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Neuroscience notes for Motor

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Department
Biology
Course
BIOLOGY 2D03
Professor
Laura Parker
Semester
Fall

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Neuroscience notes for Motor Quiz The Motor System: Lecture 1: Spinal Motor System I. Major components of motor system Parietal cortex: visual and proprioceptive processing gives positional info of an object relative to body (i.e. the hand) and sends this info to the motor cortex. Motor cortex: compute forces needed to cause desired motor action, which results in commands that are sent to the brainstem and spinal cord. Brainstem: tells spinal cord how to maintain balance during movement Spinal cord: Motor neurons send the commands received form the motor cortex and the brainstem to the muscles. During movement, sensory info from the limb is acquired and transmitted back to the cortex. Reflex pathways unsure stability of limb. A motor unit refers to a single motor neuron and the muscles fibers it controls. Each mature muscle fiber is innervated by only one motor neuron, although each motor neuron innervates many muscle fibers. Motor neurons innervating a single muscle are situated close to each other in the ventral horn, and are called a motor pool. In the ventral horn, there are two groups of motor pools. In the medial part of the ventral horn, the motor pools innervate axial muscles which help us stand up and maintain posture. In the lateral part, motor pools innervate limb muscles. Cerebellum: coordination of multi-joint movements, postural stability, and motor learning Basal ganglia: learning and stability of movements, initiation of movements, emotional and motivational aspects of movement II. Motor system diseases A) How spinal cord injury results in paralysis - Initial injury in small region  growth of damaged area  hemorrage of blood vessels  cyst, swelling, and cell death - Injured neurons release Glu at high levels  neuron excitotoxicity and glia apoptosis - Cyst and glu kill myelin producing cells. The death of the glial sells results in the demylination of healthy axons, making them unable to conduct impulses in a normal way. - After a few weeks, a wall of glial cells forms - Paralysis can be partially overcome with direct electrical stimulation from neural prosthetic B) Other diseases/conditions - Polio: virus kills motoneurons directly or allows them to survive as a giant motor unit with 10x as many sprouts. Post-polio syndrome includes motor unit enlargement followed by eventual muscle breakdown. Hypothesis is that eventual cell death is due to an overuse of the few remaining motor neurons during the previous decades (i.e. a kind of metabolic exhaustion that leads to an inability to regenerate new axon sprouts to replace degenerated ones). - ALS: slow degeneration of α-motorneurons in spinal cord and eventually in motor cortex - Motor stroke: spinal motoneurons not affected, but central control is weak - Rigor mortis: stiff muscles after death, no ATP available for myosin detachment III. Properties of muscle fibers and muscle movement - Extrafusal vs intrafusal fibers: extrafusal fibers attach to tendons, which in turn attach to the skeleton. They produce the force that acts on bones and other structures. Intrafusal fibers attach to the extrafusal fibers, produce a negligible force, and instead play a sensory role. They contain muscle spindles which, innervated by muscle spindle afferents, provide the CNS with info about muscle length. - There are two major types of motor neurons: αmotor neurons innervate large, extrafusal muscle fibers that generate force; γ motoneurons innervate intrafusal fibers that house the muscle’s sensory system. - There is an optimum force of contraction with respect to muscle length (i.e. not monotonic!) - Rapid limb movements follows a 3-phase pattern (agonist, antagonist, agonist) directed by descending commands - Types of muscle fibers: The exact content of the myosin molecule determines the functional characteristics of the muscle fibers. Type I slow (S): long contraction time and show little or no loss of force with repeated stimulation. S type motor units are composed of muscle fibers with small diameter, and are supplied by slow conducting, small diameter axons from small motor neurons. Type IIa fast fatigue resistant (FR); have intermediate contraction time and can maintain force longer than FF. Type IIx fast fatiguing (FF): have small contraction time and produce high twitch tension, but tend to fade quickly; composed of muscle fibers with relatively large diameter and are supplied by fast conducting, large diameter axons from large motor neurons. - Different motor units are composed of different ratios of fiber types - Muscle fiber type is a result of myosin isotype expr; the type can change; fast type is default - A muscle fiber cannot split to form a new fiber. So a muscle can become bulkier only if the individual fibers become thicker. This happens by addition of new myofibrils. The process starts when there is additional stress at the tendons. This triggers signaling proteins to activate genes that cause muscle fibers to make more contractile proteins (chiefly myosin). - Grading of muscle force is accomplished in two ways: 1) in voluntary contraction, as force requirements increase, new motor neurons are recruited. 2) as force requirements increase, the freq of activation of already recruited motor neurons increases. Motor units that are recruited later then to have faster contraction time and larger peak force. IV. Role of afferent neurons in motor control - Afferent neuron fiber types - Ia and II: wrap themselves around intrafusal fibers and are sensitive to muscle length changes; used for proprioception; Ia spindle afferent excites MTNs of agonist mm. and inhibits MTNs of antagonist mm. which provides the stretch reflex. Ia fibers, coming from the spindles, terminate in the part of the spinal cord wehre the motor neurons are. They have monosynaptic excitatory connections on α-motor neurons of the same muscle. A single Ia afferent sends afferents to nearly all of the MNs in the same muscle. They make excitatory synaptic input to inhibitory interneurons acting on alpha motor neurons of antagonistic muscles. - Ib: afferents innervate the junction between extrafusal muscle fibers and the tendon.; sensitive to force changes in the muscle; Golgi tendon organs (from which Ib fibers arise) measures force change. Group Ib fibers terminate in the regions of the spinal cord where interneurons are located. These interneurons inhibit alpha motor neurons that go to the same muclse. - γ motor neuron system controls spindle sensitivity. When the extrafusal muscle fibers shorten due to activation from a motor neuron, the intrafusal fibers can go slack. This would lead to a sudden loss of firing in the spindle afferents, resulting in a loss of information regarding muscle length. To prevent this, the CNS activates the γ-motor neurons during contraction to maintain tension in the intrafusal fibers. - Stretch reflex: short-loop response caused by Ia afferents responding to lengthening of muscle spindles. This produces AP in the afferents, which then synapses on the motor neurons of the stretched muscle, exciting these motor neurons and contracting the muscle. Long-loop response is a second pathways thru which a stretch can result in a compensating activity in motoneurons. This pathway begins with the Ia afferents, goes up the spinal cord thru the dorsal column-medial lemniscal pathway (DC-ML), reaches the thalamus, then the somatosensory and motor cortex and then comes back down to the spinal cord thru the cortico-spinal tract. Unlike the short loop, its activity is programmable by the brain: voluntarily we can change the response to a stretch (but loss of this control in Parkinson’s disease or ipsolateral stroke) - In absence of afferent input, accurate motor control depends strictly on visual input The Motor System: Lecture 2: Descending Tracts 0. Motor control is a high level action, e.g. it may involve complex joint motions but smooth trajectories. I. CORTICOSPINAL TRACT (CST) - Origin at premotor cortex, motor cortex (M1), somatosensory cortex (S1) - Axons run through pyramids (medulla) and 90% cross in lower medulla to form lateral corticospinal tract which projects to sensory neurons in the dorsal horn, interneurons in the intermediate zone and motor neurons innervating distal limb muscles. Therefore, the cortical motor areas have dominant control over the contralateral limbs. 10% remain ipsolateral mostly going to ventral corticospinal tract, which projects onto the ventromedial motor pools innervating axial muscles. This tract originates from the neck and trunk regions of the premotor and motor cortex. Unlike the lateral corticospinal tract, this tract has bilateral projections in the cord. A tiny minority of fibers do not cross and travel laterally in the spinal cord, and allows the motor cortex to have a small amount of control over the ipsilateral limb. The fibers that map to the dorsal horn originate in the somatosensory cortex (areas 1, 2, 3). The fibers that terminate in the ventral horn originate in the motor cortex and act on alpha and gamma motor neurons of distal muscles in primates. They have strong excitatory action. Corticospinal fibers have a small diameter, meaning they are slow conducting. They are probably involved in fine control. - Split-brain patients (surgical separation of corpus callosum) - Distribution of CST fibers provides good control of contralateral arm/hand, but poor control of ipsolateral and little control of ipso. hand - Language center is on left hemisphere, can only vocally identify items perceived by right side of body (thus left arm is an “alien arm”) - Conduction speed in CST increases early in life due to myelination but remains relatively constant afterwards despite growth/lengthening of pathway II. TECTOSPINAL TRACT - Origin at tectum (midbrain), crosses in caudal midbrain, terminates in cervical spine - Function unclear (don’t worry about this tract) The brain stem gives rise to the rubrospinal tract from the red nucleus, vesitulospinal tract, and pontine and medullary reticulo-spinal tracts. Two pathways project onto the spinal cord from the brain stem: A) a ventromedial pathway that includes the reticulospinal and vestibule-spinal tracts. These tracts terminate in the ventromedial part of the spinal cord and influence proximal muscles. They are important for maintaining balance and posture. Pontine reticulospinal tract excited extensor muscles of the lower limb (these muscles help us stand up). Medullary reticulospinal tract inhibits motor neurons at all levels. B) The dorsolateral pathway terminates in the dorsolateral part of the spinal cord and influences distal muscles of the limbs. It is important for moving our limbs and fingers. It is primarily composed of the rubrospinal fibers that originate in the red nucleus of the midbrain. The red nucleus is divided into two regions, a mgnocellular part (large cells, caudal end) and a parvoceullular part (small cells, rostral end). It has larger fibers than the corticospinal tract. The tract decussates near its origin and as it descends in the brain stem, it gives off collaterals to interpositus of cerebellum and vestibular nucleus. The red nucleus receives fibers from the cerebral cortex and the cerebellum. Projections are somatotopically organized. The cortico- rubrospinal system is composed of two parts: one originates from the leg and arm region of area 4 (primary motor cortex) and projects to the magnocellular part of the caudal red nucleus. The second, larger component projects from areas 4 and 6 to the parvocellular part of the rostral red nucleus, which in turn connects to the cerebellum thru the inferior olive in mid medulla. Outputs: Rubrospinal fibers cross completely in ventral tegmental decussation and descend to the spinal cord. In primates, its most significant projections are to the upper limbs. It is likely, though unknown, that the role of the red nucleus is important in its interaction with the cerebellum, more so than in direct spinal influence. Lesions in the red nucleus result in tremor of the arm and ataxia. III. RUBROSPINAL TRACT - Origin at red nucleus (midbrain), and receives input from cortex (M1) and cerebellum - Crosses immediately after origin, descends laterally to excite arm and hand extensors (for reaching movements) IV. RETICULOSPINAL TRACT: Function is to maintain posture. A) Pontine reticulospinal tract - Origin at pontine reticular formation (pons), and does not cross - Excites lower limb extensors and upper limb flexors (e.g. lifting) - Anticipated compensation of anti-gravity limb muscles is believed to rely on the pontine reticulospinal tract. B) Medullary reticulospinal tract (MRT) - Origin at medullary reticular formation (medulla), bilateral (both crosses and uncrossed). Descending motor tracts that originate in the medulla have an inhibitory action on the muscles. - Inhibits all upper and lower limb muscles for REM sleep - Narcolepsy (sudden, random sleep) is a defect in the MRT; it appears that high brain regions fail to properly inhibit the medulla in narcoleptics. V. VESTIBULOSPINAL TRACT: serves to regulate posture and to coordinate eye and head movements. - Origin at several vestibular nuclei (mid and lower pons and medulla) and are composed of the superior, lateral, inferior and medial nuclei. They send most of their output to the spinal cord and to the extraoccular muscles. There are two tracts: 1) Lateral VST: cerebellum input; descends down the spinal cord and excites antigravity muscles. Its function is to hold the body upright and prevent collapse. 2) Medial VST: descends only to the cervical spinal cord and functions to stabilize head when body moves, and to stabilize eyes and maintain gaze during head movments. VI. Lesions - Internal capsule: paralysis, Babinski sign, spasticity due to enlarged reflex response, some recovery of function. The symptoms are both due to a loss of corticospinal input and cortical input to the red nucleus and brain stem regions. - CST in medulla: no effect on limbs but loss of finger control, no spasticity; recovery may be mediated by rubrospinal tract. The brainstem motor centers and their descending tracts are spared. - VST/Reticulo-ST: severe postural defects, but no loss of control over arm/hand/fingers - Spinal cord: loss of descending input, areflexia (all spinal reflexes have extremely high threshold for activation) followed by spasticity (spinal stretch reflexes are hyperactive). The Motor System: Lecture 3: Posterior Patietal Cortex I. The posterior parietal cortex (PPC) determines eye-centered locations and plans movement - The receptive field of visual cortex neurons (occipital lobe) is retinocentric. A cell would have a maximum discharge at the center of the receptive field and discharge would typically decline as the image moved away from that position. The principal characteristic of a retinocentric receptive field is that the receptive field moves with the eye (i.e. the location in external space that activates a neuron will change precisely as the position of the eye changes in orbit). The receptive field does not vary with the orientation of the head or body, as long as the fixation point remains the same. - PPC neurons receive eye/head position and image location information and encode them as the gain of discharge rate and receptive field, respectively; this is all the information needed to for PPC to compute target in eye-centered coordinates. - In a delay task, PPC neurons encode target of intended movement during delay period even if the target disappears. It was found that whereas this delay period activity was present in the discharge of area 5 cells, these signals were absent among the neurons in area 2. Area 2 is one of the areas that are located rostral in the parietal love and is part of the somatosensory cortex. Activity in area 2 mostly reflected sensory feedback from the moving limb, rather than a planning-related signal, a view that is consistent with its receipt of muscle spindle signals from area 3a. Therefore, these results suggest that area PPC is involved in planning the kinematics of an intended movement, but the somatosensory cortex is not. Moreover, the presence of the cue was not necessary to sustain the delay period response. This is consistent with the idea that the neural discharge in PPC reflects something about the planning of the movement and not merely a passive response to the information that is currently available on the retina. - PPC does not encode forces needed to move to the target. PPC neurons code for movement kinematics and not dynamics. Further, PPC neurons plan for the next movement, but premotor cortex (PMd, area 6) decides whether to execute that plan or not. - The PPC also computes hand position from visual and/or proprioception input. In the PPC, proprioceptive information from the arm is aligned with visual information. The visual sight of one’s own hand is particularly meaningful, as there are PPC cells that only respond to the image of the hand in certain positions - Premotor cortex subtracts hand position from target position to determine displacement vector for hand and decides whether or not to execute the movement - In the PPC, neurons code for both location of an image on the retina and eye position. Mountcastle discovered that many cells in the PPC had activity that was both a function of the location of the stimulus and the position of the eyes in the orbit. At each new fixation point, the stimulus was always presented at the same retinocentric location (i.e. to the right and below the fixation point in the center of the receptive field). Because the monkey’s head was fixed, the animal moved its eyes to fixate the new location. Despite the fact that the stimulus’s image fell on the same patch of retina, the cell’s discharge changed. Therefore, this cell’s discharge was a function of both where the stimulus fell on the retina and where the eyes were in the orbit. - Eye position and retinal location of the image is combined as a gain field. As a fixation point changes, the discharge keeps its Gaussian shape with respect to the stimulus location of the retina. However, as the same stimulus location in retinal coordinates, discharge changed approximately linearly as a function of the fixation point. That is, discharge was scaled dependant on where the eyes were located in their orbit. - Head position and retinal location of the image is combined also as a gain field. Therefore, PPC neurons receive both eye position and head position signals. This information would be sufficient to compute where the target is located with respect to the body. Summary: target location and hand position are computed by PPC cells in terms of vectors with respect to fixation point. Proprioceptive information from the arm, head, and eyes is used to estimate hand position with respect to fixation. Proprioceptive information from the head and eyes is combines with information about retinal location of the target to estimate target position with respect to fixation. PPC neurons combine visual and proprioceptive information as a gain field. II. Effects of a lesion of the PPC - Lesion of the PPC does not affect the ability to sense the environment, but does cause agnosia (an inability to act on objects despite normal sensory processes). A particularly striking form of agnosia is neglect, which occurs in patients who suffer from a lesion to the PPC in the right hemisphere. They have deficits in perception, attention, and performing actions within the left sided visual space. Items of the left side are often ignored because, presumably, they are unable plan and carry out actions on objects on opposite side of body despite an ability to recognize an object on the left side. - Recall that individual functions in the brain are segregated, so the above should not be surprising - Rehabilitation of PPC lesion patients can be done with prism glasses, which can have a long-term effect. Due to the prism’s bending of light, the brain must recalibrate the visual sense of limb position with the proprioceptive information. The Motor System: Lecture 4: Motor Cortex I. Functions and properties of premotor cortex, motor cortex, and supplementary motor area: Neurons in the posterior parietal cortex encode target and hand position in fixation centered coordinated. In the premotor cortex, these two vectors are compared and a new vector is computer: a vector that points from the hand to the target. Finally, in the primary motor cortex, this vector is transformed into the motor commands needed to move the arm. - The premotor cortex codes object position with respect to arm, independent of fixation point and hand configuration. Neurons in the premotor cortex are sensitive to location of the target with respect to the hand and not forces. Hypothesis: If one is planning to reach for an object, cells in the ventral premotor cortex might code for where the target is located with respect to the hand, that is, the displacement vector. Importantly, if the location of the target remains invariant with respect to the location of the hand, the representation of the vector should also remain invariant. This would predict that if a monkey were to make reaching movements from different start positions of the hand, what matters is where the target is located with respect to the hand and not where the arm is located in the workspace, or where the arm is located with respect to fixation. Indeed, among nearly all the tasks related PMv cells that were found, discharge was related to the direction of the target with respect to the cursor and not affected significantly by changes in arm configuration. - Primary motor cortex is sensitive to forces needed to perform a reaching movement: Cells in PMv as a population appear to encode a movement in terms of a displacement vector with respect to the hand. Such cells are rare in M1. In M1, most cells change their discharge as the configuration of the arm is changed. Therefore, in M1 cells begin to transform the plan of movement from a displacement vector with respect to the hand to patterns of activity that are necessary for activating the muscles and moving the limb. - Some of the neurons in M1 project to the spinal cord via the corticospinal tract. - Like the somatosensory cortex, the motor cortex has a somatotopic map. - The motor map can change after amputation, a result of loss of strength of inhibitory interneurons connecting two areas in the motor cortex - Following amputation, the size of the motor region bordering amputated region enlarges; phantom limb pain (PLP) may be a result of size imbalance between the two hemispheres. Patients with PLP tend to have an imbalance in the size of the motor map between the hemispheres. - Following a lesion of a motor region, forced use of damaged region (constrained motion rehabilitation) helps restore some motor function. Rehabilitation can prevent loss of motor cortical zones outside the region of infarct: the animal in the study presented received extensive training after the infarct and it is seen that there was a prevention of the loss of hand territory adjacent to the infarct region. Functional reorganization in the undamaged motor cortex can play an important role in motor recovery by organizing itself and compensating for damaged areas. - Some primary motor cortex neurons respond to direction of muscle forces, thus primary motor cortex is responsible for determining required muscle activity to generate desired movement - Motor learning produces change in the motor map. Learning to make skilled grasping movements results in changes in the motor cortex. After training in a hard task, there was an increase in the size of the motor map associated with the digits. However, if the task was easy, there was no change. - Some cells in M1 have a discharge that correlates with forces produced by arm movements. - During a reaching movement, activity in the premotor cortex precedes activity in M1. - Supplementary motor area (SMA) is responsible for memory-guided movements whereas premotor cortex is responsible for visually-guided movements Summary of PPC, PM, and M1 1) PPC: compute hand and target position in eye centered coordinates  2) Premotor cortex: determine hand displacement trajectory  3) M1: transform desired movement to muscle activity pattern  4) Spinal cord: relay signals to muscles  5) Muscles: do the movement The Vestibular System: I. Function and properties of vestibular system - The function of the vestibular system is to sense and control motion. The vestibular receptors, located in the labyrinth of each inner ear, provide the brain with information about motion of the head and about the orientation of the head relative to gravity. - Vestibular afferents from the vestibular receptors in the bony labyrinth project to vestibular nuclei (brainstem). These secondary neurons then project to the centers responsible for control of eye, neck and trunk motion. Vestibular information is transmitted to the cortex and is used to generate a subjective measure of self-movement and of motion within the external world. - The 3 semicircular canals respond to angular acceleration and are oriented at ~ right angles with respect to each other. The otoliths (saccule and utricle) respond to linear acceleration and translational movement of the head - The vestibular nerve has superior division (to horiz., sup. semicircular canals and utricule) and inferior division (post. semicircular canal, saccule) - Information from the vestibular nerve afferents is used to control vestibular reflexes. There are two classes of vestibular reflexes: Vestibulocollic (vestibular – neck, VCR) and vestibule-ocular (vestibular – eye, VOR). The VOR is responsible for maintaining the stability of images on the fovea during head movements. - Information about angular motion of the head is encoded in the discharge rate of vestibular nerve afferent fibers innervating the semicircular canals. Each canal consists of a membranous canal within a bony canal. The membranous canal is filled with endolymph (high K, low Na) and the other vestibular space is filled with perilymph (high Na, low K), which sets up electrochemical gradient needed for signaling. - Angular motion of the head leads to inertially-driven motion of this endolymph. Each canal has an area where the hair cells are located (ampulla). Each ampulla has a region with hair cells (crista ampullaris) and a gelatinous structure that connects the hair cell region to the opposite side of the membraneous canal (capula). Motion of endolymp causes deflection of the cupula which in tern results in motion of the stereocilia towards or away from the kinocilium of the hair cells. Motion of the sterocilia towards the kinocilium results in an increase in transmitter release from the hair cell and a consequent increase in the discharge rate of the afferent nerve fiber innervating that hair cell. Conversely, motion of the stereocilia away from the kinocilium results in a decrease in transmitter release and a decrease in afferent discharge. All of the hair cells are oriented identically. - The modulation in the discharge rate of these afferent nerve fibers in response to head motion is proportional to the angular velocity of the head. The right and left horizontal canals lie in the same plane whereas the right anterior (superior) canal lies in the same plane as the left posterior canal and the left anterior canal in the same plane as the right posterior canal. These coplanar canals act as antagonists: an angular movement that leads to excitation in one will lead to inhibition in the other. II. Vestibular reflexes - Vestibulocollic (VCR) reflex stabilizes the head; vestibuloocular (VOR) reflex stabilizes the eye - The “basic” angular VOR is a three neuron arc: Vestibular nerve afferents innervating the semicircular canals carry info about angular head velocity. These afferents project to the vestibular nuclei in the brainstem (superior, lateral, medial, and descending vestibular nuclei). These second order vestibular neurons project to the extraocular motor nuclei. For horizontal motion, the axons of second order neurons cross the midline and innervate motor neurons in the contralateral abducens nucleus. There is also an ipsilateral pathway projecting in a fiber bundle known as the ascending tract of Deiters to the medial rectus subdivision of the oculomotor nucleus. These pathways allow for conjugate motion of the left and right eyes in the direction opposite to the motion of the head. There are also inhibitory connections that decrease the activation of the antagonist muscles. - Reflex pathway is a three neuron arc: vestibular nerve afferent  central vestibular neurons  extraocular neurons (III, VI)  eye muscles; cerebellum provides conscious control at level of central vestibular neurons - Reflex pathway has appropriate excitatory and inhibitory synapses to ensure proper eye coordination - The angular VOR is not hard wired but rather is highly modifiable. - VOR reflex gain is dependent on specific context (e.g. eye position, bifocal glasses) in order to prevent oscillopsia and blurred vision - Ewald’s “laws” provide principles for relating eye movements to activation of individual semicircular canals. 1) Reflex eye and head movements are in plane of affected canal 2) Larger movements are induced by excitatory stimuli rather than by inhibitory stimuli (due to larger dynamic range) III. The otolith organs respond to linear acceleration - Each otolith has a region with sensory epithelium termed the macula. Hair cells are located in the maculae and have cilia that project into a gelatinous mass with embedded calcium carbonate crystals (otoconia). Linear acceleration causes inertially-driven motion of the otoconia which results in a shear force applied to the stereocilia of the hair cells. Motion of the stereocilia towards the kinocilium results in excitation and motion of the stereocilia away from the kinocilium results in inhibition. The hair cells are oriented in opposite directions, so there are some hair cells within each otolith organ that are excited by linear acceleration in opposite directions. Most head movements for which the VOR generates compensatory eye movements involve a combination of angular and linear motion. Information about angular and translational motion is used by the central vestibular neurons to elicit an eye movement that maintains gaze stability. IV. Vestibular disorders: The symptoms and signs of vestibular dysfunction are related to the effects of pathologies on the labyrinth. - Vertigo: illusion of motion, nauseating - Oscillopsia: visualization of motion of stationary objects (e.g. in loss of VOR: When the VOR fails to produce an eye movement that compensates for a head movement, then images will move on the retina with head movements. This loss of gaze stability results in oscillopsia.). - Nystagmus: rapid beating of eyes due to imbalance of vestibular sensation. After the eye moves by about 15-20 degrees to one side, there is a rapid, resetting eye movements back towards the other side that brings the eye back close to the center of the oculomotor range. The initial eye movement is referred to as a slow compent and the rapid, resetting eye movement is the fast component. This type of nystagmus is termed spontaneous nystagmus in that it occurs without any head movement or other external event. - The slow component is directed toward weaker labyrinth and a resetting fast component is directed toward stronger labyrinth. There are three cardinal features of nystagmus due to an asymmetry between two labyrinths: 1) The naystagmus is a horizontal-torsional nystagmus with the fast components beating towards the labyrinth with greater activity. 2) It shows a dependence on eye position. It is more rapid when the patient is looking in the direction of the fast components and is diminished or extinguished when the patient is looking in the direction of the slow components. 3) It can be suppressed by visual fixation. - The caloric test provides a measure of the function of each labyrinth. The caloric test stimulates nystagmus by putting warm or cold water in ear, which causes temperature gradient across the horizontal canal which causes a gradient in density of the endolymph according to location within the canal. In the presence of gravity, there is a flow of endolymph from the more dense into the less dense regions. Endolymph will flow towards the ampulla of the horizontal canal (resulting in excitation) for warm stimuli and away for cold stimuli. Nystagmus is elicited by the caloric test. The slow component is directed opposite to the stimulated ear in the case of a warm stimulus and towards the stimulated ear in the case of a cold stimulus. Disorders of the labyrinth reflect disturbances in the underlying physiological mechanisms: - Benign paroxysmal positional vertigo: dislodged otoconia, reset by manipulation and gravity - Vestibular neuritis: sudden onset of long-lasting vertigo, affects superior vestibular nerve. Thus patients show signs of dysfunction in the horizontal and superior semicircular canals as well as the utricles. Patients may also experience oscillopsia with rapid head movements. - Meniere’s syndrome: hearing loss, ringing, aural fullness, vertigo; caused by distended endolymph spaces in the labyrinth with consequent rupture of the labyrinthine membranes. The symptoms can often be controlled with a low salt diet and diuretics. - Superior canal dehiscence syndrome: vertigo due to extra opening into superior semicircular canal; can be diagnosed with careful observation of eye nystagmus and imaging; corrected by surgically sealing hole - Bilateral vestibular hypofunction: oscillopsia symptoms; often caused by gentamicin antibiotic. The mechanism of gentamicin-induced vestibular toxicity involves gentamicin uptake within vestibular hair cells where it stays for up to 90 days. The gentamicin chelates iron and the iron-gentamicin complex causes the formation of superoxide radicals that are toxic to hair cells. Ocular Motor System The function of eye movements is to serve vision by directing gaze to an object of interest in the visual scene and the maintaining a steady image on the retina, even as the object or subject moves thru th
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