A developmental study of the effect of music training on timed movements

When people clap to music, sing, play a musical instrument, or dance, they engage in temporal entrainment. We examined the effect of music training on the precision of temporal entrainment in 57 children aged 10–14 years (31 musicians, 26 non-musicians). Performance was examined for two tasks: self-paced finger tapping (discrete movements) and circle drawing (continuous movements). For each task, participants synchronized their movements with a steady pacing signal and then continued the movement at the same rate in the absence of the pacing signal. Analysis of movements during the continuation phase revealed that musicians were more accurate than non-musicians at finger tapping and, to a lesser extent, circle drawing. Performance on the finger-tapping task was positively associated with the number of years of formal music training, whereas performance on the circle-drawing task was positively associated with the age of participants. These results indicate that music training and maturation of the motor system reinforce distinct skills of timed movement.

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Neurons in human muscles emphasize stimulation from the outside world

Stretch sensors in our muscles participate in reflexes that serve the subconscious control of posture and movement. According to a new study published in the Journal of Neuroscience, these sensors respond weakly to muscle stretch caused by one’s voluntary action, and most strongly to stretch that is imposed by external forces. The ability to reflect causality in this manner can facilitate appropriate reflex control and accurate self-perception.  

“The results of the study show that stretch receptors in our muscles indicate more than which limb is moving or how fast; these sensors also adjust their signals according to who caused the movement,” says Michael Dimitriou, who conducted this study and is currently a post doc at the Department of Integrative Medical Biology, Umeå University, Sweden.

Normally, we can easily distinguish between movements we make ourselves and movements that are imposed on our body by external forces. The ability to discriminate between self-generated and externally generated sensory events is crucial for accurate perception and the control of posture and movement. This ability is also believed to form the foundation on which conscious self-awareness is built.

Such discrimination between self and other has previously been thought to arise as a result of complex computations performed in the brain, that use prior knowledge or memories of the consequences of own actions. But the study by Michael Dimitriou shows that information on the cause of a sensory effect can be provided in real-time by so-called ‘muscle spindles’, a class of stretch receptors found in most of our skeletal muscles.

Muscle spindles differ from other sensory receptors, such as stretch receptors in the skin, because their sensitivity can be controlled by the nervous system via specialized motor neurons. The purpose of this control has been unclear. The neural data presented by Michael Dimitriou indicates that these specialized motor neurons increase the sensitivity of stretch receptors when the body is exposed to an externally imposed stretch stimulus, such as when a falling ball is caught in the hand. Because amplified spindle responses mean stronger stretch reflexes, the resulting muscle activity instantly counteracts movement of the hand. When making a voluntary movement, however, the nervous system ‘automatically’ reduces the sensitivity of spindles in the stretching muscles, thereby making it possible for us to move without setting off strong stretch reflexes that would otherwise counteract movement. Uncontrollably strong stretch reflexes are commonly referred to as ‘spasticity’.

“These results provide an explanation of how reflexes can be functionally adjusted to help us achieve our everyday tasks, without requiring conscious control of reflex sensitivity or complex computations in the brain for predicting the sensory consequences of our actions,” says Michael Dimitriou.

He believes that these new findings are important both for understanding the neural mechanisms that underlie movement control and self-perception, but also for understanding pathological states where these mechanisms are disturbed.

“With these findings, we also get new insights into mechanisms whose malfunction may contribute to neuromuscular problems such as spasticity or alien hand syndrome (also known as ‘Dr. Strangelove syndrome’), and help identify potential treatment targets for these conditions,” says Michael Dimitriou.

Research Shows How Brain Can Tell Magnitude of Errors

University of Pennsylvania researchers have made another advance in understanding how the brain detects errors caused by unexpected sensory events. This type of error detection is what allows the brain to learn from its mistakes, which is critical for improving fine motor control.  

Their previous work explained how the brain can distinguish true error signals from noise; their new findings show how it can tell the difference between errors of different magnitudes. Fine-tuning a tennis serve, for example, requires that the brain distinguish whether it needs to make a minor correction if the ball barely misses the target or a much bigger correction if it is way off.

The study was led by Javier Medina, an assistant professor in the Department of Psychology in Penn’s School of Arts & Sciences, and Farzaneh Najafi, then a graduate student in the Department of Biology. They collaborated with postdoctoral fellow Andrea Giovannucci and associate professor Samuel S. H. Wang of Princeton University.

It was published in the journal eLife.

Our movements are controlled by neurons known as Purkinje cells. Each muscle receives instructions from a dedicated set of hundreds of these brain cells. The instructions sent by each set of Purkinje cells are constantly fine tuned by climbing fibers, a specialized group of neurons that alert Purkinje cells whenever an unexpected stimulus occurs.

“An unexpected stimulus is often a sign that something has gone wrong,” Medina said, “When this happens, climbing fibers send signals to their related Purkinje cells that an error has occurred. These Purkinje cells can then make changes to avoid the error in the future.”

These error signals are mixed in with random firings of the climbing fibers, however, and researchers were long mystified about how the brain tells the difference between this noise and the useful, error-related information it needs to improve motor control.

Medina and his team showed the mechanism behind this differentiation in a study published earlier this year. By using a non-invasive microscopy technique that could monitor the Purkinje cells of awake and active mice, the researchers could measure the level of calcium within these cells when they received signals from climbing fibers.

The unexpected stimuli in this experiment were random puffs of air to the face, which caused the mice to blink. The researchers located Purkinje cells that control the mice’s eyelids and saw that calcium levels necessary for neuroplasticity, i.e., the brain’s ability to learn, were greater when the mice got an error signal triggered by a puff of air than they were after a random signal.

While being able to make such a distinction is critical to the brain’s ability to improve motor control, more information is needed to fine-tune it.  

“We wanted to see if the Purkinje cells could tell the difference not just between random firings and true errors signals but between smaller and bigger errors,” Medina said.

In their new study, the researchers used the same experimental set-up, with one key difference. They used air puffs of different durations: 15 milliseconds and 30 milliseconds.

What they found was that the eyelid-associated Purkinje cells filled with different amounts of calcium depending on the length of the puff; the longer ones produced larger spikes in calcium levels.        

In addition, the researchers saw that different percentages of eyelid-related Purkinje cells respond depending on the length of the puff.  

“Though there is a large population of climbing fibers that can give error-related information to the relevant Purkinje cells when they encounter something unexpected, not all of them fire each time,” Medina said. “We saw that there is information coded in the number of climbing fibers that fire. The longer puffs corresponded to more climbing fibers sending signals to their Purkinje cells.”

Their study could help explain how practice makes perfect, even when errors are imperceptibly small.

“If you felt a short puff and a long puff, you might not be able to say which one was which, but Purkinje cells can tell the difference,” Medina said. “The difference between a ‘very good’ and an ‘awesome’ tennis serve rests on being able to distinguish errors even as tiny as that.” 

Memories of Errors Foster Faster Learning

Using a deceptively simple set of experiments, researchers at Johns Hopkins have learned why people learn an identical or similar task faster the second, third and subsequent time around. The reason: They are aided not only by memories of how to perform the task, but also by memories of the errors made the first time.

“In learning a new motor task, there appear to be two processes happening at once,” says Reza Shadmehr, Ph.D., a professor in the Department of Biomedical Engineering at the Johns Hopkins University School of Medicine. “One is the learning of the motor commands in the task, and the other is critiquing the learning, much the way a ‘coach’ behaves. Learning the next similar task goes faster, because the coach knows which errors are most worthy of attention. In effect, this second process leaves a memory of the errors that were experienced during the training, so the re-experience of those errors makes the learning go faster.”

Shadmehr says scientists who study motor control — how the brain pilots body movement — have long known that as people perform a task, like opening a door, their brains note small differences between how they expected the door to move and how it actually moved, and they use this information to perform the task more smoothly next time. Those small differences are scientifically termed “prediction errors,” and the process of learning from them is largely unconscious.

The surprise finding in the current study, described in Science Express on Aug. 14, is that not only do such errors train the brain to better perform a specific task, but they also teach it how to learn faster from errors, even when those errors are encountered in a completely different task. In this way, the brain can generalize from one task to another by keeping a memory of the errors.

To study errors and learning, Shadmehr’s team put volunteers in front of a joystick that was under a screen. Volunteers couldn’t see the joystick, but it was represented on the screen as a blue dot. A target was represented by a red dot, and as volunteers moved the joystick toward it, the blue dot could be programmed to move slightly off-kilter from where they pointed it, creating an error. Participants then adjusted their movement to compensate for the off-kilter movement and, after a few more trials, smoothly guided the joystick to its target.

In the study, the movement of the blue dot was rotated to the left or the right by larger or smaller amounts until it was a full 30 degrees off from the joystick’s movement. The research team found that volunteers responded more quickly to smaller errors that pushed them consistently in one direction and less to larger errors and those that went in the opposite direction of other feedback. “They learned to give the frequent errors more weight as learning cues, while discounting those that seemed like flukes,” says David Herzfeld, a graduate student in Shadmehr’s laboratory who led the study.

The results also have given Shadmehr a new perspective on his after-work tennis hobby. “I’m much better in my second five minutes of playing tennis than in my first five minutes, and I always assumed that was because my muscles had warmed up,” he says. “But now I wonder if warming up is really a chance for our brains to re-experience error.”

“This study represents a significant step toward understanding how we learn a motor skill,” says Daofen Chen, Ph.D., a program director at the National Institute of Neurological Disorders and Stroke. “The results may improve movement rehabilitation strategies for the many who have suffered strokes and other neuromotor injuries.”

The next step in the research, Shadmehr says, will be to find out which part of the brain is responsible for the “coaching” job of assigning weight to different types of error.

Division of labour in the fish brain

For a fish to swim forward, the nerve cells, or neurons, in its brain and spine have to control the swishing movements of its tail with very close coordination. However, the posture of the tail, which determines swimming direction somewhat like a rudder, also needs to be fine-tuned by the brain’s activity. Using the innovative method of optogenetics, scientists from the Max Planck Institute of Neurobiology in Martinsried have now identified a group of only about 15 nerve cells which steer the movements of the tail fin. Movements of the human body are also controlled via nerve pathways in the same region of the brain, which may therefore use processing mechanisms similar to those in fish.

For a long time, neurobiologists have been trying to find out how neuronal networks control both animal and human behaviour. In this context, there is controversy as to whether the brain’s organisation is decentralised as opposed to modular. In decentralised organisation, the interaction of a large number of neurons produces a specific behaviour pattern. If this is the case, individual neurons cannot be assigned an exact function. On the other hand, if the brain has a modular structure, individual regions might possess certain competencies, each making a specific contribution to behaviour. These types of neuronal circuit modules could be combined in many ways and influence a broad range of different behavioural responses.

Switches in the fish brain?

Researchers in Herwig Baier’s Group at the Max Planck Institute of Neurobiology want to get to the bottom of the brain’s organisational structure with the aid of zebrafish larvae. A network known as the descending reticular formation is located in the brainstem of these animals. The neurons of that region are optimally suited for studying the organisation of the brain: the cells are in direct contact with motor neurons in the spinal cord of the fish and can thus directly influence tail movements. “The reticular formation is a like a ‘cockpit’ for the fish, and we asked ourselves whether there are individual ‘switches’ or ‘joysticks‘, which are used to control the movements of the tail”, is how Herwig Baier summarises this challenge.

In their search for these switches, the researchers concentrated on a small brain nucleus (nMLF) within the reticular formation. But how can the influence of individual nMLF neurons on tail movements be studied? It is only recently that such investigations even became a possibility. Using the new method of optogenetics, the activity of nerve cells can be influenced with light. Since a zebrafish larva – including its brain – is transparent, scientists can very accurately “switch on” small sets of genetically modified cells by exposing the larva to blue light. Consequently, tail movements that are induced in this way can be attributed to identified neurons.

Neurons and tillers

The first series of tests showed that the cells of the nMLF region seem to be involved in a variety of movements – from forward propulsion to rotational motion. A second experimental series using optogenetic stimulation, however, suggested that the cells control the deflection of the tail in particular. Are the nMLF cells thus part of a multifunctional centre or are they truly specialised to perform certain functions? To resolve this question, the neurobiologists performed another set of trials in which they very specifically removed small sets of nMLF cells from the circuit. “This experiment gave us our breakthrough”, recalls Tod Thiele, lead author of the now published study.

The results show that, while nMLF cells are active in many aspects of swimming, a subset of these neurons contribute to only one part of the movement: they determine swimming direction through the posture of the tail. Thus, this population of neurons in the nMLF region are more akin to a specialised module within a decentralised control system of the swimming apparatus. Herwig Baier explains it like this: “We can compare the whole setup with the propulsion of a motorboat”. The boat’s engine, which drives the propeller, determines the thrust, whereas the tiller steers the boat. It seems that the tasks in the brain are divided up in a very similar way.

Some time ago, Herwig Baier’s team discovered a small region in the hindbrain, which acts like an engine and propels the fish forwards. “With the nMLF cells, we have now also found the tiller in the fish brain”, says Herwig Baier. In the human brain, movements are also controlled by a multitude of nuclei in the reticular formation. The study therefore suggests that the allocation of tasks in our brain could be similar to that of the zebrafish.

Neymar’s brain on auto-pilot

Brazilian superstar Neymar’s brain activity while dancing past opponents is less than 10 per cent the level of amateur players, suggesting he plays as if on auto-pilot, according to Japanese neurologists.

Results of brain scans conducted on Neymar indicate minimal cerebral function when he rotates his ankle and point to the Barcelona striker’s wizardry being uncannily natural.

"From MRI images, we discovered Neymar’s brain activity to be less than 10 per cent of an amateur player," researcher Eiichi Naito said on Friday.

"It is possible genetics is a factor, aided by the type of training he does."

The findings were published in the Swiss journal Frontiers in Human Neuroscience following a series of motor skills tests carried out on the 22-year-old Neymar and several other athletes in Barcelona in February.

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(Image: Sergio Moraes / REUTERS)

New Study Shows Limited Motor Skills In Early Infancy May Be Trait of Autism

Researchers from Kennedy Krieger Institute in Baltimore, Md., announced findings that provide evidence for reduced grasping and fine motor activity among six-month-old infants with an increased familial risk for autism spectrum disorders (ASD). The research, which was published in Child Development, has important implications for our overall understanding of ASDs. Furthermore, the results suggest that subtle lags in object exploration-related motor skills in early infancy may present an ASD endophenotype - a heritable characteristic that may have genetic relation to ASD without predicting a full diagnosis- and further our understanding of the genes involved in the disorder.

“Among the infants with familial history of ASD, many were shown to have reduced fine motor skills regardless of eventual ASD diagnosis,” says Dr. Rebecca Landa, lead author and director of Kennedy Krieger’s Center for Autism and Related Disorders. “This means that reduced fine motor skills could be an ASD endophenotype without predicting full diagnosis. Identifying potential endophenotypes has important implications for future research and may improve our understanding of the neurobiology and genetics of ASDs.”

Researchers conducted two experiments examining the correlation of early motor development and object exploration in children with low risk (LR) or high risk (HR) of developing an ASD. Researchers measured key early learning skills, such as object manipulation and grasping activity, in infants at six months of age and again at 10 months. While all infants scored within the expected range and showed no difference in terms of their object manipulation, there were subtle signs that showed reduced grasping activity in HR infants as compared to their LR age-peers. These findings demonstrate that regardless of developmental outcomes, early motor skill differences in HR infants may represent an endophenotype that can be linked to ASD.

About Experiment 1

In experiment 1, participants included 129 infants, largely consisting of infant siblings of children with confirmed ASD diagnoses. During the testing period, most participants were six months old and were then followed longitudinally to the age of 36 months. Infants completed an assessment using the Mullen Scales of Early Learning (MSEL), which is a standardized assessment tool providing scores in five categories: Gross Motor (GM); Fine Motor (FM); Visual Reception (VR); Receptive Language (RL); and Expressive Language (EL). Based on the results of this assessment, infants were then divided into four groups : low-risk (LR) infants without ASD; high-risk (HR) infants without ASD, language, or social delays; HR infants showing language or social delays but not ASD; and HR infants with autism or ASD diagnosis. All children in the HR ASD group met DSM-IV diagnostic criteria for the disorder.

All four groups in Experiment 1 scored within the typical range on the MSEL subtests, meaning that none exhibited a clinical delay in their overall fine motor development at age six months. Subtle differences between HR and LR infants emerged even in HR infants who did not receive a diagnosis of ASD or other delays by age 36 months, which suggests that lower fine motor scores on the MSEL are characteristic of infants at high familial risk for ASD. In order to examine whether the HR infants would catch up to the LR infants in time, researchers conducted a second experiment with new participants.

About Experiment 2

Experiment 2 focused on a new group of six-month-old infants in both LR and HR categories and examined only their grasping behaviors in a naturalistic, free-play context, which was an important factor that emerged in Experiment 1. Participants included 42 infants who were siblings of children with ASD. The infants were observed in an unstructured play session.

The results of Experiment 2 showed reduced grasping and object exploration activity in six-month-old infants at HR for ASD. Overall, the MSEL FM T-score results observed in Experiment 2 show a similar pattern as in Experiment 1, but statistical results are somewhat weakened by an effect of gender in the LR sample. Unique to Experiment 2, was the sole focus on object manipulation-related items of the MSEL, which offered a consistent measure to identify differences between HR and LR infants. Reduced grasping activity in HR infants at age 6 months was also observed during an unstructured free-play task in Experiment 2, which provides additional evidence for the findings observed in Experiment 1. However, the HR infants caught up to the LR group in grasping, as measured in this study, by 10 months of age.

Future studies are needed to examine these preliminary findings more closely to specifically assess grasping ability in infants that receive an ASD diagnosis later in life.

(Image: Bigstock)

With the right rehabilitation, paralyzed rats learn to grip again

After a large stroke, motor skills barely improve, even with rehabilitation. An experiment conducted on rats demonstrates that a course of therapy combining the stimulation of nerve fiber growth with drugs and motor training can be successful. The key, however, is the correct sequence: Paralyzed animals only make an almost complete recovery if the training is delayed until after the growth promoting drugs have been administered, as researchers from the University of Zurich, ETH Zurich and the University of Heidelberg reveal.

Only if the timing, dosage and kind of rehabilitation are right can motor functions make an almost full recovery after a large stroke. Rats that were paralyzed down one side by a stroke almost managed to regain their motor functions fully if they were given the ideal combination of rehabilitative training and substances that boosted the growth of nerve fibers. Anatomical studies confirmed the importance of the right rehabilitation schedule: Depending on the therapeutic design, different patterns of new nerve fibers that sprouted into the cervical spinal cord from the healthy part of the brain and thus aid functional recovery to varying degrees were apparent. The study conducted by an interdisciplinary team headed by Professor Martin Schwab from the Brain Research Institute at the University of Zurich and ETH Zurich’s Neuroscience Center is another milestone in research on the repair of brain and spinal cord injuries.

“This new rehabilitative approach at least triggered an astonishing recovery of the motor skills in rats, which may become important for the treatment of stroke patients in the future,” says first author Anna-Sophia Wahl. At present, patients have to deal with often severe motor-function, language and vision problems, and their quality of life is often heavily affected.

Allow nerves to grow first, then train

On the one hand, the treatment of rats after a stroke involves specific immune therapy, where so-called Nogo proteins are blocked with antibodies. These proteins in the tissue around the nerve fibers inhibit nerve-fiber growth. If they are blocked, nerve fibers begin to sprout in the injured sections of the brain and spinal cord and relay nerve impulses again. On the other hand, the stroke animals, whose front legs were paralyzed, underwent physical training – namely, gripping food pellets. All the rats received antibody treatment first to boost nerve-fiber growth and – either at the same time or only afterwards – motor training. The results are surprising: The animals that began their training later regained a remarkable 85 percent of their original motor skills. For the rats that were trained straight after the stroke in parallel with the growth-enhancing antibodies, however, it was a different story: At 15 percent, their physical performance in the grip test remained very low.

On the one hand, the treatment of rats after a stroke involves specific immune therapy, where so-called Nogo proteins are blocked with antibodies. These proteins in the tissue around the nerve fibers inhibit nerve-fiber growth. If they are blocked, nerve fibers begin to sprout in the injured sections of the brain and spinal cord and relay nerve impulses again. On the other hand, the stroke animals, whose front legs were paralyzed, underwent physical training – namely, gripping food pellets. All the rats received antibody treatment first to boost nerve-fiber growth and – either at the same time or only afterwards – motor training. The results are surprising: The animals that began their training later regained a remarkable 85 percent of their original motor skills. For the rats that were trained straight after the stroke in parallel with the growth-enhancing antibodies, however, it was a different story: At 15 percent, their physical performance in the grip test remained very low.

Meticulous design very promising

The researchers consider timing a crucial factor for the success of the rehabilitation: An early application of growth stimulators – such as antibodies against the protein Nogo-A – triggers an increased sprouting and growth of nerve fibers. The subsequent training is essential to sift out and stabilize the key neural circuits for the recovery of the motor functions. For instance, an automatic, computer-based analysis of the anatomical data from the imaging revealed that new fibers in the spinal cord sprouted in another pattern depending on the course of treatment. By reversibly deactivating the new nerve fibers that grow, the neurobiologists were ultimately able to demonstrate for the first time that a group of these fibers is essential for the recovery of the motor function observed: Nerve fibers that grew into the spinal cord from the intact front half of the brain – changing sides – can reconnect the spinal cord circuits of the rats’ paralyzed limbs to the brain, enabling the animals to grip again.    

“Our study reveals how important a meticulous therapeutic design is for the most successful rehabilitation possible,” sums up study head Martin Schwab. “The brain has enormous potential for the reorganization and reestablishment of its functions. With the right therapies at the right time, this can be increased in a targeted fashion.

Literature:

Wahl, A.S., Omlor, W., Rubio, J.C., Chen, J.L., Zheng, H., Schröter, A., Gullo, M., Weinmann, O., Kobayashi, K., Helmchen, F., Ommer, B., Schwab, M.E. Asynchronous therapy restores motor control by rewiring of the rat corticospinal tract after stroke. Science, June 13, 2014.