Motor system

Topics

Overview of movement control.
Lower 'motor neurons' and spinal circuits
Upper 'motor neurons' and differences among cortical regions
Clinical syndromes associated with upper motor dysfunction.

Preparation for class

PN6 Chapters 16-17, 19

Topic Slide

Edward Evarts (1926-1985) was a pioneering neurophysiologist at NIH who studied the movement systems of monkeys using the single cell recording technique.

Giacomo Rizzolatti (b. 1937) is an Italian neurophysiologist who also studies the movement systems of monkeys using single cell recording. Rizzolatti is best known for his discovery of so-called mirror neurons.

Levels of control in movement

As I discussed in my first lecture, an organism's evolutionary fitness can be improved through adaptive movement. It is adaptive movement that brings an organism into purposeful contact with food sources and potential mates. The ability to plan and execute movements has been a major driving force in brain evolution.

In the broadest conceptualization, we could consider the entire brain to be involved in the the planning and execution of adaptive movements. However, here we will focus on those brain and spinal regions involved in the direct control of muscles and movements.

Motor neuron systems

The movement system is hierarchically organized with the lowest levels concerned with contracting and relaxing muscles around joints, for reflexive actions, and postural adjustments. At the highest level, it is about selecting of initiating goal directed actions, and inhibiting competing responses.

We can conceptualize the control of movements into lower motor neuron and upper motor neuron systems:

Lower motor neurons
- Alpha and gamma motor neurons in spinal cord.
- Local spinal circuits involving interneurons.
- Pattern generators.
- The final common pathway for movements, as excitation is directed to individual muscles.
Upper motor neurons
- Involves all of M1 (Brodmann Area or BA 4)
- Involves lateral and medial parts of premotor cortex (PMC) (BA 6) and parietal cortex
  - Involves the planning of movements
- Involves motor nuclei in the brainstem
  - primarily for postural adjustments and balance

Modification and learning of movements

In addition to the lower and upper motor neurons that direct excitation to the muscles, there are two 'consulting' systems that modify the motor plans. These involve two 'neuronal machines', the basal ganglia and cerebellum.

Cerebellum:

efferent control of M1 and PMC
makes movements smooth and precise
involved in motor learning

Basal ganglia:

Gates, or facilitates, desired movements
Inhibits unwanted movements

We will discuss these two structures and the manner in which they influence movements in my next lecture.

Lower motor neurons

Spinal cord

We considered the spinal cord in my lecture on the somatosensory system. A good review of spinal cord anatomy can be found here (the animations on this site require Flash).

Recall that the dorsal, or posterior, aspect of the cord was sensory. The cell bodies of the sensory neurons are located outside the spinal cord in the dorsal root ganglia. In contrast, the motor neurons are located within the ventral aspect, or anterior, aspect of the spinal cord gray matter. The axons of these neurons leave the ventral aspect of the cord and join with the sensory input fibers (or, axons) associated with the sensory neurons in the dorsal root ganglia to form spinal nerves. That is, the dorsal and ventral roots join together a short distance from the spinal cord to form the spinal nerves. A pair of dorsal and ventral roots (one per side of the spinal cord) emerge at every segment of the spinal cord.

Motor neurons in the ventral horn

The alpha motor neurons in the ventral horn of the spinal cord receive descending influence from upper motor neurons located in the cerebral cortex and from motor centers in the brainstem.

In the figure below, you can see the alpha motor neuron cell bodies in the ventral horn of the spinal cord, with efferents leaving through the ventral roots, through the spinal nerve, and synapsing on striated muscle. You can also see the proprioceptive fibers leaving the muscle spindles and entering the dorsal roots of the spinal cord. Note that the cell bodies of these sensory neurons are located in the dorsal root ganglia outside of the spinal cord.

The alpha motor neuron makes synapses with many muscle fibers within a muscle. An action potential in the alpha motor neuron causes excitation at the neuromuscular junction (the chemical synapse between the axon of the motor neuron and the muscle fiber). Other alpha motor neurons in the same motor pool would innervate other muscle fibers in that muscle. The strength of the muscle contraction is increased by higher rates of firing in individual alpha motor neurons, and by the excitation of more alpha motor neurons in that motor pool.

The degree of tension in a muscle is measured by muscle spindle fibers and Golgi tendon organs which provide proprioceptive information to the spinal cord and then upwards to the brainstem, cerebellum, and cerebral cortex.

There are interneurons in the ventral horn of the spinal cord that modulate the activity of alpha motor neurons. One such interneuron is the Renshaw cell, which is activated by collaterals of the alpha motor neuron and project back on to the same and other alpha motor neurons. This provides negative feedback to the alpha motor neuron and thus regulates the amount of excitation it produces on the muscle. The Renshaw cell is a target of the tetanus bacterium, and tetanus can cause tightening of muscles due to the loss of Renshaw cell feedback.

Joints

Joints are operated by a pair of antagonist muscles called flexors and extensors (examples from elbow joint, biceps – flexor, triceps – extensors). Joint movement requires that one of pair relax while the other of the pair contracts. For example, when the flexor contracts, the extensor relaxes.

There are many local circuits within the gray matter of the spinal cord that automate some types of movements. I had previously described the interaction of muscle spindle fibers and motor neurons in the context of the stretch reflex. In lecture, I provided an example of a more complex nociceptive reflex that coordinates the withdrawal of the the foot of one leg from a tack, while the leg on the other side extends in support. This reflex is carried out within the spinal cord and involves the interaction of nociceptive sensory input, alpha motor neurons on both sides of the ventral horn activating antagonist muscle groups in both legs, and interneurons connecting the sensory and motor neurons.

The point of this example was to show that some computations within the motor system are handled within the spinal cord and do not need coordination through the upper motor neurons of the brain. This saves the time it takes to send sensory information from the periphery to the brain and the time awaiting a motor command in response.

This idea of peripheral controllers was elaborated with the concept of a central pattern generator, which coordinates groups of muscles for more complex (but routine) activities such as ambulation. I have previously showed the example of a central pattern generator in the cat responsible for hind leg alternation in ambulation.

Upper motor neurons

The lower motor neurons are the final common pathway for controlling movements. Upper motor neurons influence the firing of lower motor neurons. However, as we know from our discussion of the Renshaw cell above, the firing of lower motor neurons is subject to feedback control, and thus movement control may be better conceptualized as a loop between upper and lower neuron systems.

Descending tracts

I provided an initial description of the corticospinal tract (sometimes referred to as the pyramidal tract) which originates in the neurons of M1 and other regions such as premotor cortex (PMC) and supplementary motor area (SMA).

The projection from M1 and PMC that is concerned with mouth and head movements is called the corticobulbar tract, and it terminates upon brainstem nuclei that give rise to the relevant cranial nerves.

About 10% of fibers of the corticospinal tract are monosynaptic, from the large Betz cells of M1 directly to alpha motor neurons in the ventral horn of the spinal cord. The axons of the corticospinal tract are part of the internal capsule, a white matter pathway that separates the caudate and putamen in the basal ganglia (which I will discuss in the next lecture).

About 90% of the axons within corticospinal tract decussate, or cross, in the ventral medulla. The pyramid shape of the crossing is why the tract is also known as the pyramidal tract (and not because Betz cells are large pyramidal neurons). The axons that cross in the pyramids form the lateral corticospinal tract that runs along the lateral aspect of the spinal cord. The ~10% of the axons that do not decussate run down the spinal cord in the anterior corticospinal tract. However, these axons cross over the cord when they reach their destination, and so still contribute to the contralateral control of the musculature.

There are other pathways that also descend in the spinal cord. These have their origins in brain stem nuclei and are not part of the pyramidal tract. They are sometimes referred to as extrapyramidal tracts.

Rubrospinal (red nucleus – less prominent in humans, controls proximal musculature)
Tectospinal (coordinates head and eye turning towards stimuli)
Vestibulospinal (balance)
Reticulospinal (posture, muscle tone, antigravity muscles)

Many of these tracts receive collaterals from the corticospinal tracts and output from the cerebellum. We will discuss this in next lecture.

Cortical regions involved in motor control

The regions of cortex most involved in movement control are as follows:

M1 or primary motor cortex which is located anterior to the central sulcus. This region is referred to Brodmann Area 4 (BA 4).
Premotor cortex (PMC) is just rostral to M1, and the region is referred to as BA 6 (lateral).
Supplementary motor area (SMA) is also referred to as BA 6, but medial, as it lies along the medial wall between the hemispheres.
Posterior parietal cortex (PPC) is an area involved in reaching, eye movements, and motor planning.
Other frontal regions are also involved in motor planning:
- Frontal eye fields (BA 8) are involved in controlling eye movements
- Mirror neuron area (BA 44) is located near Broca's area and is involved in action understanding (discussed further below).

Concepts in movement control

Motor representations are not about particular muscles – for example, your signature looks recognizably the same regardless of whether you write with your hand or your foot.

Primary motor cortex

Primary motor cortex (M1) is located on the anterior side of the central sulcus. It is also known as Brodmann Area 4. It has a body map (homunculus) just as the primary somatosensory cortex (S1, or BA 3,2,1) opposed on the posterior side of the central sulcus.

M1 is about movements, not muscles. As one drills down into homunculus map – muscle groups required for movements are colocalized. Stimulation of different regions in M1 can activate the muscles of the same joints if used in different movements.

There are extensive overlap zones where the same joint muscles can be activated from stimulating different regions.
Different combinations of muscles can be activated by stimulation of different locations.

Population vector coding of movements

Neurons in M1 are sensitive to the direction of the movement, regardless of the pattern of muscle activity necessary for the movement.

Many neurons contribute to the ‘decision’ about how a limb will move – the population vector is the vector sum of the directions contributed by each neuron. This will later become important when we discuss Brain-Computer Interfaces (BCI).

I provided one example of a BCI in a monkey, whereby the activity of neurons in M1 were analyzed in real time by a computer and used to manipulate a robotic arm.

Premotor cortex (PMC)

Premotor cortex (PMC) neuron response profiles are complex. The main distinction between neurons in PMC and M1 is that PMC neurons begin to respond prior to movement and appear to activate in both hemispheres.

I provided an example from single unit recording in reaction time and delay response task:

Some neurons responded to target of movement, some responded to movement itself, and some responded in the delay period between the target indicator and the movement itself.
Compared to M1 neurons, PMC neurons can fire before movements, and are affected by rules.
This suggests that PMC neurons participate in motor planning

Supplementary motor cortex (SMA)

Supplementary motor cortex (SMA) also has a complicated profile. SMA neurons appear to be involved in sequence of actions. Some will only fire for a specific movement if that movement occurs within a specific sequence. The same movement may not activate a SMA neuron if that movement is part of a different sequence.

What distinguishes the properties of neurons in PMC and SMA?

Internal vs. External guided movement hypothesis:

Movements guided by external stimuli – like visual percepts – are proposed to involve PMC.
Movements guided by internal stimuli – like memories – are proposed to involve SMA.

In addition, Old learned movements seem to involve more SMA than Newly Learned movements.

Lesions to the SMA:

alien hand syndrome
utilization phenomena
motor neglect

Posterior Parietal Cortex (PPC)

There is a Frontal-Parietal network for reaching and grasping:

Receptive fields for neurons in PMC and VIP (parietal lobe) spatially overlap
- the PMC tend to be tactile while the VIP are visual/perceptual.
Different types of Visuomotor neurons in parietal lobe
- Visual dominant – fire when fixated, or when manipulated in light
- Motor dominant – fire when manipulated in light or dark
- Visuomotor – fire when manipulated in light

Some parietal neurons differentiate between similar motor reaches that have different goals – e.g., to eat a peanut or put a peanut in a cup.

Some PMC neurons affected by the shape of the object – visual features.

Reaching studies in humans

Applying parietal TMS can distort reaching movements in humans.

fMRI studies show activation of the frontal-parietal network.

Lesions to parietal lobe

‘Affordances’ are parts of objects that are natural gripping/grasping points.

Parietal lobe damage affects grips. Patients do not grip according to affordances.

This function was what was preserved in patient D.F., studied by Mel Goodale, who had occipital lobe lesions (BA 18 and 19).

DF could not verbally discriminate sizes of objects that she can see.
When asked to indicate size by making an aperture between thumb and finger – she cannot do so
When asked to pick up the object – she can do so accurately. Strikingly, she makes the correct aperture as she reaches.
Intact ‘how’ pathway.

The size-weight illusion in neurologically normal captures some of this same dissociation between perception and action.

The smaller of two objects of identical weight will be judged as heavier.
This illusion persists with experience in lifting the objects.
However, the amount of force exerted to lift the objects will quickly become equal – suggesting that the motor system ‘knows’ the true weight despite the perceptual system’s illusion that the smaller one is heavier.

Mirror neurons

Mirror neurons were first discovered in PMC region F5 in monkeys by Rizzolatti and colleagues:

Mirror neurons fire when monkey performs an action.
Also fire when monkey observes another perform the action.
Some can fire even when monkey hears the action performed, but does not actually see it (ripping paper sound).
The same motion will activate or not activate depending upon goal, as mirror neurons like goals (ingestive, communicative)

Direct mapping:

You understand actions of others by the fact that observing those actions activate the same regions you would use to perform those actions.

Evidence discussed for human mirror neurons:

Not the same standard of proof as single units.
Mu rhythm is suppressed when you make a movement, OR watch another make the same movement
fMRI study of dancers watching a dance video show activation of BA 44.

Movement disorders

Motor deficits

The deficits associated with damage to movement systems will then reflect the location of the damage within its hierarchy.

Paralysis at the spinal level.
Ataxia – cerebellum and parietal lobe
Apraxia – cortical damage.
Huntington’s and Parkinson’s diseases – basal ganglia.

There are several forms of apraxia:

ideational
ideomotor
speech
constructional
ocular

I demonstrated ideational and ideomotor apraxia with two videos.

An ataxia refers to difficulty in carrying out normal coordinated movements. I will illustrate cerebellar lesioned patients to demonstrate ataxia in my next lecture.

Optic ataxia is the inability to use vision to guide motor behavior. This is associated with parietal lobe lesions and is a component of Balint's syndrome. I illustrated optic ataxia with a video of a patient of Bob Rafal’s with parietal damage cannot reach to object despite seeing object.

The Human Brain

Professor Gregory McCarthy

Lecture 11