dysfunction are more susceptible to internalizing disorders (Tramontana & Hooper, 1997). This is likely due to the complex circuits that account for emotion in the human brain. That is, there is a good probability that some of the circuits involved in emotion could be involved in the general brain dysfunction. Further, as discussed above, the indirect effects of brain dysfunction in the absence of well-developed coping skills could result in internalizing symptoms such as withdrawal and feelings of helplessness.
BEHAVIOR INHIBITION SYSTEM
Gray (1995) theorized that internalizing disorders are associated with the behavioral inhibition system (BIS). The BIS is localized in the hippocampus and amygdala of the limbic system and the dorsal and ventral striatal systems of the basal ganglia. If the BIS does not develop normally and functions in an overactive state, the individual tends to experience negative affect as well as physiological arousal (Carver & Bell, 2006). This is consistent with the tripar-tite model of internalizing disorders previously discussed. Hale and Fiorello (2004) go on to conclude that children with depression and anxiety tend to have an overactive BIS accompanied by cortical overarousal that extends to the autonomic nervous system in the form of high parasympathetic reactivity.
NEUROBIOLOGY OF ANXIETY
Anxiety is a natural response associated with fundamental, primal survival instincts and is associated with the fight-or-flight response. Specifically, the activation of the threat response system by a real threat results in feelings of anxiety and fear (Pathak & Perry, 2006). The complex brain structures and circuits that have evolved over time to protect humans are also activated in anxiety disorder in which threats are generated internally. Because the threat response is so primal, some of the phylogenetically oldest parts of the brain are engaged in the response. After sensory information enters the brain, the afferent signals synapse in the ascending reticular activating system, causing arousal and alarm. Sensory information is integrated in the thalamus and transmitted to the limbic system including the amygdala and hippocampus. The subjective interpretation of the threat signals is con-ducted in the orbitofrontal cortex in concert with limbic-mediated activity (Pathak & Perry, 2006).
Public Law 108-446, Individuals with Disabilities Education Improvement Act (IDEA; 2004) is the third reauthorization of the Education for all I Iandicapped Children Act of 1975 (PL 94-142, 1975). IDEA includes definitions for the different disabilities that can be identified to entitle individuals for services, including the development of an individualized education program (EP) and the oppor-tunity to receive an education in the least restrictive environment (LRE). Emo-tional Disturbance (In) is the category used to identify individuals with internalizing disorders such as depression and anxiety. The definition for ED is quite different from (he 16M diagnostic categories. There are three main parts to the criteria for the classi (ion of El). First, the !vhavior must occur for a long time, to a severe degree, and adversely impact the child's school functioning. Second, the behavior must fall into one of the following five categories: (1) inability to learn that can't be accounted by factors such as intellectual, sensory, or health factors; (2) inability to build interpersonal relationships with peers and teachers; (3) inappropriate behaviors or feelings under normal circumstances; (4) a general, pervasive mood of depression or unhappiness; or (5) a tendency to develop physical symptoms or fears associated with personal or school prob-lems. Finally, the term ED does not apply to children who are socially mal-adjusted unless it is determined they also have an emotional disturbance. Although vague, it is relatively clear that mood disorders and anxiety disorders qualify for services under numbers 4 and 5 in the ED definition. There is no mention of etiological considerations, so internalizing disorders secondary to brain dysfunction would qualify a child for services under IDEA.
MIXED ANXIETY-DEPRESSION
It has been argued that Major Depression and Generalized Anxiety Disorder are closely associated in children, sometimes referred to as mixed anxiety-depression, and may be variations of the same disorder (Cannon & Weems, 2006; Clark & Watson, 1991; Moffitt et al., 2007). Andrade and colleagues (2003) found major depression to be comorbid with GAD in ten countries from North America, Latin America, Europe, and Asia. Further, during the developmental period, anxiety and depression in children follows a hetero-typic course, that is, sometimes changing symptomatic patterns between anxiety and depression (Caspi, Elder, & Bern, 1988; Ferdinand, Dieleman, Ormel oz Verhulst, 2007). The issue of comorbidity has particular relevance because there is consideration being given to including Major Depression and GAD in the same diagnostic category in upcoming revisions of the DSM. It should be noted that Kessler et al. (2008) argue, based on a longitudinal, prospective study of comorbidity, that their finding of different risk factors for GAD and Major Depression suggests these two disorders are not mani-festations of the same underlying factor. Despite this finding, the majority of published studies provide convincing evidence for the association between major depression and anxiety.
TRIPARTITE MODEL OF INTERNALIZING DISORDERS
The tripartite model of anxiety and depression has been provided as a framework for interpreting the high comorbidity and heterotypic nature of these two internalizing disorders (Chorpita, Plummer, & Moffitt, 2000; Clark & Watson, 1991). The model posits that the primary feature shared by anxiety and depression is negative affect. It is further hypothesized that physiological hyperarousal is associated with anxiety and low positive affect is related to depression. Subsequent studies have shown physiological hyperarousal to be positively related to panic disorder and negatively related to generalized anxiety disorder (Brown, Chorpita, Barlow, 1998; Chorpita et al., 2000). However, Greaves_Lord and colleagues (2007) have argued, based on physi-ological measurement data that it is an oversimplification to say that physiological hyperarousal is specific to anxiety and not to depression. What appears to be clear from the literature is that negative affectivity undergirds both anxiety and depression. The research on the neural basis of negative affectivity (discussed below) is therefore particularly relevant to neuropsychological understanding of internalizing disorders.
DEVELOPMENTAL PSYCHOPATHOLOGY Applying neuropsychological methodologies to school-aged children and adolescents requires attention to developmental features of internalizing disorders. In very general terms the emergence of an internalizing disorder can be traced to the interaction of a physiological and biological vulnerability (diathesis) and the introduction of environmental stress, known as the diathe-sis-stress model (Charney & Manji, 2004; Earnheart et al., 2007; Miller, 1998). Studies indicate that the organization of the developing child may be affected by pervasive anxiety that is out of context or extreme reactions to neutral threats (Pathak & Perry, 2006). For example, parent modeling of affective responses inconsistent to the situation can produce a diathesis during critical early developmental periods. In regard to depression, the model was extended to identify cognitive diatheses, that is, a pattern of negative cognitions, and was called the cognitive diathesis-stress model (Hilsman & Garber, 1995). This notion of the development of internalizing disorders, that there is a predisposition toward psychopathology that is activated by stressful events, is c useful framework on which to link the burgeoning literature base on the develop-mental psychopathology of internalizing disorders.
BRAIN SYSTEMS AND INTERNALIZING DISORDERS
As indicated above, children with brain dysfunction are more susceptible to internalizing disorders (Tramontana & Hooper, 1997). This is likely due to the complex circuits that account for emotion in the human brain. That is, there is a good probability that some of the circuits involved in emotion could be involved in the general brain dysfunction. Further, as discussed above, the indirect effects of brain dysfunction in the absence of well-developed coping skills could result in internalizing symptoms such as withdrawal and feelings of helplessness.
BEHAVIOR INHIBITION SYSTEM
Gray (1995) theorized that internalizing disorders are associated with the behavioral inhibition system (BIS). The BIS is localized in the hippocampus and amygdala of the limbic system and the dorsal and ventral striatal systems of the basal ganglia. If the BIS does not develop normally and functions in an overactive state, the individual tends to experience negative affect as well as physiological arousal (Carver & Bell, 2006). This is consistent with the tripar-tite model of internalizing disorders previously discussed. Hale and Fiorello (2004) go on to conclude that children with depression and anxiety tend to have an overactive BIS accompanied by cortical overarousal that extends to the autonomic nervous system in the form of high parasympathetic reactivity.
NEUROBIOLOGY OF ANXIETY
Anxiety is a natural response associated with fundamental, primal survival instincts and is associated with the fight-or-flight response. Specifically, the activation of the threat response system by a real threat results in feelings of anxiety and fear (Pathak & Perry, 2006). The complex brain structures and circuits that have evolved over time to protect humans are also activated in anxiety disorder in which threats are generated internally. Because the threat response is so primal, some of the phylogenetically oldest parts of the brain are engaged in the response. After sensory information enters the brain, the afferent signals synapse in the ascending reticular activating system, causing arousal and alarm. Sensory information is integrated in the thalamus and transmitted to the limbic system including the amygdala and hippocampus. The subjective interpretation of the threat signals is con-ducted in the orbitofrontal cortex in concert with limbic-mediated activity (Pathak & Perry, 2006).
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SCHOOL-BASED CLASSIFICATION OF INTERNALIZING DISORDERS Public Law 108-446, Individuals with Disabilities Education Improvement Act (IDEA; 2004) is the third reauthorization of the Education for all I Iandicapped Children Act of 1975 (PL 94-142, 1975). IDEA includes definitions for the different disabilities that can be identified to entitle individuals for services, including the development of an individualized education program (EP) and the oppor-tunity to receive an education in the least restrictive environment (LRE). Emo-tional Disturbance (In) is the category used to identify individuals with internalizing disorders such as depression and anxiety. The definition for ED is quite different from (he 16M diagnostic categories. There are three main parts to the criteria for the classi (ion of El). First, the !vhavior must occur for a long time, to a severe degree, and adversely impact the child's school functioning. Second, the behavior must fall into one of the following five categories: (1) inability to learn that can't be accounted by factors such as intellectual, sensory, or health factors; (2) inability to build interpersonal relationships with peers and teachers; (3) inappropriate behaviors or feelings under normal circumstances; (4) a general, pervasive mood of depression or unhappiness; or (5) a tendency to develop physical symptoms or fears associated with personal or school prob-lems. Finally, the term ED does not apply to children who are socially mal-adjusted unless it is determined they also have an emotional disturbance. Although vague, it is relatively clear that mood disorders and anxiety disorders qualify for services under numbers 4 and 5 in the ED definition. There is no mention of etiological considerations, so internalizing disorders secondary to brain dysfunction would qualify a child for services under IDEA. MIXED ANXIETY-DEPRESSION It has been argued that Major Depression and Generalized Anxiety Disorder are closely associated in children, sometimes referred to as mixed anxiety-depression, and may be variations of the same disorder (Cannon & Weems, 2006; Clark & Watson, 1991; Moffitt et al., 2007). Andrade and colleagues (2003) found major depression to be comorbid with GAD in ten countries from North America, Latin America, Europe, and Asia. Further, during the developmental period, anxiety and depression in children follows a hetero-typic course, that is, sometimes changing symptomatic patterns between anxiety and depression (Caspi, Elder, & Bern, 1988; Ferdinand, Dieleman, Ormel oz Verhulst, 2007). The issue of comorbidity has particular relevance because there is consideration being given to including Major Depression and GAD in the same diagnostic category in upcoming revisions of the DSM. It should be noted that Kessler et al. (2008) argue, based on a longitudinal, prospective study of comorbidity, that their finding of different risk factors for GAD and Major Depression suggests these two disorders are not mani-festations of the same underlying factor. Despite this finding, the majority of published studies provide convincing evidence for the association between major depression and anxiety. TRIPARTITE MODEL OF INTERNALIZING DISORDERS The tripartite model of anxiety and depression has been provided as a framework for interpreting the high comorbidity and heterotypic nature of these two internalizing disorders (Chorpita, Plummer, & Moffitt, 2000; Clark & Watson, 1991). The model posits that the primary feature shared by anxiety and depression is negative affect. It is further hypothesized that physiological hyperarousal is associated with anxiety and low positive affect is related to depression. Subsequent studies have shown physiological hyperarousal to be positively related to panic disorder and negatively related to generalized anxiety disorder (Brown, Chorpita, Barlow, 1998; Chorpita et al., 2000). However, Greaves_Lord and colleagues (2007) have argued, based on physi-ological measurement data that it is an oversimplification to say that physiological hyperarousal is specific to anxiety and not to depression. What appears to be clear from the literature is that negative affectivity undergirds both anxiety and depression. The research on the neural basis of negative affectivity (discussed below) is therefore particularly relevant to neuropsychological understanding of internalizing disorders. DEVELOPMENTAL PSYCHOPATHOLOGY Applying neuropsychological methodologies to school-aged children and adolescents requires attention to developmental features of internalizing disorders. In very general terms the emergence of an internalizing disorder can be traced to the interaction of a physiological and biological vulnerability (diathesis) and the introduction of environmental stress, known as the diathe-sis-stress model (Charney & Manji, 2004; Earnheart et al., 2007; Miller, 1998). Studies indicate that the organization of the developing child may be affected by pervasive anxiety that is out of context or extreme reactions to neutral threats (Pathak & Perry, 2006). For example, parent modeling of affective responses inconsistent to the situation can produce a diathesis during critical early developmental periods. In regard to depression, the model was extended to identify cognitive diatheses, that is, a pattern of negative cognitions, and was called the cognitive diathesis-stress model (Hilsman & Garber, 1995). This notion of the development of internalizing disorders, that there is a predisposition toward psychopathology that is activated by stressful events, is c useful framework on which to link the burgeoning literature base on the develop-mental psychopathology of internalizing disorders.
BRAIN SYSTEMS AND INTERNALIZING DISORDERS
As indicated above, children with brain dysfunction are more susceptible to internalizing disorders (Tramontana & Hooper, 1997). This is likely due to the complex circuits that account for emotion in the human brain. That is, there is a good probability that some of the circuits involved in emotion could be involved in the general brain dysfunction. Further, as discussed above, the indirect effects of brain dysfunction in the absence of well-developed coping skills could result in internalizing symptoms such as withdrawal and feelings of helplessness.
BEHAVIOR INHIBITION SYSTEM
Gray (1995) theorized that internalizing disorders are associated with the behavioral inhibition system (BIS). The BIS is localized in the hippocampus and amygdala of the limbic system and the dorsal and ventral striatal systems of the basal ganglia. If the BIS does not develop normally and functions in an overactive state, the individual tends to experience negative affect as well as physiological arousal (Carver & Bell, 2006). This is consistent with the tripar-tite model of internalizing disorders previously discussed. Hale and Fiorello (2004) go on to conclude that children with depression and anxiety tend to have an overactive BIS accompanied by cortical overarousal that extends to the autonomic nervous system in the form of high parasympathetic reactivity.
NEUROBIOLOGY OF ANXIETY
Anxiety is a natural response associated with fundamental, primal survival instincts and is associated with the fight-or-flight response. Specifically, the activation of the threat response system by a real threat results in feelings of anxiety and fear (Pathak & Perry, 2006). The complex brain structures and circuits that have evolved over time to protect humans are also activated in anxiety disorder in which threats are generated internally. Because the threat response is so primal, some of the phylogenetically oldest parts of the brain are engaged in the response. After sensory information enters the brain, the afferent signals synapse in the ascending reticular activating system, causing arousal and alarm. Sensory information is integrated in the thalamus and transmitted to the limbic system including the amygdala and hippocampus. The subjective interpretation of the threat signals is con-ducted in the orbitofrontal cortex in concert with limbic-mediated activity (Pathak & Perry, 2006).
BRAIN SYSTEMS AND INTERNALIZING DISORDERS
As indicated above, children with brain dysfunction are more susceptible to internalizing disorders (Tramontana & Hooper, 1997). This is likely due to the complex circuits that account for emotion in the human brain. That is, there is a good probability that some of the circuits involved in emotion could be involved in the general brain dysfunction. Further, as discussed above, the indirect effects of brain dysfunction in the absence of well-developed coping skills could result in internalizing symptoms such as withdrawal and feelings of helplessness.
BEHAVIOR INHIBITION SYSTEM
Gray (1995) theorized that internalizing disorders are associated with the behavioral inhibition system (BIS). The BIS is localized in the hippocampus and amygdala of the limbic system and the dorsal and ventral striatal systems of the basal ganglia. If the BIS does not develop normally and functions in an overactive state, the individual tends to experience negative affect as well as physiological arousal (Carver & Bell, 2006). This is consistent with the tripar-tite model of internalizing disorders previously discussed. Hale and Fiorello (2004) go on to conclude that children with depression and anxiety tend to have an overactive BIS accompanied by cortical overarousal that extends to the autonomic nervous system in the form of high parasympathetic reactivity.
NEUROBIOLOGY OF ANXIETY
Anxiety is a natural response associated with fundamental, primal survival instincts and is associated with the fight-or-flight response. Specifically, the activation of the threat response system by a real threat results in feelings of anxiety and fear (Pathak & Perry, 2006). The complex brain structures and circuits that have evolved over time to protect humans are also activated in anxiety disorder in which threats are generated internally. Because the threat response is so primal, some of the phylogenetically oldest parts of the brain are engaged in the response. After sensory information enters the brain, the afferent signals synapse in the ascending reticular activating system, causing arousal and alarm. Sensory information is integrated in the thalamus and transmitted to the limbic system including the amygdala and hippocampus. The subjective interpretation of the threat signals is con-ducted in the orbitofrontal cortex in concert with limbic-mediated activity (Pathak & Perry, 2006).
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SEKOLAH BERBASIS KLASIFIKASI internalisasi GANGGUAN
Hukum Publik 108-446, Individu dengan Peningkatan Pendidikan Disabilities Act (IDEA; 2004) adalah reauthorization ketiga dari Pendidikan untuk semua saya Iandicapped Anak Act of 1975 (PL 94-142, 1975). IDEA mencakup definisi untuk cacat yang berbeda yang dapat diidentifikasi untuk memberikan hak individu untuk layanan, termasuk pengembangan program individual pendidikan (EP) dan oppor-kesem- untuk menerima pendidikan di lingkungan terbatas paling tidak (LRE). Gangguan Emo-nasional (Dalam) adalah kategori yang digunakan untuk mengidentifikasi individu dengan gangguan internalisasi seperti depresi dan kecemasan. Definisi untuk ED sangat berbeda dari (dia 16M kategori diagnostik. Ada tiga bagian utama kriteria untuk klasifikasi (ion dari El). Pertama, vhavior! Harus terjadi untuk waktu yang lama, untuk tingkat yang parah, dan negatif dampak fungsi sekolah anak Kedua, perilaku harus jatuh ke salah satu dari lima kategori berikut:. (1) ketidakmampuan belajar yang tidak dapat dipertanggungjawabkan oleh faktor-faktor seperti faktor intelektual, sensori, atau kesehatan; (2) ketidakmampuan untuk membangun hubungan interpersonal dengan teman sebaya dan guru; (3) perilaku yang tidak pantas atau perasaan dalam keadaan normal; (4) seorang jenderal, suasana meresap depresi atau ketidakbahagiaan, atau (5) kecenderungan untuk mengembangkan gejala fisik atau ketakutan yang berhubungan dengan-masalah pribadi atau sekolah masalah-. Akhirnya, istilah ED tidak berlaku untuk anak-anak yang mal-disesuaikan kecuali ditentukan mereka juga memiliki gangguan emosional sosial. Meskipun samar-samar, itu relatif jelas bahwa gangguan mood dan gangguan kecemasan memenuhi syarat untuk layanan di bawah nomor 4 dan 5 dalam definisi ED. Tidak disebutkan pertimbangan etiologi, sehingga gangguan internalisasi sekunder untuk disfungsi otak akan memenuhi syarat seorang anak untuk layanan di bawah IDEA.
CAMPURAN KECEMASAN-DEPRESI
Telah dikemukakan bahwa Mayor Depresi dan Generalized Anxiety Disorder yang terkait erat pada anak-anak, kadang-kadang disebut sebagai campuran kecemasan-depresi, dan mungkin variasi gangguan yang sama (Cannon & Weems, 2006; Clark & Watson, 1991;. Moffitt et al, 2007). Andrade dan rekan (2003) menemukan depresi besar untuk komorbiditas dengan GAD di sepuluh negara dari Amerika Utara, Amerika Latin, Eropa, dan Asia. Selanjutnya, selama periode perkembangan, kecemasan dan depresi pada anak-anak mengikuti kursus hetero-typic, yang, kadang-kadang mengubah pola gejala antara kecemasan dan depresi (Caspi, Elder, & Bern, 1988; Ferdinand, Dieleman, Ormel oz Verhulst, 2007) . Masalah komorbiditas memiliki relevansi khusus karena ada pertimbangan yang diberikan kepada termasuk Mayor Depresi dan GAD dalam kategori diagnostik yang sama di revisi mendatang DSM. Perlu dicatat bahwa Kessler et al. (2008) berpendapat, berdasarkan sebuah studi prospektif longitudinal komorbiditas, bahwa temuan mereka dari faktor risiko yang berbeda untuk GAD dan Depresi Mayor menunjukkan dua gangguan ini tidak mani-festations faktor dasar yang sama. Meskipun temuan ini, sebagian besar penelitian yang diterbitkan memberikan bukti yang meyakinkan untuk hubungan antara depresi berat dan kecemasan.
MODEL TRIPARTITE internalisasi GANGGUAN
Model tripartit kecemasan dan depresi telah disediakan sebagai kerangka untuk menafsirkan komorbiditas tinggi dan sifat heterotypic dari kedua gangguan (Chorpita, Plummer, & Moffitt, 2000; Clark & Watson, 1991) internalisasi. Model berpendapat bahwa fitur utama bersama dengan kecemasan dan depresi adalah negatif mempengaruhi. Hal ini hipotesis lebih lanjut bahwa hyperarousal fisiologis berhubungan dengan kecemasan dan positif rendah mempengaruhi berhubungan dengan depresi. Penelitian selanjutnya telah menunjukkan hyperarousal fisiologis secara positif berhubungan dengan gangguan panik dan berhubungan negatif dengan gangguan kecemasan umum (Brown, Chorpita, Barlow, 1998; Chorpita et al, 2000.). Namun, Greaves_Lord dan rekan (2007) berpendapat, berdasarkan data pengukuran physi-ological bahwa itu adalah penyederhanaan yang berlebihan untuk mengatakan bahwa hyperarousal fisiologis khusus untuk kecemasan dan tidak depresi. Apa yang tampaknya menjadi jelas dari literatur adalah bahwa efektifitas negatif melandasi kedua kecemasan dan depresi. Oleh karena itu penelitian atas dasar saraf efektifitas negatif (dibahas di bawah) sangat relevan dengan pemahaman neuropsikologi gangguan internalisasi.
Psikopatologi PEMBANGUNAN Menerapkan metodologi neuropsikologi untuk anak-anak dan remaja usia sekolah membutuhkan perhatian ke fitur perkembangan gangguan internalisasi. Dalam istilah yang sangat umum munculnya gangguan internalisasi dapat ditelusuri ke interaksi kerentanan fisiologis dan biologis (diatesis) dan pengenalan stres lingkungan, yang dikenal sebagai model diathe-sis-stres (Charney & Manji, 2004; Earnheart et al, 2007;. Miller, 1998). Studi menunjukkan bahwa organisasi anak berkembang dapat dipengaruhi oleh kecemasan meresap yang keluar dari konteks atau reaksi ekstrim terhadap ancaman netral (Pathak & Perry, 2006). Misalnya, orang tua pemodelan tanggapan afektif yang tidak konsisten dengan situasi dapat menghasilkan diatesis selama periode perkembangan kritis awal. Dalam kaitan dengan depresi, model diperpanjang untuk mengidentifikasi diatesis kognitif, yaitu, pola kognisi negatif, dan disebut kognitif Model diatesis-stres (Hilsman & Garber, 1995). Gagasan pengembangan gangguan internalisasi, bahwa ada kecenderungan ke arah psikopatologi yang diaktifkan oleh peristiwa stres, adalah c kerangka kerja yang bermanfaat yang menghubungkan dasar literatur yang berkembang pada mengembangkan-jiwa psikopatologi gangguan internalisasi.
SISTEM OTAK DAN internalisasi GANGGUAN
seperti ditunjukkan di atas, anak-anak dengan disfungsi otak lebih rentan terhadap gangguan internalisasi (Tramontana & Hooper, 1997). Hal ini mungkin disebabkan oleh sirkuit kompleks yang menjelaskan emosi di otak manusia. Artinya, ada kemungkinan yang baik bahwa beberapa sirkuit yang terlibat dalam emosi bisa terlibat dalam disfungsi otak umum. Selanjutnya, seperti yang dibahas di atas, efek tidak langsung dari disfungsi otak dalam ketiadaan berkembang dengan baik keterampilan coping dapat mengakibatkan internalisasi gejala seperti penarikan dan perasaan tak berdaya.
SISTEM PERILAKU INHIBISI
Gray (1995) berteori bahwa gangguan internalisasi berhubungan dengan perilaku sistem inhibisi (BIS). BIS terlokalisir di hipokampus dan amigdala dari sistem limbik dan dorsal dan sistem striatal ventral dari ganglia basal. Jika BIS tidak berkembang secara normal dan fungsi dalam keadaan yang terlalu aktif, individu cenderung mengalami dampak negatif serta gairah fisiologis (Carver & Bell, 2006). Hal ini konsisten dengan model Tripar-tite gangguan dibahas sebelumnya internalisasi. Hale dan Fiorello (2004) pergi untuk menyimpulkan bahwa anak-anak dengan depresi dan kecemasan cenderung memiliki BIS terlalu aktif disertai overarousal kortikal yang meluas ke sistem saraf otonom dalam bentuk reaktivitas parasimpatis tinggi.
Neurobiologi KECEMASAN
Kecemasan adalah respon alami terkait dengan fundamental, naluri survival primal dan berhubungan dengan respon fight-or-flight. Secara khusus, aktivasi sistem respon ancaman oleh ancaman nyata menghasilkan perasaan cemas dan takut (Pathak & Perry, 2006). Struktur otak yang kompleks dan sirkuit yang telah berevolusi dari waktu ke waktu untuk melindungi manusia juga diaktifkan dalam gangguan kecemasan di mana ancaman yang dihasilkan secara internal. Karena respon ancaman begitu primal, beberapa bagian filogenetis tertua otak yang terlibat dalam respon. Setelah informasi sensorik memasuki otak, sinyal aferen sinaps dalam sistem pengaktif retikuler naik, menyebabkan gairah dan alarm. Informasi sensorik terintegrasi dalam thalamus dan dikirim ke sistem limbik termasuk amigdala dan hippocampus. Penafsiran subjektif dari sinyal ancaman adalah con-menyalurkan di korteks orbitofrontal dalam konser dengan kegiatan limbik-dimediasi (Pathak & Perry, 2006).
Hukum Publik 108-446, Individu dengan Peningkatan Pendidikan Disabilities Act (IDEA; 2004) adalah reauthorization ketiga dari Pendidikan untuk semua saya Iandicapped Anak Act of 1975 (PL 94-142, 1975). IDEA mencakup definisi untuk cacat yang berbeda yang dapat diidentifikasi untuk memberikan hak individu untuk layanan, termasuk pengembangan program individual pendidikan (EP) dan oppor-kesem- untuk menerima pendidikan di lingkungan terbatas paling tidak (LRE). Gangguan Emo-nasional (Dalam) adalah kategori yang digunakan untuk mengidentifikasi individu dengan gangguan internalisasi seperti depresi dan kecemasan. Definisi untuk ED sangat berbeda dari (dia 16M kategori diagnostik. Ada tiga bagian utama kriteria untuk klasifikasi (ion dari El). Pertama, vhavior! Harus terjadi untuk waktu yang lama, untuk tingkat yang parah, dan negatif dampak fungsi sekolah anak Kedua, perilaku harus jatuh ke salah satu dari lima kategori berikut:. (1) ketidakmampuan belajar yang tidak dapat dipertanggungjawabkan oleh faktor-faktor seperti faktor intelektual, sensori, atau kesehatan; (2) ketidakmampuan untuk membangun hubungan interpersonal dengan teman sebaya dan guru; (3) perilaku yang tidak pantas atau perasaan dalam keadaan normal; (4) seorang jenderal, suasana meresap depresi atau ketidakbahagiaan, atau (5) kecenderungan untuk mengembangkan gejala fisik atau ketakutan yang berhubungan dengan-masalah pribadi atau sekolah masalah-. Akhirnya, istilah ED tidak berlaku untuk anak-anak yang mal-disesuaikan kecuali ditentukan mereka juga memiliki gangguan emosional sosial. Meskipun samar-samar, itu relatif jelas bahwa gangguan mood dan gangguan kecemasan memenuhi syarat untuk layanan di bawah nomor 4 dan 5 dalam definisi ED. Tidak disebutkan pertimbangan etiologi, sehingga gangguan internalisasi sekunder untuk disfungsi otak akan memenuhi syarat seorang anak untuk layanan di bawah IDEA.
CAMPURAN KECEMASAN-DEPRESI
Telah dikemukakan bahwa Mayor Depresi dan Generalized Anxiety Disorder yang terkait erat pada anak-anak, kadang-kadang disebut sebagai campuran kecemasan-depresi, dan mungkin variasi gangguan yang sama (Cannon & Weems, 2006; Clark & Watson, 1991;. Moffitt et al, 2007). Andrade dan rekan (2003) menemukan depresi besar untuk komorbiditas dengan GAD di sepuluh negara dari Amerika Utara, Amerika Latin, Eropa, dan Asia. Selanjutnya, selama periode perkembangan, kecemasan dan depresi pada anak-anak mengikuti kursus hetero-typic, yang, kadang-kadang mengubah pola gejala antara kecemasan dan depresi (Caspi, Elder, & Bern, 1988; Ferdinand, Dieleman, Ormel oz Verhulst, 2007) . Masalah komorbiditas memiliki relevansi khusus karena ada pertimbangan yang diberikan kepada termasuk Mayor Depresi dan GAD dalam kategori diagnostik yang sama di revisi mendatang DSM. Perlu dicatat bahwa Kessler et al. (2008) berpendapat, berdasarkan sebuah studi prospektif longitudinal komorbiditas, bahwa temuan mereka dari faktor risiko yang berbeda untuk GAD dan Depresi Mayor menunjukkan dua gangguan ini tidak mani-festations faktor dasar yang sama. Meskipun temuan ini, sebagian besar penelitian yang diterbitkan memberikan bukti yang meyakinkan untuk hubungan antara depresi berat dan kecemasan.
MODEL TRIPARTITE internalisasi GANGGUAN
Model tripartit kecemasan dan depresi telah disediakan sebagai kerangka untuk menafsirkan komorbiditas tinggi dan sifat heterotypic dari kedua gangguan (Chorpita, Plummer, & Moffitt, 2000; Clark & Watson, 1991) internalisasi. Model berpendapat bahwa fitur utama bersama dengan kecemasan dan depresi adalah negatif mempengaruhi. Hal ini hipotesis lebih lanjut bahwa hyperarousal fisiologis berhubungan dengan kecemasan dan positif rendah mempengaruhi berhubungan dengan depresi. Penelitian selanjutnya telah menunjukkan hyperarousal fisiologis secara positif berhubungan dengan gangguan panik dan berhubungan negatif dengan gangguan kecemasan umum (Brown, Chorpita, Barlow, 1998; Chorpita et al, 2000.). Namun, Greaves_Lord dan rekan (2007) berpendapat, berdasarkan data pengukuran physi-ological bahwa itu adalah penyederhanaan yang berlebihan untuk mengatakan bahwa hyperarousal fisiologis khusus untuk kecemasan dan tidak depresi. Apa yang tampaknya menjadi jelas dari literatur adalah bahwa efektifitas negatif melandasi kedua kecemasan dan depresi. Oleh karena itu penelitian atas dasar saraf efektifitas negatif (dibahas di bawah) sangat relevan dengan pemahaman neuropsikologi gangguan internalisasi.
Psikopatologi PEMBANGUNAN Menerapkan metodologi neuropsikologi untuk anak-anak dan remaja usia sekolah membutuhkan perhatian ke fitur perkembangan gangguan internalisasi. Dalam istilah yang sangat umum munculnya gangguan internalisasi dapat ditelusuri ke interaksi kerentanan fisiologis dan biologis (diatesis) dan pengenalan stres lingkungan, yang dikenal sebagai model diathe-sis-stres (Charney & Manji, 2004; Earnheart et al, 2007;. Miller, 1998). Studi menunjukkan bahwa organisasi anak berkembang dapat dipengaruhi oleh kecemasan meresap yang keluar dari konteks atau reaksi ekstrim terhadap ancaman netral (Pathak & Perry, 2006). Misalnya, orang tua pemodelan tanggapan afektif yang tidak konsisten dengan situasi dapat menghasilkan diatesis selama periode perkembangan kritis awal. Dalam kaitan dengan depresi, model diperpanjang untuk mengidentifikasi diatesis kognitif, yaitu, pola kognisi negatif, dan disebut kognitif Model diatesis-stres (Hilsman & Garber, 1995). Gagasan pengembangan gangguan internalisasi, bahwa ada kecenderungan ke arah psikopatologi yang diaktifkan oleh peristiwa stres, adalah c kerangka kerja yang bermanfaat yang menghubungkan dasar literatur yang berkembang pada mengembangkan-jiwa psikopatologi gangguan internalisasi.
SISTEM OTAK DAN internalisasi GANGGUAN
seperti ditunjukkan di atas, anak-anak dengan disfungsi otak lebih rentan terhadap gangguan internalisasi (Tramontana & Hooper, 1997). Hal ini mungkin disebabkan oleh sirkuit kompleks yang menjelaskan emosi di otak manusia. Artinya, ada kemungkinan yang baik bahwa beberapa sirkuit yang terlibat dalam emosi bisa terlibat dalam disfungsi otak umum. Selanjutnya, seperti yang dibahas di atas, efek tidak langsung dari disfungsi otak dalam ketiadaan berkembang dengan baik keterampilan coping dapat mengakibatkan internalisasi gejala seperti penarikan dan perasaan tak berdaya.
SISTEM PERILAKU INHIBISI
Gray (1995) berteori bahwa gangguan internalisasi berhubungan dengan perilaku sistem inhibisi (BIS). BIS terlokalisir di hipokampus dan amigdala dari sistem limbik dan dorsal dan sistem striatal ventral dari ganglia basal. Jika BIS tidak berkembang secara normal dan fungsi dalam keadaan yang terlalu aktif, individu cenderung mengalami dampak negatif serta gairah fisiologis (Carver & Bell, 2006). Hal ini konsisten dengan model Tripar-tite gangguan dibahas sebelumnya internalisasi. Hale dan Fiorello (2004) pergi untuk menyimpulkan bahwa anak-anak dengan depresi dan kecemasan cenderung memiliki BIS terlalu aktif disertai overarousal kortikal yang meluas ke sistem saraf otonom dalam bentuk reaktivitas parasimpatis tinggi.
Neurobiologi KECEMASAN
Kecemasan adalah respon alami terkait dengan fundamental, naluri survival primal dan berhubungan dengan respon fight-or-flight. Secara khusus, aktivasi sistem respon ancaman oleh ancaman nyata menghasilkan perasaan cemas dan takut (Pathak & Perry, 2006). Struktur otak yang kompleks dan sirkuit yang telah berevolusi dari waktu ke waktu untuk melindungi manusia juga diaktifkan dalam gangguan kecemasan di mana ancaman yang dihasilkan secara internal. Karena respon ancaman begitu primal, beberapa bagian filogenetis tertua otak yang terlibat dalam respon. Setelah informasi sensorik memasuki otak, sinyal aferen sinaps dalam sistem pengaktif retikuler naik, menyebabkan gairah dan alarm. Informasi sensorik terintegrasi dalam thalamus dan dikirim ke sistem limbik termasuk amigdala dan hippocampus. Penafsiran subjektif dari sinyal ancaman adalah con-menyalurkan di korteks orbitofrontal dalam konser dengan kegiatan limbik-dimediasi (Pathak & Perry, 2006).
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