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BIOL 2P94 (40)

lecture 2

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Dirk De Clercq

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 regrowth.  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 motor units.  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 movements.  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 neuron input.  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 too forceful.  In the stretch reflex, the sensory neuron synapses with the motor neuron and an inhibitory interneuron.  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 neuron.  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).  Corticospinal tract: 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 contralateral limbs. 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 short latency. 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 “alien hand.” 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 its function. 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 semi-circular canals).  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 moves.  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 cortex.  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 presented with.  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 action.  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 proximal arm).  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 whiskers’ region.  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 the changes.  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
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