CNS

Motor Control

CNS - Motor Control

• The brain is, first and foremost, a movement control device.

• All other aspects of brain organization are subservient to the organism's need to be able to take action.

• In this lecture, the functional characteristics of the neural systems that provide for postural and voluntary movements will be discussed.

The Nature of Motor Control

• Different motor pathways (brown arrows) provide for different "modalities" of movement.

• The cerebellum and basal ganglia, which do not project directly to lower motor neurons (LMNs), are critical for successful motor performance.

• Their output is directed to upper motor neurons (UMNs).

The Nature of Motor Control

• All levels of the motor hierarchy receive information from somatic sensory receptors (green arrows).

• These receptors, especially the proprioceptors, continually inform the motor system about the position and movement of the body and limbs.

Upper Motor Neurons (UMNs)

• UMNs are cells that carry signals (motor commands) from supraspinal centers to the lower motor neurons (LMNs) of the spinal cord.

• UMNs synapse directly (monosynaptically) on LMNs or influence them indirectly via interneurons.

• UMN cell bodies are found in the cerebral cortex and in the brainstem; they contribute to three motor pathways that are more-or-less functionally distinct.

The Three Upper Motor Neuron Pathways

UMNs contribute to three functionally distinct motor pathways, each of which subserves a different 'modality' of movement.

The Three Upper Motor Neuron Pathways

The newest pathway, the corticospinal motor pathway, arises in the cerebral cortex and provides for fine, precise movements, especially those produced by distal muscle groups (e.g., movements of individual digits).

The Three Upper Motor Neuron Pathways

The next pathway, the lateral brainstem pathway, arises in the red nucleus and provides for limb and hand movements, but not movements of individual digits.

The Three Upper Motor Neuron Pathways

• The oldest pathway, the medial brainstem motor pathway, arises from cells in the reticular formation, the vestibular nuclei and the tectum.

• This motor pathway provides for movements of posture and equilibrium usually involving many muscle groups, particularly antigravity muscles.

UPPER MOTOR NEURONS ACTIONS

UMNs have six actions at the cranial nerve or segmental level:

1. EXCITATIONDirectly (i.e., monosynaptically) or indirectly (via interneurons), UMNs excite alpha and gamma motor neurons.

2. INHIBITIONUMN inhibition of LMNs is carried out mostly (or entirely) via inhibitory interneurons. Postsynaptic and presynaptic mechanisms of inhibition are involved.

UPPER MOTOR NEURONS ACTIONS

3. GATING OF REFLEXES Neurons involved in reflexes can be influenced to change the pattern of or enhance or eliminate the reflex.

For example, UMN axons influencing a stretch reflex arc by exciting a Group Ia presynaptic inhibitory interneuron or a gamma motor neuron innervating the muscle spindle.

UPPER MOTOR NEURONS ACTIONS

4. EFFERENCE COPY (corollary discharge)In addition to effects on motor neurons and reflexes, UMN signals are carried into other areas of the brain to let them know that an active movement is occurring.

For example, cells in the pontine nuclei receive a copy of the motor commands and send them to the cerebellum, thus apprising it of the intended movement. Efference copy is also sent to cells of origin of the ventral spinocerebellar tract.

UPPER MOTOR NEURONS ACTIONS

5. Activation of other UMNs

• Some corticospinal tract fibers influence red nucleus neurons or reticular formation neurons.

• The cells of origin of the medial brainstem pathways are richly interconnected.

UPPER MOTOR NEURONS ACTIONS

6. Activation of pattern generators. Signals from UMNs can activate intrinsic neuronal circuits that produce a stereotyped pattern of response.

For example, the spinal cord of cats contains a pattern generator for walking. It is likely that a similar pattern generator exists in primate spinal cord.

UMN Terminations in the Spinal Cord

Signs of UMN Damage

• Damage to UMNs can produce two kinds of neurological signs: negative signs and positive signs.

• Negative signs are the loss or absence of function that would be expected from the loss of or damage to UMNs.

• A negative event, the lesion, has a negative consequence, the loss or reduction of a function. Weakness is a typical negative neurological sign of UMN dysfunction.

Signs of UMN Damage

• In contrast, some lesions cause the appearance of signs not normally present or cause an increase in some function.

• Such new or enhanced signs are referred to as positive neurological signs (also called "release of function“).

Signs of UMN Damage

• Increased muscle tone is typical example of positive neurological signs that usually accompany UMN lesions.

• Positive neurological signs, such as paresthesia (pins and needles) or pain (thalamic pain), may occur following lesions of the somatosensory system.

Features of Motor Pathways

The following features of the motor pathways are especially important:

1. Location of cells of origin.2. Trajectory of axons, especially in the spinal cord white matter.3. Terminal distribution fields in the spinal gray matter.4. Muscle groups (proximal or distal) towards which their main action is directed.

Medial Brainstem Motor Pathway

Cells of origin:Reticular formation, vestibular nuclei,

tectum, and locus coeruleus.

• 1. Main action is via interneurons onto motor neurons for axial (postural) muscles, especially those for antigravity muscles. Reticulospinal action is excitatory or inhibitory; vestibulospinal actions are mainly excitatory. Locus coeruleus neurons are nor-adrenergic.

Medial Brainstem Motor Pathway

• 2. Divergence characterizes this pathway. Individual neurons give off collaterals at several segmental levels. Many fibers end bilaterally.

• 3. The medial brainstem motor pathway controls the concerted action of many muscle groups. It is especially important in the control of posture and muscle tone.

Lateral Brainstem Motor Pathway

Cells of origin:red nucleus,

magnocellular (large-celled) division.

• 1. Main action is via interneurons to motor neurons of proximal and distal limb muscles, especially flexor muscles.

Lateral Brainstem Motor Pathway

• 2. Less divergent than the medial brainstem pathway.

• 3. Controls the action of a few muscle groups. In primates other than humans, this pathway provides for limb movements, but not for independent digit movements. This pathway is not well developed in the human brain.

Corticospinal Motor Pathway

Cells of origin:Layer V of motor cortex, i.e., the precentral gyrus of the frontal lobes (Brodmann's areas 4 and 6).

• 1. This motor pathway acts on motor neurons of all muscle groups, but is especially strong and direct to LMNs of distal muscles. For example, there are many monosynaptic connections to LMNs of digit muscles.

Corticospinal Motor Pathway

2. The overall terminal distribution field of the corticospinal motor pathway overlaps those of the medial and lateral brainstem motor pathways. Individual corticospinal tract fibers are less divergent than fibers in other motor pathways.

Corticospinal Motor Pathway

3. The lateral corticospinal tract provides precise control of individual muscles, particularly distal muscles. The discrete, fractionated movements provided for by this pathway reflect its monosynaptic control of LMNs.

Examples of UMN Problems

Decerebrate Rigidity• Decerebrate "rigidity" is a

condition of increased muscle tone and stretch reflexes, particularly in extensor muscles.

• It is produced by intercollicular brainstem transection. This disconnects certain reticulospinal neurons from their most important source of excitatory synaptic drive, eliminates rubrospinal inhibition, and leads to the appearance of the positive neurological signs of increased muscle tone and stretch reflexes.

• Disinhibition of extensor motor neurons is the major culprit, but ongoing excitation from the vestibulospinal tract is also important.

Decerebrate RigidityDecerebrate rigidity comes about through the following

interactions: • 1. The pontine reticular formation (N. reticularis pontis

oralis and caudalis) facilitates alpha and gamma motor neurons of extensor muscles. Pontine reticulospinal neurons receive excitatory drive from somatosensory receptors as well as from the cerebral cortex (forebrain). These reticulospinal neurons continue to fire even when they are disconnected from the forebrain.

• 2. The medullary reticular formation (N. reticularis gigantocellularis) facilitates flexor LMNs and inhibits, via inhibitory interneurons, alpha and gamma motor neurons of extensor muscles. Medullary reticulospinal neurons do not receive much excitatory drive from somatosensory receptors and thus depend on excitatory drive from the cerebral cortex for maintaining their normal rate of firing. Medullary reticulospinal neurons cease firing when disconnected from the forebrain, so inhibitory synaptic drive onto extensor motor neurons is decreased.

Decerebrate Rigidity

• 3. Tonic reciprocal inhibition of extensor motor neurons from rubrospinal tract axons is eliminated by brainstem transection. This further disinhibits the extensor LMNs.

• 4. The net result of the transection is to cause an imbalance in descending influences onto alpha and gamma extensor motor neurons: excitation outweighs inhibition. This occurs because inhibitory action from the medullary reticular formation and the red nucleus is much reduced while excitatory action from the pontine reticular formation and the lateral vestibular nucleus persists.

• 5. Because gamma motor neurons are most excitable (recall the "size principle") the stretch reflex arc becomes spontaneously active. This causes a large, tonic increase in extensor muscle tone (hypertonia) with increased stretch reflexes (decreased threshold and increased amplitude, referred to as hyperreflexia).

UMN Disease

• Positive neurological signs may be marked in the case of UMN disease. The most common positive signs include spasticity and the Babinski Sign.

• Weakness is the predominant negative sign. Spasticity refers to a set of signs where muscle tone is increased and the resistance to passive movement is velocity sensitive during its initial phase. Stretch reflexes are, of course, hyperactive and clonus may be present.

UMN Disease

Weakness is always present and the Clasp knife phenomenon and the Babinski sign may be present.

UMN Disease

• The best explanation of spasticity is that it is similar to decerebrate rigidity, i.e., due to disinhibition of alpha and gamma extensor motor neurons in the presence of ongoing excitation from other sites (pontine reticular formation and lateral vestibular nucleus).

• Another factor that contributes is the disfacilitation of Group Ia presynaptic inhibitory interneurons. They normally receive excitatory synaptic drive from collaterals of UMNs. When they are depressed, impulse transmission through the stretch reflex arc is enhanced and the increased excitatory drive to LMNs worsens the hyperreflexia and hypertonia.

Spinal Cord Transection (I)

Complete spinal cord transection produces the following:

1. Spinal Shock:

Immediately following the transection, spinal reflexes below the level of cord transection are lost (areflexia). This is a classic negative sign due to profound disfacilitation of LMNs, as well as interneurons in reflex circuits. These cells are disfacilitated due to transection of all motor pathways.

Spinal Cord Transection (II)

2. Mass Reflex:With time, somatic and autonomic reflexes return and may become hyperactive. Flexion reflexes return before stretch reflexes. Light tactile stimulation may produce bilateral flexion of legs and trunk accompanied by bladder and bowl evacuation. Hyperactive reflexes probably arise due to two reasons:1) development of denervation supersensitivity in spinal cord neurons, 2) sprouting of the central terminals of primary afferent fibers.

The Motor (MI) Cortex and Corticospinal Tract

• The primary motor (MI) cortex is considered to be Brodmann's area 4 in the precentral gyrus.

• The motor cortex is the executant, but not the highest level of control, of the motor system. Its output neurons in layer V, which project to the spinal cord, must fire for a voluntary movement to occur.

• These corticospinal neurons carry the motor commands to LMNs (and to UMNs of the brainstem motor pathways). Their pattern and frequency of firing encodes the nature, speed, and amplitude of the movement.

The Motor (MI) Cortex and Corticospinal Tract

• The motor cortex receives input about the desired goal from the limbic system via the prefrontal association areas of the cerebral cortex.

• In addition, it receives inputs from sensory association areas, parts of the basal ganglia and cerebellum, and the premotor and supplementary motor areas.

• These areas provide for planning and programming, i.e., they specify a complex motor program suitable to the desired goal and set a posture that will support the intended movement.

The Motor (MI) Cortex and Corticospinal Tract

• Actual movement tactics, i.e., selection of appropriate muscle groups, are specified by the primary motor cortex (MI) in conjunction with its inputs from premotor cortex, as well as from the spinocerebellum.

• The signals from the spinocerebellum provide periodic correction of on going movements.

• Most, if not all, motor pathways become involved in the execution of the movement.

The Motor (MI) Cortex and Corticospinal Tract

• Given the number and complexity of the circuits antecedent to the motor cortex, it is not surprising that motor preparation time is long.

• In fact, when scalp electrodes are placed over the arm area, a negative going readiness potential occurs over the premotor and motor cortex beginning 1,000 to 800 msec before a brief voluntary movement.

• The actual firing of corticospinal tract cells in area 4 (MI), which designates the pattern and strength of LMN activation, occurs along with a positive shift in the potential (the premotor positivity) 90 to 100 msec prior to movement onset.

Thank YouFor Your Attention!