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309 Cards in this Set
- Front
- Back
3 levels of control for motor systems
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-cerebral cortex
-brainstem -spinal cord (ventral horn grey matter) |
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Subcortical structures the modulate motor systems
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-basal ganglia (caudate nucleus, putamen, etc)
-cerebellum (motor learning) |
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thalamus and motor info
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-relay system for info from
basal ganglia--> cortex and cerebellum--> cortex |
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spinal cord role in motor systems
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- execute movement
-bottom of hierarchy -motor neurons and interneurons |
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lower motor neurons
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-in ventral horn, project to muscles and ultimately cause muscle contraction
-somatotopics: medial=proximal mm; laterla= distal mm |
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Interneurons from spinal cord
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-in intermediate zone btw dorsal and ventral horns
-segmental (project within a level) and propriospinal (project between levels to motor neurons) -form circuits that help connect and coordinate motor neurons that contract groups of muscles for specific tasks |
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brainstem role in motor systems
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- modulates the action of spinal motor circuits
- motor nuclei with motor neurons that directly innerv facial mm -groups on neurons that project down and terminate on neurons in spinal cord grey matter -- upper motor neurons --> medial and lateral descending brainstem pathways |
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medial brainstem pathways
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-reticulospinal, vestibulospinal, tectospinal tracts
-descend in medial ventral white matter and terminate in ventromedial area of ventral spinal cord -axial, proximal mm for basic postural control |
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lateral brainstem pathways
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-rubrospinal tract
-descends in dorsolateral white matter and temrinates in dorsolateral area of the ventral horn -distal muscles of limbs for goal-directed limb movements like reaching and manipulating |
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cerebral cortex and motor systems
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-modulates action of motor neurons in the brainstem and spinal cord
-top of hierarchy -gives ability to organize complex motor acts -primary motor cortex, premotor cortex, supplementary motor area -also primary somatosensory cortex and posterior parietal cortex |
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primary motor cortex
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-executes commands to motor neurons-- command center
-coordinates force and direction -somatotopic map -contralateral |
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premotor cortex
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-integrates motor movements with sensory input (mainly from visual system)
-coordinates complex sequences of movement (motor learning) |
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Supplemental motor area
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-internally-driven, will-driven movements
-planning -will have an increase in blood flow just thinking about performing a complex action |
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primary somatosensory cortex (SI)
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-regulates incoming sensory info in the dorsal horn
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posterior parietal cortex
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-helps localize where an object is with respect to body
(helps motor system reach in correct direction for an object) |
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Cerebral cortex acts on motor neurons via:
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-two descending pathways
-lateral corticospinal -ventral corticospinal |
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lateral corticospinal tract
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-descending pathway from cortex to contralateral limb/digits
-goal-directed reaching |
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ventral corticospinal tract
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-descending pathways from cortex to neck/trunk muscles
-postural control |
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hierarchy of motor systems
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-cortex--> brainstem--> spinal cord--> muscle movement
-lower structures=more simple tasks like reflexes -cognitive motor= slow, but more options |
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parallel motor systems
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-motor pathway between cortex and spinal cord
-motor pathways between cortex-brainstem-spinal cord -if one is lesioned, other can partially compensate -redundancy gives flexibility and plasticity |
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3 general types of movements
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-reflex
-automatic postural adjustments -voluntary movements |
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Reflex movement
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-simple, involuntary coordinated patterns of muscle contract and relax d/t peripheral stimuli
-spinal cord, motor neurons, sensory neurons, brainstem neurons sometimes |
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Automatic postural adjustments
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-more complex and flexible than reflexes
-involve brainstem, spinal cord, motor neurons -posture info to vestibular system--> descending pathways from brainstem to spinal cord make compensatory shifts -contextual controlled |
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voluntary movements
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-goal-directed
-cerebral cortex, brainstem, spinal cord, motor neurons -most complex and flexible -improve with practice -much longer response time |
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skeletal muscle
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-execute vol movement, maintain posture, produce heat and metabolic energy
-parallel bundles of fascicles- fascicles made of fibers |
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Motor unit
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-one motor neuron and all of the muscle fibers it innervates
-smallest functional element of the motor system -provides smallest increment of tension that can be generated |
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alpha and gamma motor neurons
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-alpha: extrafusal muscle fibers
-gamma: muscle spindles |
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motor units in normal muscle
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-motor neuron innervates many muscle fibers in DIFF fascicles within one muscle
-efficiently activate entire muscle -recruit more units as more force is needed to create smooth movement |
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what does the CNS recognize with regards to muscle
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-motor units-- uses them as increments of force generation to produce smooth, fluid, energy-efficient movement
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Motor unit innervating many muscle fibers within ONE fascicle
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-indicates pathology where deinnervation-reinnervation occurred
-produces jerky movements that are too powerful for force needed |
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Electromyogram
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-record motor unit action potentials while patient contracts muscles
-a large single motor unit can mean denervation-reinnervation |
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neuropathic disorders on EMG
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-fasciculations
-denervation causes adjacent neurons to sprout and innervate larger area--> larger motor units -large EMG -reduced interference pattern because of reduced total number of motor units |
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Motor neuron organization
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-in vertical columns called motor nucleus
-motor neurons innervating same muscle are found in same motor nucleus -1 muscle can be innervated by many motor neurons in one nucleus |
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medial motor nuclei
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-axial muscles of neck, back
-connect across many segments by propriospinal neurons (long axons, branch extensively) |
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lateral motor nuclei
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-limb muscles
-most medial innerv proximal limb muscles -most lateral innerv distal limb mm -connected across few segments by propriospinal neurons (short axons, less branching) |
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flexors and extensors
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-flexors closer to center of spinal cord
-extensors are more peripheral |
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upper motor neurons
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-neurons that originate in brainstem and motor cortex
-descend and synapse on lower motor neurons to convey descending control of movement -"premotor" neurons |
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upper motor lesions
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-weakness
-no atrophy -no fasciculations -increased reflexes and tone |
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lower motor lesions
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-weakness
-atrophy -fasciculations -decreased relfexes and tone |
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slow-twitch motor units
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-innerv red, slow, type 1 fibers
-smaller fibers, small MN, slow contraction -oxidative metabolism: use glucose and O2 via mitoch and myoglobin -small tension for long duration without fatigue |
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fast fatigable motor units
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-innerv white, fast type IIb fibers
-large fibers, large MNs -fast, large contraction -anaerobic catabolism from glycogen stores-- lactic acid -specialized for speed and strength |
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fast fatigue-resistant motor units
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-innerv intermed IIa fibers
-combines fast twitch with enough aerobic capacity to resist fatigue for several minutes -exercise with endurance |
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ultimate force exerted depends on:
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-rate of firing (freq of APs in a single MN)
-recruitment (number of motor units firing) -size principle |
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Size principle
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-smallest motor units fire first (low threshold for firing)
-largest motor units fire last (high threshold for firing) |
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Motor unit recruitment order
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-smallest-->largest
-small force: slow twitch fibers recruited -more force: fast fatigue-resist units recruited -max force: fast fatigable units -fibers stop firing in reverse order |
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advantages of size principle
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-allows a smooth increase in force output by muscle
-minimizes fatigue -keeps power in reserve until needed -allow appropriate recruitment of fibers for job |
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general components of a reflex
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-sense status of muscle via spindles and golgi tendon organs
-cause an effect via efferent motor neurons -sometimes modify info via interneurons and descending neurons |
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muscle spindle
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-parallel to extrafusal fibers
-sense muscle LENGTH -key for proprioception -discharge best when muscle is stretched -silent when muscle shortens -composed of intrafusal fibers |
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types of intrafusal fibers
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-dynamic nuclear bag fibers: sense change in length
-static nuclear bag fibers and nuclear chain fibers: sense steady response over time |
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Ia afferents
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-innervate all 3 types of intrafusal fibers
-sense muscle length and rate of change of length -convey fast, phasic, dynamic response of muscle fibers -velocity of stretch, very sensitive to small changes |
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II afferent (spindle)
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-innervate static bag and nuclear chain fibers
-sense muscle length, not rate -convey slow, tonic, static responses -code duration of stretch |
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when intrafusal fibers are stretched....
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-sensory endings are stretched and increase firing rate
(when fibers are not stretched, sensory endings stop firing) |
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why do we need dynamic and static intrafusal fibers in the muscle spindle
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-need to know angle of joint
-dynamic sense when muscle is changing and static fibers sense when muscle has stabilized at a new length -both are sensitive to small changes -CNS uses muscle spindles to sense and correctly change position of body segments |
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golgi tendon organ
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-@ jx btw extrafusal muscle fibers and tendon
-sense muscle TENSION -innervated by a single Ib afferent neuron which branches and intertwines with collagen fibers |
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golgi tendon organ and muscle contraction
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-stretches tendon--> straightens collagen--> compress nerve endings--> AP firing
-very sensitive -precisely measures force in contracting muscle |
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why do we need golgi tendon organs
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-continuously measure tension from force in a contracting muscle
-gives NS precise info about state of contraction -protects muscle from too much muscle tension |
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gamma motor neurons
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-dynamic: innervate dynamic nuclear bag fibers
-static: innervate static nuclear bag and nuclear chain fibers -activation causes shortening of intrafusal fibers, stretches central region of intrafusal fibers, increases firing of afferent fibers |
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role of gamma motor neurons
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-adjust dynamic and static sensitivity of muscle spindle and their afferents
-keep spindles sensitive |
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alpha-gamma co-activation
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-both are activated during voluntary movement
-maintains spindle sensitivity -automatically maintains muscle spindle sensitivity over all muscle lengths |
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Monosynaptic excitatory reflex (deep tendon reflex)
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-stim= stretch of muscle increases its length--> activation of spindles
-afferent= Ia from spindle -spinal cord=Ia to alpha MNs that control same muscle and project to/excite synergistic mm -efferent= alpha MNs fire and cause contraction of homoymous and synergistic mm |
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why do we need the monosynaptic reflex
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-maintain muscle tone for posture
-allows us to hold still -smooths out movements -increases efficiency for locomotion |
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Flexion and crossed extension reflex (Flexor Reflex)
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-role= withdrawal from painful stimulus; polysynaptic
-stim=activation of Ad nociceptors -spinal cord=nociceptors excite ipsi flexors and inhibit extensors; interneurons cross cord and excite contra extensors and inhibit flexors |
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Golgi tendon reflex
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-inhibits alpha MN via inhibitory interneuron
-stim= tensions on Golgi tendon activates Ib inhib interneuron--> inhibits original muscle that was stretched = autogenic inhibition -adjust forces (ie picking up a delicate object wo/crushing it) and prevents overly forceful movements |
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Inhibitory interneurons modulating spinal reflexes
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-help coordinate reflex actions
-mediate reciprocal innervation -receive many convergent inputs from muscle afferents and descending pathways |
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inhibitory interneurons in stretch reflex
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-Ia interneurons inhibit antagonist muscles
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inhibitory interneurons in golgi tendon reflex
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-Ib interneurons receive input from Golgi tendon organs, muscle spindles, joint, and cutaneous receptors and descending pathways
-inhibit agonist muscles |
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descending control modulating spinal reflexes
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-regulate the strength of reflex by changing the tonic level of activity
-sites for modulation: alpha MNs, interneurons, and presynaptic terminals of afferent fibers |
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myopathic diseases
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diseases arising from intrinsic abnormalities in the skeletal muscle (ie DMD)
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neuropathy
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diseases that cause abnormalities in peripheral nerves; symptoms more pronounced distally
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neurogenic
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disease that interrupts normal innervation of muscle (dennerv or reinnerv); abnormality in muscle is secondary to abnormality in nerve; ie guillain-barre
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Duchenne's
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most common for children; xlinked recessive; usually onset at walking age
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Duchenne's clinical symptoms
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waddling or lurching; muscle wasting; lordosis; scoliosis; contractures in gastrocnemius
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Duchenne's diagnostic test
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Gowers maneuver-- push up from ground; high creatine kinase in blood before clinical symptoms
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Duchenne's cause
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lack of gene for protein dystrophin which anchors actin in cytoskel membrane to stabilize sarcolemma, allowing influx of Ca2+ and necrosis
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Duchenne's treatment
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no cure; PT, surgery, corticosteroids to slow rate of muscle degeneration
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Myasthenia gravis- autoimmune form pathophysiology
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-ab's made against nicotinic Ach RECEPTOR;
-cross links receptors and triggers internalization and degradation of receptor; -reduced junctional fold size, larger synaptic cleft |
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Myasthenia gravis net effect of reduced functional Ach receptors
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-reduced amplitude of end-plate potentials;
-APs fails to fire in some muscles; -Ach depletes with repeated firing; -muscle power is reduced |
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mysathenia gravis clinical symptoms
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-weakness and fatigue in muscles esp cranial and oropharyngeal like ptosis;
-unstable or waddling gait; -severity varies over day and day-day; -assoc with other autoimmune diseases |
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Myasthenia gravis and thymus gland
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-tumors;
-lymphocytes in thymus produce ab's against Ach receptor; -myoid cells in thymus express Ach receptors and are antigenic |
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Myasthenia gravis treatment
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-Achase inhibitors;
-corticosteroids to suppress ab production; -plasmaphoresis to remove ab's |
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disorders of lower motor neurons
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atrophy, fasciculations, decreased muscle tone, loss of tendon reflexes (weak, wasted, twitching muscles)
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disorders of upper motor neurons
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spasticity, overactive tendon reflexes, abnormal plantar extension reflex (Babinski)
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Amyotrophic lateral sclerosis
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progressive degeneration of both upper and lower MN's; hardness from proliferation of astrocytes, scarring of lateral columns of spinal cord
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pathophysiology of ALS
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-disease of corticospinal tracts;
-loss of MN's in ventral horn of spinal cord; -loss of motor nuclei in lower brainstem; -loss of Betz and pyramidal cells in layer V of cortex; -usually spares ocular muscles and bladder sphincters |
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spinal cord of ALS
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-lightened lateral and ventral corticospinal tract and ventral horn indicating loss of neuronal cell bodies
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ALS symptoms
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-Upper (spasticity, hyperreflexemia, Babinski, dysarthria- slow clumsy speech, dysphagia);
-Lower (progressive weakness, atrophy, fasciculations, cramps); -brainstem MN's (resp muscle weakness/fatigue, head droop); -pseudobulbar affect |
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ALS causes
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-unknown, could be accumulation of oxidative free radicals, 90% die within 6 years of onset
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ALS treatment
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-riluzole: blocks glutamine release to protect MN's;
-neurotrophic/GFs, antioxidants |
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Guillain-Barre
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-acute inflamm demyelinating polyneuropathy;
- often 1-2 weeks after viral infection |
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G-B pathophysiology
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-inflamm cells and ab's attack myelin sheath around peripheral nerves --> myelin breaks down --> axons damaged
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G-B symptoms
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-paresthesia, rapid onset loss of motor in legs/arms; weakness/paralysis of breathing muscles;
-loss of stretch reflex |
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G-B causes
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-unknown, may be microbial resp or GI infection, autoimmune mechanisms, inappropriate activation of immune system by virus/bact
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G-B treatment
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plasmaphoresis; most recover weeks to months and return to normal life
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Ataxia
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-lack of order
-uncoordinated movements indicating cerebellar injury |
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Cerebellum blood supply
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-Superior cerebellar a
-PICA -AICA |
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Cerebellar lobes
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-Anterior (in front of primary fissure)
-Posterior (behind primary fissure, with tonsils) -Flocconodular lobe (1 nodule part of vermis, 2 flocculi-- separated from posterior lobe by posterolateral fissure) |
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Flocculonodular lobe
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-1 nodule, 2 flocculi
-forms the vestibulocerebellum -control of equilibrium, balance, and eye movements (VOR) |
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Vermis
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-along the midline
-part of the spinocerebeelum → control of axial and proximal limb movements |
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Intermed zone of cerebellar hemisphere
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-part of spinocerebellum
-controls distal limb movement |
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Lateral zone of cerebellar hemisphere
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-part of cerebrocerebellum
-planning and initiation of movements |
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5 major cell types of cerebellum
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-Purkinje cells, granule cells, golgi cells, basket cells, stellate cells
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Purkinje cells
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-inhibitory
-major output neurons of cerebellar cortex -largest neurons in brain |
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Granule Cells
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-excitatory
-only cell type in cerebellum thats excitatory |
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Basket cells
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-inhibitory
-inhibit Purkinje cell bodies |
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Golgi cells
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-inhibitory
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Stellate cells
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-inhibitory
-inhibit Purkinje cell dendrites |
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Climbing fibers
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--one afferent fiber type in cerebellum
-from contralateral inferior olivary nucleus |
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Mossy fibers
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-one afferent fiber type in cerebellum
-from all sources except contralateral inferior olivary nucleus |
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Molecular layer of cerebellum
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-dendrites of Purkinje cells
-parallel fibers from axons of granule cells (excitatory) -climbing fibers from inf olivary nucleus (excitatory) - stellate cells (inhibit Purkinje cell dendrites) -basket cells (inhibit Purkinje cell bodies) |
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Purkinje layer of cerebellum
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-Purkinje cells- inhibitory, GABA
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Granular cell layer of cerebellum
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-Granule cells- excitatory
-Golgi cells- inhibitory (inhibit synpase btw mossy fiber input) -Mossy fiber (excitatory)- glomeruli |
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Deep cerebellar nucleus
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-Major output neurons of the cerebellum
-Excitatory |
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Where do deep cerebellar nuclei receive input from?
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-Receive collaterals from extrinsic afferents to cerebellar cortex
-receive input from the cerebellar cortex |
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Dendate nucleus
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-largest
-most lateral |
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Emboliform and Globose nuclei
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-part of interposed nuclei
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Fastigial nucleus
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most medial
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climbing fibers synaptic circuits
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- climbing fibers (excitatory) → Purkinje cells (inhibitory) → deep cerebellar nuclei
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mossy fibers synaptic circuits
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- mossy fibers (excitatory) → granule cells (excitatory) → parallel fibers (excitatory) → Purkinje cells (inhibitory) → deep cerebellar nuclei
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inhibitory interneurons
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-Basket and stellate cells in the molecular layer
-Golgi cells in the granule cell layer |
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Major cerebellar afferent: vestibular nuclei
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- vestibular nuclei → vestibulocerebellum
-from ipsilateral vestibular labyrinth and vestibular nuclei to vestibulocerebellum or flocculonodular lobe |
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Major cerebellar afferent: visual centers
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- superior colliculus and visual cortex → pons → vestibulocerebellum to control eye movements
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Inferior cerebellar peduncle (restiform body)
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-spinal cord → spinocerebellum
-dorsal spinocerebellar tract (from ipsilateral spinal cord and lower medulla) -cuneocerebellar track (from ipsilateral spinal cord and lower medulla → upper arm and neck info) -olivocerebellar tract (from CONTRAlateral inf olivary nucleus) |
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Superior cerebellar peduncle (brachium conjunctivum)
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-spinal cord → spinocerebellum
-Ventral spinocerebellar tract (from CONTRAlateral spinal cord, projects to contralateral spinocerebellum) |
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Lesion of superior cerebellar peduncle
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-double crossing results in ipsilateral effects
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Middle cerebellar peduncle (brachium pontis)
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-cortex → cerebrocerebellum
-cortico-ponto-cerebellar tract → cerebrocerebellum (from contralateral cortex, via pontine nuclei to cerebrocerebellum) |
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Monoaminergic fibers from the brainstem
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-serotoninergic fibers from raphe nuclei (along midline)
-noradrenergic fibers fro locus ceruleus |
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Major cerebellar efferent: floccuonodular lobe
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-flocc lobe → vestibular nuclei
-reciprocal connections -controls eye movements and body equil while standing or moving |
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Major cerebellar efferent: cerebellar cortex
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- cerebellar cortex → deep cerebellar nuclei → superior cerebellar peduncle
-input from neck and trunk -vermis → fastigial nucleus → brainstem regions → medial descending systems → axial and proximal muscles -vermis → fastigial nucleus → thalamus → motor and premotor cortex -axial and proximal motor control -control ongoing execution of movement |
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Major cerebellar efferent: intermediate zones
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-input from limbs
-intermediate zones → interposed nucleus → brainstem regions (red nucleus) → laterla descending tract → distal limb muscles -intermed zones → interposed nucleus → thalamus → motor and premotor cortex → corticospinal tract → distal limb muscles -distal motor control; controls ongoing execution of movements |
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Major cerebellar efferent: lateral zones
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-lateral zones → dentate nucleus → red nucleus or directly → thalamus → motor and premotor cortex → corticospinal tract → spinal cord or corticopontine tract → back to lateral zone
-initiation, planning, timing of voluntary movements |
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General functional significance of cerebellum
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-control of balance and eye movement
-regulates movement and posture indirectly by modulating the output of major descending motor systems -compares intention with actual movement and compensates for errors -function is changed by experience- motor learning |
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Corticopontocerebellar tract
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-how cerebellum receives info about plans for movement from motor and premotor cortex
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Ventral spinocerebellar tract
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-how the cerebellum monitors the integration of descending and peripheral info regarding movement in the spinal cord
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Dorsal spinocerebellar tract
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-how the cerebellum receives feedback info from sensory periphery
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Dentatorubrothalamic tract
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-how the cerebellum projects to motor centers that send fibers to the spinal cord to adjust output of the motor system
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Cerebellar lesions
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-disruption of coordinated limb and eye movements, impaired balance, reduced muscle tone
-IPSIlateral -can impair motor learning -ataxia, hypotonia, intentional tremor, dysdiadochokinesia, dysmetria, nystagmus, titubation |
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Components of basal ganglia
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-striatum (caudate nucleus and putamen)
-globus pallidus (GPi and GPe) -subthalamic nucleus -substantia nigra (SNc and SNr) -nucleus accumbens |
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Basal ganglia blood supply
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-anterior cerebral
-middle cerebral -posterior communicating |
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Basal ganglia direct pathway
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-Striatum (GABA and substance P) → inhibits Gpi and Snr (GABA) → less inhibition → thalamus → premotor and SMA
-thalamus is disinhibited (excited) = movement facilitated |
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Basal ganglia indirect pathway
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-striatum (GABA and enkephalin) → inhibits Gpe (GABA) → no inhibition of subthalamic nucleus (glutatmate) → activates Gpe, Gpi, and Snr (GABA) → inhibit thalamus → premotor and SMA
-thalamus is inhibited = movement inhibited |
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Nigrostriatal pathway
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-dopaminergic
-facilitates movement by acting on both direct and indirect pathways |
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Dopamine effect on D1 dopamine receptors
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-involved in exciting the direct pathway → facilitates movement
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Dopamine effect on D2 dopamine receptors
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-involved in inhibiting the indirect pathway → facilitates movement
|
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Acetylcholine in striatum
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-only acts within striatum
-inhibits direct pathway and excited indirect → inhibition of movement -Huntington's = Ach path destroyed so no inhibition of movement |
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Extrinsic inputs to basal ganglia come from:
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-cerebral cortex (motor, sensory, association, limbic): topographical projections, corticospinal pathway
-intralaminar nuclei of thalamus (topographic, thalamostriate pathway) -terminate in striatum |
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Extrinsic output from basal ganglia
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-arise from globus pallidus and SNr
-project to motor nuclei of thalamus or superior colliculus of midbrain (for eye movement) |
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Caudate and putamen connections within basal ganglia
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-project to globus pallidus (striatopallidal pathway)
-reciprocally connected with substantia nigra (SNc → striatum → SNr) |
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Subthalamic nucleus connections within basal ganglia
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-receives input from the motor and premotor cortices
-reciprocally connected with the globus pallidus -projects to SNr |
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Substantia nigra connections within basal ganglia
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-receives info and projects to striatum
|
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General functional significance of basal ganglia
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-regulates movement through direct and indirect connections with cerebral cortex
-forms major component of extrapyramidal motor system -involved in control of eye movements and in the memory of orientation in space -contributes to cognition -related to limbic functions |
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Basal ganglia disorders causes
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-usually a disruption of transmitter metabloism
-abnormal movements are often from release of system from inhibition |
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Symptoms of basal ganglia disorder
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-involuntary movements: tremor at rest, athetosis, chorea, ballism, dystonia
-akinesia and bradykinesia -changes in posture and muscle tone, muscular rigidity |
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Parkinson's
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-disease of basal ganglia
-degeneration of dopaminergic cells in Snc -tremor at rest, rigidity, bradykinesia |
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Huntington's
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-degeneration of cholinergic and GABAergic neurons in the striatum
-inherited, mutation in chrom 4 causing lots fo CAG repeats -chorea, athetosis, dystonia |
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Tardive dyskinesis
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-results from longterm use of antipsychotic agents that block dopamine transmission
-involuntary movement of tongue and face |
|
Hemiballismus
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-lesion of subthalamic nucleus
-uncontrollable “ball-throwing” movement -contralateral |
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Cerebellum and spinal cord
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-direct input
-no direct output |
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Basal ganglia and spinal cord
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-no input or direct output
|
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Cortex input and cerebellum vs basal ganglia
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-cerebellum: indirect input from cortex
-basal ganglia: direct input from cortex |
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Output of cerebellum/ basal ganglia
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-cerebellum: excitatory
-basal ganglia: inhibitory |
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Cerebellar lesion in general
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-ipsilateral symptoms
-ataxia, impaired balance, intentional tremor |
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Basal ganglia lesion in general
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-often contralateral symptoms, or bilateral
-too much or too little movements -tremor at rest |
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Basal ganglia general function
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-planning and execution of complex motor strategies
-amplitude and velocity of movements |
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Cerebellum general function
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-coordinates the execution of movements
-compares intended with executed |
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Cerebellum integration
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-integrates input from multiple regions of cortex, brainstem, and spinal cord
-vision, proprioception, muscle strength, muscle tone, vestibular, pressure |
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Patients with a suspected cerebellar disorder must first be examined to rule out:
|
-muscle weakness
-vestibular dysfunction -impaired proprioception |
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Appendicular ataxia
|
-agonist/antagonist muscles aren't coordinated
-movements are jerky, irregular, not smooth -affected extremity is IPSIlateral to cerebellar lesion |
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Dysdiadochokinesia
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-pt is asked to rapidly alternate one hand between supination and pronation
-pts with cerebellar disorder will be clumsy with the hand that is IPSIlateral to the lesion |
|
Titubation
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-patients are unable to sit upright
-unable to coordinate agonist/antagonist muscles of trunk to maintain an upright posture -irregular, jerky movements of head and thorax -localizes lesion to vermis/flocculonodular lobe (midline lesion) |
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Suppression of VOR
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-VOR is normally suppressed by vermis when you are watching a moving object so you can continue to fixate on it
|
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Impaired suppression of VOR
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-midline cerebellar lesions
-can't suppress VOR → unable to fixate on a moving object without it becoming blurred from intermittent triggering of the VOR |
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Gait imbalance
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-patients have wobbly and erratic gaits due to combinations of leg ataxia and impaired suppression of VOR
|
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Scanning dysarthria
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-Patients asked to repeat multi-syllable words
-Cerebellar dysfunction will mean clipped words, slight hesitations between each syllable |
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Examples of cerebellar disorders
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-tumors (ie hemangioblastoma)
-ischemic stroke (ie embolism to PICA) -hemorrhage (ie secondary to arterio-venous malformation) -infectino (ie abscess) -atrophy (ie alcoholic or idiopathic) |
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Pt with ischemic stroke, ataxia of R upper extremity and R lower extremity, cannot suppress VOR when object moves from R to L, what was damaged?
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-R lateral cerebellar hemisphere and L vermis
|
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R cerebellar injury, can't watch vehicles moving in which direction?
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Left to Right
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Lesion in basal ganglia direct pathway
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Hypokinesis (no thalamus stimulation)
|
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Lesion in basal ganglia indirect pathway
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Hyperkinesis (no thalamus inhibition)
|
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Gross pathological changes seen in Huntington's
|
-caudate and putamen atrophied
-very large ventricles (butterfly shaped instead of boomerang) -indirect pathway problems → hyperkinetic |
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Events in lesion in indirect pathway
|
dec GABA from striatum → more active Gpe → inc GABA from Gpe → inhibits STN → less glutamate release by STN → inhibits Gpi → no GABA release from Gpi → thalamus is not inhibited → hyperkinesis
|
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Huntington's disease characteristics
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-progressive
-invol movements, chorea, athetosis -memory loss and cognitive dysfunction -psychiatric disturbances -autosomal dominant |
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Parkinson's clinical triad
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-Tremor at rest (resolves with kinesis)
-rigidity -bradykinesis |
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Parkinson's characteristics and treatment
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- loss of dopaminergic neurons in the Snc
-treated with dopamine-replacing medications to improve bradykinesia |
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What kind of surgery can be performed for bradykinesia and rigidity?
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-Pallidotomy: Create lesion to indirect pathway by burning globus pallidus
or -Deep brain stimulation: inhibits STN, facilitates movement |
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What kind of surgery can be performed for severe tremor?
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-Thalamotomy
-Create lesion on thalamus to dampen excessive movement |
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Motor circuits in spinal cord are regulated by input from:
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-primary motor cortex
-prefrontal cortex -somatosensory and parietal assoc cortex -basal ganglia -cerebellum -thalamus -brainstem |
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Lateral motor pathways
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-goal directed limb movement
-lateral corticospinal tract -rubrospinal tract |
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Medial motor pathways
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-posture, head and neck movement, eye movement
-Ant. corticospinal tract -Lat vestibulospinal tract -Med vestibulospinal tract -corticotectal and tectospinal tract -reticulospinal tract |
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Somatotopy of primary motor cortex
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-feet-legs-hip-trunk-arm-hand-forehead-chin-tongue
-disproportionally large representation for hand for fine motor movements |
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Corticospinal tract main characteristics
|
-primary motor cortex connects to alpha LMNs
-innervate particular muscle for voluntary control of distal extremities -allows for skilled movements -excites flexors -inhibits extensors |
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CST axons arise from...
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-primary motor cortex
-Betz cells -premotor cortex and supplementary motor cortex -parietal lobe |
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CST axons pass through...
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-corona radiata
-post limb of internal capsule -middle of cerebral peduncle (crus cerebri) -medullary pyramids |
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Where do 90% of CST fibers descend-- Lateral CST?
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-in pyramidal decussation and descend in lateral funiculus to all sp cd levels
|
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Where do 10% of CST fibers descend-- Medial CST?
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-do NOT decussate in pyramids
-descend in anterior funiculus -decussate in ventral white commissure to thoracic spinal cord |
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What do lesions to CST above pyramidal decussation result in?
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- CONTRAlateral weakness
|
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What do CST lesions BELOW the pyramidal decussation result in?
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IPSIlateral weakness
|
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CST lesion in cortex
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-contralateral paresis of a particular part of body corresponding to area of cortical damage
|
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CST lesion in the posterior limb of internal capsule
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-contralateral hemiplegia
|
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CST lesion in the cerebral peduncle (crus cerebri)
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-Weber Syndrome (occlusion of PCA)
-contralateral paralysis of lower face, tongue, arm, leg -ipsilateral CN III damage (eye deviates laterally, ptosis, pupil dilated and fixed) |
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Possible cause of Weber syndrome
|
-occlusion of PCA
|
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CST lesion in medullary pyramid
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-medial medullary syndrome (occlusion of ant spinal or vertebral aa)
-contralateral hemiparesis, sparing face -ipsilateral CN XII lesion (paralysis and atrophy of tongue) -medial lemniscus injury (contralateral loss of touch, vibration, proprioception) |
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CST lesion in spinal cord
|
-ipsilateral spastic paralysis
-ipsilateral Babinski sign |
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Rubrospinal tract function
|
-cerebral cortex and cerebellum indirectly influence motor activity in the spinal cord
-excites motor neurons innervating distal flexors in upper limb |
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Red nucleus
|
-locates in tegmentum of midbrain at sup colliculus
-receives input from cortex and cerebellar nuclei |
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Where does rubrospinal tract decussate and descend?
|
-decussates in ventral tegmentum
-descends in lateral brainstem and lateral funiculus (intermingles with corticospinal tract) |
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Where does the rubrospinal tract project to and terminate?
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-projects to spinal cord and brainstem nuclei
-terminates directly and indirectly on alpha-LMNs and gamma-LMNs |
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Decorticate Posturing/rigidity
|
-injury to cerebral cortex or internal capsule
-upper limbs flexed at elbow, lower limbs extended -no cortical input to red nucleus -do have cerebellar input to red nuc and rubrospinal tract |
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Benedikt's syndrome
|
-unilateral lesion of red nucleus
-CN III injury (ipsilateral occulomotor injury) -contralateral tremor |
|
T1-weighted MRI
|
-shows anatomical resolution highest
-good grey/white matter differentiation -not as good at showing some types of pathology -called SPGR also |
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Fluid Attenuated Inversion Recovery (FLAIR) image
|
-multiparameter imaging
-highlights tumors better -also show edema -less defined grey/white matter |
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Threshold FLAIR + SPGR
|
-allows detailed anatomy from SPGR and better image of tumor from FLAIR overlayed
|
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Functional MRI
|
-highly localized changes in blood flow and oxygenation that are driven by changes in the net neural activity due to a sensory, motor, or cognitive event
|
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Blood Oxygenation Level Dependent (BOLD) mech for fMRI
|
-neural activty--> local vasodilation --> highly oxygenated Hb
-water protons within blood are induced to emit radio freq that are high when the local magnetic field created by the scanner is undisturbed but are low when the local field is disrupted by presence of highly oxygenated Hb -thus, neural activity --> increased blood flow--> removes poorly oxyg Hb --> allows protons to emit strong signal |
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Caveats to BOLD fMRI
|
-how neural activity triggers the blood flow change is not fully understood
-fMRI signals are slow compared to neural events |
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fMRI mapping of the visual field
|
-visual stim consisting of flickering, checkered annulus slowly expands
-colors identify locations in the visual field not the amplitude of the fMRI response |
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MRI and "no-fly zone"
|
-grey and white matter structures within 5-10 mm of a resection site are likely to be at risk for damage caused by the surgery
|
|
Therapeutic brain stimulation
|
-use 3D CT scans to show a set of 6 surface markers to guide surgeon
-use fMRI to identify optimal location for stimulating electrode placement |
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Intra-op guidance
|
-can track location of surgical instruments relative to images of brain
|
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Shapes radiation treatment
|
-shaping of radiation to maximally impact tumor while minimizing dosage to eloquent cortex nearby
|
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Lateral vestibulospinal tract
|
-maintain upright posture and balance
-excites neurons for extensors (antigravity) mainly of lower limb |
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Lateral vestibulopsinal tract path
|
Lateral vestib nucleus --> ipsilateral projection to all levels of spinal cord, synapsing on more medial part of ventral horn --> alpha and gamme LMNs that innervate extensors of trunk and limbs
|
|
Modifying lateral vestibulopsinal tract
|
-input form cerebellum (floccular and nodular lobes)
-sensory receptors in utricle, saccule, semicircular canals via CN VIII |
|
Lesion of vestibular nerve or vestibular nuclei
|
-stumbling or falling toward side of lesion
|
|
Causes of lateral medullary syndrome of Wallenberg
|
-vertebral artery or PICA occlusion
|
|
Lateral medullary syndrome of Wallenberg
|
-IPSI: dysphagia, dysarthria (nucleus ambiguus CN XI and X), loss of pain and temp from face (spinal tract of V), vertigo, nasea, nystagmus (vestib nuc)
-CONTRA: loss of pain and temp from body (anterolateral system) key: checkerboard loss of pain temp (ipsi face/ contra body) |
|
Medial vestibulospinal tract functions
|
-adjusts head position in response to posture changes
-coordinates eye movements with each other -VOR |
|
medial vestibulospinal tract path
|
medial vestibular nuc --> axons project bilaterally --> ventral horn of cervical spinal cord and LMNs assoc with spinal accessory nerve --> axonds descend in MLF to inhibit alpha and gamma LMNs controlling neck and axial mm
|
|
Modulating medial vestibulopsinal tract
|
-sensory info to medial vestib nuclei modulates pathway to adjust head in response to posture changes
|
|
Superiorly projecting axons from medial vestibular nuclei
|
-in MLF to nuclei of CNs III, IV, VI
-coordinates eye movement with each other and VOR |
|
Internuclear opthalmoplegia (INO)
|
-lesion in MLF
-side of lesion: eyes can't adduct -contralat: eye has nystagmus -from interruption of input to medial rectus btw abducen nuclei and contra occulomotor nuc -often from MS, pontine infarcts, tumor, trauma |
|
VOR afferent and efferents
|
-afferent: neck proprioception and CN VIII
-efferent: MVST projects to abducens nuclei and via MLF to occulomotor nucleus |
|
Lesion of R CN VI
|
eye deviates medially (no lateral rectus)
|
|
lesion of R CN III
|
eye deviates laterally (no medial rectus)
|
|
Lesion of R abducens nucleus
|
-lose R lateral rectus
-lose info along MLF to contralateral occulomotor nuc -thus, can't turn eyes to R |
|
Corticotectal tract
|
-fibers arise in retina, visual cortex and inf parietal lobe
-project to superior colliculus -facilitate reflexive turning of eye and head |
|
Tectospinal tract
|
-fibers arise in sup colliculus
-decussate in dorsal tegmentum -terminate in contralateral cervical spinal cord (CN XI nuc= SCM) -facilitate reflexive head and eye movements and upward gaze |
|
Parinaud's syndrome/ dorsal midbrain syndrome/ Collicular syndrome
|
-lesion in sup colliculi or posterior commissure = eye abnormalities
-impaired vertical gaze -large, irreg pupils -eyelid abnormalities -convergence- retraction nystagmus -from pineal gland tumors or hydrocephalus |
|
Reticular formation
|
-scattered groups of neuron cell bodies and fibers that extend throughout interior of brainstem
-input from widespread areas of cerebral cortex |
|
Reticulospinal tracts (lateral/medullary and medial/pontine)
|
-help maintain upright posture by influencing voluntary and reflexive movements
-inhibit (LRST) or excite (MRST) motor neurons innervating axial muscles -convery autonomic info |
|
Lateral (medullary) reticuospinal tract
|
-axons descend bilaterally through lat funiculus
-suppresses extensors--> mellow -ascending fibers project to intralaminar and thalamic nuclei for arousal/sleep |
|
Medial (pontine) reticulospinal tract
|
-axons descend ipsilaterally in ant funiculus to all spinal cord levels
-excite axials mm and leg extensors -pumped up |
|
Decerebrate posturing/ rigidity
|
-increased muscle tone
-extension of limbs -removal of excitatory input to the inhibitory LRST --> only MRST intact--> facilitation of extensors |
|
Locked in syndrome
|
patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eye
|
|
Corticonuclear/ corticobulbar tract functions
|
controls muscles of head and face
|
|
Corticonuclear path
|
fibers from precentral gyrus --> through corona radiata, internal capsule genu, cerebral peduncle --> project bilaterally --> terminate on brainstem motor nuclei of CNs V, VII, XII, nuc ambigus (X and XI), access nuc
-VII and XII are contralateral, not bilateral |
|
Pseudobulbar palsy
|
-bilateral lesion of corticobulbar tract
-dysphagia, dysarthria, paresis of tongue, loss of emotional control, jaw jerk reflex -from brainstem infarcts, MS, ALS |
|
Corticonuclear pathway to facial nucleus
|
-upper portion receives bilateral innervation
-lower portion only receives contralateral innerv |
|
LMN lesion: Peripheral CN VII
|
-Bell's palsy
-ipsilateral face, entire half -lesion occurs after nucleus |
|
UMN lesion: central CN VII
|
-upper half still receives some cortical input
-results in CONTRAlateral lower quadrant weakness |
|
UMN corticonuclear tract lesion to XII nucleus
|
-contralateral tongue weakness
|
|
Peripheral lesion of CN XII
|
-ipsilateral tongue weakness
|
|
Midbrain CN
|
-CN III (eye movement problems)
|
|
Pons CN
|
-CN V at midpoint (chewing problems)
-bottom= CN VI, VII, VIII |
|
Medulla CN
|
-CN IX, X, XI
-difficult swallowing, drooping palate -further down: CN XII (tongue movement) |
|
Midbrain contents
|
-sup and inf colliculi
-PAG and cerebral aqueduct -red nucleus -cerebral peduncle (tegmentum, sustantia nigra, crus cerebri) -corticospinal tract -spinothalamic tract -oculomotor nucleus |
|
Pons contents
|
-4th ventricle
-corticospinal tract -medial lemniscus -spinothalamic tract -sensory and motor nuc of V -spinal nuc of V -facial nuc -abducens nuc -lateral vestibular nuc |
|
Medulla contents
|
-4th ventricle
-central canal -hypoglossal nuc -inf olivary nuc -dorsal motor nuc of X -nucleus ambiguus -vestibular nuc -spinal nuc of V -corticospinal tract -spinothalamic tract -medial lemniscus -nucleus gracilis -nucleus cuneatus -decussation of pyramids |
|
Foveation
|
-highest visual acuity
-the purpose of eye movements is to maintain it |
|
functional classes of eye movements
|
-pursuits (slow, steady)
-saccades (very fast, pizza hamburger) -vestibular -vergence (maintain focus as objects approach/recede) -optokinetic (stabilize) -fixation (maintain foveation on stationary object) |
|
Smooth pursuits
|
-follow my finger as I move it
-eyes should track with smooth, uninterrupted movements |
|
Smooth pursuit lesion
|
-ipsilateral occipital-temporal lobe
-jerky pursuits on gaze to R = R hemisphere lesion |
|
Saccades
|
-initiated by frontal eye fields in frontal lobe
-pt wants to look R--> L frontal eye field sends impulse to contra PPRF in pons --> subnucleus for CN VI for R LR muscle and subnuc for VI to activate MLF to CN III nuc for L MR muscle |
|
Hypoactive eye field
|
-ie from infarct
-eyes deviate towards affected eye field |
|
Hyperactive eye field
|
-ie from seizure
-eyes deviate away from affected eye field |
|
Eyes deviate to L, R hemiparesis, where's the lesion?
|
-L frontal eye field and L motor cortex
|
|
Eyes deviate to R and R hemiparesis, where's the lesion?
|
-damage to brainstem: L CN VI nucleus or PPRF and to L corticospinal tract
|
|
How can you determine whether the lesion involves CN VI or the PPRF?
|
-check VOR
-if intact, lesion is in PPRF -VOR: CN VIII nucleus sends signal to CN VI nucleus, bypasses PPRF |
|
If patient can look up and down, what does this indicate?
|
-CN III and IV are intact
|
|
One-and-a-half syndrome
|
-cannot gaze R at all
-R eye cannot adduct to look L -R CN VI nuc or PPRF (R eye abduction, L eye adduction) and R MLF (R eye adduction) |
|
Locked-in syndrom
|
-infarct in anterior pons
-damages corticopsinal tracts and CN VI nerves -CN III and IV (in midbrain) and reticular formation are spared -can look up and down and understand (but that's all) |
|
How many motor neurons are involved in the transmission of a nerve impulse from cortex to a muscle fiber?
|
Two:
-UMN -LMN |
|
Where does synpase btw UMN and LMN take place?
|
-ventral horn of spinal cord aka anterior horn cell
|
|
When are UMNs and LMNs firing?
|
-LMN is always firing, tonically stimulating muscle to contract
-UMN inhibits LMN, allowing muscle to relax |
|
What is the pathway for the stretch (deep tendon) reflex?
|
-afferent limb sends sensory stimulus back to integration center
-efferent limb transmits a motor command in response to sensory stimulation |
|
Why do patients with diabetic peripheral neuropathy have reduced ankle reflexes?
|
-the sensory nerve (afferent limb) is damaged
-no weakness, but don't get the sensory input |
|
What is the UMN pattern of weakness?
|
-Arms: extensors more affected, flexors=stronger --> tonically flexed at elbow, wrist, fingers
-Leg: flexors are less affected, extensors=stronger --> tonically extended at knee, ankle |
|
What are the possible localization for a LMN lesion?
|
-anterior horn cell = neuronopathy (ALS, polio, spinal musc atrophy)
-nerve root (disc herniation) -nerve plexus (brachial plexitis, Pancoast's tumor, lumbosacral plexopathy) -Peripheral nerve (carpal tunnel) -NMJ (myasthenia gravis, Lambert-Eaton, botulism) -muscle (myopathy, myositis) |
|
ACA stroke signs
|
-leg weakness more prominent
(midline of cortex where leg motor signals come from is more affected) |
|
MCA stroke signs
|
-face and arm weakness more prominent
(periphery of cortex where these motor signals come from is more affected) |
|
What distribution will the weakness be in an ACA-MCA watershed stroke
|
-arm>leg weakness
|
|
A pt suffers from R paresis of arm and leg with no other effects, diagnosis?
|
-Lacunar stroke in medulla
(if in frontal lobe, internal capsule or pons would see facial weakness as well) |
|
Testing CN I
|
-unilaterally with a commonly recognized odor
|
|
Bilateral anosmia after falling
|
-most likely shearing of nerves at cribiform plate
-could be an olfactory groove mass |
|
Pt with seizure disorder smells strange odor prior to onset, aura localizes where?
|
Piriform/periamygdaloid/entorhinal cortex (Uncus)
|
|
CN 3, 4, 5
|
-function to keep both eyes fixated on the same object
-images from each retina fused together to relay the perception of a single object |
|
Horizontal diplopia, which CN is dysfunctional
|
CN VI
|
|
Oblique diplopia, which CN is dysfunctional?
|
-CN III or IV
|
|
Headache, binocular diplopia, massive ptosis, eye deviates out, large pupil
|
CN III (down and out)
|
|
CN III supplies what and what is the main finding in a lesion?
|
-SR, MR, IR, IO, levator palpebrae, sphincter pupillae
-down and out, with ptosis |
|
Aneurysms and CN III
|
-CN III btw PCA and SCA
-will press on parasymp for pupil dilation then CN III palsy -common for post communicating artery to outpouch and compress |
|
Pupillary-sparing CN III palsy
|
-down and out, massive ptosis, no pupil dilation
-ischemia of CN III fascicles from vasa nervorum -parasymp's have diff blood supply |
|
CN V supplies
|
-facial sensation
-muscles of mastication (x buccinator= VII): BITEM |
|
How to examine masseter muscle
|
-have patient clench teeth
-feel bulge over angle of jaw -try to pry open jaw by pressing down on chin |
|
how to examine temporalis muscle
|
-have patient clench teeth
-feel bulge over temple -try to pry open jaw by pressing down on chin |
|
What muscle are you testing when you try to CLOSE a pt's open jaw?
|
-lateral pterygoid (lowers manible, opens jaw, helps move side-side)
|
|
Medial pterygoid
|
-elevates mandible
-closes jaw -helps move jaw side-side |
|
Vascular decompression surgery
|
-Janetta procedure
-fat/ teflon between affected nerve and artery to protect nerve |
|
CN VII functions
|
-facial expression mm
-dampen loud sounds (stapedius) -lacrimation -salivatoin -taste ant 2/3 tongue |
|
Testing CN VII
|
-Frontalis: wrinkle forehead
-Orbicularis oculi: close eyes tight and don't let me open them -Buccinator: pull back corners of your mouth like smiling -Platysma: wrinkle skin on neck, pull down hard on corners of mouth |
|
What features should you pay attention to when assessing facial weakness?
|
-Naso-labial fold
-palebral fissure -forehaed? -buried eyelases with eyelid closure |
|
Functions of CN IX
|
-stylopharyngeus
-pharyngeal constrictors -post 1/3 tongue taste and pharynx -somatic senationof TM, eust tube, mastoid region -carotid body -parotid gland |
|
Functions of CN X
|
-sensation of concha, dura of post fossa
-pharynx and soft palate mm -taste for epiglottis, palate, pharynx -cricothyroid muscle -sensation to larynx -all other laryngeal muscles -cardiac, pulm, esophageal, abdominal visceral plexi |
|
Glossopharygneal neuralgia can be caused by
|
compression by R internal carotid artery
|
|
PICA can compress...
|
-CN IX (neuralgia) or X (asystole)
|
|
CN XI supplies
|
SCM and trapezius
|
|
Pt tries to rotate their head against your hand on the their L cheek but you can push their head back to the R, which SCM is weak?
|
R SCM (b/c it's attached to post part of the skull)
|
|
Arm elevation about the horizontal
|
-limited by the acromion
-requires a functional trapezius to rotate scapula superiorly so that deltoid can continue working |
|
Shrugging shoulders
|
-doesn't tell you if CN XI is working properly because levator scapulae (C3-5) can elevate shoulder without a functioning trap
-must have them raise arm above horizontal |
|
Cavernous Sinus Thrombosis
|
-Chemosis/proptosis: congested opthalmic vein
-Blindness: compression of central retinal artery -deficits of CN 3, 4, V1, V2, 6 -usually secondary to mastoiditis or sinusitis |