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Home , Corticobulbar tract, Extrapyramidal system, Motor system, Red nucleus, Reticular formation, Righting reflex

Brainstem and Cortical Control Of Movement Richard M. Costanzo, Ph.D.

OBJECTIVES

After studying the material of this lecture, the student should be able to:

1. Identify fiber tracts belonging to the Pyramidal and Extrapyramidal pathways. 2. Describe the role that each of the following centers play in the control of posture and spatial orientation. a. Red b. Pontine c. Medullary reticular formation d. e. 3. Describe the effects of a transection at different levels of the brainstem and . 4. Explain the underlying cause of decerebrate rigidity. 5. Describe the role of the primary (area 4) in the control of voluntary movement. 6. Describe the role of the premotor and (area 6) in the control of voluntary movement

I. MOTOR CENTERS AND PATHWAYS

Historically, the has been divided into Pyramidal and Extrapyramidal pathways. Pyramidal pathways have fibers that pass through the medullary "pyramids", and include the corticospinal and corticobulbar tracts. The carries information from motor cortex directly to the spinal cord, the corticobulbar projects to centers in the brainstem.

All other motor pathways are considered to be extrapyramidal and originate in centers primarily within the brainstem. These brainstem structures are responsible for the control of posture and spatial orientation. They include the , pontine and medullary reticular formation, vestibular nuclei, and superior colliculus.

Figure 1: Motor Centers and Descending Pathways (From Berne & Levy)

A.

This tract originates in the red nucleus. Fibers project to in the lateral region of the spinal cord. Stimulation of the red nucleus causes facilitation of flexors and inhibition of extensors.

B. Pontine (Medial) Reticulospinal Tract

This tract originates from cells in the nucleus reticularis pontis caudalis and nucleus reticularis pontis oralis located in the medial two thirds of the (Pontine reticular formation). Fibers project to the ventromedial spinal cord where they have a general excitatory effect on both extensor and flexor motoneurons, although maximal excitation is on the extensors.

C. Medullary (Lateral) Reticulospinal Tract

Cells originate in the medullary reticular formation (nucleus reticularis gigantocellularis) and terminate on spinal cord interneurons in the intermediate gray. The medullary reticulospinal tract has the opposite effect of the Pontine reticulospinal tract, in that it has a general inhibitory effect on motoneurons with a stronger inhibition on extensors.

D. Lateral

Cells originate in the lateral vestibular nucleus (Deiters' nucleus) and project to ipsilateral motoneurons and interneurons. Stimulation of cells in Deiters' nucleus produces a powerful excitation of extensors and inhibition of flexors It plays an important role in the control of antigravity muscles and the maintenance of posture. E.

Cells of origin are in the superior colliculus. Fibers project to the cervical spinal cord where they control muscles involved in head movement.

II. BRAINSTEM CONTROL OF POSTURE

Transections at different levels of the brainstem have been used to demonstrate the importance of brainstem centers in the control of posture. Isolation of centers below the transection from central influences above, reveals the regulatory functions of the intact centers.

A. Spinal Transection

If the spinal cord is cut three things happen.

1. Complete loss of voluntary movements

This results from the interruption of descending pathways from motor centers located in the brainstem and higher centers. Following spinal transection is a total paralysis of all muscles below the level of the lesion, a condition referred to as paraplegia.

2. Loss of conscious sensations

Sensory information from the body regions below the cut (spinal dermatome regions) can not reach higher centers and those regions appear to be anesthetized.

3. Initial loss of

Immediately following transection the sudden loss of tonic background facilitation provided by descending pathways results in a loss of and the limbs become flaccid. If the spinal transection is high (above C3) respiratory muscles will be disconnected from control centers in the brainstem and breathing will stop. This is a rather serious condition and, without a respirator, death due to anoxia will occur. If the cut were to occur around the level of C7, sympathetic tone to the heart would decrease and bradycardia and hypotension would develop.

The loss of reflexes and flaccid limbs following spinal cord lesion is called spinal shock. It is the direct result of removal of strong background facilitation provided by higher centers, primarily on alpha and gamma motoneurons. Partial recovery from spinal shock may occur after a few weeks with the return of some of the basic reflexes (knee jerk, Babinski's ).

B. Decerebrate Rigidity (Mid-Collicular Transection)

Two brainstem centers that are very important to the maintenance of muscle tone in antigravity muscles (primarily extensors) are the pontine reticular formation (medial reticulospinal tract), and Deiter's nucleus (lateral vestibulospinal tract). Both centers have an excitatory influence on extensors. Stimulation of cells in the pontine reticular formation has a very powerful excitatory effect on extensors, but its activity is normally modulated (inhibited) by central (cortical) projections. If the spinal cord is cut above the level of the pontine reticular formation (mid collicular), the inhibitory influence is removed and there is an exaggerated activation of muscle tone in extensors (antigravity muscles). This produces a rigid posture which is referred to as decerebrate rigidity. In humans arms and legs are extended, back is arched, head dorsiflexed, and feet ventroflexed (curling of toes lifts against gravity). This stiff posture does not permit joints to bend and the body is capable of standing upright. This is very different from spinal transection, where extensor muscle tone is abolished and the body becomes limp.

1. Gamma rigidity

Cutting the dorsal roots abolishes decerebrate rigidity. Cutting the Ia spindle afferents interrupts the myotatic . This demonstrates that the decerebrate rigidity was primarily due to the hypersensitivity of muscle spindles resulting from descending excitation of gamma motoneurons. Removal of the gamma contribution abolishes the rigidity. Therefore, decerebrate rigidity is considered primarily a gamma rigidity.

2. Alpha rigidity

A selective increase in alpha motoneuron activity can produce what is referred to as alpha rigidity. This can be demonstrated after reversing decerebrate rigidity caused by gamma excitability (cutting the dorsal roots) and increasing the excitation of alpha motoneurons. Since cells in the lateral vestibular nucleus (Deiters' nucleus) are normally inhibited by projections from the , removal of cerebellar projections increases the activity of these cells. The result is an increase in descending excitation of extensors and rigidity is restored by alpha motoneurons (gammas may fire too, but they are ineffective since the dorsal roots have been cut).

3. Positional (postural) reflexes

Changing the position of the head can alter the distribution of muscle tone throughout the body. There are two reflexes that do this. The are antagonistic to one another.

a. Tonic neck reflexes - align body with head b. Tonic labyrinth reflexes - restore head to a normal (vertical) position

C. Animal (Transection above midbrain)

Transection of the brainstem above the level of the red nucleus does not result in decerebrate rigidity. This is the direct result of the inhibitory influences of the red nucleus (via the rubrospinal tract) on extensor activity. This inhibitory influence on extensors offsets the excitatory influence of lower brainstem centers. In addition, the rubrospinal tract has a facilatory effect on flexors muscles.

A significant feature of the midbrain animal is its ability to reflexively right itself from any abnormal position. This is referred to as the . This reflex occurs in stages. First the input from the vestibular organs allow the head to orient into a normal vertical position. Next distortion from the neck muscles provide information to allow the trunk to come into alignment with the head. Thus the midbrain animal is capable of maintaining normal body posture and reflexively (without voluntary control from higher centers).

Figure 2: Diagram illustrating major stem centers controlling posture.

III. CONTROL OF VOLUNTARY MOVEMENT

Three major brain centers work together to control voluntary movement. They are: 1. the motor regions of the (premotor cortex, supplementary motor area, and ) 2. the , and 3. the cerebellum.

These centers have direct (pyramidal system) or indirect () projections to the "lower motor ". The lower motor neurons in turn make direct connections with muscle fibers (via neuromuscular junctions) and provide the "final common pathway" for all motor movement.

IV. CORTICAL MOTOR CENTERS

Cortical centers that control voluntary movement are located in the frontal lobe (anterior to the ). They include the primary motor cortex (area 4), premotor cortex and supplementary motor area (area 6). Although the (areas 9-12) is concerned with "strategy" for movement, it is not part of the agranular motor cortex.

Figure 3: From Berne and Levy, 1998, Fig. 14-2B

A. Primary Motor Cortex

The primary motor cortex is located in the (area 4) and is responsible for the execution of movement. It serves as a staging center for motor programs that are generated in motor association areas. Programmed patterns of motor neurons are activated in motor cortex resulting in the execution of the programmed movement. Excitation of cells in the motor cortex (upper motorneurons) is transferred to the brainstem () and spinal cord (corticospinal tract) where it excites the "lower motor neurons" that have direct control over specific muscle groups.

The primary motor cortex (precentral gyrus) is somatotopically organized (motor homunculus). Muscles from different parts of the body are represented in specific areas of the cortex. Those areas that represent parts of the body capable of fine delicate movements (e.g., , , face) have larger cortical representation. The deeper layers of the cortex project to single or small muscle groups, whereas cells located near the surface appear to project to more diffuse groups of muscles needed for more complex movements.

Hulings Jackson was one of the first to propose that motor functions were localized in particular regions of the motor cortex. He observed that epileptic events in motor cortex resulted in a progressive spread of contractions beginning with the fingers and then moved to the wrist, forearm, arm and, regions. This sequence of events illustrates the somatotopical organization of motor cortex and is referred to as a "Jacksonian Seizure" or "Jacksonian March".

B. Premotor Cortex and Supplementary Motor Area (Area 6)

The premotor cortex and supplementary motor areas are responsible for the generation of patterns or programs for movement. They receive information from a variety of sources including sensory association cortex and lateral cerebellum. This information is used to formulate programs and patterns for movement which are transferred to the primary motor cortex for execution.

The Supplementary motor area is located on the dorsomedial surface of the cerebral hemisphere and plays an important role in programming complex motor sequences often involving muscles on both sides of the body. The supplemental motor area appears to play a role in the preparation for movement and has been found to be active during the "mental rehearsal" of a sequence of movements. This activity can occur even if a movement is not actually executed by the primary motor cortex.

C. Prefrontal Cortex (Areas 8-12)

Although not part of the "motor cortex" per se, the prefrontal cortex plays an important role in providing the motivation and correct strategies for movement. This area of the frontal cortex receives complex sensory information from many areas of the brain including sensory and posterior parietal cortex. Because of the extensive inputs received by the prefrontal cortex it can combine learned or remembered motor responses (e.g., memory) with changing events. It receives "limbic" input that affects motivation.

D. Posterior Parietal Cortex

The posterior parietal cortex provides motor regions of the brain with information about one's environmental surroundings and external space achieved through complex multimodal sensory integration. Although this region is not considered part of "motor cortex", it plays an important role in providing information needed to generate correct strategies for movement. Without essential sensory information, such as the spatial coordinates of nearby objects, it is difficult, if not impossible, for the motor cortex to generate appropriate motor signals. Patients with lesion in frontal association areas or posterior parietal cortices are unable to execute simple motor acts such as eating with a knife and fork. The inability to correctly execute learned sequences despite intact pathways is called "apraxia".

E. Diseases (Lesions) of the Motor Cortex

A which disrupts the blood supply to motor cortex or the corticospinal tract fibers, results initially in of limbs on the side contralateral to the lesion. Paralysis is gradually replaced by spastic paralysis. Fine motor control of movement is often lost in lesions involving motor cortex. Epileptic events in motor cortex usually begin with movement of the fingers on one hand and progress to the hand, arms, and eventually the whole body (Jacksonian March).

V. BASAL GANGLIA AND CEREBELLUM

The basal ganglia and cerebellum have an important influence on the production and coordination of normal (smooth) movements. They work together with motor centers in the cortex to help program and execute motor plans.

A. Basal Ganglia

The major structures of the basal ganglia include the (caudate nucleus and ), (internal, GPi and external GPe segments), (, SNr and , SNc) and the , STN. The striatum receives input from the cortex (corticostriates, areas 3, 1, 2, 4 and 6) related to plans for an intended movement and ultimately generates signals facilitating the initiation of movement programs. A major function of the basal ganglia is to modulate the flow of activity from the to the motor cortex.

Cells in the striatum normally have low spontaneous activity. When stimulated by excitatory corticostriate (glutamate) inputs from the cortex they increase their activity. GABAergic inhibitory projections from the striatum to the globus pallidus reduce the activity of the cells in the globus pallidus. Normally, the globus pallidus have high spontaneous activity. GABAergic inhibitory projections from the globus pallidus to the subthalamic and thalamic nuclei reduce the activity of these cells. When GABAergic inhibitory projections from the striatum to the globus pallidus cells are active, globus pallidus cells are inhibited. This decrease in globus pallidus cell activity results in decreased activity of their GABAergic projections to the and thalamus. This results in less inhibition/more activity of the cells in the subthalamic and thalamic nuclei (inhibition of inhibition = excitation).

There are two major projection pathways through the basal ganglia, a direct and an indirect. The (striatum output nuclei (GPi and SNr) thalamus) causes stimulation of thalamic neurons and facilitates movement. The indirect pathway (striatum GPe subthalamus output nuclei (GPi and SNr) thalamus) cause inhibition of thalamic neurons and decrease or inhibits movement. The mechanisms by which the basal ganglia modulate thalamic outflow is based on the release of excitatory and inhibitory transmitters by projection neurons.

Figure 4: Direct and indirect projection pathways through the Basal Ganglia (From Costanzo, 2006, Fig. 3-34).

The increased activity in thalamic projections to the premotor and supplementary motor cortex is thought to serve as a "facilitator" to initiate execution of movement by cells in the motor cortex.

When normal control of thalamic activity is altered, movement disorders are observed. Disorders of the basal ganglia that causes a reduction in the inhibitory control of the thalamus result in hyperkinetic movement disorders (e.g., Ballism and Huntington's disease). When there is an increase in inhibition of thalamic activity by the basal ganglia, hypokinetic movement disorders are observed (e.g., Parkinson's disease). Cells in the dark pigmented zone of the substantia nigra pars compacta (SNc) send fibers back to the striatum (nigrostriatals) and use as a . Degeneration of cells in the SNc and reduced dopamine levels in the striatum (e.g., Parkinson's disease) results in a reduced activity in GABAergic inhibitory projections to GPi and SNr [less inhibition] and an increased activity in inhibitory projections to GPe [more inhibition]. Inhibition of GPe activity permits cells in the subthalamic nucleus (STN) to increase their firing rate which in turn acts to further increase the activity of the output nuclei (GPi and SNr cells). This increased activity in GPi and SNr acts to inhibit cells in the thalamus and the thalamocortical projections to motor cortex. This can lead to hypokinetic movement disorders such as those observed in Parkinson's disease (e.g., bradykinesia, slowness and delayed movement, and resting ).

Table 1: DISORDERS OF THE BASAL GANGLIA DISORDER LESIONS CHEMICAL NEUROLOGICAL CLINICAL ISSUES CHANGES SIGNS

Parkinson's Nigrostriatal Dopamine Resting Common disorder Disease (3-6/sec) RX: L-Dopa or pathway Bradykinesia dopamine agonists shuffling gait (bromocriptine)

Huntington's Intrastriatal and Choline acetyl- Chorea (to dance) Autosomal dominant Disease cortical transferase writhing movements (chromosome 4) and usually fatal GABAergic neurons No treatment: GABA dopamine antagonists to control chorea

Hemiballism Infarct or Glutamate Uncontrollable flinging Neuroleptics hemorrhage of movements of the subthalamic nucleus contralateral limb

B. Cerebellum

The cerebellum has the ability to "eaves drop" on most motor pathways and thus is one of the best informed structures in the CNS. It continuously receives input about ongoing movement (cortico-ponto-cerebellar pathway), proprioceptive (spinocerebellars) and vestibular inputs (vestibulocerebellars) which are essential for the coordination of smooth movements. This allows the cerebellum to continuously update and correct motor signals so that the programmed motor plan is correctly executed. Lesions of the cerebellum often result in or asynergia (lack of coordination due to errors in the rate, range, force, and direction of movement. Lesions can also produce "intention" (action) tremors (e.g., shaking upon attempt to perform motor task). VI. VOLUNTARY MOVEMENT

Ideas, strategies, and motivation for movement originate in a variety of brain centers (sensory and association cortex) and in concert with the prefrontal cortex are responsible for the earliest planning stages for voluntary movement.

The basal ganglia (trigger or "go" signals) together with the lateral regions of the cerebellum (pontocerebellum) help to assemble a program or motor plan within the premotor cortex.

Motor plans are executed by the primary motor cortex which projects to "lower motor neurons" that in turn activate specific muscle fibers or muscle groups that results in movement. The intermediate region of the cerebellum (spinocerebellum) helps to coordinate the activity of specific muscle groups by monitoring the output of the motor cortex and making corrections and adjustments so that movements match the "motor plan". The cerebellum does this by receiving proprioceptive feedback from muscle and joint receptors. It shares this information with the motor cortex and motor neurons in the spinal cord so that adjustments can be made

PLANNING EXECUTION

Basal Ganglia

Sensory and Motor Association Premotor Movement Cortex Cortex

Cerebellum Cerebellum (Pontocerebellum) (Spinocerebellum)

Figure 5: General Scheme for Voluntary Movement

ADDITIONAL REFERENCES

Costanzo, L.S. Physiology , 3rd Edition, Saunders Elsevier, 2006, pp. 101-107.

Kandel, E.R., Schwartz, J.H., and Jessell, T.M. Principles of Neural Science (4th ed), McGraw- Hill, 2002, Chapter 36 (pp. 713-736), Chapter 38 (pp. 756-781), Chapter 41 (pp. 816-831) and Chapter 43 (pp. 853-867).