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motor hierarchy (3 main components)
lower motor neurons, upper motor neurons, extrapyramidal system
lower motor neurons (final common pathway)
spinal reflexes (proprioceptors and spinal interneurons)
cranial nerves
skeletomuscular efferents
autonomic efferent
upper motor neurons (descending control)
pyramidal (primary) motor system — planning, initiating, and directing voluntary movements
brainstem systems — basic movements and postural control
extrapyramidal system
basal ganglia
cerebellum
parts of midbrain
motor hierarchy movement path
basal ganglia — gates proper initiation of movement; cerebellum — sensory motor coordination; premotor/parietal/parts of the midbrain — coordinate transforms, planning → upper motor neurons (motor cortex, brainstem centers) → 1. local circuit neurons (sensory inputs → spinal cord and brainstem circuits) — reflex coordination → lower motor neurons → skeletal muscles; or 2. lower motor neurons → skeletal muscles
upper motor neurons; ex: lateral corticospinal pathway (pyramidal, primary motor)
provide descending (central) control over lower motor neurons and spinal reflexes
other (extrapyramidal) parallel pathways are important for other functions
ex. corticobulbar tract for facial movements, vestibulospinal tract for postural adjustments
primary motor cortex (M1, BA 4)
source of origin of corticospinal tracts (70%) — large specialized pyramidal cells in La V (Betz cells)
contralateral movement —> somatotopic mappings
motor seizures — “march” down the body; orderly progression — when seizure spreads, spreads in a somatotopic way
what is coded in M1?
m1 microstimulation elicits particular movements of combinations of muscle groups; neurons will code for a bunch of muscles; lower in the spinal cord is more 1:1, but going higher elicits more complex combinations
neurons fire before movement is made (stimulates spinal cord, when then is the proximal cause of the movement (lower motor neurons))
target brainstorm/spinal cord for complex (multi-joint) movement
what else is coded in M1?
Magnitude and direct of force to be exerted
direction of visually-guided movements determined by population coding
relative discharges in large number of neurons yields direction sensitivity
how can action potential & silencing be seen with neurons
how neurons move and what direction they prefer — neurons all favor different directions, but subject wants to move in a specific direction, so neurons that prefer this direction will start firing, and this collective firing results in movement
upper motor neuron syndromes
somatotopic paresis (weakness/hypotonia), especially for extremities, which partially recovers due to plasticity in motor representations — neurons overlap and some can take over representations
in children, long myelinated fibers are not completely developed; this is tested, normal plantar response will be flexion (toes going down), Babinski sign will be a fanning of the toes bc of damage to descending corticospinal pathways
spasticity/decerebrate rigidity (loss of inhibitory control over vestibulospinal/reticulospinal tracts)
hyperreflexia of sensory-motor reflexes
lateral corticospinal damage = loss of fine motor control = lack movement control, no strong movements
support systems for upper motor neurons
premotor/parietal
parietal cortex transforms sensory inputs into a body-centric space to guide action
parietal cortex, somatosensory system
retinatopic system coordinate transform → somatosensory system → parietal takes in sensory inputs → body-centric space → guides action
damage to parietal cortex can disrupt goal-directed reaching and eye movement (optic ataxia — making clumsy movements based on visual input)
the visual system in not in the somatosensory system, but is tuned into the retinatopic system (where you are looking)
parts and functions of the premotor cortex (BA 6)
30% of corticospinal tracts arise from this region
lateral premotor cortex (externally guided)
medial premotor cortex (internally guided)
neurons respond maximally during movement planning: more respond earlier compared to those in the motor cortex, neurons shut off once motor movement is made
more activation in supplementary motor area (medial premotor cortex) in self-initiated movement versus visually triggered movement
lateral premotor cortex function
initiates externally guided motor movements; based on visual input to make motor response = sensory cue → particular movement
visuomotor learning (e.g. red vs green traffic lights)
control of eye movements (frontal eye fields)
medial premotor cortex (supplementary motor cortex) function
initiates internally-guided motor movements
damage = reduced self-initiated movements (e.g., chosen altering driving paths on a whim — change of plans (like getting coffee instead of going straight home)
readiness potential (scalp EEG)
precedes both intentions and actions
starts out anterior and bilateral (premotor), then shifts posterior and contralateral (motor)
enhanced when attention is focused on motivations to act rather than action itself — recruits medial premotor, dorsolateral, prefrontal, and parietal cortices)
basal ganglia anatomy
collections of subcortical structures at the base of the forebrain
neostriatum (corpus striatum,)
paleostriatum (globus pallidus)
sub thalamus (diencephalon)
substantia nigra (midbrain)
output of basal ganglia system: Globus Pallidus internal (GPi)/ Substantia Nigra pars reticulata
protect to thalamus (VA/VL) and superior colliculus
basal ganglia has to remove tonic inhibition to generate action (mostly internal self-initiated)
one of few brain areas without reciprocal connections to the cortex
output is inhibitory with high resting activity
disengagement of output neurons needed to release goal-directed movements in a direct pathway
parallel pathways in basal ganglia anatomy (car analogy)
direct vs indirect pathways
indirect involves subthalamus, which serves as an emergency brake and engages tonic inhibition
direct involves thalamus, which serves as the accelerator → disinhibition on direct pathway
basal ganglia disorders
hemiballismus
parkinson’s disease
huntington’s disease
hemiballismus
disease of the subthalamus
removes brake of indirect pathway so no tonic inhibition = spontaneous, uncontrolled movements on contralateral side
tonic, phasic
tonic: at rest
phasic: once region becomes activated by cortex, inhibition is temporarily released so movement can be executed
Parkinson’s disease
DA (dopamine) nigrostriatal pathway degenerates (50-80%)
linked to neurotransmitter dysfunction
loss of dopamine input to caudate containment → increased inhibitory outflow to thalamus = removes accelerator and simultaneously engages brakes
motor symptoms of parkinson’s
slow movements, lack of movement, difficulty initiating movements, starting a movement but cannot initiate stop, adjusting force (ballistic movements)
impacts postural muscles (gait, posture) — “shuffling” locomotion
special difficulty with internally-drvien motor plans (medial premotor cortex)
treatments for parkinson’s
behavioral: use external sensory cues to help initiate movement
pharmacological: replace DA, but problem with blood-brain barrier, so use L-DOPA as precursor, but problem is non-specific, so can produce schizophrenic-like symptoms, and can target other things
implanted deep brain stimulators (inhibitory or excitatory: thalamus, Globus Pallidus (internal)/subthalamus — impact of degeneration = more tonic movement → increases inhibitory outflow to thalamus so implanted deep brain stimulation to help
Huntington’s disease
progressive degenerative disorder, late adult onset (40s-50s)
inherited
loss of medium spiny neurons that project to Globus Pallidus external (indirect pathway) — so cannot apply the brakehu
Huntington’s disease motor symptoms
excess movements, coordination across multiple areas and not just contralateral control, difficult to test motor functions
irregular gestures because movement is less goal-oriented
loss of sustained muscular contraction
the cerebellum components
nuclear group (deep nuclei) OUTPUT
codex (anterior lobe (paleocortex), flocculonodular lobe (archicortex), lateral lobes
anterior lobe
spinocerebellum (muscle tone/reflexes)
vermis (proximal)
paramedian zone (distal)
flocculonodular lobe: vestibulocerebellum (balance)
lateral lobes: cerebrocerebellum (sensorimotor coordination/timing/errors)
the cerebellum
body representation in cerebellum is IPSILATERAL
spinocerebellar and vestibular axons don’t cross
descending projections from cortex cross in peduncles and then cross back
somatotopic maps in spinocerebellum
large fibers interconnecting cerebrum and cerebellum (20x corticospinal tract)
results of damage to the lateral cerebellar cortex (neocortical)
ataxia - clumsy, uncoordinated movements; no error correction (feedback)
hypermetria — rapid pointing movements extend beyond target
problems switching between gestures (irregular complex movements)
poorly timed movements, especially for over practiced ones (e.g., tennis serve)
abnormal reflect conditioning/motor learning
error-correcting role of cerebellum
cerebellum involved in on-line and feedback-based guidance of movement trajectories and movement correction following termination
lateral cerebellar activity, motor skill accuracy
participants track position of target with random jumps (simulates hypermetria)
cerebellum signals the difference between motor commands issued and actual movements produced
can be used to help generate accurate internal models of outcomes of motor processes
cerebellar versus basal ganglia loops
externally-guided versus internally-guided sequences/target actions
termination (correction) vs initiation of movements
interaction of each level of motor processing for different aspects of action (e.g., planning, sequencing, executing force, and timing)
what is motor system divided into
upper and lower motor neurons and modulatory circuits
how does primary cortex work
indexes both the direction and force of movements through population coding
medial vs lateral premotor cortices response
movement initiation: medial is internal cues, lateral is external cues
complex movements and coordination
complex movements require coordination across disparate motor components — transformation of coordinate systems into somatomotor space in parietal cortex, planning and selection in the premotor cortex, movement initiation in the basal ganglia and sensorimotor coordination in the cerebellum
basal ganglia pathways
both direct and indirect processing pathways act antagonistically
cause of parkinson’s disease
degeneration of dopamine in nigrostriatal pathway, other syndromes emerge due to imbalance in processing pathways within the basal ganglia
cerebellum has…
parallel pathways for vestibular, balance, sensorimotor control
error-correction mechanisms, which contribute to smooth trajectories of movements and appropriate stopping at target locations, and motor learning