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| {{:Structural Image.png|}} | {{:Structural Image.png|}} | ||
| - | //This image highlights the areas of the brain that show structural abnormalities in patients with ADHD (Greenberg, 2015)// | + | //Figure 1: This image highlights the areas of the brain that show structural abnormalities in patients with ADHD (Greenberg, 2015)// |
| ==== Functional ==== | ==== Functional ==== | ||
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| {{:Function Image.png|}} | {{:Function Image.png|}} | ||
| - | //This image highlights the areas of the brain that show functional abnormalities in patients with ADHD (Greenberg, 2015)// | + | //Figure 2: This image highlights the areas of the brain that show functional abnormalities in patients with ADHD (Greenberg, 2015)// |
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| === Inattentive === | === Inattentive === | ||
| - | <box 32% round right | > {{:DSM-5_3D.jpg|}} </box| The Diagnostic Statistical Manual 5 (DSM-5) >This must include at least 6 of the following symptoms of inattention that must have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level (American Psychiatric Association, 2013): | + | <box 32% round right | > {{:DSM-5_3D.jpg|}} </box| Figure 3: The Diagnostic Statistical Manual 5 (DSM-5) >This must include at least 6 of the following symptoms of inattention that must have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level (American Psychiatric Association, 2013): |
| * Often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities | * Often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities | ||
| * Often has difficulty sustaining attention in tasks or play activities | * Often has difficulty sustaining attention in tasks or play activities | ||
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| Diagnostic tools are used to determine if an individual has ADHD and which treatments are appropriate for their conditions. Physicians use scales and checklists obtained from parents, teachers and other regarding symptoms and functioning in various settings. It is important to note that the use of scales and checklists are only one component of the evaluation. Other components include a medical examination and interview (CHADD, 2016). | Diagnostic tools are used to determine if an individual has ADHD and which treatments are appropriate for their conditions. Physicians use scales and checklists obtained from parents, teachers and other regarding symptoms and functioning in various settings. It is important to note that the use of scales and checklists are only one component of the evaluation. Other components include a medical examination and interview (CHADD, 2016). | ||
| - | === Conners Comprehensive Behavior Rating Scale === | + | == Conners Comprehensive Behavior Rating Scale == |
| The Conners Comprehensive Behavior Rating Scale (Conners CBRS) is a questionnaire that assesses children from ages 6-18 who may potentially have ADHD. It observes behaviors, emotions, academic and social problems in children (Conners, 2013). Three forms assess behavior, one for the parents, one for the teachers and a self-report conducted by the child if between the ages of 8-18. The Conners CBRS is made up of many components, including DSM-5, symptoms scales, content scales, other clinical indicators, critical items and impairments items (Conners, 2013). This diagnosis tool aims to assist with the diagnostic process, identifies and qualifies children for special education, assists with the development of intervention and treatment plans and evaluates its effectiveness (Conners, 2013). | The Conners Comprehensive Behavior Rating Scale (Conners CBRS) is a questionnaire that assesses children from ages 6-18 who may potentially have ADHD. It observes behaviors, emotions, academic and social problems in children (Conners, 2013). Three forms assess behavior, one for the parents, one for the teachers and a self-report conducted by the child if between the ages of 8-18. The Conners CBRS is made up of many components, including DSM-5, symptoms scales, content scales, other clinical indicators, critical items and impairments items (Conners, 2013). This diagnosis tool aims to assist with the diagnostic process, identifies and qualifies children for special education, assists with the development of intervention and treatment plans and evaluates its effectiveness (Conners, 2013). | ||
| | | ||
| - | === Barkley Home & School situations questionnaire === | + | == Barkley Home & School situations questionnaire == |
| The Barkley Home Situations Questionnaire (HSQ) and Barkley School Situations Questionnaire (SSQ) were developed by Dr. Russell Barkley. According to the DSM-5, symptoms of ADHD must be visible in at least two environments thus these questionnaires are designed to gather information from both parents and teachers (Bailey, 2016). The HSQ measures how symptoms of ADHD disrupt regular home situations such as watching TV or conducting chores (Bailey, 2016). Parents must rate problems on a scale from 1-9 in sixteen different areas (Bailey, 2016). The SSQ measures 12 common school situations such as listening to instructions, sitting at desks, paying attention in the classroom etc. Physicians use these questionnaires along with complete evaluations to determine the correct diagnosis. Results from these questionnaires along with the results from the DSM-5 will help the physician determine if a child has ADHD. (Bailey, 2016) | The Barkley Home Situations Questionnaire (HSQ) and Barkley School Situations Questionnaire (SSQ) were developed by Dr. Russell Barkley. According to the DSM-5, symptoms of ADHD must be visible in at least two environments thus these questionnaires are designed to gather information from both parents and teachers (Bailey, 2016). The HSQ measures how symptoms of ADHD disrupt regular home situations such as watching TV or conducting chores (Bailey, 2016). Parents must rate problems on a scale from 1-9 in sixteen different areas (Bailey, 2016). The SSQ measures 12 common school situations such as listening to instructions, sitting at desks, paying attention in the classroom etc. Physicians use these questionnaires along with complete evaluations to determine the correct diagnosis. Results from these questionnaires along with the results from the DSM-5 will help the physician determine if a child has ADHD. (Bailey, 2016) | ||
| - | === Wender Utah Rating Scale === | + | == Wender Utah Rating Scale == |
| The Wender Utah Rating Scale created by Paul Wender is another questionnaire used to assess adults with ADHD. The questionnaire consists of 61 questions about the patient’s childhood, which must be answered on a scale of 0-4. Twenty-five of the questions are associated with ADHD. According to the Wender Utah Rating Scale, a score of 46 or higher indicates patients having ADHD during their childhood (Ward, 1993). | The Wender Utah Rating Scale created by Paul Wender is another questionnaire used to assess adults with ADHD. The questionnaire consists of 61 questions about the patient’s childhood, which must be answered on a scale of 0-4. Twenty-five of the questions are associated with ADHD. According to the Wender Utah Rating Scale, a score of 46 or higher indicates patients having ADHD during their childhood (Ward, 1993). | ||
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| In most cases physicians use behavior to diagnose patients with ADHD but when the physician requires confirmation of diagnosis or the diagnosis is questionable more testing is approached. In these cases the use of imaging techniques are used as the next approach to diagnosis patients. However it is important to note, these imaging tools cannot be used alone to make a final diagnosis. It must be combined with other test results such as the behavioral questionnaires. | In most cases physicians use behavior to diagnose patients with ADHD but when the physician requires confirmation of diagnosis or the diagnosis is questionable more testing is approached. In these cases the use of imaging techniques are used as the next approach to diagnosis patients. However it is important to note, these imaging tools cannot be used alone to make a final diagnosis. It must be combined with other test results such as the behavioral questionnaires. | ||
| - | === Single Photon emission computed tomography (SPECT) === | + | == Single Photon emission computed tomography (SPECT) == |
| - | <box 40% round right | > {{:SPECT.png|}} </box| This image shows a 17 year old with ADHD SPECT results, showing hypoperfusion in bilateral frontal cortices and bilateral medial temporal lobes. (Santra & Kumar, 2014)>SPECT is the most common testing technique to measure for ADHD. SPECT is a 20 minute neuroimaging technique that measures the blood flow within the brain. It shows regions in the brain that are active (hot) and quiescent (cold) while patients complete various tasks (Sherman, 2015). | + | <box 50% round right | > {{:SPECT.png|}} </box| Figure 4: This image shows the SPECT results of a 17 year old with ADHD, showing hypoperfusion in bilateral frontal cortices and bilateral medial temporal lobes. (Santra & Kumar, 2014)>SPECT is the most common testing technique to measure for ADHD. SPECT is a 20 minute neuroimaging technique that measures the blood flow within the brain. It shows regions in the brain that are active (hot) and quiescent (cold) while patients complete various tasks (Sherman, 2015). |
| - | === Quantitative electroencephalography (qEEG) === | + | == Quantitative electroencephalography (qEEG) == |
| qEEG measure brain activity by observing distinctive brain patterns. Patients wear an electrode-studded cap and gel is applied to the head to conduct electrical impulses (Sherman, 2015). The brain waves show physicians abnormalities in the frontal area of the brain. ADHD patients show excess slow waves while others may have way too fast-wave activity (Sherman, 2015). This testing helps physicians determine which medication to prescribe and which will be most effective. | qEEG measure brain activity by observing distinctive brain patterns. Patients wear an electrode-studded cap and gel is applied to the head to conduct electrical impulses (Sherman, 2015). The brain waves show physicians abnormalities in the frontal area of the brain. ADHD patients show excess slow waves while others may have way too fast-wave activity (Sherman, 2015). This testing helps physicians determine which medication to prescribe and which will be most effective. | ||
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| ===== Pathophysiology and Etiology ===== | ===== Pathophysiology and Etiology ===== | ||
| - | <box 45% round right | > {{:etiology.jpg.png|}} </box| The Biopsychosocial model of ADHD >The biopsychosocial model of ADHD portrays a broad view which attributes the disorder outcomes to the interaction of three factors: biological, psychological, and environmental. | + | <box 45% round right | > {{:etiology.jpg.png|}} </box| Figure 5: The Biopsychosocial model of ADHD >The biopsychosocial model of ADHD portrays a broad view which attributes the disorder outcomes to the interaction of three factors: biological, psychological, and environmental. |
| Pathophysiology of ADHD is unclear and the roots have yet to be discovered. Drugs used to treat ADHD have led to hypothesizing the involvement of certain areas in the brain involved in attention have some sort of neural transmission deficits. The underlying brain regions are thought to be involved distributed over various brain regions as opposed to a single area. Indicated though PET scan imaging, the most notable structural and functional alterations are in parietal lobes and cerebellum (Cherkasova & Hechtman, 2009). Specifically, the neurotransmitters dopamine and norepinephrine are associated with ADHD. | Pathophysiology of ADHD is unclear and the roots have yet to be discovered. Drugs used to treat ADHD have led to hypothesizing the involvement of certain areas in the brain involved in attention have some sort of neural transmission deficits. The underlying brain regions are thought to be involved distributed over various brain regions as opposed to a single area. Indicated though PET scan imaging, the most notable structural and functional alterations are in parietal lobes and cerebellum (Cherkasova & Hechtman, 2009). Specifically, the neurotransmitters dopamine and norepinephrine are associated with ADHD. | ||
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| Temperament is the behavioral style that individuals consistently exhibit as a response to their environments (Foley, McClowry & Castellanos, 2008). It is evident early in life, relatively stable across time and various situations, biologically-driven and genetically-linked. For children with ADHD, three aspects of temperament are evident (Foley, McClowry & Castellanos, 2008): 1. Neuroticism (intensity and frequency of the expression of negative response to stress); 2. Conscientiousness (persistence in task performance); and 3. Extraversion/Activity (highly outgoing/overactive). | Temperament is the behavioral style that individuals consistently exhibit as a response to their environments (Foley, McClowry & Castellanos, 2008). It is evident early in life, relatively stable across time and various situations, biologically-driven and genetically-linked. For children with ADHD, three aspects of temperament are evident (Foley, McClowry & Castellanos, 2008): 1. Neuroticism (intensity and frequency of the expression of negative response to stress); 2. Conscientiousness (persistence in task performance); and 3. Extraversion/Activity (highly outgoing/overactive). | ||
| - | <box 95% round white centre|>{{:temperament.jpg|}}</box|ADHD individuals score higher on Activity and Negative Reactivity, and lower on Task Persistence, compared to non-ADHD controls (Foley, McClowry & Castellanos, 2008).> | + | <box 95% round white centre|>{{:temperament.jpg|}}</box|Figure 6: ADHD individuals score higher on Activity and Negative Reactivity, and lower on Task Persistence, compared to non-ADHD controls (Foley, McClowry & Castellanos, 2008).> |
| A study by Jensen and Rosen (2004) performed a study involving parent-ratings, where mothers of children with ADHD were asked to rate the intensity and frequency their child’s emotional responses. They found that children with ADHD were rated to be significantly more emotionally reactive to both immediate and future events compared to children without ADHD. In addition, children with ADHD showed a greater response to negative emotional events (both in immediate and future time periods) compared to positive emotional events. However, when rating the responses to the consequences of their behavior, children with ADHD were rated as less emotionally reactive than children without ADHD (Jensen & Rosen, 2004). | A study by Jensen and Rosen (2004) performed a study involving parent-ratings, where mothers of children with ADHD were asked to rate the intensity and frequency their child’s emotional responses. They found that children with ADHD were rated to be significantly more emotionally reactive to both immediate and future events compared to children without ADHD. In addition, children with ADHD showed a greater response to negative emotional events (both in immediate and future time periods) compared to positive emotional events. However, when rating the responses to the consequences of their behavior, children with ADHD were rated as less emotionally reactive than children without ADHD (Jensen & Rosen, 2004). | ||
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| === Response Inhibition === | === Response Inhibition === | ||
| - | <box 40% round right | > {{:gonogotask.png|}} </box| An example of the experimental setup of the ‘Go/No-go’ task > Response inhibition is the cognitive process of inhibiting oneself from making a dominant response when it is not appropriate in the situation (an example is a child with ADHD who persistently moves around the classroom despite being told by the teacher to sit quietly, and the rest of the children are sitting down). This process is impaired in individuals with ADHD. A study by Wodka et al. (2007) examined response inhibition in children with ADHD using three ‘go/no-go tests’: one with high cognitive demand, one with low cognitive demand, and one that is motivation-linked (have rewards and response costs). In ‘go/no-go’ tasks, test subjects are presented with a continuous stream of stimuli and they are asked to perform a binary decision on each stimulus. One of the stimuli requires participants to make a motor response (‘go’), whereas the other requires participants to withhold a response (‘no-go’). Accuracy and reaction times are measured for each event, and the dominant response is established by presenting a higher proportion of the ‘go’ stimuli, where the subjects are supposed to make the motor response (Wodka et al., 2007). | + | <box 40% round right | > {{:gonogotask.png|}} </box| Figure 7: An example of the experimental setup of the ‘Go/No-go’ task > Response inhibition is the cognitive process of inhibiting oneself from making a dominant response when it is not appropriate in the situation (an example is a child with ADHD who persistently moves around the classroom despite being told by the teacher to sit quietly, and the rest of the children are sitting down). This process is impaired in individuals with ADHD. A study by Wodka et al. (2007) examined response inhibition in children with ADHD using three ‘go/no-go tests’: one with high cognitive demand, one with low cognitive demand, and one that is motivation-linked (have rewards and response costs). In ‘go/no-go’ tasks, test subjects are presented with a continuous stream of stimuli and they are asked to perform a binary decision on each stimulus. One of the stimuli requires participants to make a motor response (‘go’), whereas the other requires participants to withhold a response (‘no-go’). Accuracy and reaction times are measured for each event, and the dominant response is established by presenting a higher proportion of the ‘go’ stimuli, where the subjects are supposed to make the motor response (Wodka et al., 2007). |
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| ==DRD4 gene== | ==DRD4 gene== | ||
| <box 63% round white right|>{{:drd4structure.png|}} | <box 63% round white right|>{{:drd4structure.png|}} | ||
| - | </box|The DRD4 gene codes for a G-protein-coupled receptor with 7 transmembrane subunits. The activation of this protein leads to a cascade of second-messenger pathways involved in regulation of higher-level cognition.>DRD4 is a G protein-coupled receptor belonging to the dopamine D2-like receptor family, which act to inhibit adenylyl cyclase (Gizer, Ficks & Waldman, 2009). The DRD4 gene has been mapped to position 15.5 of the p-arm of chromosome 11. It is mostly expressed in the frontal lobe regions of the brain, such as the orbitofrontal cortex and anterior cingulate, thus playing a role in the regulation of higher-level cognitive functions such as reward anticipation, decision-making, impulse control, and emotion. Association studies have linked this gene to the personality trait of novelty seeking, and has been likened to the high levels of impulsivity and excitability seen in the diagnosis of ADHD. In addition, DRD4 knockout mice have been shown to exhibit a heightened response to cocaine and metamphetamine compared to control groups, as seen through increases in their locomotor activity. The most widely studied DRD4 polymorphism is the 48-bp variable number of tandem repeats (VNTR) in exon 3 of the gene. This VNTR has been shown to play a role in secondary messenger systems (i.e. cyclic AMP) and in responses to antipsychotic medication such as clozapine (Gizer, Ficks & Waldman, 2009). | + | </box|Figure 8: The DRD4 gene codes for a G-protein-coupled receptor with 7 transmembrane subunits. The activation of this protein leads to a cascade of second-messenger pathways involved in regulation of higher-level cognition.>DRD4 is a G protein-coupled receptor belonging to the dopamine D2-like receptor family, which act to inhibit adenylyl cyclase (Gizer, Ficks & Waldman, 2009). The DRD4 gene has been mapped to position 15.5 of the p-arm of chromosome 11. It is mostly expressed in the frontal lobe regions of the brain, such as the orbitofrontal cortex and anterior cingulate, thus playing a role in the regulation of higher-level cognitive functions such as reward anticipation, decision-making, impulse control, and emotion. Association studies have linked this gene to the personality trait of novelty seeking, and has been likened to the high levels of impulsivity and excitability seen in the diagnosis of ADHD. In addition, DRD4 knockout mice have been shown to exhibit a heightened response to cocaine and metamphetamine compared to control groups, as seen through increases in their locomotor activity. The most widely studied DRD4 polymorphism is the 48-bp variable number of tandem repeats (VNTR) in exon 3 of the gene. This VNTR has been shown to play a role in secondary messenger systems (i.e. cyclic AMP) and in responses to antipsychotic medication such as clozapine (Gizer, Ficks & Waldman, 2009). |
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| ==DAT1 gene== | ==DAT1 gene== | ||
| - | <box 30% round white right|>{{:dat1structure.png|}}</box|The DAT1 gene codes for DAT transporter protein, which plays a role in dopamine reuptake.> The DAT1 gene is located in position 15, in the p-arm of chromosome 5 (Gizer, Ficks & Waldman, 2009). The gene codes for a carrier protein that is responsible for the recycling of dopamine from the synaptic cleft back to the presynaptic neuron. This protein is widely distributed in the corpus striatum and the nucleus accumbens, and represents the basis of dopamine regulation in these brain areas. Stimulant medications for ADHD such as methylphenidate have been shown to inhibit the function of DAT1, thereby increasing the levels of available dopamine in the synapse and decreasing the manifestation of ADHD symptoms. In addition, mice that were genetically modified to have a higher density of the DAT1 gene presented the phenotypic behaviors of ADHD, such as increased motor activity compared to wild-type controls. The most widely investigated polymorphism of DAT1 is a VNTR sequence in the 3’ untranslated region of the gene. Several studies show that the dopamine transporter availability and binding potential are influenced by genotype at this VNTR (Gizer, Ficks & Waldman, 2009). | + | <box 30% round white right|>{{:dat1structure.png|}}</box|Figure 9: The DAT1 gene codes for DAT transporter protein, which plays a role in dopamine reuptake.> The DAT1 gene is located in position 15, in the p-arm of chromosome 5 (Gizer, Ficks & Waldman, 2009). The gene codes for a carrier protein that is responsible for the recycling of dopamine from the synaptic cleft back to the presynaptic neuron. This protein is widely distributed in the corpus striatum and the nucleus accumbens, and represents the basis of dopamine regulation in these brain areas. Stimulant medications for ADHD such as methylphenidate have been shown to inhibit the function of DAT1, thereby increasing the levels of available dopamine in the synapse and decreasing the manifestation of ADHD symptoms. In addition, mice that were genetically modified to have a higher density of the DAT1 gene presented the phenotypic behaviors of ADHD, such as increased motor activity compared to wild-type controls. The most widely investigated polymorphism of DAT1 is a VNTR sequence in the 3’ untranslated region of the gene. Several studies show that the dopamine transporter availability and binding potential are influenced by genotype at this VNTR (Gizer, Ficks & Waldman, 2009). |
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| The **catecholamine hypothesis of ADHD** states that the three main neurotransmitters that play a role in ADHD are the catecholamines: norepinephrine, serotonin, and dopamine, and that there is a significant impairment in the dynamics of these catecholamines in the neural synapse, which is correlated with the symptomatology of the disease (Pliszka, McCracken & Maas, 1996). The central norepinephrine system may be dysregulated in ADHD, such that the system does not sufficiently prime the cortical posterior attention system to external stimuli in the environment. Also, reduced activity of norepinephrine in the reticular formation puts the brain in a ‘sleepy’ state. The effective mental processing of information involves the anterior executive system (i.e. the prefrontal cortices) which largely depend on dopaminergic circuits. Dopamine is also the basis of regulating the reward/gratification of the brain. Again, these are deficient in the brain of an individual with ADHD. Serotonin has an inhibitory effect on the other two catecholamines. It is hypothesized that ADHD individuals have too much serotonin activity, leading to an excessive deactivation of norepinephrine and dopamine (Pliszka, McCracken & Maas, 1996). | The **catecholamine hypothesis of ADHD** states that the three main neurotransmitters that play a role in ADHD are the catecholamines: norepinephrine, serotonin, and dopamine, and that there is a significant impairment in the dynamics of these catecholamines in the neural synapse, which is correlated with the symptomatology of the disease (Pliszka, McCracken & Maas, 1996). The central norepinephrine system may be dysregulated in ADHD, such that the system does not sufficiently prime the cortical posterior attention system to external stimuli in the environment. Also, reduced activity of norepinephrine in the reticular formation puts the brain in a ‘sleepy’ state. The effective mental processing of information involves the anterior executive system (i.e. the prefrontal cortices) which largely depend on dopaminergic circuits. Dopamine is also the basis of regulating the reward/gratification of the brain. Again, these are deficient in the brain of an individual with ADHD. Serotonin has an inhibitory effect on the other two catecholamines. It is hypothesized that ADHD individuals have too much serotonin activity, leading to an excessive deactivation of norepinephrine and dopamine (Pliszka, McCracken & Maas, 1996). | ||
| - | <box 60% round centre | > {{:neurotransmitters.jpg|}} </box| The three catecholamines: Dopamine, Norepinephrine, and Epinephrine are the main neurotransmitters involved in ADHD etiology. | + | <box 60% round centre | > {{:neurotransmitters.jpg|}} </box| Figure 10: The three catecholamines: Dopamine, Norepinephrine, and Epinephrine are the main neurotransmitters involved in ADHD etiology. |
| > | > | ||
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| Various environmental factors are thought to contribute as risk factors to the development of ADHD such as including food additives/diet, pre- and postnatal toxin exposure or mercury or lead, cigarette and alcohol exposure, maternal smoking during pregnancy, and low birth weight. Many recent studies have specifically examined the relationships between ADHD and these extraneous factors (Banerjee et al, 2007). However, it is to be noted that these studies show that these environmental risk factors and potential gene–environment interactions increase the risk for developing ADHD. In addition to this, even if one does not have a high expression of the candidate genes of risk, but were exposed to an environmental risk factor, there is also a risk for developing ADHD. | Various environmental factors are thought to contribute as risk factors to the development of ADHD such as including food additives/diet, pre- and postnatal toxin exposure or mercury or lead, cigarette and alcohol exposure, maternal smoking during pregnancy, and low birth weight. Many recent studies have specifically examined the relationships between ADHD and these extraneous factors (Banerjee et al, 2007). However, it is to be noted that these studies show that these environmental risk factors and potential gene–environment interactions increase the risk for developing ADHD. In addition to this, even if one does not have a high expression of the candidate genes of risk, but were exposed to an environmental risk factor, there is also a risk for developing ADHD. | ||
| - | <box 85% round centre | > {{Risk factors.jpg}} </box| Environmental risk factors for ADHD > | + | <box 85% round centre | > {{Risk factors.jpg}} </box| Figure 11: Environmental risk factors for ADHD > |
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| ====Methylphenidate (e.g. Ritalin)==== | ====Methylphenidate (e.g. Ritalin)==== | ||
| - | <box 40% round right | > {{:ritalin.jpg|}} </box| Methylphenidates like Ritalin are most commonly used for the treatment of ADHD.> Methylphenidate (MPH) is the most commonly prescribed drug for the treatment of ADHD (Volkow et al, 2002). It is a stimulant drug that blocks dopamine and norepinephrine transporters in the brain, thereby increasing the levels of dopamine in the brain (Volkow et al, 2002). | + | <box 40% round right | > {{:ritalin.jpg|}} </box| Figure 12: Methylphenidates like Ritalin are most commonly used for the treatment of ADHD.> Methylphenidate (MPH) is the most commonly prescribed drug for the treatment of ADHD (Volkow et al, 2002). It is a stimulant drug that blocks dopamine and norepinephrine transporters in the brain, thereby increasing the levels of dopamine in the brain (Volkow et al, 2002). |
| - | Though the exact mechanism of action is widely unknown, it may help increase attention and decrease impulsiveness and hyperactivity (FDA, 2013). Methylphenidate potentiates, or strengthens, dopaminergic signalling by increasing the effect of dopamine cell firing on the concentration of dopamine in the synaptic cleft (Tripp & Wickens, 2008). The Dopamine Transfer Deficit (DTD) theory suggests that there are specific alterations in the magnitude and timing of this anticipatory dopamine cell firing in children with ADHD (Tripp & Wickens, 2008). This anticipatory dopaminergic cell firing is important for behavioural reinforcement in learning (Tripp & Wickens, 2008). The DTD theory predicts that for children with ADHD, there is a dopamine transfer dysfunction. Specifically, the phasic dopamine cell response to the cue that predicts reinforcement is reduced in amplitude to the point of being ineffective (Tripp & Wickens, 2008). Consistent with the DTD theory, it is beneficial to block the dopamine transporter, DAT, so there is less dopamine reuptake and more dopamine present in the synaptic cleft (Tripp & Wickens, 2008). | + | Though the exact mechanism of action is widely unknown, it may help increase attention and decrease impulsiveness and hyperactivity (FDA, 2013). Methylphenidate potentiates, or strengthens, dopaminergic signalling by increasing the effect of dopamine cell firing on the concentration of dopamine in the synaptic cleft (Tripp & Wickens, 2008). |
| + | |||
| + | The Dopamine Transfer Deficit (DTD) theory suggests that there are specific alterations in the magnitude and timing of this anticipatory dopamine cell firing in children with ADHD (Tripp & Wickens, 2008). This anticipatory dopaminergic cell firing is important for behavioural reinforcement in learning (Tripp & Wickens, 2008). The DTD theory predicts that for children with ADHD, there is a dopamine transfer dysfunction. Specifically, the phasic dopamine cell response to the cue that predicts reinforcement is reduced in amplitude to the point of being ineffective (Tripp & Wickens, 2008). | ||
| + | |||
| + | Consistent with the DTD theory, it is beneficial to block the dopamine transporter, DAT, so there is less dopamine reuptake and more dopamine present in the synaptic cleft (Tripp & Wickens, 2008). | ||
| This type of drug treatment should not be used for children under six years of age because it has not yet been studied for this age group (FDA, 2013). Some side effects of Ritalin include, headache, decreased appetite, stomach ache, nervousness, trouble sleeping and nausea. | This type of drug treatment should not be used for children under six years of age because it has not yet been studied for this age group (FDA, 2013). Some side effects of Ritalin include, headache, decreased appetite, stomach ache, nervousness, trouble sleeping and nausea. | ||
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| - | <box 40% round right | > {{:treatment.jpg|}} </box| Dexymethylphenidate affects the dopaminergic system. This diagram illustrates how the neurotransmitter dopamine is packaged into vesicles in the presynaptic neuron. Dopamine is released from the vesicles into the synaptic clef, and then binds to receptors on the post synaptic neuron.> | + | <box 40% round right | > {{:treatment.jpg|}} </box| Figure 13: Dexymethylphenidate affects the dopaminergic system. This diagram illustrates how the neurotransmitter dopamine is packaged into vesicles in the presynaptic neuron. Dopamine is released from the vesicles into the synaptic clef, and then binds to receptors on the post synaptic neuron.> |
| Most cases of ADHD persist into adulthood. This dug is a safe and effective treatment for ADHD among children and adults (Spencer et al, 2007). | Most cases of ADHD persist into adulthood. This dug is a safe and effective treatment for ADHD among children and adults (Spencer et al, 2007). | ||
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| It was noted that dopamine levels were elevated in the nucleus accumbens as well (Bymaster et al., 2002). The nucleus accumbens is involved in the reward circuit, thereby increasing the susceptibility of abuse of psychostimulants; stimulants are considered a Schedule II drug meaning that there is a high potential for abuse (Allen et al., 2005). | It was noted that dopamine levels were elevated in the nucleus accumbens as well (Bymaster et al., 2002). The nucleus accumbens is involved in the reward circuit, thereby increasing the susceptibility of abuse of psychostimulants; stimulants are considered a Schedule II drug meaning that there is a high potential for abuse (Allen et al., 2005). | ||
| - | The downside is that some children reported to feel embarrassed at school when taking the medication and would often skip it (Tripp & Wickens, 2008). Another pitfall is that individuals with ADHD are often forgetful and may miss a dosage of their medication and thus impairs the efficacy of the drug (Tripp & Wickens, 2008). | + | The downside is that some children reported to feel embarrassed at school when taking the medication and would often skip it (Tripp & Wickens, 2008). |
| + | |||
| + | Another pitfall is that individuals with ADHD are often forgetful and may miss a dosage of their medication and thus impairs the efficacy of the drug (Tripp & Wickens, 2008). | ||
| In a specific study, the only side effects experienced were a dry mouth (Spencer et al., 2007). | In a specific study, the only side effects experienced were a dry mouth (Spencer et al., 2007). | ||
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| ====Non stimulants==== | ====Non stimulants==== | ||
| Non stimulants are also prescribed to treat ADHD. An example is Atomoxetine, which has high selectivity for noradrenergic reuptake transporters and low selectivity for dopaminergic transporters in the nucleus accumbens, thereby increasing norepinephrine specifically in the prefrontal cortex (Allen et al., 2005). This is important because it does not disrupt sleep as severely; a side effect of stimulants (Allen et al., 2005). In addition, the low selectivity for dopamine means that the nucleus accumbens is not affected as severely as with stimulants, so there is less potential for abuse of this drug (Allen et al., 2005). | Non stimulants are also prescribed to treat ADHD. An example is Atomoxetine, which has high selectivity for noradrenergic reuptake transporters and low selectivity for dopaminergic transporters in the nucleus accumbens, thereby increasing norepinephrine specifically in the prefrontal cortex (Allen et al., 2005). This is important because it does not disrupt sleep as severely; a side effect of stimulants (Allen et al., 2005). In addition, the low selectivity for dopamine means that the nucleus accumbens is not affected as severely as with stimulants, so there is less potential for abuse of this drug (Allen et al., 2005). | ||
| + | |||
| + | ===== Conclusions and Future Implications ===== | ||
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| =====References===== | =====References===== | ||
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