Unit 3 - Motor Control Flashcards
Lower motor neurons
Motor neuron projecting from spinal cord to the motor end plate on muscle,
Synapses with upper motor neuron in ventral horn
Upper motor neuron
Projects from cortical areas to spinal cord, synapses with lower motor neuron
Higher cortical areas
–> no direct contact with spinal cord, so influence = indirect.
ie: association cortex, basal ganglia, and cerebellum
(Signal via thalamus)
Spinal circuit reflex
Most simple motor circuit,
Sensory receptors –> spinal grey matter –> muscle
(Cutaneous, pain or muscle spindles)
ie: stretch reflex
Central pattern generator (CPG)
Moderately complex motor circuit;
Generated at brainstem or spinal cord,
INdependent of descending input, but turned on/off by cortex
Ex: walking or breathing
ballistic movement
rapid movement that MUST go to completion
(can’t withdraw action once started)
ie: saccades (eyes), hemiballismus
organization of motor neurons in spinal cord
Medial: axial muscles – control balance/stability
Lateral: distal muscles – fine motor control
dorsal: flexor mm.
ventral: extensor, mm.
motor unit
a single alpha motor neuron, along with all muscle fibers innervated by it (3-1,000)
- small size = fine motor control
- increase muscle force by recruiting motor units
2 types of alpha motor neurons (+ function)
“red” (small): slow, low force, fatigue-resistant
“pale” (large): fast, fatiguable
monosynaptic/myotactic reflex
- passive stretch of tendon
- a) contract muscle (via muscle spindle Rs)
b) relax opposing muscle (“reciprocal inhibition”)
nocioceptive withdrawal reflex
1. nocioRs sense pain (ie: step on tack)
(--> Lissauer's tract)
2. a) ipsilateral flexor contracts
b) contralateral extensor contracts
* provides support for opp. limb to "escape"Muscle proprioceptive pathway
- muscle spindle (stretch R)
- ipsilateral dorsal column - spinal cord
- dorsal column nucleus
* decussate!* - contralateral medial lemmniscus
- VPL of thalamus –> S1 (cortex)
muscle spindle
in parallel with mm., w/ stretch Rs;
- -> passive stretch/increase muscle length
- 1a and II axons
- gamma mns change length to increase sensitivity (via intrafusal fibers)
- stimulated by vibration (lengthening illusion)*
Golgi tendon
in series w/ mm (at end, inside collagen);
- -> isometric contraction (tension on muscle)
- 1b axons to inhib. interneurons, compensate for fatigue
Lesion to posterior parietal cortex
- apraxia (loss of learned/skilled movements)
2. optic ataxia (mis-reaching)
Lesion to premotor/supplementary motor cortex
poor planning and sequencing,
decreased spatial organization
* feet = medial, head = lateral
lesion to basal ganglia
- akinesia/bradykinesia (slowed mvmt)
- ballismus
(responsible for selection and initiation of mvmt)
lesion to cerebellum
ataxia (uncoordinated mvmt)
* normally responsible for mvmt smoothness and coordination
Cortical circuits involved in voluntary movement
Direct to spinal neurons:
1. corticospinal tract; 2. corticobulbar (*bilateral!)
INdirect to spinal neurons:
1. corticorubral tract; 2. corticoreticular tract
Thalamic motor control
- VPL = somatosensory (proprioceptive/cutaneous info)
2. VA/VL = timing/coordination
Major cortical motor areas
1.Primary motor cortex (BA 8)
2. Supplementary motor cortex (BA 6)
3. Premotor cortex (BA 6)
4. Cingulate Motor area (BA 24)
Req’s: thin granular layer (IV), & electrical stim. to area –> mvmt
Neurons in primary motor cortex (M1)
each = directionally tuned,
fire: just before & during mvmt, (latency = 100-150 ms)
* population vector of neurons matches direction of mvmt*
- - increase firing rate = increase force
lesion to pyramidal tract
decrease in hand control, ie:
- thumb-finger opposition
- precise grip (=> “scoop hand”)
- single digit extension
lesion to primary motor cortex
- -> spastic paresis (bc = upper motor neurons)
- lose fine motor control
- increase tone/hyper-reflexia
- adjacent representations fill in void! (modified by use/experience)
Function of Premotor cortex (BA 6)
1) learned visual stimulus-response associations
2) rule-based actions
3) motor planning (to instructional cue)
* ventral (PMv) = hand grasp & mirror neurons
* dorsal (PMd) = arm reach
Supplementary motor area function (SMA):
self-initiated mvmts, mental mvmt rehearsal, and learned motor sequences.
- single neurons = selective for specific mvmt sequences (Bop-it);
- – “bereitshift potential” = from EEG over SMA.
“distributed processing” for motor cortex:
Multiple distinct cortical areas responsible for motor processing,
* all areas have different but overlapping function*
–> damage to 1 area = mild/transient,
BUT damage to >1 area = severe, persistant
input to inferior cerebellar peduncle:
- vestibular nuclei
- brainstem
- spinal cord
* output = vestibular nuclei
input to Middle Cerebellar Peduncle:
- Pontine Relay Nuclei
- Cerebral cortex
(output = cerebellum)
Cellular organization of the cerebellum
3 layers, 5 total cell types.
- Purkinje layer: 1 cell thick (purkinje cell bodies)
- Molecular layer: purkinje dendrites, parallel fibers, and interneurons
- Granular layer: granule cells (= cell bodies of parallel fibers),
* inhibited by Golgi cells (interneurons, NT = GABA)
synapses on Purkinje cells
all use glutamate as excitatory NT,
1. Climbing fibers (from Inf. Olive) –> short AP burst
= motor error signal (teaching)
2. Granule cells (become parallel fibers) –> single AP
= sensory feedback/motor commands
** Purkinje cells = INhibitory to Deep Cerebellar Nuclei **
Climbing fibers
neurons connecting Inferior Olive to Purkinje Cells (excitatory),
for signaling motor errors;
input to Inf.O. from:
Cerebral cortex, Red Nucl., Spinal Cord, Deep Cerebellar Nuclei
Mossy Fibers
neurons in cerebellum connecting input to Purkinje cells (excit.),
via Granule cells/parallel fibers.
Input from: Cerebral cortex, Brainstem and Spinal cord.
Long-term Depression
phenomenon where parallel fiber signaling is weakened by simultaneous firing of climbing fibers.
Output from cerebellum
info from cerebellum to a) motor thalamus, b) Red Nucleus
via Superior Cerebellar Peduncle.
Inferior Olive (relation to cerebellum)
Receives input from Cortex, Red Nucleus, Spinal Cord, and Deep Cerebellar Nuclei (“Loop Circuit”).
* sends to CONTRAlateral cerebellar hemisphere.
Inferior Olive –> Climbing Fibers –> Purkinje Cell(s)
unilateral lesions in cerebellum cause…
Hypotonia (if decrease gamma motor neuron activity via thalamus),
= IPsilateral deficits bc cross twice (in SCP and after M1)
Vestibulocerebellum
= vermis and flocculonodular lobe.
controls balance and eye mvmts,
Inputs: vestibular nuclei, visual cortex, motor cortex (for posture)
Output: Vestibular nucleus
Lesion deficits:
- balance: fall to side of lesion,
- Eyes: spontaneous nystagmus, poor smooth pursuit (eyes(
Spinocerebellum
= vermis and medial hemispheres;
Receives somatosensory info.
Input: spinal cord (ipsilateral limb tracts)
Output: to Reticular Formation (via Fastigial nucleus)
Lesion Deficits:
Ataxia, dysmetria (poor coordination), hypotonia, tremor, poor rapid alt. mvmts/decomposed mvmt.
Cerebrocerebellum
= lateral hemisphere; helps w/ voluntary mvmt.
Input: Motor cortex, somatosensory cortex, Association cortex
Output: Motor thalamus (via dentate nucleus)
Lesion Deficits: fine mvmt ataxia, cognitive deficits
Basal Ganglia
“Gates” mvmt (selection and initiation); somatotopic organization.
= Striatum, Globus Pallidus, Subthalamic nucl, and Substancia Nigra.
– Direct Path: suppress inhibition –> increase motor output.
— Indirect: inhibit direct path –> decrease motor output.
lesion to caudate nucleus
deficit = robotic walking
Lesion to putamen
deficit = vulgar and impulsive personality shift, hypersexuality
striatum neurons
= medium spiny neurons (“MSNs”) –> inhibitory projections to globus pallidus, NT = GABA.
(+ some interneurons)
* somatotopic organization
Nigrostriatal pathway
from STN (subthalamic nucleus) to Striatum;
D1 Rs: + to MSNs in Direct path.
D2 Rs: - to MSNs in INdirect path
==> promote movement (aka motor output)
** Dopamine deficit in Parkinson’s limits this pathway.
Parkinson’s Disease
–> akinesia, bradykinesia, slow rest tremor
= Dopamine deficit to nigrostriatal pathway,
From oxidative stress, mimicked by MTPT drug.
Treatment: L-DOPA, Pallidotomy (decrease inhibitory GPi output), DeepBrain Stimulation
Huntington’s Disease
autosomal dominant mutation (CAG repeat on chrom.4 short arm)
-> MSNs and cerebral cortical neurons die
==> chorea, athetosis (slow writing), Dementia, and personality changes.
* 30-50 yr. onset
Direct Basal ganglia pathway
Cortex –> (+) striatum –I (-) GPi/SNr -/-I Thalamus
==> suppress inhibition = increase motor output
INdirect Basal Ganglia pathway
Cortex–> striatum–I GPe -/-I (-)STN –> (+)GPi/SNr –I Thalamus
==> inhibit direct pathway = Decrease motor output
Lesion to Globus pallidus
–> dystonia (sustained muscle contractions, abnormal postures, etc.)
lesion to Subthalamic Nucleus (STN)
–> hemiballismus (involuntary flinging motion in extremities)
bc lesion causes LOSS in mvmt inhibition (via INdirect pathway)
Muscle groups used for postural tone
(tonic activity in muscles opposing gravity)
- Upper limb flexors
- Lower limb extensors
2 routes for postural control
- Direct: via vestibulospinal tract to alpha mns
- Reflex Route: via corticospinal or reticulospinal tracts to gamma mns
==> act on muscle spindles to increase tone via alpha mns
Reticulospinal tract and postural control:
to modulate gamma mns –> affect alpha mns;
a) Cortex –I Pontine Reticular Formation –> + gamma mns
= increase m. tone.
b) Cortex –> Medullary Reticular Formation –I - gamma mns
= DEcrease tone.
Lesion to “MRF” (medullary reticular formation):
INcreased tone bc DISinhibit gamma neurons
(so increase alpha mn work too)
Median Vestibular tract (“MST”)
carries bilateral cervical information from semicircular ducts,
=> stabilize head position, influence alpha mns to neck muscles.
(maintain center of gravity)
Lateral Vestibular tract (LVST)
ipsilateral to all levels of spinal cord,
=> stabilize stance/maintain balance and posture.
to alpha mns of legs
(anti-gravity and tilt reflexes)
Lesion to vestibulospinal tracts
loss of balance,
will fall towards side of lesion
Decortication
lesion above the red nucleus, so red nuc = DISinhibited;
(ie: cerebral cortex, internal capsule, thalamus)
Sx –> flex arms and extend legs
decerebration
lesion below the red nucleus, disrupts the rubrospinal tract
(loss of tonic input from cortex –> hyperactive stretch reflex)
-> increase gamma mn activity = increase postural tone
Sx –> extend arms and legs, arch head back
Treatment: cut dorsal roots to decrease rigidity
Reasons for return of sensation >2 months after lesion
to descending systems
- -> hyperactive reflexes and hypertonic bc…
1. denervation sensitivity (increase sensitivity to input)
2. synaptic void filled by nearby neurons (increase strength of proximal circuits)
saccade
ballistic mvmt to rapidly redirect fovea,
*not modifiable once started, = CPG reflex.
** CAN perform on verbal command**
During mvmt: blurry image and no f(x)al vision
Latency: 150-200 ms, Duration: 20-50 ms
Velocity: ~400 degrees/second
Smooth pursuit (eye mvmt)
eye mvmt to follow moving target – eyes match speed of target;
“retinal slip” = speed mismatch
* canNOT perform on visual command (uses saccadic tracking)
DO have f(x)al vision while move eyes
= voluntary cortical modulation of reflex mech in brainstem
Lesion to cortical eye fields and/or brainstem visual centers
1 or other: mild, transient saccade deficits
Both areas: severe and persistent saccade deficits
Cortical eye fields
code direction and amplitude of eye movement,
each neuron = directionally tuned.
= frontal/supplementary eye fields and lateral intraparietal area;
*project to: a) brainstem (saccade reflex)
b) pontine relay nuclei/cerebellum (smooth pursuit)
Superior colliculus
1 of 2 visual centers in brainstem, = on tectum of midbrain;
F(x): reflexive, contralateral saccades
- superficial layer: stimulus position
- deep layer: direction/amplitude of saccade
reticular formation
1 of 2 visual centers in brainstem, = saccade central pattern generator a) midbrain (riMLF) = vertical component - output: abducens nucleus b) pons (PPRF) = horizontal component - output: occulomotor nucleus *output goes 1st to nucleus of IPsilateral eye!
“Pulse-step” pattern for visual saccades
= firing pattern in abducens and occulomotor nuclei;
- pulse: burst –> saccade
- step: tonic activity –> fixation/tension
pathway for smooth pursuit:
- cortical eye fields/extrastriate visual cortex
- via Pontine Relay Nuclei - - Cerebellum: Flocculum
- Vestibular nuclei
- Brainstem nuclei (direct to abducens, INdirect to occulomotor)
- Eye muscles
Function of Vermis (cerebellum) in saccades
adjusts amplitude of saccade to match target
(so gaze lands accurately on target)
*Lesion ==> dysmetric saccades (miss/overshoot target)
Lesion to flocculum (cerebellum)
–> smooth pursuit = abolished!
but saccades not affected.
(so use saccadic tracking to overcome deficit)
