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