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use your braaaaaain

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houseofmind:

Attention-Deficit/Hyperactivity Disorder
In the US, ADHD has a prevalence of around 5-12% during childhood. Approx. 5 million children and adolescents in the US have ADHD, while only 2 million are being treated (mostly through psychostimulants). ADHD has long been characterized by its well-known pervasive behavioral symptoms: hyperactivity, impulsivity and inattention, which begin in childhood. There are 2 types of ADHD according to the DSM-IV: Hyperactive/Impulsive ADHD and Inattention ADHD.
Hyperactive/Impulsive ADHD Symptoms: ADHD 1
Fidgeting/squirming
Inability to remain seated
Restless
Loud and noisy (difficulty playing quietly)
Excessive talking
Impulsive
Intrusive 
“Always on the go”
Inattention Symptoms: ADHD2
Careless errors
Inattention to detail
Sustains attention poorly
Appears to not be listening
Disorganized
Trouble following through with directions/obligations
Loses needed objects
Dislikes sustained mental effort
Easily distracted 
Forgetful
In order for criteria to be met, +6 of the symptoms mentioned above (according to ADHD type) need to be present for 6 months or more and cause impairments in more than 1 setting (social, academic, occupational). These symptoms must also not be attributable to any other condition (i.e. depression, anxiety, substance use, etc)  and can cause impairment in children by the age of 7. Other characteristics that are important in the understanding and diagnosis of ADHD patients include: age, sex, comorbidity with other psychiatric disorders, intelligence, prematurity, exposure to toxins during early life, locomotor hyperactivity, differences in delay aversion, reward salience, motor inhibition tasks, error processing and working memory compared to controls. Moreover, ADHD is a disorder that’s characterized by high intra-subject variability (which is thought to be mediated by competition among functional neural networks). 
Although the underlying cause of ADHD is currently unknown, there is a belief that both genetic (mostly dopaminergic and noradrenergic genes) and environmental factors (i.e. parental smoking, brain injury) play a role in ADHD. Moreover, some have suggested that gene-environment interactions account for about 70-80% of ADHD cases. 
ADHD has strongly been linked to developmental, volumetric and functional differences in several brain structures/areas. For example, brain imaging studies of children with ADHD have found smaller sizes in the corpus callosum, caudate nucleus, and right frontal cortex. Overall, the brains of children with ADHD are significantly smaller and that the brain volume reduction in ADHD is widespread and also affects the cerebrum and cerebellum. Other studies from different disciplines have implicated disruption of the frontostriatal pathway and other circuitry in diverse areas like the prefrontal cortex, the basal ganglia and the cerebellum. Additionally, other studies have found delayed cortical maturation in children with ADHD-meaning that they take longer and are slower to develop compared to normal brains.
More recently, disruptions in other brain networks and their relation to ADHD are starting to be explored. The diagram above is taken from Castellanos et. al (2008). Dr. Castellanos is an NYU clinician who employs neuroimaging techniques like fMRI to study differences in brain circuitry and wiring in patients with ADHD. In the ADHD brain, the precuneus (red part towards the posterior end of the brain), which is involved in high-level integration of posterior association processes with anterior executive function, appears to be enlarged. ADHD related differences in brain regions are shown at the right. The authors suggest that functional circuits linking the anterior cingulate cortex to the precuneus and posterior cingulate cortex and their long range connections should be considered as dysfunctional center in the ADHD brain. 
Sources:
Castellanos et. al. 2008. Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder. Biological Psychiatry. 63 (3): 332-7. 
Castellanos and Tannock. 2002. Neuroscience of attention-deficit/hyperactivity disorder: The search for endophenotypes. Nature Reviews Neuroscience. 3: 617-626. 
Castellanos, XF. 2011. The Restless Brain: Spontaneous Brain Fluctuations and Variability in ADHD. Disorders of the Nervous System Lecture. 
Kieling et. al. 2008. Neurobiology of attention deficit hyperactivity disorder. Child and Adolescent Psychiatric Clin N America. 17: 285-307. 

houseofmind:

Attention-Deficit/Hyperactivity Disorder

In the US, ADHD has a prevalence of around 5-12% during childhood. Approx. 5 million children and adolescents in the US have ADHD, while only 2 million are being treated (mostly through psychostimulants). ADHD has long been characterized by its well-known pervasive behavioral symptoms: hyperactivity, impulsivity and inattention, which begin in childhood. There are 2 types of ADHD according to the DSM-IV: Hyperactive/Impulsive ADHD and Inattention ADHD.

Hyperactive/Impulsive ADHD Symptoms: ADHD 1

  • Fidgeting/squirming
  • Inability to remain seated
  • Restless
  • Loud and noisy (difficulty playing quietly)
  • Excessive talking
  • Impulsive
  • Intrusive 
  • “Always on the go”

Inattention Symptoms: ADHD2

  • Careless errors
  • Inattention to detail
  • Sustains attention poorly
  • Appears to not be listening
  • Disorganized
  • Trouble following through with directions/obligations
  • Loses needed objects
  • Dislikes sustained mental effort
  • Easily distracted 
  • Forgetful

In order for criteria to be met, +6 of the symptoms mentioned above (according to ADHD type) need to be present for 6 months or more and cause impairments in more than 1 setting (social, academic, occupational). These symptoms must also not be attributable to any other condition (i.e. depression, anxiety, substance use, etc)  and can cause impairment in children by the age of 7. Other characteristics that are important in the understanding and diagnosis of ADHD patients include: age, sex, comorbidity with other psychiatric disorders, intelligence, prematurity, exposure to toxins during early life, locomotor hyperactivity, differences in delay aversion, reward salience, motor inhibition tasks, error processing and working memory compared to controls. Moreover, ADHD is a disorder that’s characterized by high intra-subject variability (which is thought to be mediated by competition among functional neural networks). 

Although the underlying cause of ADHD is currently unknown, there is a belief that both genetic (mostly dopaminergic and noradrenergic genes) and environmental factors (i.e. parental smoking, brain injury) play a role in ADHD. Moreover, some have suggested that gene-environment interactions account for about 70-80% of ADHD cases. 

ADHD has strongly been linked to developmental, volumetric and functional differences in several brain structures/areas. For example, brain imaging studies of children with ADHD have found smaller sizes in the corpus callosum, caudate nucleus, and right frontal cortex. Overall, the brains of children with ADHD are significantly smaller and that the brain volume reduction in ADHD is widespread and also affects the cerebrum and cerebellum. Other studies from different disciplines have implicated disruption of the frontostriatal pathway and other circuitry in diverse areas like the prefrontal cortex, the basal ganglia and the cerebellum. Additionally, other studies have found delayed cortical maturation in children with ADHD-meaning that they take longer and are slower to develop compared to normal brains.

More recently, disruptions in other brain networks and their relation to ADHD are starting to be explored. The diagram above is taken from Castellanos et. al (2008). Dr. Castellanos is an NYU clinician who employs neuroimaging techniques like fMRI to study differences in brain circuitry and wiring in patients with ADHD. In the ADHD brain, the precuneus (red part towards the posterior end of the brain), which is involved in high-level integration of posterior association processes with anterior executive function, appears to be enlarged. ADHD related differences in brain regions are shown at the right. The authors suggest that functional circuits linking the anterior cingulate cortex to the precuneus and posterior cingulate cortex and their long range connections should be considered as dysfunctional center in the ADHD brain. 

Sources:

Castellanos et. al. 2008. Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder. Biological Psychiatry. 63 (3): 332-7. 

Castellanos and Tannock. 2002. Neuroscience of attention-deficit/hyperactivity disorder: The search for endophenotypes. Nature Reviews Neuroscience. 3: 617-626. 

Castellanos, XF. 2011. The Restless Brain: Spontaneous Brain Fluctuations and Variability in ADHD. Disorders of the Nervous System Lecture. 

Kieling et. al. 2008. Neurobiology of attention deficit hyperactivity disorder. Child and Adolescent Psychiatric Clin N America. 17: 285-307. 

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