Lecture 1: Motor I
Ultimately, we move because there’s some sensory state that’s more rewarding than the
present. Once you decide to move, you trigger a cascade of events in different structures
including: Basal ganglia (motivation of movement), Cerebellum (coordination), Thalamus
(relay), Posterior Parietal Cortex (use visual cues to plan voluntary movement), Motor Cortex
(initiate and direct voluntary movement), Brainstem (posture), Spinal Cord (reflex), Motor
Neurons and Skeletal muscle.
Cervical spinal cord nerves control breathing, head/neck movement, heart rate, and upper
limb. Thoracic spinal cord nerves control sympathetic tone, temperature regulation and trunk
stability. Lumbar spinal cord nerves control ejaculation, hip/knee/foot movement. Sacral
spinal cord nerves control penile erection and bowel/bladder activity.
Generally in the spinal cord, sensory stuff is dorsal, motor stuff is ventral.
With spinal cord injury, only a small region is damaged. Hemorrhaging causes swelling and
pressure on healthy neurons. Also, injured neurons release lots of glutamate and you get
excitotoxicity. A cyst from swelling and glutamate kill myelin producing cells BELOW the
level of the injury, and soon you get demyelination and a wall of glial cells forms preventing
Whiplash often occurs at C5-C6. Just below this are motor neurons to triceps, so you tend to
be unable to extend the arm, though you may be able to flex it. Hand and finger movements
are also below C6. You can give neural prosthetics like functional electrical stimulation
(FES) under the skin that cause the hand to grip when you raise the contralateral shoulder.
The problem isn’t with the muscle, only with the innervation.
Sarcomeres are strung together as filaments, which are bundled into myofibrils, which go
into one muscle fiber. Bundles of fibers make up the fascicles of a muscle. Motor neuron
pools innervate a single muscle. Proximal and axial muscles are innervated by more medial
motor neurons, whereas distal muscles and limbs are innervated by lateral motor neurons.
A motor unit is a motor neuron and the muscle fibers it innervates. Where you need fine
control, motor units only have a few muscle fibers. For less control, you can have many.
Poliovirus invades motor neurons and kills them, so muscle fibers in the motor unit are
paralyzed. Neighboring motor neurons branch and take over these fibers, resulting in giant
In motor stroke, damage to the brain causes the loss of neurons that descend to the spinal
cord. So the discharge of motor neurons is severely reduced.
There are two kinds of motor neurons. α motor neurons go to extrafusal muscle fibers and
produce force. γ motor neurons go to intrafusal muscle fibers that contribute to the function
of the muscle spindle (measure length and changes in length of a muscle).
Muscle force depends on the rate of APs, with high frequency impulses leading to
summation (greater force) and tetanus. Muscle force also depends on muscle length. Since
force is modified by AP frequency and muscle length, you have to know limb positions and
their muscle lengths to make a well controlled movement.
To move a limb slowly, you just contract the agonist muscle. But to move it quickly, you
must forcefully activate the agonist, then stop the limb movement by quickly activating the
antagonist. The timing of this is crucial. There is normally a “3 burst” pattern typical of
rapid movement in which the agonist (induce movement), then antagonist (slow movement), then agonist (stabilize movement) muscles fire. You get an essential tremor if a cerebellar
condition causes a delayed 2 agonist burst, leading to instability after a movement.
Different types of extrafusal muscle fibers have different myosin isoforms, and include:
o Type I: “slow contracting,” lower force, slower rise time for force, little or no fatigue.
o Type IIa: “fatigue resistant,” intermediate properties.
o Type IIx: “easily fatigued,” higher force, fast rise time for force.
Muscle compositions usually reflect muscle function. Endurance athletes have more slow
muscle types and sprinters have more fast types in their quads. Strength training stresses
tendons signaling increased myosin production. You can slowly transform IIx fibers into IIa
fibers. With paralysis, type I fibers transform into type IIx. To measure muscle types you
look at how quickly and forcefully they contract.
With need for more force, you first recruit slow motor units and increase their firing rate.
Subsequently, you also recruit more motor units (type IIa and IIx, depending on how much
force you need). So basically, you recruit more motor units and increase the activity of each
one, and the ones you recruit later are faster and more forceful.
The dominant hand has more type I muscle fibers to produce smaller, more refined
The muscle’s sensory system allows measurement of muscle force and muscle length. The
Golgi tendon organ and its tendon organ afferent (type Ib) detect and relay information about
muscle force. The muscle spindle is innervated by γ motor neurons and its spindle afferents
(type Ia and II) relay info on muscle length and changes in length.
We use the muscle spindles to sense limb position. If you activate the spindle afferents in the
biceps with vibrations, you feel like the muscle is stretched and your arm is extended.
To maintain sensitivity to changes in length over a broad range, γ motor neurons control the
intrafusal muscles in parallel to the muscle spindle so that there’s always an appropriate
amount of tension on it. The spindle is sensitive to extrafusal muscle length and γ motor
Spindle afferents excite α motor neurons of the same muscle (stretch reflex). Golgi tendon
afferents go through interneurons to inhibit the same muscle and stop it if contractions get
In the stretch reflex, the sensory neuron synapses with the motor neuron and an inhibitory
Reflex loop pathways have a fast involuntary response that is mediated at the spinal cord, but
also a slower voluntary response that is processed in the brain. Even the fast response takes
around 30ms. Short latency path: spindle afferents → motor neuron. Long latency path:
spindle afferents → dorsal column nuclei → thalamus → cortical motor neuron → motor
The long latency (voluntary, cortical) response can take ~100ms, so you don’t always wait
for the stimulus. Sometimes you predict how something will be and respond accordingly. If
you expect a glass to be full and it’s not, you pick it up too forcefully.
A patient with a right brainstem stroke can have no long latency reflexes. They will have
poor joint position sensing and 2 point discrimination.
Patients with no large fiber afferents for proprioception can still move fine if they can still
see their hand. The movement of flexors and extensors is centrally programmed, so is still functional, and they’re getting visual feedback. But, if they can’t see it, they get no feedback
on where it is and their limb just drifts off course.
Lecture 2: Motor II
Actions are represented in the brain as desired trajectories of the effector, so writing with
your wrist, elbow or shoulder all look like your characteristic handwriting.
Also, when we move from one point to the next, the motion itself is quite smooth despite
complicated joint movements. So we plan a simple movement in the posterior parietal cortex
and let the motor system translate that into the necessary motions.
To write something: You decide to write in the prefrontal cortex and basal ganglia. The
posterior parietal cortex integrates somatosensory and visual info to see where the pen is and
where your hand is relative to your visual fixation point. The premotor cortex determines
where the pen is with respect to your hand, and plans the action. Cerebellum formulates the
details and dynamics of the movement. Primary motor cortex sends impulses down spinal
cord. Brainstem maintains proper posture.
Descending tracts include: corticospinal tract (from motor/somatosensory cortex),
rubrospinal tract (from red nucleus), vestibulospinal tract (from pons/medulla), pontine
reticulospinal (from pons, excitatory control of posture) and medullary reticulospinal (from
medulla, inhibitory control of posture).
o Fibers originate from primary motor (30% - area 4), premotor (30% - area 6) and
somatosensory (30% - areas 1,2,3) areas of cortex. All are excitatory, small/slow fibers.
o 90% of these fibers cross at the lower medulla, then enter the lateral corticospinal tract.
These generally control distal parts of limbs. So, most cortical areas control the
o Of the 10% of fibers that don’t cross, 8% form the ventral corticospinal tract which
innervates the axial muscles bilaterally.
o 2% of neurons stay in the ipsilateral lateral corticospinal tract.
o Stimulation of the primary motor cortex (M1) induces contraction of distal arm muscles
very effectively, with a less prominent response in proximal muscles. The response is
o Stimulation of the supplementary motor area (SMA) affects distal and proximal muscles
equally. It is much weaker, and a little slower.
o Split brain patients have no corpus callosum. The right visual field will go to the left
hemisphere, and info won’t be shared with the right hemisphere. Show someone a target
in the right visual field and it registers in the left hemisphere. They can use that
hemisphere for good control of the right arm, ok control of the proximal left arm muscles
(reach), and poor control of the left fingers (since most axons go contralateral).
o Split brain patients may have trouble making one hand follow their will, resulting in
o The left hemisphere usually houses language centers. If a split brain patient sees
something in the right visual field, he/she can describe it. If it’s in the left visual field,
info goes to the right hemisphere, and the language side of the brain has seen nothing. So when asked what they saw, they respond “nothing,” even though they can pick out the
object they’ve seen by feeling for its shape.
o You can examine the corticospinal tract by stimulating the cortex or spine and measuring
the muscle response in the extremities.
Ventromedial (Medial) brain stem pathways include the tectospinal tract (from tectum),
reticulospinal tract (from pontine and medullary reticular formations), and the vestibulospinal
tract (from lateral and medial vestibular nuclei).
o The tectospinal tract crosses the midline, descends and ends in the cervical spinal cord.
It may be involved in turning the head toward a light stimulus, though little is know about
o Reticulospinal tracts from the pons and medulla are large axons that control posture,
balance and “anti-gravity” muscles. The brain predicts postural consequences of planned
movement and acts to prevent loss of balance. So if you are going to lift something that
might tip you forward, gastrocnemius muscles will contract before you do to maintain
balance. But if you know you’re stabilized, it won’t do this, so it takes into account the
state of the body and isn’t automatically programmed.
The pontine reticulospinal tract has excitatory synapses on leg extensors and arm
flexors. It is medial to the medullary reticulospinal tract.
The medullary reticulospinal tract has inhibitory synapses for almost all limb
muscles. This medullary tract shows high activity in narcolepsy. It is lateral to
the pontine reticulospinal tract.
o The vestibulospinal tract coordinates eye and head movements to maintain gaze while the
head is rotating, as well as keeping the head upright and body vertical (with info from
The lasteral VST descends the length of the spinal cord to excite anti-gravity
muscles of the lower limbs.
The medial VST descends to cervical levels to stabilize the head as the body
The Dorsolateral (Lateral) brain stem pathway is the rubrospinal tract (from red nucleus). It
has large fibers. Input comes in from the cortex and cerebellum, and outputs cross then
descend to cervical and lumbar spinal cord. They control the distal musculature, primarily
the extensors of the arm and hand.
Lesion of the internal capsule is a common disruption of cortical input to spinal cord and
brainstem pathways. It is characterized by paralysis and the Babinski sign (extension and
fanning of toes w/ plantar reflex test) at around 12 hours. The corticospinal tract usually
inhibits the muscle contractions producing the Babinski sign, so you normally flex the toes.
With this lesion you also get spasticity in the leg extensors and arm flexors, producing
abnormally strong resistance to passive movement as a result of more active stretch reflexes.
You can recover some function after 3 weeks from reduced swelling and increased
contralateral hemisphere activity.
Lesion of the corticospinal tract produces a deficit in fine finger movements. But, animals
show some quick recovery. The rubrospinal tract which had mostly stimulated extensors
now facilitates flexion and extension of arm muscles after the lesion. During reach, this
region is stimulated, so it may have some degree of plasticity that is important for recovery.
Lesion of vestibulospinal and reticulospinal tracts produces postural deficits. Lesions of the spinal cord can compromise all descending input, resulting in areflexia
followed by spasticity.
Lecture 3: Motor III
To reach for something, you must figure out where the target is by integrating visual info
with proprioceptive info from the eye/head/neck muscles. To figure out where your hand is
relative to a visual fixation point you also you use proprioception and vision. Before you do
something, you also consider the task’s rewards and costs.
When you point to something, you don’t actually have your arm directed right at the target.
You align your finger so that your finger and the target are at the same location on the retina.
So really, the way the world is represented in your brain is based on input from your eyes.
Retinocentric receptive fields are at a specific orientation relative to the fixation point. If a
target (light) is at the receptive field, the neuron with that RF will discharge.
Combining eye position, head position and retinal input with proprioceptive joint angle
perception, you determine where you hand is relative to the fixation center. Using input from
the retinas, you determine where the target is positioned relative to the fixation point. You
then calculate how you should move to get your hand to the target.
The posterior parietal cortex integrates visual and proprioceptive information to determine
where the hand is and where the target is relative to the fixation point. Certain neurons in the
posterior parietal cortex fire only when hand and target are in a specific location relative to
the fixation point. But, their relative position to each other is determined in the premotor
Damage to the right parietal lobe makes it harder to reach left. Tests of reaching error after
parietal lobe damage suggest that the ability to reach appropriately is coded with respect to
visual fixation point and doesn’t depend on targets’ positions relative to the subject’s body.
Neurons in the posterior parietal cortex encode image location and eye/head position. Even
if a light is shined in a cell’s RF and stays in the same position relative to the fixation point,
moving the fixation point by moving one’s eyes or head changes how strongly the cell
responds. Eye/head position changes the gain on the discharge due to receptive field
changes. So depending on how the eyes and head are positioned, it just magnifies receptive
field info differently without really changing the pattern of the response.
Posterior parietal cortex neurons appear to encode an intended movement if you know what
movement to make but have a delay before you execute the action. The same neurons light
up during the delay as during the action itself. In the somatosensory cortex, there is no
proprioceptive response until you actually move, suggesting that these cells are merely
responding to the movement. So, PPC appears important for planning movement.
Even if you remove the target of an intended movement during the delay period, PPC
continue to fire as though it were still there. The target leaves a neural imprint even after it’s
gone, so the planned response can still be carried out in its absence.
Although the PPC neurons encode the target’s location, they don’t encode the force
necessary to carry it out. Activity of primary motor cortex neurons and the muscle cells
themselves do reflect the force required. PPC neurons also encode an internal value of the visual stimulus and the action that may take
place. It an animal knows a certain stimulus in a certain RF will give it a reward, the cells
with that RF will fire in response to the stimulus. But, if the animal knows the stimulus
won’t give it a reward, the same stimulus can fail to elicit a response from the neurons. This
is an example of neuroeconomics and using sensory information to makes decision based on
it. The concept of value is important regarding different stimuli.
Patients with lesions in the right hemisphere may exhibit “neglect” of the left visual space.
They’ll only respond to, copy or even register the right halves of different things they’re
Neglect of personal space (combing hair, shaving, lipstick) occurs with right parietal cortex
lesions, whereas neglect of extrapersonal space (drawing, writing, etc) occurs with right
frontal lobe lesions.
People with neglect will point away from the neglected side when told to point straight
ahead. By using prism glasses that make them see everything as though it’s farther away
from the neglected side, upon removal you can produce a compensatory shift in focus toward
the neglected side. In a normal person this adaptation would quickly be undone, but in these
patients it helps them permanently reduce the neglect.
Damage to the right hemisphere causes neglect of the left side, because the right hemisphere
is important for visual input from the world.
Damage to the left hemisphere’s parietal cortex can cause apraxia. This is the inability to
perform skilled movements, particularly those involving the use of tools, which occurs in the
absence of elementary motor deficits (weakness, posture, muscle tone).
A theory of mind is the awareness that others have beliefs, desires and perceptions different
from our own. We can guess their goals and intentions from their actions. “Mirror neurons”
in the PPC discharge when the animal does some action, but are also excited when the animal
watches someone else do the same action. These may play a role in understanding the
intentions of others, and may be related in some way to autism.
Lecture 4: Motor IV
The primary motor cortex is at the precentral gyrus. Anterior to that medially is the
supplementary motor area, and laterally is the premotor cortex.
The PPC determines hand and target locations relative to the fixation point of vision, the
premotor cortex encodes a movement plan based on their relation to each other, and the
primary motor cortex figures out what force and which muscles must be used to carry out the
Regardless of how the arm is positioned relative to the body, premotor cortex neurons will
respond comparably if the arm and target are in the same positions relative to each other.
Similarly, the premotor cortex codes for the goal of a movement, regardless of the motor
processes necessary to carry it out. The same cells respond when a monkey tries to move a
cursor on a screen to the right when it moves the sensor with the hand supinated or pronated,
even though they require the use of totally different muscles.
In the primary motor cortex, neurons fire in relation to the forces and muscles that are being
used. So in the above test, different M1 neurons would fire with the hand in different
positions. Also, if you make a monkey resist different forces, you find different cells respond
when it has to apply force in different directions, due to using different muscles. During a reach, you first activate the premotor cortex, then the primary motor cortex, then the
muscle, then finally you see a movement.
The supplementary motor area is more active when a series of steps is memory guided,
whereas the premotor cortex is more active when a task is visually guided. The primary
motor cortex responds the same way in either case, because you’re using the same muscles.
Corticospinal neurons project to multiple spinal cord levels and contact motor pools for
multiple muscles. 1 cortical motor neuron probably goes to ~3 muscles on the arm or hand,
(more likely on lateral ventral horn neurons to the hand or fingers than medial ones to the
Stimulation of the cortex shows that there’s some sort of somatotopic map, though areas for
different parts of the body are not entirely segregated from one another and follow complex
patterns. Stimulating the motor cortex produces twitches of muscles on the contralateral
side. Stimulation of the hippocampus, in contrast, evokes memory recall.
Epilepsy monitoring of cortical activity is good to localize the source of a seizure, but it’s
also useful for observing excitatory patterns with various activities.
The motor map isn’t static. Damage to peripheral nerves can cause changes in the map. If
you cut motor nerves to a rat’s whiskers, adjacent areas of the motor cortex invade the
The mechanism for this plasticity is due to the fact that cortical neurons usually have
excitatory outputs to adjacent motor neurons and adjacent inhibitory neurons. Usually the
inhibitory neurons prevent the excitatory signal from activating nearby motor neurons.
Damage to peripheral nerves somehow reduces the efficacy of the inhibitory pathway, so
excitatory connections to adjacent regions are unmasked.
Amputation also changes the motor map. If you amputate a right arm at the wrist, you expect
to see effects in the contralateral hemisphere. In the left hemisphere, you see that stimulation
of what used to be “wrist” areas now send excitatory signals to adjacent bicep regions. So
effectively, the “biceps” area of the cortex has expanded.
With amputated hands, the elbow regions take over the hand’s motor areas. But if you graft
hands back on, elbow and hand innervations return to their normal locations.
Patients with phantom limb pain have an expanded motor area on the side contralateral to the
amputation. So hand amputees with phantom limb pain often have a disproportionately large
biceps motor area.
A stroke can cause loss of some motor cells controlling the digits, for example. But, this
often leads to less use of the digits that causes other digital motor areas to disappear as well.
If you’re forced to use the affected digits, you recruit more areas for them. Since a lack of
use seems to make the problem worse, constrained motion rehab is sometimes employed. In
this, the unaffected arm is restrained for 8 hours a day for 12 days, and the benefits for the
affected arm are long lasting.
There is also some motor cortex plasticity that comes with training. After training to do a
task that requires fine finger movements (move stuff to/from a small well), a monkey shows
expanded motor areas for its fingers, and the efficiency at this task increases over time. With
an easy task, you don’t get a change in the motor cortex of efficiency over time. This
plasticity is much better at youth.
Lecture 5: Vestibular System Vestibular receptors provide info on head orientation and motion, and it’s been highly
evolutionarily conserved. The receptors are in the labyrinth of each inner ear, and they send
afferents to secondary neurons in the vestibular nuclei of the brainstem. These project to
centers controlling eye, neck and trunk movements.
Vestibular receptors include 3 semicircular canals that detect angular acceleration and 2
otolith organs (utricle and saccule) that respond to linear acceleration and orientation. The
vestibular nerve, which gets input from these receptors, has a superior subdivision (utricle,
horizontal and superior semicircular canals) and inferior division (saccule and posterior
semicircular canals). Each subdivision has a ganglia of Scarpa.
Head movements control the vestibulocollic (neck, VCR) and vestibulo-ocular (eyes, VOR)
reflexes, which stabilize the head and eyes during movement. VOR maintains an image on
the fovea during head movement. It is very accurate in normal function.
There is a membranous canal within a bony canal. The membranous canal is filled with
endolymph (high K, low Na), and the space between the bone and membrane is filled with
perilymph (low K, high Na). Each canal has an ampulla with sensory hair cells, and within
the ampulla is a cupula with ciliated receptors.
With head movement, inertia-driven motion of the endolymph in the semicircular canals
causes deflection of the cupula, which moves the stereocilia. If they move toward the
kinocilium, hair cells release transmitter and discharge afferent nerve fibers. If they move
away from the kinocilium, they release less transmitter and nerves fire less. Afferent nerves
have a resting discharge rate, which may be increased or decreased.
L and R horizontal canals are in the same plane. L anterior and R posterior semicircular
canals are in the same plane, as are L posterior and R anterior. Movement that leads to
excitation in one of these co-planar pairs will lead to inhibition in the other.
The basic vestibulo-ocular reflex is a three-neuron arc. The sensory afferents go from the
inner ear to the vestibular nuclei in the brainstem. They synapse with second order neurons
that project to extraocular muscle motor nuclei (abducens, trochlear, occulomotor). These
second order neurons go to some motor nuclei ipsilaterally and some contralaterally to
coordinate the reflex. So if you move the ipsilateral medial rectus (occulomotor nucleus
innervated via tract of Deiters), you will also want that neuron to innervate the contralateral
lateral rectus (abducens nucleus) so that both eyes move in the same direction. Inhibitory
connections decrease activity in the antagonist muscles. VOR is very fast and accurate.
VOR is modifiable, so can be calibrated to specific situations and contexts. When you wear
bifocals with miniaturizing portions and magnifying portions, the VOR must respond
differently in those regions. This is regulated by motion of images on the retina (retinal slip),
which creates blurring called oscillopsia. Retinal slip is a cue for adaptation of the VOR, and
the vestibulocerebellum (flocculus and paraflocculus) plays an important role in carrying out
Ewald’s laws: Semicircular canals are sense eye and head movements in the same plane as
the canal. Stimuli that result in excitation of receptors or afferents are responsible for
producing the larger eye and head movements.
Horizontal canals move the eyes medial/lateral, whereas superior and posterior canals move
the eyes up/down with an additional rotation around the visual axis.
Each otolith organ (utricle/saccule) has a region with sensory epithelium called the macula.
The macula’s hair cells have cilia that project into a gelatinous mass with CaCO c3ystals
called otoconia. With linear acceleration, inertia leads to shearing force on the stereocilia. As with the semicircular canals, these cilia moving toward the kinocilium produces an
excitatory output, and movement away from the kinocilium produces an inhibitory output.
Whereas hair cells in the ampulla of each semicircular canal are oriented in the same
direction, some hair cells in each otolith organ are oriented in opposite directions from one
another. So, with a given linear acceleration, some hair cells are excited and others inhibited.
Vertigo is the illusion of motion when none is present, usually a result of vestibular disorder.
Oscillopsia is a visualized motion of objects known to be stationary, and if this is induced by
head movement it is often indicative of vestibular dysfunction. If VOR doesn’t compensate
for head movement, the images move on the retina resulting in oscillopsia.
Nystagmus is a rapid beating of the eyes with slow and fast components. The slow
component results from imbalance in the vestibular signals from the two labyrinths. Since
movement inhibits semicircular canals on one side and inhibits them on the other, any
imbalance in signaling will be interpreted as movement, even if the head is still. This
“movement” will evoke a VOR. The eye will drift slowly toward the side with decreased
signaling, then quickly reset. If, as in this case, it occurs with no head movement or external
stimulus, it’s termed spontaneous nystagmus.
Three cardinal features of spontaneous nystagmus: It is horizontal/torsional with fast
components moving toward the labyrinth with greater activity. It is more rapid with the
patient looks in the directio