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1. Motor System PENZA STATE UNIVERSITY Department of Neurology, Neurosurgery and Psychiatry

2. The Main Points Types of movements The central part of motor system The features of main motor pathways Corticospinal tract Corticobulbar tract The peripheral part of motor system The main syndromes of the motor system damage Upper motor neuron syndrome Lower motor neuron syndrome

3. 3 Major Types Of Movements • Reflexes ( Spinal cord circuits ) • Postural adjustments ( Spinal & Brain stem ) • Voluntary movements (from simple to complex ) ( Spinal cord, Brainstem, & cortex )

4. Reflex is a stimulus-evoked involuntary motor muscle contraction • Monosynaptic reflex • Knee-jerk • Jaw-jerk • Disynaptic reflex • withdrawal

5. Postural Adjustments • Context important • Can reorganize depending on context • Feedback control-reactive • Error correction • Response lags stimulus; sometimes too late; sometimes vicious circle • Feed-forward control-predictive • Response anticipates stimulus • More timely, but depends on practice • Depends on cerebellum , brain stem pathways & spinal cord • More complex neural representation

6. Voluntary Movements • Organized around purposeful acts • Flexible input-output relationships • Limitless • Price to pay: whole brain • Recruits all motor systems components & much of the association cortex

7. Voluntary movements are organized by motor programs • Translate goal into action • Formation of a movement representation, or motor program • Premotor cortex --> Primary motor cortex • Program • To produce the desired goal, which muscles should contract and when • 2 Key movement characteristics that are programmed • Spatial (hand path; joint angles) Kinematic program • Force Dynamic program

8. Central Components of the Motor System the primary motor cortex (area 4) the adjacent cortical areas ( particularly the premotor cortex, area 6), the corticobulbar and corticospinal tracts to which these cortical areas give rise

9. The Motor Cortex

10. Motor Cortical Areas The primary motor cortex is a band of cortical tissue that lies on the opposite side of the central sulcus from the primary somatosensory cortex (in the postcentral gyrus) and, like it, extends upward and past the superomedial edge of the hemisphere onto its medial surface. The area representing the throat and larynx lies at the inferior end of the primary motor cortex ; above it, in sequence, are the areas representing the face, upper limbs , trunk , and lower limbs. This is the inverted “ motor homunculus ,” corresponding to the “somatosensory homunculus” of the postcentral gyrus. Motor neurons are found not only in area 4 but also in the adjacent cortical areas . The fibers mediating fine voluntary movements, however, originate mainly in the precentral gyrus. This is the site of the characteristic, large pyramidal neurons (Betz cells) , which lie in the fifth cellular layer of the cortex and send their rapidly conducting, thickly myelinated axons into the pyramidal tract . The pyramidal tract was once thought to be entirely composed of Betz cell axons, but it is now known that these account for only 3.44 % of its fibers.

11. Cortical Motor Paths • Lateral corticospinal tract Limb control mostly • Ventral corticospinal tract Proximal muscle control; mostly upper body •Corticobulbar tract For cranial muscle control

12. The Corticospinal Tract

13. Corticospinal Tract (Pyramidal Tract) This tract originates in the motor cortex and travels through the cerebral white matter (corona radiata ), the posterior limb of the internal capsule (where the fibers lie very close together), the central portion of the cerebral peduncle ( crus cerebri ), the pons , and the base (i.e., the anterior portion) of the medulla , where the tract is externally evident as a slight protrusion called the pyramid . The medullary pyramids (there is one on either side) give the tract its name. At the lower end of the medulla, 80 - 85% of the pyramidal fibers cross to the other side in the so-called decussation of the pyramids . The fibers that do not cross here descend the spinal cord in the ipsilateral anterior funiculus as the anterior corticospinal tract ; they cross farther down (usually at the level of the segment that they supply) through the anterior commissure of the spinal cord. At cervical and thoracic levels, there are probably also a few fibers that remain uncrossed and innervate ipsilateral motor neurons in the anterior horn , so that the nuchal and truncal musculature receives a bilateral cortical innervation . The majority of pyramidal tract fibers cross in the decussation of the pyramids , then descend the spinal cord in the contralateral lateral funiculus as the lateral corticospinal tract . This tract shrinks in cross-sectional area as it travels down the cord, because some of its fibers terminate in each segment along the way . About 90% of all pyramidal tract fibers end in synapses onto interneurons , which then transmit the motor impulses onward to the large α motor neurons of the anterior horn, as well as to the smaller γ motor neurons .

14. Features Of The Corticospinal Tract ( how to learn ) It’s descending It begins in the motor cortex It goes to the muscles of limbs and body It consists of two neurons: upper/central/first motor neuron lower/peripheral/second motor neuron The synapses are in the anterior horn of the spinal cord The upper neuron goes to the other side The decussation is at the level of brainstem (in the pyramids) for the most fibers, and at the level of the segment they supply (in the anterior commissure of the spinal cord) for the others. Is it ascending or descending? Where does it begin? Where does it go? How many neurons does it consist of? Where are the connections between the neurons? What neuron goes to the other side? What is the level of decussation?

15. Corticobulbar Tract

16. Corticonuclear (Corticobulbar) Tract Some of the fibers of the pyramidal tract branch off from the main mass of the tract as it passes through the midbrain and then take a more dorsal course toward the motor cranial nerve nuclei . The fibers supplying these brainstem nuclei are partly crossed and partly uncrossed . The nuclei receiving pyramidal tract input are the ones that mediate voluntary movements of the cranial musculature through cranial nerves V (the trigeminal nerve), VII ( the facial nerve), IX, X, and XI (the glossopharyngeal, vagus , and accessory nerves ), and XII (the hypoglossal nerve).

17. Features Of The Corticobulbar Tract ( how to learn ) It’s descending It begins in the motor cortex It goes to the cranial muscles It consists of two neurons: upper/central/first motor neuron lower/peripheral/second motor neuron The synapses are in the each level of the brainstem The upper neuron PARTLY goes to the other side The PARTLY decussation is upper brainstem nuclei of CN V (the trigeminal nerve), VII (the facial nerve), IX, X, and XI (the glossopharyngeal, vagus , and accessory nerves), and XII (the hypoglossal nerve ) . Is it ascending or descending? Where does it begin? Where does it go? How many neurons does it consist of? Where are the connections between the neurons? What neuron goes to the other side? What is the level of decussation?

18. Other Central Components Of The Motor System A number of central pathways beside the pyramidal tract play major roles in the control of motor function. One important group of fibers (the corticopontocerebellar tract ) conveys information from the cerebral cortex to the cerebellum , whose output in turn modulates planned movements . Other fibers travel from the cortex to the basal ganglia ( mainly the corpus striatum = caudate nucleus and putamen), the substantia nigra , the brainstem reticular formation , and other nuclei (e. g., in the midbrain tectum ). The motor tracts in the spinal cord are anatomically and functionally segregated into two groups: a lateral group , comprising the corticospinal and rubrospinal tracts, and a medial group , comprising the reticulospinal , vestibulospinal , and tectospinal tracts). The lateral tracts mainly project to the distal musculature (especially in the upper limbs) and also make short propriospinal connections. They are primarily responsible for voluntary movements of the forearms and hands, i.e., for precise , highly differentiated, fine motor control. The medial tracts, in contrast , innervate motor neurons lying more medially in the anterior horn and make relatively long propriospinal connections. They are primarily responsible for movements of the trunk and lower limbs ( stance and gait ).

19. Peripheral Components Of The Motor System The peripheral portion of the motor system comprises the motor cranial nerve nuclei of the brainstem, the motor anterior horn cells of the spinal cord, the anterior roots, the cervical and lumbosacral nerve plexuses , the peripheral nerves , and the motor end plates in skeletal muscle.

20. Anterior Horn Cells The fibers not only of the pyramidal tract but also of the nonpyramidal descending pathways (the reticulospinal , tectospinal , vestibulospinal , and rubrospinal tracts, among others), as well as afferent fibers from the posterior roots, terminate on the cell bodies or dendrites of the larger and smaller α motor neurons. Fibers of all of these types also make synaptic contact with the small γ motor neurons, partly directly, and partly through intervening interneurons and the association and commissural neurons of the intrinsic neuronal apparatus of the spinal cord. Some of these synapses are excitatory, others inhibitory. The thin, unmyelinated neurites of the γ motor neurons innervate the intrafusal muscle fibers. In contrast to the pseudounipolar neurons of the spinal ganglia, the anterior horn cells are multipolar. Their dendrites receive synaptic contact from a wide variety of afferent and efferent systems. The functional groups and nuclear columns of neurons in the anterior horn are not separated from one another by anatomically discernible borders . In the cervical spinal cord, the motor neurons for the upper limbs lie in the lateral portion of the gray matter of the anterior horn; those for the truncal muscles lie in its medial portion. The same somatotopic principle applies in the lumbar spinal cord, where the lower limbs are represented laterally , the trunk medially.

21. Anterior Roots. The neurites of the motor neurons exit the anterior aspect of the spinal cord as rootlets (fila radicularia ) and join together, forming the anterior roots . Each anterior root joins the corresponding posterior root just distal to the dorsal root ganglion to form a spinal nerve, which then exits the spinal canal through the intervertebral foramen.

22. Peripheral Nerve And Motor End Plate There is one pair of spinal nerves for each segment of the body. The spinal nerves contain afferent somatosensory fibers , efferent somatic motor fibers, efferent autonomic fibers from the lateral horns of the spinal gray matter, and afferent autonomic fibers. At cervical and lumbosacral levels, the spinal nerves join to form the nerve plexuses , which , in turn, give rise to the peripheral nerves that innervate the musculature of the neck and limbs. The thick , myelinated , rapidly conducting neurites of the large α motor neurons are called α1 fibers. These fibers travel to the working musculature , where they divide into a highly variable number of branches that terminate on muscle fibers. Synaptic impulse transmission occurs at the neuromuscular junctions (motor end plates).

23. Motor Unit An anterior horn cell, its neurites, and the muscle fibers it innervates are collectively termed a motor unit (Sherrington). Each motor unit constitutes the final common pathway for movement-related impulses arriving at the anterior horn cell from higher levels: its activity is influenced by impulses in a wide variety of motor tracts that originate in different areas of the brain, as well as by impulses derived from intrasegmental and intersegmental reflex neurons of the spinal cord. All of these movement-related impulses are integrated in the motor unit, and the result of this integration is transmitted to the muscle fibers . Muscles participating in finely differentiated movements are supplied by a large number of anterior horn cells, each of which innervates only a few (520 ) muscle fibers; such muscles are thus composed of small motor units . In contrast , large muscles that contract in relatively undifferentiated fashion, such as the gluteal muscles, are supplied by relatively few anterior horn cells, each of which innervates 100500 muscle fibers ( large motor units ).

24. Upper Motor Neuron Syndrome Damage to any part of the motor system hierarchy above the level of alpha motor neurons (not including the side loops) results in a set of symptoms termed the upper motor neuron syndrome. Upper motor neuron disorders typically arise from such causes as stroke, tumors, and blunt trauma. For example, strokes to the middle cerebral artery, lateral striate artery, or the medial striate artery can cause damage to the lateral surface of cortex or to the internal capsule, where the descending axons of the corticospinal tract collect.

25. The Symptoms o f Upper Motor Neuron Syndrome : The effects extend to large groups of muscles.   М uscles from different body parts are activated by stimulation of parts of motor cortex, consistent with the notion that motor cortex represents movements that are controlled by many joints, rather than individual muscles. Thus, a stroke in a particular part of motor cortex will affect the activation of many muscles in the body. Likewise, a stroke that affects the internal capsule or crus cerebri could affect muscles on the entire contralateral side of the body.  

26. Atrophy is rare.   Because alpha motor neurons are present, muscles will continue to receive trophic agents necessary for their survival. A mild amount of atrophy may result from disuse, but it will not be as pronounced as that resulting from a lower motor neuron disorder.   Weakness.  Upper motor neuron disorders produce a graded weakness of movement ( paresis ), which differs from the complete loss of muscle activity caused by paralysis ( plegia ).   The Symptoms o f Upper Motor Neuron Syndrome :

27. Absence of fasciculations .  Because alpha motor neurons themselves are spared, fasciculations do not occur.  Absence of fibrillations.  Likewise, fibrillations do not occur.  Hypertonia .  Upper motor neuron disorders result in an increase in muscle tone. Recall that descending motor pathways can modulate the intrinsic circuitry that is present in the spinal cord. This modulatory input can be either inhibitory or excitatory. Through mechanisms that are not well understood, the loss of descending inputs tends to result in an increased firing rate of alpha and/or gamma motor neurons. The higher firing rate causes an increase in the resting level of muscle activity, resulting in hypertonia.  Hyperreflexia .  Because of the loss of inhibitory modulation from descending pathways, the  myotatic (stretch) reflex  is exaggerated in upper motor neuron disorders. The stretch reflex is a major clinical diagnostic test of whether a motor disorder is caused by damage to upper or lower motor neurons.  The Symptoms o f Upper Motor Neuron Syndrome :

28. Absence of fasciculations .  Because alpha motor neurons themselves are spared, fasciculations do not occur.  Absence of fibrillations.  Likewise, fibrillations do not occur.  Hypertonia .  Upper motor neuron disorders result in an increase in muscle tone. Recall that descending motor pathways can modulate the intrinsic circuitry that is present in the spinal cord. This modulatory input can be either inhibitory or excitatory. Through mechanisms that are not well understood, the loss of descending inputs tends to result in an increased firing rate of alpha and/or gamma motor neurons. The higher firing rate causes an increase in the resting level of muscle activity, resulting in hypertonia.  Hyperreflexia .  Because of the loss of inhibitory modulation from descending pathways, the  myotatic (stretch) reflex  is exaggerated in upper motor neuron disorders. The stretch reflex is a major clinical diagnostic test of whether a motor disorder is caused by damage to upper or lower motor neurons.  The Symptoms o f Upper Motor Neuron Syndrome :

29. The symptoms of upper motor neuron syndrome are : Initial contralateral flaccid paralysis.  In the initial stages after damage to motor cortex, the contralateral side of the body shows a flaccid paralysis. Gradually, over the course of a few weeks, motor function returns to the contralateral side of the body. This gradual recovery of function results from the ability of other motor pathways to take over some of the lost functions. Recall that there are multiple descending motor pathways by which high-order information can reach the spinal cord. Thus, descending pathways such as the rubrospinal and the reticulospinal tracts, which receive direct or indirect cortical input, can take over the function lost by the damage to the corticospinal tract. Moreover, primary motor cortex itself is capable of reorganizing itself to recover some lost function. Thus, if the part of motor cortex that controls a certain body movement is damaged, neighboring parts of the motor cortex that are undamaged can, to some extent, alter their function to help compensate for the damaged areas. The one major exception to the recovery of function is that fine control of the distal musculature will not be regained after a lesion to the corticospinal tract. Recall that there are direct connections from primary motor cortex neurons to alpha motor neurons controlling the fingers. These connections presumably underlie our abilities to manipulate objects with great precision and to do such tasks as playing a piano and performing microsurgery. None of the other descending pathways have direct connections onto spinal motor neurons, and none of them can compensate for the loss of fine motor control of the hands and fingers after damage to the corticospinal tract. 

30. The symptoms of upper motor neuron syndrome are : Clonus.  Sometimes the stretch reflex is so strong that the muscle contracts a number of times in a 5-7 Hz oscillation when the muscle is rapidly stretched and then held at a constant length. This abnormal oscillation, called clonus, can be felt by the clinician . Spasticity .  A clinical sign of upper motor neuron disorder is a velocity dependent resistance to passive movement of the limb. If the clinician moves a patient’s limb slowly, there may be little resistance to the movement. As the passive movement becomes quicker, however, at a certain point the muscle will sharply resist the movement. This is referred to as a “spastic catch.” The mechanism for this spasticity is not entirely known, but altered firing rate of gamma motor neurons and their regulating interneurons may be involved, as well as an increase in alpha motor neuron activity, causing an inappropriately powerful stretch reflex to a fast stretch of the muscle. Sometimes, the resistance becomes so great that the autogenic inhibition reflex is initiated, causing a sudden drop in the resistance; this is referred to as the  clasp-knife reflex . 

31. Lower Motor Neuron Syndrome Motor system dysfunction can result from damage or disease at any level of the motor system hierarchy and side-loops. Differences in the symptoms that result from damage at different levels allow the clinician to localize where in the hierarchy the damage is likely to be. Damage to  alpha motor neurons  results in a characteristic set of symptoms called the lower motor neuron syndrome (lower motor neurons refer to alpha motor neurons in the spinal cord and brain stem; all motor system neurons higher in the hierarchy are referred to as upper motor neurons). This damage usually arises from certain diseases that selectively affect alpha motor neurons (such as polio) or from localized lesions near the spinal cord. Lower motor neuron syndrome is characterized by the following symptoms

32. Lower motor neuron syndrome The effects can be limited to small groups of muscles.  Recall that a  motor neuron pool  is a nucleus of alpha motor neurons that innervate a single muscle. Furthermore, nearby motor neuron pools control nearby muscles. Thus, restricted damage to lower motor neurons, either within the spinal cord or at the ventral roots, will affect only a restricted group of muscles.  Muscle atrophy.  When alpha motor neurons die, the muscle fibers that they innervate become deprived of necessary trophic factors and eventually the muscle itself atrophies. 

33. Lower motor neuron syndrome Fasciculation.  Damaged alpha motor neurons can produce spontaneous action potentials. These spikes cause the muscle fibers that are part of that neuron’s motor unit to fire, resulting in a visible twitch (called a fasciculation) of the affected muscle.   Fibrillation .  With further degeneration of the alpha motor neuron, only remnants of the axons near the muscle fibers remain. These individual axon fibers can also generate spontaneous action potentials; however, these action potentials will only cause individual muscle fibers to contract. This spontaneous twitching of individual muscle fibers is called a fibrillation. Fibrillations are too small to be seen as a visible muscle contraction. They can only be detected with electrophysiological recordings of the muscle activity (an electromyogram). 

34. Lower motor neuron syndrome Weakness.  Because of the damage to alpha motor neurons and the atrophy of muscles, weakness is profound in lower motor neuron disorders.  Hypotonia .  Because alpha motor neurons are the only way to stimulate extrafusal muscle fibers, the loss of these neurons causes a decrease in muscle tone.  Hyporeflexia .  The  myotatic (stretch) reflex  is weak or absent with lower motor neuron disorders, because the alpha motor neurons that cause muscle contraction are damaged.