House of Mind

"Biology gives you a brain. Life turns it into a mind" - Jeffrey Eugenides

  • 27th May
    2011
  • 27
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. 

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. 

  • 3rd May
    2011
  • 03
Anatomically Distinct Dopamine Release During Anticipation and Experience of Peak Emotion to Music
Music has long been recognized as both an abstract and rewarding stimulus that produces feelings of euphoria and pleasure in many listeners.  Music may also elicit emotional responses from listeners and alter affective states. While music has been present across multiple cultures and societies throughout time, the experience of pleasure while listening to music is highly specific, personal and subjective. In a study featured in Nature Neuroscience last February, Salimpoor and others set out to study what goes on in the brain of individuals while they listened to enjoyable/pleasurable music. 
For the study, subjects were asked to bring their own pleasurable music, and the other subjects’ music was used as neutral music for comparison. Dopamine release while listening to music was estimated indirectly by using ligand-based positron emission tomography (PET) scan in which 11C raclopride, a radioactively labeled ligand, competes with endogenous dopamine for D2 receptor binding. The assumption is that if brain areas are experiencing surges of dopamine release, they binding capacity of 11C raclopride will decrease in these areas. The experience of feeling chills, a marker of peak emotional responses to music, was self-reported by the subjects. In addition, psychophysiological measurements (i.e. respiration rate, heart rate, skin conductance, temperature) were also conducted while the subjects listened to music while undergoing PET scanning. 
PET scanning revealed changes in 11C raclopride binding in the striatum, specifically in the right caudate and the right nucleus accumbens. There was also a significant positive correlation between reports of chills and feelings of overall pleasure, perhaps indicating that chills may serve as an objective measure of pleasure while listening to music. The experience of overall greater pleasure while music listening was also correlated with greater autonomic nervous system arousal, as indexed by changes in psychophysiological measurements. 
To assess the temporal dynamics in dopamine release, the group employed functional magnetic resonance imaging (fMRI) while subjects listened to neutral or pleasurable music. Subjects were asked to press a button whenever they felt chills (typically during pleasurable moments), and the 15s prior to the pressing of the button, which indicated chills + pleasure, were denoted as the anticipation window. Thus, dopamine release was studied in two different time periods: anticipation period (15s before reported pleasure and chills), and peak response (chills/pleasure). 
When the fMRI scans were conjoined with the PET masks, the group was able to identify a temporally mediated BOLD response in the right side of dorsal (caudate) and ventral (nucleus accumbens) striatum that corresponded with anticipation epochs and peak experience, respectively. Moreover, as demonstrated above, behavioral measures like the number of reported chills were more correlated with 11C raclopride binding changes in the right caudate while intensity of chills and overall degree of reported pleasure were more significantly correlated with changes in 11C raclopride binding potential in the right nucleus accumbens. 
In summary, the experience of pleasure while listening to music acts on the brain similarly to other rewards like food, sex and drugs. Listening to pleasurable music targets striatal areas associated with mesolimbic reward circuitry and dopaminergic neurotransmission. 
Source:
 
Salimpoor, et al. 2011. Anatomically Distinct Dopamine Release During Anticipation and Experience of Peak Emotion to Music. Nature Neuroscience. doi:10.1038/nn.2726

Anatomically Distinct Dopamine Release During Anticipation and Experience of Peak Emotion to Music

Music has long been recognized as both an abstract and rewarding stimulus that produces feelings of euphoria and pleasure in many listeners.  Music may also elicit emotional responses from listeners and alter affective states. While music has been present across multiple cultures and societies throughout time, the experience of pleasure while listening to music is highly specific, personal and subjective. In a study featured in Nature Neuroscience last February, Salimpoor and others set out to study what goes on in the brain of individuals while they listened to enjoyable/pleasurable music. 

For the study, subjects were asked to bring their own pleasurable music, and the other subjects’ music was used as neutral music for comparison. Dopamine release while listening to music was estimated indirectly by using ligand-based positron emission tomography (PET) scan in which 11C raclopride, a radioactively labeled ligand, competes with endogenous dopamine for D2 receptor binding. The assumption is that if brain areas are experiencing surges of dopamine release, they binding capacity of 11C raclopride will decrease in these areas. The experience of feeling chills, a marker of peak emotional responses to music, was self-reported by the subjects. In addition, psychophysiological measurements (i.e. respiration rate, heart rate, skin conductance, temperature) were also conducted while the subjects listened to music while undergoing PET scanning. 

PET scanning revealed changes in 11C raclopride binding in the striatum, specifically in the right caudate and the right nucleus accumbens. There was also a significant positive correlation between reports of chills and feelings of overall pleasure, perhaps indicating that chills may serve as an objective measure of pleasure while listening to music. The experience of overall greater pleasure while music listening was also correlated with greater autonomic nervous system arousal, as indexed by changes in psychophysiological measurements. 

To assess the temporal dynamics in dopamine release, the group employed functional magnetic resonance imaging (fMRI) while subjects listened to neutral or pleasurable music. Subjects were asked to press a button whenever they felt chills (typically during pleasurable moments), and the 15s prior to the pressing of the button, which indicated chills + pleasure, were denoted as the anticipation window. Thus, dopamine release was studied in two different time periods: anticipation period (15s before reported pleasure and chills), and peak response (chills/pleasure).

When the fMRI scans were conjoined with the PET masks, the group was able to identify a temporally mediated BOLD response in the right side of dorsal (caudate) and ventral (nucleus accumbens) striatum that corresponded with anticipation epochs and peak experience, respectively. Moreover, as demonstrated above, behavioral measures like the number of reported chills were more correlated with 11C raclopride binding changes in the right caudate while intensity of chills and overall degree of reported pleasure were more significantly correlated with changes in 11C raclopride binding potential in the right nucleus accumbens. 

In summary, the experience of pleasure while listening to music acts on the brain similarly to other rewards like food, sex and drugs. Listening to pleasurable music targets striatal areas associated with mesolimbic reward circuitry and dopaminergic neurotransmission. 

Source:

Salimpoor, et al. 2011. Anatomically Distinct Dopamine Release During Anticipation and Experience of Peak Emotion to Music. Nature Neurosciencedoi:10.1038/nn.2726


  • 24th February
    2011
  • 24
mindovermatterzine:

poculum:

Brain tractography: visualising neuronal tracts. Neuronal  tractography image showing the neuronal tracts in the brain of a  45-year-old male brain viewed from above. Tractography is an imaging  technique that highlights the neural tracts within the brain. It uses a  branch of magnetic resonance imaging (MRI), and computer-based image  analysis to define the structure and location of neuronal bundles. This  process is possible by tracking the movement of water molecules similar  to diffusion tensor imaging (DTI). The colour is assigned to make the  image more accessible and is based on the direction of the fibres.
Picture: Nuada Medical  / Wellcome Images

Total geek-gasm right now.

mindovermatterzine:

poculum:

Brain tractography: visualising neuronal tracts. Neuronal tractography image showing the neuronal tracts in the brain of a 45-year-old male brain viewed from above. Tractography is an imaging technique that highlights the neural tracts within the brain. It uses a branch of magnetic resonance imaging (MRI), and computer-based image analysis to define the structure and location of neuronal bundles. This process is possible by tracking the movement of water molecules similar to diffusion tensor imaging (DTI). The colour is assigned to make the image more accessible and is based on the direction of the fibres.

Picture: Nuada Medical / Wellcome Images

Total geek-gasm right now.

(via hellosugarmouse)

  • 8th February
    2011
  • 08
  • 31st January
    2011
  • 31