motor systems & tracts - wikispaces systems... · descends in medial longitudinal fasiculus...
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Motor Systems & Tracts
UMNs & Tracts
Vestibulospinal tracts
gaze stablility
postural stability
nuclei
pons/medulla junctionsuperior (SVNu)
inferior (IVNus, aka spinal: SPNu)
medial (MVNu)input from SEMI-CIRCULAR CANALS (angular acceleration)
gives rise to medial vestibulospinal tract (MVesSp)
lateral (LVNu)input from OTOLITH'S MACULA (linear acceleration)
gives rise to lateral vestibulospinal tract (LVesSp)
MVesSp(semi-circular input,angular accel)
descends in medial longitudinal fasiculus
stops in THORACIC segments
INHIBITS EXTENSORS of the neck/back
inhibits (medial tract) andexcites (lateral tract) EXTENSORS
LVesSp(OTOLITH input,linear accel)
LVNu doesn't go through a fasiculus, descends directly as LVesSp
goes all the way to LUMBOSACRAL region
EXCITES EXTENSORS
righting reaction: R head tilt -> right otolith stim ->LVesSp increases R extensors
Corticospinal(pyramidal)
ONLY direct descending path to alpha motor neuron pools
does voluntary and discrete skilled movements
alpha and gamma co-activation, "fractionated movements
gets info about equally from primary motor, pre-motor, sensory
primary neurons go all the way to the spinal cord level without being affected or doing any effecting
Pathway1) corona radiata
2) posterior limb of internal capsule
3) crus cerebri (lumbar segments lateral)
4) basilar pons
5) medullary pyramids
Decussation80% cross and become lateral corticospinal tract
20% stay ipsilateral, become anterior (medial) corticospinal tract(more involved in POSTURE than lateral)
also synapses on INTERNEUONS and dorsal horn (sensory) neurons/interneuons
Rubrospinal tractarises from red nucleus (paired structure in rostral midbrain)
input from deep cerebellar nuclei (interposed) and motor cortex
excitatory to FLEXORS
probably involved in distal limb muscle coordination
involved in decorticate rigiditydecorticate = too much rubrospinal (FLEXORS) in upper extremity
ALSO, decorticate = not enough lateral corticospinal -> too much extension in lower
Reticulospinal tract
reticular nuclei help mediate attention/arousal, loacted in brainstem
pontine reticular nucleusorigin of MEDIAL reticulospinal tract
stays IPSILATERAL, innervates extensors
medullary reticular nucleusorigin of LATERAL reticulospinal tract
IPSI and CONTRALATERAL inhibition of extensors
disruption can cause excessive extension in gait
innervates EXTENSORS(as does vestibulospinal)
Motor Disorders
UMN lesionsweakness without atrophy
spacticity
abnormal reflexes (babinski)
normal reflexes present as well
LMN lesionsweakness with atrophy
hyporeflexia
no spacticity
flaccid paralysis
pre v. post plexuspre = segmental (dermatomal/myotomal) pattern loss
post = mixed segment peripheral nerve pattern
Basal Ganglia
hypokinetic
secondary to loss of dopaminergic neurons in SNpc
Parkinson's
rigidity
bradykinesia (decreased spontaneous movement)
resting tremor
normally dopamine stimulates the DIRECT path and inhibits the INDIRECT path
direct path increases thalamic activity, indirect path decreases it
so loss of domapine means DIRECT path is UNDERstimulated, and INDIRECT path is OVERstimulated
so, in effect, both pathways are contributing to excessive inhibition of thalamic motor activity
postural instability
choreiform disorders
Hemiballismusdecrease in activity at STN, which normally excites GPi
jerky, involuntary movements
Huntington'sjerky, involuntary, dance-like movements
basically lose the indirect pathway, which is inhibitory
overstimulation at the thalamus because inhibitory outflow from GPi is diminished
deficiency of striatal neurons, especially striatal matrix (D2, indirect path)
Spinal cord lesions
anterior cordbilateral loss of motor, pain, temp
central cordbilateral loss of pain, temp near level of the lesion
brown-sequardhalf of cord
at level of lesion: loss of all sensory and motor
IPSILATERAL below lesion: paralysis and loss of touch & proprioception
CONTRALATERAL below lesion: loss of pain and temp
cauda equinaPNS lesion!
analgesia; areflexia; denervation atrophy; flaccid bladder
PolioLMN lesion
attacks ventral horn neurons
ALSUMN and LMN lesion
attacks ventral horn and lateral corticospinal tracts
ASIA
complete = no S4/5, anal sensation
motor levelsC5 = biceps
C6 = wrist extensors
C7 = elbow extensors
C8 = finger flexors
T1 = pinky finger abduction
L2 = hip flexors
L3 = knee extensors
L4 = ankle dorsiflexors
L5 = long toe extensors
S1 = ankle plantar flexors
if can't move biceps, motor level of injury = C4
sensory levels
C5 = lateral arm elbow and above
C6 = lateral forearm, dorsal thumb
C7 = dorsal middle finger
C8 = dorsal pinky finger
T1 = medial forearm, elbow
L2 = anterior medial thight
L3 = medial epicondyl femur
L4 = medial malleolus ankle
L5 = dorsum of foot
S1 = lateral calcaneus
S2 = popliteal fossa
ASIA A = no motor or sensory in S4-5
ASIA B = incomplete; sensory but not motor preserved below the neurological level
ASIA C = incomplete: motor funtion is preserved below the neurological level, more than half of key muscles have grade less than 3
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Cerebellum
Spinocerebellar lesionipsilateral truncal and limb ataxia
gait disturbace
scanning speech
Vestibulocerebellar lesiondistorted equillibrium
nystagmus
ataxia
falling
Cerebrocerbellar lesiondistal ataxia
intention tremor
hypotonia
delay in initiation of motor task
dysdiadochokineasia (rapid alternating)
can't estimate weight
LMNs
axons leave the CNSalpha-motor neurons
final common pathway
Motor neuron poolscranial
anatomically distinct clusters
still column-like
spinal cord,not cranial
clustered within the ventral horn (lamina IX)
somatotopylateral in cord = more distal
medial in cord = more proximal
ventral in cord = extensor
dorsal in cord = flexor
Control of LMNs Interneuronsnot contained within the motor neuron pools
excitatory interneurons
inhibitory interneurons
"gating" by interneurons can allow descending control over reflexes
help with rhythmic motion by stimulating one muscle while blocking its opposite
Renshaw cellsglycinergic inhibitory interneurons which feed back onto motor neurons, and neighboring neurons
important for localized control
Descending tractsprimary target is interneurons
also target some motor neurons directly
can influence reflexes through "gating" interneurons, or direct presynaptic inhibition
firing depends on total summation of IPSPs and EPSPsIA afferents from muscle spindles have a lot of influence (synapse on proximal dendrites)
Reflex networks
reflex = stereotyped involuntary responseactivated by specific sensory stimulus
reflex arc = sensory receptor, afferent link, integrative center, efferent link, effector
monosynaptic reflexonly the strech reflex (spindles)
receptor organs
muscle spindleIA afferents monitor rate of change of muscle
type II afferents detect static length, have different DRG neurons, involved in "slowly adapting response"
gamma motor neurons end on infrafusal fibers, keeping the spindle sensitive after changes in length
golgi tendon organ (GTO)contained in the tendon of the extrafusal muscle
IB primary afferent (70m/s) axon proprioceptor intertwined in collagen
muscle CONTRACTION causes the collagen to tighten, activating the GTO
passive stretch doesn't do much
both are proprioceptors which signal via the dorsal column and dorsal spinocerebellar tracts, in addition to the local reflex circuits
stretch reflex(spindles)
1) stretch of the spindle by filling glass that is being held
2) IA afferents project to spinal cord to directly activate biceps motor neurons
3) IA collaterals and type II afferents make excitatory connections thru interneurons to synergist muscles
4) also, IA collaterals contact inhibitory interneurons for antagonist muscles
5) gamma motor neuons tune the intrafusal fibers so that the spindle is still sensitive to further changes
lengthening reflex(GTO)
1) very forceful muscle contraction
2) IB afferents terminates on IB inhibitory interneurons
3) IB afferents also terminate on excitatory interneurons to antagonist muscle
basically, a protective reflex against excessive force
Flexion reflexdriven by pain fibers, unmylinated type C and small myelinated delta fibers
1) cutaneous nociceptors DRG cells produce polysynaptic (chains of interneurons) excitation of ipsilateral flexors (dorsal cord!), and inhibition of extensors (ventral cord!)
2) on contralateral side, extensors are stimulated and flexors are inhibited; to preserve balance
this is what happens when you step on a nail
Motor Unit
each muscle fiber receives synapses from 1 spinal motor neuron
motor neuron will contact ~100 muscle fibers
motor unit = motoneuron + all the fibers it innervates
muscle fibers of one motor unit are normally dispersed
after injury, motor units lose that dispersion and get larger
size principle: smaller motor units get recruited first
tetanuspartial/unfused: still some display of single contractions
fused: no individual contractions are evident
tentanus in general: successive action potentials produce a cumulative effect
starts happening when the frequency of APs exceeds the rate which calcium can be pumped out
Basal Ganglia & Cerebellum
Basal GangliaMacroscopic
dorsal striatumcaudate
putamen
ventral striatumnucleus accumbens
olfactory tubercle
amygdala
globus pallidus interal
globus pallidus external
subthalamic nucleus (STN)
substantia nigrapars compacta
pars reticulara
Microscopic
striatum composed of:striasomesmedium spiny neurons
express D1 receptor
GABA in association with substance P and dynorphin
matrixGABA in association with encephalin
medium spiny neurons
express D2 receptor
giant aspiny neurons, with ACh
Pathways
dopamine
from substantia nigra pars COMPACTA to the striatum
dopamine is excitatory at the D1 receptors of striasomes
dopamine is inhibitory at the D2 receptors of striatal matrix
direct pathway 1) striasome neurons are inhibitory at GPi using GABA/substance P, dynorphin
2) GPi neurons are inhibitory at thalamus with GABA
Net effect: INCREASE in thalamic activity; more striasome inhibition of GPi, less GPi inhibition of thalamus
indirect pathway 1) striatal matrix neurons are inhibitory at GPe using GABA/enkephalin
2) GPe neurons are inhibitory at STN with GABA
3) STN neurons are excitatory at GPi with glutamate
4) GPi neurons are inhibitory at thalamus with GABA
Net effect: DECREASE in thalamic activity; matrix inhibition of GPe -> less GPe inhibition of STN -> more STN excitation of GPi -> more GPi inhibition of thalamus
coordinate motor activity in parallel with the cerebellum
extrapyramidal system
modifies pyramidal through thalamus
Cerebellum
Nuclei
fastigialassociated with vestibular and spinocerebellum
postural maintenance in standing/walking
modulation of saccade and smooth pursuit
interposedmodulation of stretch reflex (distal)
associated with spinocerebellum
dentateassociated with cerebrocerebellum
fine, precise motor movements
vestibularassociated with vestibulocerebellum
static and dynamic stabilization of gaze and posture
Peduncles
SCP
incomingventral spinocerebellar tract (golgi tendon info) to vermis
outgoing fastigial to contra cerebelluminterposed to contra red nucleusdentate to contra red nucleus (loop) and VL thalamus (loop)
MCP incomingfrom contra pontine relaying nuc to neocerebellum
ICPincoming
primary vestibular afferents
vestibulocerebellar projection
olivocerebellar tract from contra olivary nuc (climbing fibers)
dorsal spinovestibular tracts from dorsal nuc of Clarke (muscle spindles)
outgoingCerebellobulbar tract to ipsi vestibular nucleus
Functional divisions
Vestibulocerebellum
Territory: nodulus and bilateral folcculi
inputsmainly vestibular nerve and vestibular nucleus (ICP)
outputs (purkinje cells)
bilateral vest nuc (ICP, SCP)
contra cerebellum (SCP)
brainstem ret formation
Associated nuclei: fastigial and vestibular
Functions: equilibrium, static and dynamic gaze stabilization, static and dynamic posture
Spinocerebellum
Territory: Vermis and intermediate hemispheres
Associated nuclei: fastigial and interposed
Functions: controls muscle tone, synergy, and stretch reflexes
inputsdorsal spinocerebellar tract from dorsal nuc of Clarke (spindles) via ICP to paravermian
ventral spinocerebellar tract from bilateral dorsal cord to bilateral spinocerebellum (golgi) via SCP
cuneocerebellar tract, merges with dorsal spinocerebellar tract
auditory, visual, vestubular and cerebral
outputs(purkinje cells)
vermis to fastigial to lateral vest nuc to contralateral VL thalamus and brainstem ret formation
paravermian to interposed nuc to conta red nuc (SCP) and contra VL thalamus
CorticopontocerebellumAssociated nucleus: dentate
Territory: lateral cerebellar hemispheres
Functions: compares planned and actual motion, ensures smoothness of complex motion
inputscorticopontocerebellar tract from cortex to contra cerebellar hemisphere
olivocerebellar tract from inferior olive (climbing fibers) to contra ICP to posterior cerebellar hemisphere
outputsdentatorubrothalamic tract (SCP) to parvocellular red nuc and VL thalamus