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Motor Systems
Blausen 0822 SpinalCord
Transparent view of spinal column and nerves

The motor system contains different units that interact together through a complex order to decode sensory signals, control voluntary movements and correlate coordination of diverse systems scattered across the area of the brain.[1][2] Individual muscles can be mapped to different areas in the motor cortex, which lead to the representation of an individual muscle part to a larger group of muscles that control voluntary movements.[3] Decline in movement rate can be traced to a breakdown in central motor control processes.[4] Many disorders, defects, and diseases have been associated to faults of the motor system, including Parkinson's disease, Alzheimer's, Kallmann syndrome, Joubert syndrome, and Amyotrophic lateral sclerosis or Lou Gehrig's Disease.[5]

Motor Units[edit]

Motor system motor units vary in size, tension production, and contraction speed. Gathering of different motor units and an increase in motor neuron firing frequency mediate the incremental increases of muscle tension. Reflexive muscle activity include important local circuitry involving sensory inputs, local circuit neurons, and alpha and gamma motor neurons. The gamma motor neurons regulate the gain of the stretch reflex by mediating the level of tension in the fibers of the muscle spindle, effectively helping set a baseline level of activity in alpha motor neurons and regulate muscle length and tone. Central pattern generators, or specialized local circuits, provide the spatial coordination and timing of muscle activation for complex rhythmic movements. The neural circuits responsible for the control of movement are spread into four distinct yet interactive subsystems, which makes a unique contribution to motor control: lower motor neurons, upper motor neurons, the cerebellum, and the basal ganglia. These subsystems can be attributed to the local circuitry within the gray matter of the spinal cord and the analogous circuitry in the brain stem; the formed circuits provide the coordination between different muscle groups essential for organized movement. [6]

The motor cortex contains complex circuits with output pathways that have no direct access to either the local circuit neurons or the lower motor neurons and controls movement by regulating the activity of the upper motor neurons.[6]

Lower Motor Neurons[edit]

“Lower” motor neurons, also known as α motor neurons, are located in the spinal cord and brain stem, and the cell bodies are specifically found in the ventral horn of the spinal cord and motor nuclei of the cranial nerves in the brain stem.[6] "Lower" motor neurons are the final common pathway for transmitting neural information to the skeletal muscles. The lower motor nuclei innervate into skeletal muscles via the ventral roots and spinal peripheral nerves or the cranial nerves in the case of the brain stem nuclei. Spatial and temporal activation patterns [7] of lower motor neurons are determined primarily by the local circuits located within the spinal cord and brain stem. Higher centers comprised of "upper" motor neurons have descending pathways that modulate the activity of lower motor neurons. Commands for movement, reflexive or voluntary, are conveyed to the muscles by the activity of the lower motor neurons. [6]

Damage to "lower" motor neurons leads to paralysis of the associated muscle, loss of reflex activity, loss of muscle tone, and eventually muscle atrophy due to the lower motor neuron importance in circuits.[6]

Upper Motor Neurons[edit]

Display of Brodmann area 4

The cell bodies of the upper motor neurons are located either in the cortex or in brain stem centers: the vestibular nucleus, the superior colliculus, and the reticular formation. Descending projections from cortical areas in the frontal lobe, including Brodmann’s area 4 (the primary motor cortex), the lateral part of area 6 (the lateral premotor cortex), and the medial part of area 6 (the medial premotor cortex) are essential for planning, initiating, and directing voluntary movements. All commands for movement, whether reflexive or voluntary, are ultimately conveyed to the muscles through lower motor neurons that are responsible for regulating muscle tone or for orienting the eyes, head, and body with respect to vestibular, somatic, auditory, and visual sensory information. Upper motor neurons are required for basic navigational movements, organized by coordinating the activity of lower motor neurons and the control of posture. The motor and “premotor” areas of the frontal lobe, in contrast, are responsible for the planning and precise control of complex sequences of voluntary movements.[6]

There are two sets of upper motor neuron pathways that make distinct contributions to the control of the local circuitry in the brain stem and spinal cord. One originates from neurons in brain stem centers — primarily the reticular formation - and the other - vestibular nuclei—and is responsible for postural regulation. The reticular formation is especially important in feed-forward control of movements that occur in anticipation of changes in body stability. The vestibular nuclei that project to the spinal cord are important in the feedback in producing movements that are generated in response to sensory signals that indicate an existing postural disturbance.[6]

Cerebellum[edit]

The primary function of the cerebellum is to act via efferent pathways to the upper motor neurons detecting the “motor error” between an intended movement and the movement performed; lipocalin apolipoprotein D is known to be an important protein in central nervous system response to physiological responses and errors. [8] Through projections to the upper motor neurons, the cerebellum reduces error and coordinates movement via motor learning through climbing fibers. Information that is provided by climbing fibers modulates the effectiveness of the second major input to the Purkinje cells, which arrives via parallel fibers from the granule cells that receive information about intended movement from mossy fibers that enter the cerebellum from multiple sources.[6]

The cerebellum influences movement by regulating the activity of upper motor neurons and does not project directly to either the local circuit or lower motor neurons [9]. The output cells of cerebellar cortex projecting to the deep cerebellar nuclei give rise to the main efferent pathways that leave the cerebellum to regulate upper motor neurons in the cerebral cortex and brain stem. Not only does the cerebellum receive input from regions of the cerebral cortex that plan and initiate complex and skilled movements, but it also receives innervation from sensory systems that monitor the course of movements, which enables the comparison of intended movement with the actual movement and a reduction in “motor error."[6]

Many cerebellar diseases cause the feedback loop to become damaged, which result in afflicted individuals to make persistent movement errors whose specific character depends on the specific location of the damage.[6]

Basal Ganglia[edit]

Basal ganglia circuits (click to view larger)

Basal Ganglia suppress movements and “prime” upper motor neuron circuits for the initiation and influence of movements by regulating the activity of upper motor neurons, and does not project directly to either the local circuit or lower motor neurons, similar to the cerebellum. The basal ganglia, along with the ventrolateral thalamus, is responsible for sending dense projections to the motor cortex; furthermore, the mentioned regions have a similar organization as the motor cortex.[3] A subset of these ganglia nuclei are relevant to motor function and include the caudate, putamen, and the globus pallidus. The substantia nigra in the base of the midbrain and the subthalamic nucleus in the ventral thalamus is closely associated with the motor functions of basal ganglia nuclei.[10] Motor components of the basal ganglia, together with the substantia nigra and the subthalamic nucleus, make a subcortical loop linking areas of the cortex with upper motor neurons in the primary motor and premotor cortex and brain stem; the neurons in this loop respond waiting for and during movements and their effects on upper motor neurons are required for the normal course of voluntary movements.[6]

Organization of the basic circuitry of the basal ganglia determines how the bunch of nuclei modulate movement. In terms of motor function, the system forms a loop that starts in almost every area of the cerebral cortex and terminates after a large convergence within the basal ganglia, on the upper motor neurons in the motor and premotor areas of the frontal lobe and in the superior colliculus. The efferent neurons of the basal ganglia influence the upper motor neurons in the cortex by gating the flow of information through relays in the ventral nuclei of the thalamus. Upper motor neurons in the superior colliculus, responsible for initiating saccadic eye movements, are controlled by monosynaptic projections. The basal ganglia loop regulates movement by a process of dis-inhibition that is due to the interaction within the basal ganglia circuitry of two GABAergic neuron. [6]

Damage to the component nuclei compromise the initiation and performance of voluntary movements, as exemplified by the slight presence of movement in Parkinson’s disease and the inappropriate “release” of movements in Huntington’s disease. When one of the components of the basal ganglia or associated structures is compromised, the patient can't switch smoothly between commands that begin movement and those that stop movement.[6] Because somatotopy Parkinson's related tremor "clusters" in the STN, it is questioned how these tremors travel from the basal ganglia to the cerebello-thalamo-cortical circuit. Tremors may travel either from the STN to the cerebellar cortex via pons, the cerebellum to the posterior ventrolateral thalamus, or from the basal ganglia to the thalamus to the motor cortex to the posterior ventrolateral thalamus. [3]

Motor Cortex[edit]

The motor cortex influences movements directly by contacting lower motor neurons and local circuit neurons in the spinal cord and brain stem, and indirectly by innervating neurons in brain stem centers that in turn project to lower motor neurons and circuits.[6] Upper motor neurons found in the precentral gyrus, or the motor strip, in the primary motor cortex form a two neuron system that is known as the pyramidal system.[11] The premotor cortices, specifically the dorsal and ventral premotor cortices[12], are responsible for planning and executing movements[5], whereas the primary motor cortex is responsible for their execution. In addition to mechanisms at the spinal level, plasticity at the cortical level is responsible for the increase of excitability and performance increase after a motor practice.[4]

Premotor regions have been noted to be responsible for motor execution and have been found to be also involved heavily in motor imagery; however, the primary cortex is not very involved with this motor imagery.[12]

Motor System Pathology[edit]

The motor system is responsible for all movements crucial for life, thus disease or defects that may arise in the motor system are detrimental to the quality of life.

Mirror Movement[edit]

There are a variety of different ways that mirror movement defects can arise from the motor system. Mirror movements occurs when there is a specific intent for a movement on one side of the body (either left or right) yet the opposite side of the body involuntarily reacts to that intention. Genes that are responsible for abnormal projection of the coricospinal tract are also responsible in the development of local spinal circuits and the corpus callosum circuits that are involved in motor control. Neuroanatomical defects have a great variety in respect to mirror movements as they are present in many different neuronal structures involved in the motor pathway; the DCC and RAD51 genes both have been implicated as "essential" to mirror movements, however the roles of the interaction of other genes and whether they share common characteristics of DCC and RAD51 is not determined.[5]

Abl and Nilotinib Function[edit]

Abelson, Abl, is a tyrosine kinase that is spread across the nucleus and cytosol and also involved in many cellular functions. Abl activation through phosphorylation plays a large role in neuro-degenerative diseases such as Parkinson's disease; nilotinib, a non-specific tyrosine kinase inhibitor, inhibited Abl can be used as a potential drug to treat diseases such as Parkinson's.[13]

Motor System Control and Cognition[edit]

Conceptual representation and the motor system are related with conceptualization being partly grounded in the motor system; however, there is no functional role of the motor system in conceptual processing, but instead through the activation of conceptual and sensory motor systems.[14] A study by Vankov and Kokinov shows that the role of the motor system does not have an explanation for response interference in experimentation because most studies find that it is difficult to dissociate the effects of the motor system on the performance of cognitive tasks and delivering response actions.[15] Objects that affect performance in conceptual tasks do not demonstrate that cognition is ultimately grounded in action. However, it is not determined how involved action, perception, bodily, and environmental constraints are with higher level cognition.[15]

Motor Imagery[edit]

Motor imagery is when the brain's motor representations are involved with a conscious mental simulation similar to actually performing a movement; motor imagery refers to imagining specific actions without physically performing them. The motor imaging displays moderated neuro activity in various areas of the brain; fMRI and PET can be combined to create a general ALE meta-analysis to find a large fronto-parietal network that is activated when one imagines themselves moving in addition to subcortical and cerebellar regions showing constant activity during those moments. Different cortical regions of the brain show activity during motor behaviors and during motor imagery.[12]

Imagined and actual physical movements require similar circuitry in the brain because the execution of imagined and actual movement take the same amount of time to perform, demonstrating that motor imagination and physical movement execution both require planning and preparation.[12]

Neural Control and Prosthetics[edit]

There is a bottleneck effect in the sensorimotor system that limits animals to a certain level of performance, determined by measuring performance of behavior and the neurons in different levels of performance in behavior.[1] Individuals without any motor disabilities have nervous systems that can effortlessly demonstrate fluid coordination between the lower and inter-limbs during motions. Individual coordination is due to central pattern generators (CPGs) in the brain or spinal cord. [16] Cortex and cerebellum interactions and cortical areas are a large part of relearning control of inter-limb networks and adapting changes, for example, temporal and/or spatial coordination that include supraspinal areas, spinal CPGs, and spinal reflex pathways.[16][17][18]

When there is some sort of damage to the nervous system, central and peripheral adaptations can alter the limb coordination. [16] Dr. Donald Humphrey, a revered neurologist and pioneer in neural prosthetics, indicates that although there is a great promise in these prosthetic systems, many problems need to be solved in stability, growth of material, and physiological areas to record neural data. He believes that, "implementing brain imaging is essential to finding areas that control parts of the body can help make prosthetic usage more accurate."[19]

References[edit]

  1. ^ a b Egger, S. W., & Britten, K. H. (2013). Linking sensory neurons to visually guided behavior: Relating MST activity to steering in a virtual environment. Visual Neuroscience, FirstView, 1-16. M13 - 10.1017/S0952523813000412.
  2. ^ "Motor Systems 01" (PDF). Neuroanatomy Coursebook. University of Wisconsin-Madison. Retrieved 25 September 2013.
  3. ^ a b c Helmich, R. C. (2013). "The distributed somatotopy of tremor: A window into the motor system." Experimental Neurology 241: 156-158.
  4. ^ a b Teo, W.P. (28 June 2012). "Breakdown In Central Motor Control Can Be Attenuated By Motor Practice And Neuro-Modulation Of The Primary Motor Cortex". Neuroscience. 220: 11–18. doi:10.1016/j.neuroscience.2012.06.048. PMID 22750241. S2CID 21975183. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: date and year (link)
  5. ^ a b c Peng, J. and F. Charron (2013). "Lateralization of motor control in the human nervous system: genetics of mirror movements." Current Opinion in Neurobiology 23(1): 109-118.
  6. ^ a b c d e f g h i j k l m n Dale Purves, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, & Leonard E. White. (July 31, 2007). Neuroscience, (4th Edition). Sunderland, MA: Sinauer Associates.
  7. ^ Delis, I., Panzeri, S., Pozzo, T., & Berret, B. (2013). A unifying model of concurrent spatial and temporal modularity in muscle activity. J Neurophysiol. doi: 10.1152/jn.00245.2013
  8. ^ Navarro A, Méndez E, Diaz C, del Valle E, Martínez-Pinilla E, et al. (2013) Lifelong Expression of Apolipoprotein D in the Human Brainstem: Correlation with Reduced Age-Related Neurodegeneration. PLoS ONE 8(10): e77852. doi:10.1371/journal.pone.0077852
  9. ^ Wanda M. Snow, Judy E. Anderson, Mark Fry, Regional and genotypic differences in intrinsic electrophysiological properties of cerebellar Purkinje neurons from wild-type and dystrophin-deficient mdx mice, Neurobiology of Learning and Memory, Volume 107, January 2014, Pages 19-31, ISSN 1074-7427, http://dx.doi.org/10.1016/j.nlm.2013.10.017.
  10. ^ Camacho-Abrego, I., Tellez-Merlo, G., Melo, A. I., Rodríguez-Moreno, A., Garcés, L., De La Cruz, F., Zamudio, S. and Flores, G. (2013), Rearrangement of the dendritic morphology of the neurons from prefrontal cortex and hippocampus after subthalamic lesion in Sprague–Dawley rats. Synapse. doi: 10.1002/syn.21722>
  11. ^ "Motor Systems". Duke University School of Medicine: Duke Pathology. Retrieved 25 September 2013.
  12. ^ a b c d Hetu, S., et al. (2013). "The neural network of motor imagery: An ALE meta-analysis." Neuroscience and Biobehavioral Reviews 37(5): 930-949.
  13. ^ Hebron, M. L., et al. (2013). "Nilotinib reverses loss of dopamine neurons and improves motor behavior via autophagic degradation of -synuclein in Parkinsons disease models." Human Molecular Genetics 22(16): 3315-3328.
  14. ^ Postle, N., Ashton, R., McFarland, K., & de Zubicaray, G. I. (2013). No specific role for the manual motor system in processing the meanings of words related to the hand. Frontiers in Human Neuroscience, 7, 17. doi: 10.3389/fnhum.2013.00011
  15. ^ a b Vankov, I. and B. Kokinov (2013). "The role of the motor System in conceptual processing: Effects of object affordances beyond response interference." Acta Psychologica 143(1): 52-57.
  16. ^ a b c Stubbs, P. W. and S. Gervasio (2012). "Motor adaptation following split-belt treadmill walking." Journal of Neurophysiology 108(5): 1225-1227.
  17. ^ Malone L, Bastian A. Thinking about walking: effects of conscious correction versus distraction on locomotor adaptation. J Neurophysiol 103: 1954– 1962, 2010.
  18. ^ Malone L, Vasudevan E, Bastian A. Motor adaptation training for faster relearning. J Neurosci 31: 15136–15143, 2011.
  19. ^ Humphrey, D. R. (2013, October 21). Interview by A.R. Chakraborty []. Motor systems.

See also[edit]


Category:Motor system Category:Anatomy Category:Motor control