Motor skill consolidation

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Motor skill consolidation represents the process by which motor skills are transformed from an initial fragile state, in which they are especially prone to being disrupted or lost, to a more solid or permanent state. [1] Any newly formed motor skill, such as learning to play a musical instrument or adjusting one's running stride, is subject to a consolidation period. The time course of this period during which new motor skills are susceptible to disruption appears to be on the order of a few hours. [1] [2]

Contents

Distinctions between procedural and declarative memories

Motor skills, also known as procedural memories, are distinct from declarative memories, which involve memories of events, people, places, etc. Both types of memories are, however, subject to a consolidation period, though the neural mechanisms appear to differ. Some of the earliest evidence pointing to a distinction between procedural and declarative memories came from the famous neurology patient HM. As a treatment for severe epilepsy, portions of HM's temporal lobes, including both hippocampi, were removed. This left him unable to form new declarative memories (anterograde amnesia), while his ability to learn novel motor tasks remained intact. [3]

Motor skills and the internal model

It is believed that motor skill acquisition requires learning a new internal model of limb dynamics. [4] [5] For instance, in order to reach for a cup of coffee, a person must have an implicit understanding of the mass of their own arm, and how specific patterns of muscle activation will change the position of that limb. A common model for studying motor learning and consolidation involves perturbations to reaching tasks using robotic arms to impart forces on the limb during reaches, forcing the subject to learn new internal representations of the limb to take these new external forces into account. [4] [6]

Role of sleep in motor memory consolidation

A number of recent studies have begun to demonstrate the importance of sleep in the process of consolidation of both procedural and declarative memories. [7] [8] [9] For instance, it was recently shown that even a short 90 minute nap after training in a skilled finger task prevented interference two hours after the task when compared to subjects that did not nap. [10] During night sleep, REM sleep and slow-wave sleep both contribute to the motor memory consolidation process through an increase in neuromodulatory activity, as well as regular field potential oscillations such as sleep spindles (reviewed by Diekelmann and Born, 2010 [11] ).

Pathologies and processes affecting motor memory consolidation

While the precise neural basis for motor skill consolidation is not fully understood, many of the structures necessary for the process have been identified. As the process of learning a motor skill requires both initial execution of the skill, as well as long storage of the consolidated memory, a complex network of brain areas are involved, including the primary motor cortex, the cerebellum, the prefrontal cortex, and the basal ganglia. [5] [12] [13] [14] Given that motor skill consolidation is a distributed process, the ability to form new procedural memories is susceptible to the effects of a number of processes and pathologies.

Cerebellar diseases

The cerebellum, and especially the cerebellar cortex, is critical for coordinating motor outputs during skilled tasks, as well as the process of stabilizing newly formed motor skills. [15] Damage to the cerebellum can occur through a number of causes including trauma, alcoholism, chronic degenerative diseases such as olivopontocerebellar atrophy, and genetic developmental disorders. [16] [17]

Parkinson's disease

Parkinson's disease, which affects the basal ganglia, has been shown to cause an impairment in the ability to consolidate new motor skills. [18] For instance, when Parkinsonian patients were tested in force field reaching tasks, they showed significantly less retention of the motor skill than controls during later testing. [19] This points to the importance of the basal ganglia, the primary target of Parkinson's disease, in creating the new sensory/motor mappings that are necessary for the long term retention of a motor skill.

Stroke

A stroke is the damage of a volume of brain tissue resulting from restricted blood supply, which is often a result of occluded blood vessels leading to the brain. Given the large number of brain areas involved in the motor skill acquisition, strokes affecting any of these areas can lead to deficits in motor skill consolidation. Therapies for stroke have focused on modified practice techniques to allow the reacquisition of important skills after the damage has occurred. [20]

Aging

Aging has been shown to have an effect on declarative memory consolidation, which appears to be related to disruptions of sleep patterns, [21] as well as hippocampal degeneration. [22] However, aging does not appear to have a direct effect on motor skill consolidation, with subjects up to 95 years of age showing the ability to retain newly formed motor skills up to two years after acquisition. [23]

Related Research Articles

Multiple hypotheses explain the possible connections between sleep and learning in humans. Research indicates that sleep does more than allow the brain to rest. It may also aid the consolidation of long-term memories.

Cerebellum Structure at the rear of the vertebrate brain, beneath the cerebrum

The cerebellum is a major feature of the hindbrain of all vertebrates. Although usually smaller than the cerebrum, in some animals such as the mormyrid fishes it may be as large as or even larger. In humans, the cerebellum plays an important role in motor control. It may also be involved in some cognitive functions such as attention and language as well as emotional control such as regulating fear and pleasure responses, but its movement-related functions are the most solidly established. The human cerebellum does not initiate movement, but contributes to coordination, precision, and accurate timing: it receives input from sensory systems of the spinal cord and from other parts of the brain, and integrates these inputs to fine-tune motor activity. Cerebellar damage produces disorders in fine movement, equilibrium, posture, and motor learning in humans.

Motor learning refers broadly to changes in an organism's movements that reflect changes in the structure and function of the nervous system. Motor learning occurs over varying timescales and degrees of complexity: humans learn to walk or talk over the course of years, but continue to adjust to changes in height, weight, strength etc. over their lifetimes. Motor learning enables animals to gain new skills, and improves the smoothness and accuracy of movements, in some cases by calibrating simple movements like reflexes. Motor learning research often considers variables that contribute to motor program formation, sensitivity of error-detection processes, and strength of movement schemas. Motor learning is "relatively permanent", as the capability to respond appropriately is acquired and retained. Temporary gains in performance during practice or in response to some perturbation are often termed motor adaptation, a transient form of learning. Neuroscience research on motor learning is concerned with which parts of the brain and spinal cord represent movements and motor programs and how the nervous system processes feedback to change the connectivity and synaptic strengths. At the behavioral level, research focuses on the design and effect of the main components driving motor learning, i.e. the structure of practice and the feedback. The timing and organization of practice can influence information retention, e.g. how tasks can be subdivided and practiced, and the precise form of feedback can influence preparation, anticipation, and guidance of movement.

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

Muscle memory is a form of procedural memory that involves consolidating a specific motor task into memory through repetition, which has been used synonymously with motor learning. When a movement is repeated over time, the brain creates a long-term muscle memory for that task, eventually allowing it to be performed with little to no conscious effort. This process decreases the need for attention and creates maximum efficiency within the motor and memory systems. Muscle memory is found in many everyday activities that become automatic and improve with practice, such as riding bicycles, driving motor vehicles, playing ball sports, typing on keyboards, entering PINs, playing musical instruments, poker, martial arts, and dancing.

Kinesthetic learning, kinaesthetic learning, or tactile learning is a learning style in which learning takes place by the students carrying out physical activities, rather than listening to a lecture or watching demonstrations. As cited by Favre (2009), Dunn and Dunn define kinesthetic learners as students who require whole-body movement to process new and difficult information. However, scientific studies do not support the claim that using kinesthetic modality improves learning in students identified as kinesthetic learners.

Explicit memory is one of the two main types of long-term human memory, the other of which is implicit memory. Explicit memory is the conscious, intentional recollection of factual information, previous experiences, and concepts. This type of memory is dependent upon three processes: acquisition, consolidation, and retrieval. Explicit memory can be divided into two categories: episodic memory, which stores specific personal experiences, and semantic memory, which stores factual information. Explicit memory requires gradual learning, with multiple presentations of a stimulus and response.

Dysmetria is a lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia. It can also include an inability to judge distance or scale.

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The cerebellothalamic tract or the tractus cerebellothalamicus, is part of the superior cerebellar peduncle. It originates in the cerebellar nuclei, crosses completely in the decussation of the superior cerebellar peduncle, bypasses the red nucleus, and terminates in posterior division of ventral lateral nucleus of thalamus. The ventrolateral nucleus has different divisions and distinct connections, mostly with frontal and parietal lobes. The primary motor cortex and premotor cortex get information from the ventrolateral nucleus projections originating in the interposed nucleus and dentate nuclei. Other dentate nucleus projections via thalamic pathway transmit information to prefrontal cortex and posterior parietal cortex. The cerebellum sends thalamocortical projections and in addition may also send connections from the thalamus to association areas serving cognitive and affective functions.

The neuroanatomy of memory encompasses a wide variety of anatomical structures in the brain.

Procedural memory is a type of implicit memory which aids the performance of particular types of tasks without conscious awareness of these previous experiences.

Basal ganglia disease Group of physical problems resulting from basal ganglia dysfunction

Basal ganglia disease is a group of physical problems that occur when the group of nuclei in the brain known as the basal ganglia fail to properly suppress unwanted movements or to properly prime upper motor neuron circuits to initiate motor function. Research indicates that increased output of the basal ganglia inhibits thalamocortical projection neurons. Proper activation or deactivation of these neurons is an integral component for proper movement. If something causes too much basal ganglia output, then the ventral anterior (VA) and ventral lateral (VL) thalamocortical projection neurons become too inhibited, and one cannot initiate voluntary movement. These disorders are known as hypokinetic disorders. However, a disorder leading to abnormally low output of the basal ganglia leads to reduced inhibition, and thus excitation, of the thalamocortical projection neurons which synapse onto the cortex. This situation leads to an inability to suppress unwanted movements. These disorders are known as hyperkinetic disorders.

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Sleep and memory Relationship between sleep and memory

The relationship between sleep and memory has been studied since at least the early 19th century. Memory, the cognitive process of storing and retrieving past experiences, learning and recognition, is a product of brain plasticity, the structural changes within synapses that create associations between stimuli. Stimuli are encoded within milliseconds; however, the long-term maintenance of memories can take additional minutes, days, or even years to fully consolidate and become a stable memory that is accessible. Therefore, the formation of a specific memory occurs rapidly, but the evolution of a memory is often an ongoing process.

A motor program is an abstract representation of movement that centrally organizes and controls the many degrees of freedom involved in performing an action.p. 182 Signals transmitted through efferent and afferent pathways allow the central nervous system to anticipate, plan or guide movement. Evidence for the concept of motor programs include the following:p. 182

Cerebellar cognitive affective syndrome (CCAS), also called Schmahmann's syndrome is a condition that follows from lesions (damage) to the cerebellum of the brain. It refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

Wolfgang Grodd German radiologist

Prof. Dr. med. Wolfgang Grodd is a German neuroradiologist and professor emeritus of the University hospital at the University of Tübingen. He is known for his scientific works on the development and application of structural and functional magnetic resonance imaging in metabolic diseases, sensorimotor representation, language production, and cognitive processing, cerebellum, thalamus, and basal ganglia. Currently, Wolfgang Grodd is a research scientist at the Department of the High-Field MR at the Max Planck Institute for Biological Cybernetics.

Anne Schaefer is a neuroscientist, professor of Neuroscience, vice-chair of Neuroscience, and director of the Center for Glial Biology at the Icahn School of Medicine at Mount Sinai in New York City. Schaefer investigates the epigenetic mechanisms of cellular plasticity and their role in the regulation of microglia-neuron interactions. Her research is aimed at understanding the mechanisms underlying various neuropsychiatric disorders and finding novel ways to target the epigenome therapeutically.

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