Amygdala Medial Prefrontal Cortex Disconnect

A great amount of research has been conducted exploring how sleep deprivation weakens systems such as the immune system, weight control, cognitive processing (memory and learning) but there has been little inquiry into how sleep loss effects our emotional brain. Sleep deprivation has been commonly associated with several psychiatric disorders. It is thought that psychiatric and mood disorders, such as bi polar disorder, cause sleep loss. However, Mathew Walker and colleagues new study show that this isn’t necessarily the case as sleep deprivation, as the results from their study indicate, can itself be the cause of psychological instability.

The Study:
The study involved 26 healthy participants ages 18-30. The 26 subjects were divided in two groups: 12 were assigned to a sleep control group and the other 14 to a sleep deprivation group. All subjects had to refrain from ingesting caffeinated and alcoholic beverages for a total of 72 hours and followed a normal sleep/wake pattern for one week prior to the study (7 to 9 hours of sleep per night, waking hours: 6am -9pm). Their sleep/wake pattern was monitored by an actigraphy, a wristwatch movement sensor.

Pre-Study:
The sleep control group subjects had a normal night of sleep the night before the scanning. The sleep deprivation group remained awake for the entire night and the entire day before the scanning at 5pm (total of 35 hours of sleep deprivation).

Study/ fMRI Scanning:
The subjects were shown 100 images ranging from neutral to gruesome (i.e. basket on table to images of burn victims). Each image was shown for 10 seconds and the subjects were asked to quickly rate their emotional response through a button system, this was also to insure that all subjects remained awake and alert during the experiment. The subjects were in fMRI scanners during this whole process. Mathews and his colleagues were particularly looking for reactions in the amygdala, and curious to see if there were any significant differences between the sleep control group and the sleep deprivation group.

Results:
Both groups had similar emotional responses to the neutral images, but as the images became more and more aversive the fMRI scans showed that there were indeed great differences in how the brains were firing in the sleep-deprived subjects. In both groups the amygdala, as hypothesized, showed greater activity in response to the intense images, yet the sleep deprived subjects amygdala’s were 60% more active than the sleep control group subjects. Not only were the sleep deprived subjects amygdalas showing a stronger activation but also the volume of the amygdala that was activated (greater amount of neurons being activated) was three times that of the sleep control subjects.


It also became evident when observing the fMRI scans that there was a difference in the brain wiring of the control subjects and the sleep control subjects. The control subjects amygdalas maintained normal communication with the medial-prefrontal cortex (MPFC), however; the sleep deprivation participants amygdalas appeared to have lost connectivity with the MPFC and were instead communicating with regions of the autonomic nervous system.



Why is this loss of connectivity with the MPFC significant?

The MPFC communicates with the amygdala as it sends connections to the amygdalas central nucleus and brain stem outputs of the central nucleus. The MPFC serves as an “inhibitory, top-down control of amygdala function, resulting in contextually appropriate emotional responses.”






Maria Morgan, working in Joseph LeDoux’s lab, researched damaged MPFC and found that some lesions of MPFC resulted in exaggerated fear reactions. When the amygdala is reacting to fear the MPFC remains inactive and vice versa. When the MPFC is damaged increased anxiety occurs as the amygdala is left “unchecked” by the MPFC. This often leads to a difficulty with decision making in emotional situations. This research supports Mathews and colleagues’ findings. However, in their case study a lack of connectivity between the MPFC and amygdala wasn’t caused by lesions in the MPFC but rather by a lack of sleep.



The heightened emotional state occurs when threatening or in this case disturbing stimuli goes unchecked by the MPFC, and this greater activation of the amygdala communicates with the autonomic nervous system that in turn can lead to fight or flight responses.

Stimuli that activate the fight or flight response trigger the brains periventricular system PVS, commonly known as the brains punishment circuit. The PVS is composed of the hypothalamus, the thalamus, and the gray substance around the Sylvius. Acetylcholine activates emission of a hormone known as adrenal cortico-trophic ACTH which activate the adrenal glands to release adrenalin that prepares the body for fight or flight response.

This case study highlights the great importance of sleep. While more research must be done on the connection of sleep deprivation and mood disorders it is clear that sleep loss affects those without symptoms of psychiatric disorders as well. Most of us have experienced the altered state after pulling an all nighter. Now there is evidence that our brains are literally rewiring to create a heightened emotional state. As more research is conducted sleep might be taken more seriously in terms of psychological instabilities. Perhaps certain careers that often keep employees awake for hours on end who’s decision making is crucial will be reconsidered. For example, medical workers.

Sources:

LeDoux, Joseph. Synaptic Self: How Our Brains Become Who We Are. New York: Penguin Books, 2002.

Swaminathan Nikhil. “Can a Lack of Sleep Cause Psychiatric Disorders? Study shows that sleep deprivation leads to a rewiring of the brain’s emotional circuitry” Scientific American. October 23 2007. Get link

Walker, Mathew P. et al. “The human emotional brain without sleep- a prefrontal amygdala disconnect.” Current Biology. Vol 17 No 20.

Walker, Mathews P. et al “ Supplemental Data: The human emotional brain without sleep- a prefrontal-amygdala disconnect” Current Biology. Vol 17 No 20.

“The Amygdala and its Allies.” The Brain from Top to Bottom
http://thebrain.mcgill.ca/flash/i/i_04/i_04_cr/i_04_cr_peu/i_04_cr_peu_1a.jpg

article for april 14th

http://www.sciencedaily.com/releases/2009/03/090304160400.htm

Article for 4/14

Here's my article for April 4th

Autism and Music

Autism Spectrum disorders affect about 6 in every 1,000 people with varying severities. The prevalence has been drastically increasing since the 1980’s, but most people believe that is not due to an actual increase in the disorder but simply a change in diagnostic criteria.
Autism starts affecting children before the age of three. It is characterized by difficulty with social interactions, repetitive behaviors, and difficulty in acquiring and using language. About 0.5% to 10% of autistic individuals are called autistic savants. They are extremely gifted in one skill set or talent. Though scientists are not in agreement with the causes of autism, there are many theories that dominate the general discourse. It is commonly assumed to be a combination of environmental and genetics with differing emphasis between the two. The research that is compelling for the genetics autism paradigm involves studies of identical twins which proved that there was a 60% chance that the twin of an autistic child would develop autism. These results are staggering considering that .6% of the population has autism and fraternal twins showed no significant increase in autism prevalence.
Further, many researchers have found physical irregularities in several parts of the brain including the levels of serotonin in the brain. Specifically, research centers called “Centers of Excellence in Autism Research” have shown that connections in the brain are often impaired in autistic children. “Research is now being conducted all over the world to determine specific genes that increase the likelihood of someone developing autism. A group known as the International Molecular Genetic Study of Autism Consortium, which includes clinicians and researchers from the USA, UK, France, the Netherlands, Denmark, Italy, and Greece, has pinpointed four chromosomes which they believe play critical roles in autism. The chromosomes they identified are numbers 2, 7, 16 and 17. The evidence for involvement of chromosomes 2 and 7 is particularly strong as these had also been previously identified by other independent researchers (2,3,4,5). Chromosome 7 is known to be associated with many language disorders and chromosome 2 plays an important role in early brain development. These findings are further demonstrated by research showing dyslexia patients also have abnormalities on these chromosomes. This is not surprising as dyslexia also produces deficits in learning ability and information processing in the brain”
The problem with autism is something that we take for granted. Most of us learn how to make sense of our environment through an unconscious ability to combine our sensory information. What we hear, see, feel and know all merge to create spatial maps that allow us to understand our relative place in space. In childhood, we learn how to put our senses together to respond more efficiently to impediments presented to us in our environment. Children with autism have trouble learning to do this. They have greater difficulty creating a synthesis of all the sensory information and therefore have more difficulty responding to the environmental impediments. Sensory integration therapy is a type of occupational therapy that places children in a room specifically designed to stimulate and challenge all of the senses. This therapy is based on the assumption that the child is either overstimualted or understimulated by the environment. Specifically music therapy seeks to stimulate the auditory processing in autistic children so that the overall sensory integration will be more efficient. Music therapy seeks to regulate a common trend in autism; acute lack of total sensory integration. This is reflected and materialized in many ways in the brain.

Auditory Processing of Music
The majority of symptoms in children and adults include attention deficits, learning disabilities, autism, obsessive-compulsive disorder, depression, anxiety, chronic pain and many more are all directly a result of an imbalance of electrical activity in the brain. There are many environmental factors that can produce an imbalance of electrical activity and function of the two sides of the brain documented as either an increase of activity on one side or a decreased activity on the other.
Adverse activity is the right hemisphere which autism is expected to be specifically stimulated by low frequency tones, negative or downbeat music. Specifically, autism is a common sensory processing disorder (SPD). In children with autism, sensory integration is very difficult to accomplish. Music therapy can work as a way to increase the integration of the main sensory areas. The sensory system is broken up into three main areas: the tactile, vestibular, and the proprioceptive sense. The tactile system is your sense of touch. The vestibular system is responsible for movement and the body’s position in space. The proprioceptive system deals with muscles and joints. There are other sensory systems but they are not as commonly associated with sensory dysfunction.
The vestibulocochlear system informs us of sound, movement and orientation of space. The cochlear portion of the system turns sound or vibration into electrochemical messages that are relayed throughout the central nervous system and is critical to auditory processing. The vestibular portion serves to provide stabilization, influences attention and arousal, posture, movement, thus being critical to sensorimotor integration. It is the integration of our senses that allows us to understand what we are experiencing in our world.
Specifically, the vestibular system contributes to our balance and our sense of spatial orientation that provides input about movement and equilibrioception. (equilibrioception is what experiencial information from the vestibular system is called.) It is anatomically joined with cochlear system, and the systems lie closely together throughout the nervous system and together elaborate the general labyrinth of the inner ear.



Further, there is a profound connection between vestibular functioning and language processing. This allows for many close neuronal associations with auditory processing and language. The vestibular system sends signals primarily to the neural structures that control our eye movements, and to the muscles that keep us upright.
Decreased vestibular processing can impact on the area of speech and language development, particularly auditory processing. It is associated with autistic disorder, which are generally categorized by decreased electrical neurotransmitting activity. Research has found that therapy to improve the function of the vestibular system can also result in improved language development.


Musical Processing and Emotional Understanding
Vestibular complications are not the only ways that music can affect autism. A benefit to music therapy for autistic children aids them in verbal communication and social interaction deficits. A proposed study by Molnar Szakacs and Overy wants to compare musical processing on a neurological basis to communication, language and action. This is determined by the mirror neuron system, which allows us to abstract musical sounds similar to the ways in which humans form language when speaking and interacting. “The mirror neuron system has been proposed as a mechanism allowing an individual to understand the meaning and intention of a communicative signal by evoking a representation of that signal in the perceivers own brain “(p.235.) Spatial maps created in the brain, specifically the parietal lobe, are influenced by these mirror neurons and contribute to an overall understanding of actions and intentions. Essentially, mirror neurons enable humans to understand emotions through facial and body expressions.
Music is closely connected with motor activity. Producing music involves developed spatial maps and a physical understanding of vibrations and sounds. The mirror neuron system that allows someone to understand musical experiences is the same set of neurons that is present in motor functioning and mapping. There have been recent neuro-imaging studies that show that people with musical expertise have a change in their fronto-parietal mirror neuron system. Music is also inherently similar to language. Music is pitches composed into symphonies the way that language is words composed into novels.
The proposed study by Molnar Szakacs emphasizes the important connection between an understanding of language with an understanding of music. This is further emphasized by research conducted on other language disorders like dyslexia. The main point that Molnar Szakacs intends to look at is if language and music are so similar and if they are dictated by similar mirror neural patterns, then why can’t autistic savants with high pitch sensitivity understand facial emotions and social communications?
Mirror neurons are cells that enable normally developing people to decipher meaning and intention in actions as well as replicate those actions. Autistic children are typically noted to have a decreased or altered mirror neural system. This affects the ways in which the limbic system, which is responsible for emotions, interacts with those mirror neurons. This comes back to the point that these same mirror neurons are involved in the understanding of music. 

Music Based Therapies

So it makes sense that a program that would stimulate and help to integrate the cochlear and vestibular systems might be very helpful for the autistic child’s emotional understanding. This does not present a cure for autism, but The Listening Program (TLP) can be an effective intervention for children on the autistic spectrum.
TLP is a music-based sound stimulation program that currently consists of 8 one hour audio CD’s that contain specially processed classical music and nature sounds plus a 112 page guidebook. Listening sessions are typically fifteen minutes in length, done once or twice a day, five days a week, using high quality stereo headphones.

1- Increases engagement- The individuals experience an improvement in their self-image and an improved sense of their body in space. This enables them to feel more comfortable interacting with their surroundings. They show an increase in the toleration and need for physical contact. There is also an increase in attentiveness and initiation of eye contact.
2- Emerging Skills- When used in conjunction with other forms of therapy, it allows for better integration of the motor and sensory systems which in turn leads to a faster rate of skill acquisition.
3- Auditory Processing- It improves the accuracy and speed at which individuals process sound. This leads to better overall communication skills.
4- Reduced Sound Sensitivity- Many autistic individuals experience hypersensitivity to sounds because their nervous system is unable to regulate the sensory input. This program helps the nervous system be able to better process sensor info, which reduces sound sensitivity.

Obesity: Reviving the Promise of Leptin

The History of Leptin

• Discovered by Douglas Coleman (The Jackson Laboratory, Bar Harbor, Maine)

• Parabiosis of normal mice with either diabetic or overweight mice.

• Found that there was a "satiety factor" circulating in the blood. Hypothesized that db mice lacked the receptor to the factor, while ob mice did not produce it.
  

• It could not be extracted from the blood because it was present in tiny amounts. However, the gene responsible for it was eventually isolated and the "satiety factor", leptin, was produced in a lab. The leptin gene is spliced into bacteria and the bacteria sets to work producing the protein.
  

• By the mid 1990s it was greeted as a possible miracle cure for the rising obesity epidemic. 1995 New York Times headline read: "Researchers find hormone causes a loss of weight". Leptin is discussed as a "magic bullet", which would hopefully "change the image of obesity, helping people to see it not as a punishment for gluttony but rather as a metabolic disorder, treatable with a remedial hormone just as diabetes is treated with insulin."

• By the end of 90s none of the new research had panned out. All experiments that had been done on obese humans had found that leptin rarely caused weight loss, and if it did it was only temporary. New York Times headline from 1999 read: "Hormone that slimmed fat mice disappoints as panacea in people". Researchers determined that obese people were somehow resistant to leptin, so it was not effective in their brain.

• Since then most research has focused on understanding the metabolic pathways of leptin, and little thought has been given as to how it might be used as a treatment for obesity.

How is Appetite Controlled?

• Hypothalamus is the main organ involved in regulation of appetite; specifically the arcuate nucleus (situated at the base).

• The neurons involved primarily employ serotonin as a neurotransmitter, although neuropeptide Y and Agouti-Related peptide are also involved.

• The hypothalamus uses Ghrelin, Leptin, Insulin and PYY as markers to influence how hungry we feel.

• Ghrelin is excreted by the stomach may also be produced in the brain. Causes feelings of hunger and is associated with regular meal times. Ghrelin levels rise immediately before a meal and fall sharply after eating.
  

• Ghrelin Factoids: Those suffering from anorexia nervosa have higher blood levels of ghrelin. - Individuals who have undergone gastric bypass surgery produce less ghrelin. - Ghrelin acts not only on neurons in the arcuate nucleus but also activates reward circuitry in the brain associated with dopamine.

• Leptin is mainly produced by white adipose tissue. Leptin blood level is proportional to body fat. The more body fat on the body the more leptin that is produced.

• Differences in brain activity during eating in people with leptin deficiency and those with normal leptin levels.
  

• When leptin is given to genetically obese mice they lose 30% of their body weight in 2 weeks. When leptin is given to lean mice they lost all their body fat in 4 days.
  

• Human trials with leptin were unsuccessful. Except at the highest doses (several tablespoons a day) there were no significant changes in weight.

• Why was it so unsuccesful? Obese humans develop a resistancy to leptin in their brain.

Explaining and Reversing Leptin Resistance

• Umut Ozcan - Harvard - Endoplasmic Reticulum Stress Plays a Central Role in Development of Leptin Resistance

• General Hypothesis: The hypothalamus has become resistant to leptin through a process called Endoplasmic Reticulum Stress (ER Stress) which ultimately results in reduced ER function. This causes reduced function of Leptin Receptor signaling. To resensitize the brain to leptin it is necessary to improve function in the ER. Chemical chaperones have been shown to do this.

• The Endoplasmic Reticulum is an organelle responsible for protein folding and transportation of proteins to the cell membrane.

• If the normal processes of the ER are disturbed misfolded proteins accumulate in the cell. This activates cellular stress mechanism called the Unfolded Protein Response (UPR) is activated.

• UPR halts protein translation and causes an increase in the production of molecular chaperones involved in protein folding. If this mechanism is unsuccessful, UPR leads to apoptosis.
  

• How ER stress is induced and how this leads to UPR is not well understood. The main theory suggests that increased levels of circulating cytokines, fatty acids, excess nutrition and activation of the rapamycin pathway (involved in cellular homeostasis) contribute.
  

• What they demonstrated in the paper:

1. Leptin Acts on a Subset of Hypothalamic neurons
2. ER Stress Inhibits Leptin Receptor Signaling
3. ER Stress Creates Leptin Resistance in the Brain of Lean Mice
4. Improvement of ER Function Enhances Leptin Signaling
5. ER Capacity of the Brain Links Obesity to Leptin Resistance
6. Chemical Chaperones are Leptin Sensitizers.

2. ER Stress Inhibits Leptin Receptor Signaling

• Cells that presented the Leptin Receptor (LepRB) were exposed to tunicamycin (a chemical that induces ER stress) and then treated with leptin for 45 minutes.

• There was no evidence of leptin-stimulated tyrosine phosphorylation of LepRB or Stat3 phosphorylation (both cellular events that occur as a result of leptin binding to LepRB).

• This indicates that UPR inhibits LepRB signaling at all steps.

• Since LepRB is folded in the ER they next investigated ER stress blocks LepRB translocation from the ER to the cell membrane as a possible explanation of the block in leptin signaling.

• They induced ER stress in cells using tunicamycin and then used immunflorescence staining to analyze LepRB levels in the cell membrane. They found that ER stress does not decrease LepRB translocation to the membrane nor does it cause a misfolding of LepRB.

3. ER Stress Creates Leptin Resistance in the Brain of Lean Mice

• First - Showed that injecting tunicamycin into the hypothalamus of lean mice caused ER Stress.

• Second - Showed that ER stress in the brain's of lean mice completely blocked activation of Stat3.

• Third - Noted that the food uptake of lean mice with induced ER stress in the hypothalamuc increased.

5. ER Capacity of the Brain Links Obesity to Leptin Resistance

• Bred XNKO mice that produced less of the regulators involved in protein folding in the ER therefore making them more susceptible to ER stress (deletion of the XPB1 gene).

• On a normal diet they had a slightly lower body weight. Blood glucose and leptin levels were normal. Glucose homeostasis was maintained within a normal range.

• On a high fat diet the XNKO mice gained weight more quickly. A sharp increase in leptin level was maintained through out the experiment. They consumed more food, had a higher total fat amount and a significantly lower lean mass.

• These results support the hypothesis that ER capacity of the brain is involved in regulating body weight, leptin sensitivity and metabolic homeostasis.

6. Chemical Chaperones are Leptin Sensitizers

• Chemical chaperones are compounds that have been found to increase ER function and decrease the accumulation of misfolded proteins in the ER, thereby reducing the likelihood that ER stress will occur.
  

• 2 FDA approved chemical chaperones for humans are 4-phenyl butyrate (PBA) and tauroursodeoxycholic acid (TUDCA). Past studies have shown that these chemicals can relieve ER stress in the liver and adipose tissues, as well as enhancing insulin sensitivity in mouse models.
  

• Attempted to reverse ER stress in the hypothalamus of mice who had been on a high fat diet. Normal mice were kept on a high-fat diet for 25 weeks and then treated with PBA for 10 days, followed by daily leptin administration.
  

• Control mice rapidly lost weight and then rapidly regained it. Mice treated with PBA rapidly loss weight, they also consumed less food.

• Similar results were obtained with TUDCA.
  

• Both PBA and TUDCA also had some success in increasing leptin sensitivity in genetically obese mice (ob/ob mice).

What This Means

• After years of searching for leptin-sensitizing agents, chemical chaperones have been identified as potential novel treatment options for obesity.

Music evokes emotion in children with autism

Here's my article.


Music and Autism

Musical Behavior in a Neurogenetic Developmental Disorder

Evidence from Williams Syndrome

Daniel J. Levitin

Daniel J. Levitin's paper reviews a series of studies performed to assess the musical abilities and behaviors of individuals with Williams Syndrome- a neurogenetic developmental disorder.

What is Williams Syndrome (WS)?

Williams Syndrome is created by a small genetic accident which occurs during meiosis, when a segment of DNA containing 25 genes is lost. The result of which affects abstract thought, so that many WS have a bad concept of spacial, quantitative, reasoning, attention, eye-hand coorination, and reading abilities. WS people tend to be very talkative, and will talk with everyone; they completely lack a sense of social fear. Functional brain scans have shown that the amygdala in WS people shows no reaction when they see angry or worried faces.

Here is an image taken from the National Institutes of Health website depicting the difference in amydala activity scanned in reaction to threatening scenes and faces in WS participants and controls (http://www.nih.gov/news/pr/jul2005/nimh-10.htm)

Abnormal regulation of the amygdala in participants with Williams Syndrome (right) compared to controls (left). The amygdala activates more for threatening scenes (bottom), but less for threatening faces (top).

What is the connection between WS and music?
Not only do WS people show extreme friendliness and near-normal speaking skills, they also tend to be more engaged in musical activities and musicality than others. Levitin reports in this paper a possible neuroanatomical correlate of this engagement, with increased activation in the right amydala to music and to noise.

Based on Levitin and his team's observations, claims of musicality involve many aspects of music including frequent music listening, music performance (for example: a WS person can be able to play the clarinet despite not knowing how to tie their shows) , a deep emotional engagement with msuic, or an above-average musical memory and sound sensitivities (hyperacusis) involving unusual sensitivity to sound, categorization or labelling of sounds that others can't, or anxiety and fear of sounds that non-WS people do not find aversive.

Levitin says that WS can help us better understand the links between genes, brain, and musical behaviors and that WS hypersociability and lack of social inhibitions might be related to their musicality.

The Studies

1st Step:
Characterizing the musical phenotype in WS
The Questionnaire.
Levitin administered a questionnaire to the caregivers of 130 WS participants, 130 Down syndrome participants, 130 autistic participants, and to 130 normal controls. The questionnaire gathered information about physical variables, interest in music, emotional responses to music, musical training, the amount of time engaged in musical activities, and the age of onset of musical activities.

Individuals with WS showed a significantly younger age of onset of musical interest, spent more time per week listenign and playing, and were reported to experience higher levels of emotion when listening to music.

A prinical components analysis revealed seven underlying orthogonal factors that contributed to the profile obtained from the questionnaire. This can be divided up into 7 factors including content related to musical complexity, reproduction, sensitivity, musical theory and achievement, listening habits, positivity, and emotions.

Study of Neural Correlates of Auditory Perception in WS using fMRI

Levitin hypothesized that he would find differences in brain activation bewteen people with WS and controls, and that WS people would show a wider and more diffuse pattern of activation to music and noise stimuli than controls, and that they would show a greater amygdaloidal activation, indexing their heightened emotional reations to music and noise.

Study was conducted usuing a desensitization program that involved a professionally proudced video introdcution to the fMRI scanning procedure, usuing a child's-eye-view of the facility and a child's narration. This was followed to a visit fo an fMRI simulator in which the participants could become acclimated to the noises and enclosed space. 5 WS participants were recruited for an fMRI study of differential processing of music and noise, and five age- and sex-matched controls.
Participants listened to to excerpts from familiar and unfamiliar classical music, as well as the types of noisy sounds that WS people are often sensitive to, such as fans, motors, and leaf blowers.

Results:

Comparing music to noise, WS individuals showed a significantly lower voxel intensity bilaterally in the superior temporal cortex, middle temporal gyri, and superior temporal sulcus. In a comparison of responses to music-minus-rest vs. noise-minus-rest, control participants showed significantly higher temporal lobe activations to the music than the noise, while the WS participants showed virtually indistinguishable activation levels.

He also observed marked differences between WS patients and controls in the right amydala, with WS patients exhibiting far greater activation intensity in the music-minus-noise contrast. This points to a possible neural basis for the unusal acoustical and musical sensitivities observed in affected individuals. Overall, WS participants showed more variable and diffuse activations throughout the brain, and the showed increased activation in the amygdala and cerebellum.

The test of musical skills:

Rhythmic Production Ability

To test rhthym, Levitin and his team presented 8 WS individuals and 8 mentally age-matched controls with a set of clapped rhythums in increasing complexity. The participant had to clap back the rhythm as accurately as possible. Independent coders, blind to hypothesis, and group membership, analyized audio tapes of the test sessions and scored each trial as correct or incorrect or incorrect but very musical nonetheless.

The results showed that the WS and control participants obtained an equal number of correct trials about 66%. However, WS indiviuduals were three times more likely when incorrect to supply a musically compatible rhythm. This was interpreted as a marker of rhythmic ability or creative rhythmicity among the WS participants.

Melodic Production Ability

Levitin presented 12 WS individuals, 12 chronologically age-matched NCs, and 12 individuals with DS a set of melodies increasing in complexity, to assess their melodic reproduction ability. WS and NC were statistically better at melodic repetition than the DS, and not significantly different from one another. He then presented all participants with a set of melodic fragments and instructed them to complete the melodies. The WS individuals were not as good at melodic completion as the NCs. Thus, WS individuals are better at rhymic production than melodic production.

Sources:

Levitin, Daniel J.  (2005) Musical Behavior in a Neurogenetic Developmental Disorder, Retrieved March 15, 2009 from Daniel J. Levitin's Website: http://www.psych.mcgill.ca/levitin/

Dobbs, David "The Gregarious Brain." The New York Times July 8, 2007. Retrieved on March 15, 2009 from nytimes.com