control term three Flashcards
what are the two main types of upper motor neurons in pyramidal tracts?
what’s the difference?
why is the difference clinically relevant?
vetz cells (bigger): - synapse directly on to LMNs
non-vetz cells:
- synapse with an interneuron which then synapses with LMN
if there’s damage to a vetz cell then the LMN has no innervation and so looses function/dies but if there’s damage to a non-vetz cell then another UMN can take over its function as interneurons synapse with a lot of UMNs
what are the two types of LMNs?
what’s the difference?
alpha motor neurons
- directly responsible for the generation of force by muscle
- extrafusal
- form bulk of muscle
gamma motor neurons
- proprioception (sensory)
- intrafusal
- basically just muscle spindles
nb intrafusal means inside capsule
how many LMN axons control each muscle fibre
each fiber is innervated by a single axon (helps give fine control)
but each axon can innervate multiple fibres
where do upper motor neurons synapse with lower motor neurons?
ventral horn in the spinal cord around the level at which the LMN exit the spinal cord
nb the size of the ventral horn is much larger in the cervical and lumbar sections of the spinal cord as these supply the upper and lower limb
what is a motor neuron pool?
why is this clinicaly relevant?
all the motor neurons that innervate a single muscle
the LMN cell bodies are distributed through several sections of spinal cord
means that if you have a lesion in one segment then you loose some control to the musscle but not all control
what is the segmental distribution of LMNs in the ventral horn of the spinal cord compared to peripheral musculature?
within the ventral horn…
LMNs that control flexors (eg biceps brachii) lie dorsal to extensors (eg triceps brachii)
LMNs that control axial muscles lie more medial to those controlling distal muscles
what is a motor unit?
the muscle fibres that are innervated by one alpha motor neuron
it is the smallest unit of force that can be activated to produce movement
nb the muscle fibres that a single LMN innervates are spread out evenly over the extent of the muscle to ensure even contractility
- this also ensures that damage to a single motor axon will not necessarily reduce the muscle’s ability to contract
what are the three different sizes of muscle units?
what is the difference in function of the different sizes?
small motor unit:
- eg extraoccular muscles
- 3 muscle fibres per LMN
- high precision, low power
medium motor unit:
- eg soleus muscle (posture)
- 180 muscle fibres per LMN
- med precision, med power
large motor unit:
- eg gastrocnemius
- 1500 muscle fibres per LMN
- low precision, high power
what is the size principle of motor units?
the higher the number of motor units recruited the greater the increase in force
small motor units are recruited before large ones, producing increases in force
what are the two main types of muscle fibres?
how does this relate to the concept of motor units?
fast twitch
- large force
- easily fatigued
- mainly anaerobic
- look pale
slow twitch
- less force
- not easily fatigued
- mainly aerobic
- look red (high blood supply, myoglobin + mitochondria)
motor units differ in the type of muscle fibres that they innervate
- so slow motor units consist mainly of slow twitch fibres etc
what procedure is used to record motor unit activity?
an electromyograph (EMG)
nb can be used for clinical diagnosis of certain UMN + LMN conditions
in the context of muscle contraction, what does Hz mean?
a higher Hz means that the LMNs are firing more frequently
what are the 4 levels of muscle contraction?
incl approximate Hz
muscle twitch:
- <5Hz
- contration followed by complete relaxation
summation of the twitch:
- > 10Hz
- another AP is firing before muscle fibre has time to relax -> summation + actually being able to generate enough force to move muscle
smoothing of muscle contraction:
- > 20Hz
- this is normal muscle contraction
fused tetanus:
- > 40Hz
- constant contraction, no relaxation at all
what are the three main sources of input to alpha motor neurons?
- sensory inputs from peripheral proprioreceptors
- local inputs from spinal interneurons (originally from UMNs)
- direct input from UMNs
what are the two main types of proprioceptive receptors?
- what detect change in?
- where lie?
- innervation?
muscle spindle
- detects change in muscle LENGTH
- intrafusal (inside capsule)
- lies parallel to muscle fibres
- gamma motor neurons (Ia + II)
golgi tendon organ
- detects change in muscle TENSION/contraction
- lies in tendon part of muscle
- Ib afferents
what is responsible for ensuring there is also a baseline level of muscle tone (even when muscles aren’t actually moving)?
interaction between muscle spindles and alpha motor neurons ensure muscles are always under some degree of stretch = muscle tone
what are the two main classes of spindle fibres?
- types of fibres?
- what measure?
chain:
- Ia + II afferent fibres
- fire as long as the muscle is stretched
bag:
- Ia afferent fibres
- fire when there is a CHANGE in stretch
nb both gamma motor neurons
describe the interaction between the alpha and gamma motor neurons
- activation of alpha MN -> contraction + shortening of muscle fibre
- shortening of extrafusal muscle fibre -> collapse of the intrafusal muscle spindle + loss of sensitivity
- this is corrected by the gamma MN which then fires so muscle spindle contracts to match length of extrafusal muscle fibres
in changing the size of the muscle spindles to match the extrafusal fibres this tells body how much muscle has contracted and so where body parts are in space (proprioception)
what is the difference between isometric and isotonic muscle contraction?
which proprioceptive receptors fire during which?
isometric:
- increase in tension without a change in muscle length
- golgi tendon active (Ib)
isotonic:
- increase in length without a change in muscle tension
- muscle spindle active (Ia)
what are the axons which supply muscle spindles and golgi tendon organs all subtypes of?
subtypes of A alpha fibres
(fastest type of neuron)
proprioception is fast!!
nb difference in naming: axons from skin vs axons from muscles (skin is letters)
Aa = I AB = II Ad = III C = IV
what are the four clinical signs which are seen a few days after UMN damage?
- positive babinski sign
- spasticity
- hypereflexia
- loss of fine movements
nb muscles which control fine movements are often directly supplied by UMN (no interneuron) + LMN and so if damage to UMN then get loss of fine movements
nb INITIAL symptoms are muscle flacidity
why do babies have a positive babinski sign?
their corticospinal tract has not finished developing yet
ALS:
- what is it?
- pathogenesis?
- cause?
a type of motor neurone disease
- gradual loss of all voluntary movement
progressive alpha motor neurone degeneration
10% is familial, 90% sporadic
via what pathway is sensory innervation from the face?
trigeminal thalamic
nb corticobulbar is motor