motor control and disease Flashcards
motor control hierarchy
basal ganglion and cerebellum –>
descending systems (upper motor neurons): motor cortex and brainstem centres –>
spinal cord and brainstem circuits (lower motor neurons): local circuit neurons (sensory inputs here) and motor neuron pools (output to skeletal muscles)
circuits for simple reflexes
local circuit control of spinal motor neurons by spinal sensory neurons
all movements from skeletal muscle are initiated by LMNs
spinal cord has central pattern generators - complex behaviour without input from brain
upper vs lower motor neurons
UMN:
motor cortex = planning, initiating, directing voluntary movements
brainstem centres = basic movements and postural control
control motor function in brain
LMN:
local circuit neurons = integration of LMNs and sensory inputs
motor neuron pools = output to skeletal muscles
UMNs always synapse on LMNs (or their interneurons) and LMNs always synapse on muscle fibres
somatotopic mapping of motor cortex
lower body represented medially
upper body represented laterally
mapped on cortex in similar way to somatosensory map
somatic motor system (3 types of muscles and where they innervate)
control of LMNs in ventral horn of spinal cord - innervation of striated muscle to control movement
axial muscles = head and trunk movement
proximal muscles = shoulder, elbow, pelvis, knee movement
distal muscles = hands, feet, digits movement
LMNs - connection to muscle fibres
each fibre receives input from a single alpha LMN
each LMN innervates fibres of just one muscle - can innervate more than one fibre
LMN - motor unit and motor neuron pools
motor unit = motor neuron and all the muscle fibres it innervates
motor neuron pool = all the motor neurons that innervate a single muscle
grouped in rod-shaped cluster in spinal cord - over several vertebral segments (found using retrograde tracing in the muscle
LMN - somatotopic organisation of motor pools
mediolateral position of a motor pool reflects whether it innervates proximal or distal muscle
therefore organised mediolaterally and rostro-caudally
LMN - CST
LMNs have direct input from UMNs which project axons down spinal cord
corticospinal tract (CST) is a lateral pathway of spinal cord for voluntary movement
CST axons originate in layer V of motor cortex
CST axons project directly from cortex to ventral horn
axons cross the midline in pyramidal decussation in medulla –> project laterally in spinal cord –> synapse laterally to LMN circuits which control distal muscles
LMN - pyramidal cells and CST
pyramidal cells of the motor cortex project axons into the corticospinal tract
axons of CST derive from large pyramidal cells in layer V aka Betz cells
motor cortex has 6 layers -> main inputs in layer IV, main outputs from layers III, V, VI
UMN - in motor cortex
fine voluntary control of more distal structures
mainly project contralaterally via CST to muscles for precise limb movement
also project via corticobulbar tract to hypoglossal nucleus in brainstem to control movements of tongue - human speech
UMN - in brainstem
to medial motor pools
for posture and balance
ventromedial pathways project mainly ipsilaterally and medially in spinal cord:
- vestibulospinal tract = head balance and turning - with inputs from vestibular system
- tectospinal tract = orienting response - inputs from visual system via superior colliculus
- reticulospinal tract = antigravity reflexes
synapse to medially located LMN circuits which control axial muscles
integration of postural control and voluntary movement
when lifting a lever, the first muscles to contract are in the legs
anticipatory feedforward mechanism - preadjusts body posture to compensate for forces that will be generated when lifting the lever
indirect cortical control of LMNs (from 2 areas of motor cortex)
feedforward mechanisms - UMNs influence spinal cord circuits by 2 routes:
- from area 6 (premotor area - PMA) = anticipate movement –> indirect projection to axial muscles via reticular formation
- from area 4 (primary motor cortex) = activates voluntary movement –> direct to spinal cord via CST
activity in PMA (anticipation) precedes area 4 (voluntary movement)
motor neuron disease (MND)
aka amyotrophic lateral sclerosis (ALS)
degenerative disease of motor neurons
amyotrophic = no nourishment of muscles so muscle atrophy (wastes away)
sclerosis = hardening/scarring of lateral spinal cord from degeneration of axons in CST
famous case = Lou Gehrig - baseball player, development can be seen by decrease in batting rate. died 3 years after contracting
MND - neuropathology - effect on UMNs and LMNs
lower motor neuron disease:
- muscle paresis or paralysis
- loss of muscle tone - loss of stretch reflexes
- severe muscle atrophy
- usually die from lung dysfunction (due to atrophy in intercostal muscles)
upper motor neuron disease:
- muscle paresis
- increased muscle tone = spasticity - from failure to modulate stretch reflex - too tight
- hyperactive reflexes
- loss of fine voluntary movement
- usually die from loss of input to bulbar muscles (tongue and pharynx) via corticobulbar tract
intellect is never compromised - Stephen Hawking
MND - aetiology (cause)
neurodegenerative disease
cause not well understood
one theory = excitotoxicity - overstimulation (typically by glutamate) leads to neuronal cell death
vicious cycle of glutamate release - particularly in hypoxic conditions (too little oxygen e.g. after cardiac arrest, stroke, brain trauma)
drug therapy = Riluzole which blocks glutamate relase - only delays disease by a couple months
10% have a clear genetic basis:
mutation in gene encoding superoxide dismutase (SOD1) - enzyme that clears up free radicals that accumulate in metabolically active cells
other genes affect variety of cellular processes - not fully understood
brain components in initiation of movement
motor cortex (AF4) - telencephalon
basal ganglia - forebrain
- caudate putamen
- globus pallidus
- subthalamic nucleus
ventral lateral nucleus of thalamus - diencephalon
substantia nigra (midbrain)
basal ganglia - motor loop
motor cortex connects to the basal ganglia - feeback to premotor area (area 6) via ventrolateral complex of the thalamus (VLo) to control initiation of movement
can take 2 pathways: direct and indirect
basal ganglia - motor loop - direct pathway
with no cortical input:
globus pallidus internal segment (GPi) tonically (continually) inhibits the VLo
with input from cortical regions:
1. input converges on the striatum (contains caudate putamen - CP)
2. caudate putamen inhibits the GPi
3. GPi no longer inhibits VLo
4. VLo activates area 6 and initiates movement
allows integration of many cortical inputs
high speed - idea that the engine is running with the GPi as the “break” which is released
basal ganglia - motor loop - indirect pathway
modulates the direct pathway with the substantia nigra (SN) and GP external segment (GPe)
GPe inhibits the GPi - but GPe is inhibited by CP
SN acts via CP to maintain balance between inhibition and activation of VLo - has input from decision making and emotion centres - risk reward judgements to slow an otherwise fast circuit
modulation of direct pathway:
excitatory element of SN –> inhibits GPi –> stops inhibition of VLo –> activates area 6 for movement - through DIRECT pathway
indirect pathway:
inhibitory element of SN –> SN inhibits CP –> stops inhibition of GPe –> inhibits GPi –> stops inhibition of VLo –> activation of area 6 for movement
degeneration here leads to Huntingtons
cerebellum role in motor learning
modulates UMNs - no direct connections to spinal cord
used in learned execution of planned, voluntary, multi-joint movements
instructs motor cortex about direction, timing, and force of movement
based on predictions of outcomes based on past experience of movements - therefore practice helps with motor learning
cerebellum and “muscle memory”
strengthening or weakening of existing neural pathways - no new pathways being made
memory is in the neurons - not the muscles
muscle memory = motor learning in cerebellum
there is evidence for memory within muscles but in relation to speed of regaining muscle mass e.g. stop going gym then start again
cerebellum loop with motor cortex
cerebellum receives input from many cortical areas (esp sensory cortex) via corticopontocerebellar projection
also receives sensory info from spinal cord and vestibular system
projects back into motor cortex (area 4) via the thalamus (VLc - ventrolateral) (no direct output to spinal cord)
function = detect and correct differences between intended and actual movement (motor-error) and records this to build into prediction for next time movement is made
cerebellum lesion = cerebellar ataxia - poorly integrated movement (dyssynergia)