Spinal reflexes and upper motorneurons Flashcards
What are the Two sensory receptors associated with muscles monitor length and tension?
Muscle spindles
stretch (length) receptors
In parallel with muscle fibers
Golgi tendon organs
tension (force) receptors
In series with muscle fibers
What is Muscle spindles? and what type of receptor it has ?
– stretch receptors
i’s a fibrous, fluid filled capsule surrounds “intrafusal” muscle fibers
the spindle receives sensory and motor innervation
sensory axons have stretch-sensitive ion channels
(group la sensory neuron_
Intrafusal vs Extrafusal muscle fibres
Two fiber types are in parallel
Extrafusal fibres are responsible for force generation
Intrafusal fibres are responsible for changing spindle length (and therefore sensitivity)
Need to know where our limbs are can be achieved by
And what does it help with?
monitoring muscle length and muscle tension.
This also helps maintain constant muscle length and tension, preventing muscle overload and compensating for fatigue.
Particularly common in muscles used for fine movements (like in fingers)
Depend on stretch sensitive ion channel.
How muscle spindle encodes the length ?
Action potential rate encodes muscle length and/or velocity
Longer muscle / lengthening of muscle = higher firing rate
Shorter muscle / shortening of muscle = lower firing rate
Intrafusal fibres are responsible for
And how do are they involved to signal for change of length?
changing spindle length (and therefore sensitivity)
Fibrous capsule of the muscle spindle contains specialized “intrafusal” fibers.
They are contractile, so they have inputs from a motor neuron, but they’re also associated with sensory neurons.
These sensory neurons have stretch sensitive ion channels, to signal muscle length.
Fusiform => having a spindle shape
Gemma motor neurons and it’s difference with alpha motor neuron
Gamma motor neurons target intrafusal fibers, shortening the muscle spindle.
Alpha motor neurons target extrafusal muscle fibers, shortening bulk of muscle.
- alpha activation decreases sensory Ia activity;
- gamma activation increases sensory Ia activity.
How is Gamma co-activation important in Maintaining sensitivity of the spindles
Activation of the alpha motor neuron causes a contraction (shortening) of the extrafusal fibers. This reduces firing in the 1a axon.
Problem: after contraction of extrafusal fibers, muscle spindle is “slack” => loses its ability to signal muscle length
Co-activation of the gamma motor neuron shortens the intrafusal fibers.
This increases firing in the 1a axon.
Feedback loop model Gemma
Gamma feedback loop: tries to maintain a “set-point” of constant muscle length.
Simple feedforward system: co-activation of alpha and gamma to change set-point (like a form of adaptation).
Does CO-activation occur with unexpected change in muscle length?
NO, Co-activation only occurs when there are planned changes to muscle length. So if muscle has an unexpected change in length, the change in AP rate of the 1a sensory fibre signals that change.
Why not just have a spindle system that is sensitive throughout the complete range of muscle lengths?
Simply not sensitive enough. We have firing rate range of 0-100 spikes/s – can reasonably only code 100 different lengths. By changing sensitivity, we can effectively code 1000s of different lengths.
The myotatic reflex
Group Ia sensory neurons synapse on alpha motor neurons and interneurons.
A monosynaptic feedback loop mediates the myotatic reflex.
spinal-cord mediate reflexes are modulated by descending inhibition
The myotatic reflex is diagnostic test of :
- 1 - Normal spindle and sensory fiber function
- 2 – spinal cord synapses (and response gain)
- 3 – motorneuron function
- 4 – muscle contraction.
when tendon jerk is the largest?
and when is this relevent?
- Tendon jerk is largest when muscle length is optimal length for contraction. If muscle is short, tendon is slack. If muscle is long, spindles have high background activity and don’t signal additional stretch.
- Size of jerk is also susceptible to descending control from the brain (i.e., we can consciously inhibit it to some degree). This is the basis of the Jendrassik manouever.
- When is this relevant – maintaining posture. If body leans forwards, it stretches the ankle extensors, leading to contraction and the body leans back.
- Similarly, if the body leans too far back, ankle flexors are stretched, leading to contraction.
Reciprocal inhibition
Sensory inputs from Ia axons are used to inhibit contraction of antagonist
=> contraction of one muscle automatically relaxes the second .This also prevents the myotatic reflex from resisting intentional movement
occurs during voluntary muscle contraction
prevents the myotatic reflex to engage in voluntary movement
Reflex Action of Ia Fibre activation
- Monosynaptic excitation of homonymous muscle
- Excitation of synergist muscles
- Inhibition of antagonist muscles
- Restricted to muscles in the same “myotatic unit” (no effect at other joints).
why Myotatic reflex must be suppressed during voluntary movement?
Myotatic reflex must be suppressed during voluntary movement – otherwise the intentional contraction of one muscle, which leads to stretch of the antagonist muscle, will be counteracted.
What is Homonymous muscle, Synergist, Antagonist
Homonymous muscle = muscle from which original signal originated
Synergist = muscle performing the same action as the homonymous muscle
Antagonist = opposing muscle
primary role of muscle spindle
This reflex is not the primary role of the muscle spindles (which is to provide information about muscle length), but it illustrates a simple way that their signals can be used to modulate movement.
Golgi tendon organs signal muscle tension
where does is synapse to?
types of ion channel
what happens when tension increases?
Innervated by Ib sensory axons, which synapse onto interneurons in ventral horn.
Increased tension => increased firing rate
Golgi tendon organs are in series with extrafusal muscle fibers
have stretch-sensitive ion channels
During which type of contraction Golgi tendon organ only signal change and spindle doesn’t
- During an isometric contraction - No change in muscle length – this is what happens when we grip an object or hang from a bar.
- Thus muscle spindle doesn’t change its firing rate, but Golgi tendon organ signals change in tension.
Autogenic inhibition
Maintains muscle tension within an optimal range (allows precise control of tension) Autogenic inhibition (as implemented by the circuit shown on the slide) is a negative feedback circuit.
Reflex Action of Ib Fibre activation
- Disynaptic inhibition of homonymous muscle
- Inhibition of synergist muscles.
- Excitation of antagonist muscles
- Affects other myotatic units (more widespread than Ia fibres)
- Context dependent (autogenic inhibition is suppressed during locomotion)
what happens with Increase muscle length and Increased muscle tension
Increase muscle length => activates alpha motor neuron => muscle contraction
Increased muscle tension => inhibits alpha motor neuron => muscle relaxation.
Proprioceptive sensation
Muscle spindles
-signal information about muscle length
innervated by Type Ia sensory neurons
in parallel with extrafusal muscle fibers
gamma co-activation maintains sensitivity
Golgi tendon organs
- signal information about muscle tension
innervated by Type Ib sensory neurons
in series with muscle fibers
no direct motor innervation
Flexor & crossed-extensor reflexes
A spinal cord mediated reflex can withdraw (flex) a limb in response to a painful stimulus.
Flexion (withdrawal) of the ipsilateral limb is compensated by extension of the contralateral limb.
Adelta (glutamate)
Adelta (glutamate) - Pain fibers synapse in multiple spinal segments, activating alpha motor neurons controlling all flexors in the limb.
What affects conduction velocity?
- diameter; myelination; temperature; damage.
- Motor alpha and Group Ia/b fibers are large diameter (13-20um)
How are movements controlled?
Movement requires more than just contracting muscles
- Plan the movement
- Initiate the movement
- Co-ordinate multiple muscles in space and time
- Refine the movement using sensory feedback
- Optimise and learn repeated movements
Upper versus Lower Motor neurons
Lower motor neurons:
involved in all movements (voluntary and reflexive).
directly innervate muscle
cell bodies in spinal cord
Upper motor neurons
- control voluntary movements
do not directly innervate the muscle
cell bodies in brain, project down spinal cord to lower motor neurons
Upper motor neurons can also modulate reflexes, since they synapse onto the neurons involved in mediating the reflexes
Main descending pathway for upper motor neurons is
the lateral corticospinal tract
- Upper motor neurons (pyramidal ) , with cell bodies in cortex or brainstem
- Lateral corticospinal tract is the primary pathway through which fine, skilled movements are controlled.
medullary pyramid versus pyramidal Betz cells.
- Motor cortex contains large projection neurons that originate in layer V and project directly to the anterior horn cells of the spinal cord via the corticospinal tract. When this tract passes through the medulla, it forms a pyramid like shape, and is thus sometimes called the pyramidal tract. This should not be confused with the pyramidal neurons (of which Betz cells are a subtype), which are the projection neurons in the cerebral cortex.
Cortical areas are distinguishable based on their
cytoarchitecture (cellular structure)
Sensory cortex: enlarged layer IV (inputs)
Motor cortex: enlarged layer V (outputs)
-Descending control is predominantly from neurons with cell bodies in the primary motor cortex.
-Again, multiple names – M1, Brodmann’s area 4, precentral gyrus, primary motor cortex.
layer V
Layer V is an output layer – in motor cortex, it’s thick, and contains many large pyramidal cells.
Betz cells represent about 10% of the total pyramidal cell population in layer Vb of the human primary motor cortex
Coarse somatotopic organization: the motor homunculus (little man)
There are 3 major representations in M1 – face; arms; legs.
Adjacent muscle groups are targeted by adjacent regions of cortex
Surface area in cortex is proportional to level of fine muscular control
Electrical stimulation of the cortex revealed somatotopic organisation
Fritsch & Hitzig (1870): in anaesthetized dogs, electrical stimulation of frontal cortex elicited contralateral movements Wilder Penfield (1930-1950s): weak electrical stimulation in area 4 elicits contralateral muscle twitches
Question: how is primary motor cortex organised?
One approach: electrical stimulation.
The concept of a cortical region systematically organized to control movements of different body parts was first hypothesized by Hughlings Jackson in the 1870s, based on his observations of certain epileptic patients in whom convulsive movements systematically marched from one part of the body to adjacent parts
Penfield’s experiments: awake patient. Probing cortex to remove epilepsy foci – but don’t want to remove “important” parts of the brain. So they map the brain – electrically stimulate and observe where they twitch or feel some sensation when cortex is stimulated.
Penfield’s results revealed somatotopic organisation
– adjacent regions of cortex control adjacent muscle groups (to a degree)
Note – there is not a direct correspondence between a region of cortex and a specific muscle – upper motor neurons are more associated with simple movements that involve related muscle groups
There is no sequentially ordered representation of adjacent muscles!
We rarely activate a single muscle – motor cortex is set up to facilitate control of multiple muscles
(In contrast, somatosensory cortex is very precisely organized)
Localising motor neuron damage
Lateral corticospinal tract – 80-90% of fibres decussate in medullary pyramids
Anterior corticospinal tract – remainder of fibres decussate where they exit the spinal cord
Unilateral lesions:
UMN lesions above pyramidal decussation
UMN lesions above pyramidal decussation affect contralateral side
UMN lesions below the decussation affect
the ipsilateral side
LMN lesions produce
ipsilateral paralysis and atrophy
control of muscles in the head and neck
(mediated by cranial nerve nuclei rather than spinal cord).
cervical lesions will affect
thoracic lesions will affect
Lesion in brain =>
Lesion below decussation =>
cervical lesions will affect all 4 limbs
-thoracic lesions will affect lower limbs
Lesion in brain => Contralateral paralysis
Lesion below decussation => ipsilateral paralysis
Hemiplegia / paraplegia / quadraplegia
Hemiplegia
Hemiplegia is a condition caused by brain damage or spinal cord injury that leads to paralysis on one side of the body. It causes weakness, problems with muscle control, and muscle stiffness
Lower motor neuron lesions
Caused by trauma, ischemia or infection
Flaccid Paralysis (-plegia)
lesion in all of the lower motor neuron associated with a muscle
• Loss of motor control
• e.g. hemiplegia / paraplegia / quadraplegia
Paresis
lesion in some of the lower motor neuron associated with a muscle Weakness / incomplete paralysis Voluntary power is impaired over time we can observe Muscle atrophy •muscle fibers lose their contractile proteins Areflexia •Loss of reflexes (circuitry is missing)
hemiplegia due to damage in spinal cord or cortex?
spinal cord injury as it involves lower motor neuron lesion
Maintenance of muscle bulk depends on receiving
inputs
Motor neuron disease / Amytrophic lateral sclerosis / Lou Gherig’s disease
Progressive degeneration of upper & lower motor neurons
Muscles weaken and denervate, leading to fasiculations and atrophy
Eventually lose the ability to control all voluntary movement
Upper motor neuron lesions have different short-term and long-term symptoms
First day - Immediate symptoms (spinal shock)
Flaccidity
Hypotonia (decreased spinal cord activity)
Areflexia
Subsequent long-term symptoms
Loss of fine / fractionated movements
Spasticity (hyper-reflexia and hyper-tonia)
Babinski sign
Hyper-reflexia
- Descending pathways normally inhibit or dampen reflexive responses
- Upper motor neuron damage (loss of descending inhibition) leads to exaggerated reflexes
- Clonus - sustained stretch causes rhythmic cycles of reflexive contraction + relaxation
Hypertonia
Increased resistance to passive muscle stretch e.g. increased activation of bicep and triceps making it harder to move - ongoing
reflects ongoing contractile activity in muscle (antagonist muscle groups)
due to hyper-excitability and tonic input from muscle stretch receptors
Babinski sign
Pathological dorsiflexion + toe fanning
Reflects damage to upper motor neurons / corticospinal damage
(Not evident in infants, as corticospinal pathways immature)
In normal adults, stroking the sole of the fit leads to plantar-flexion, especially in the big toes.
Following damage to upper-motor neuron pathways, stimulation of the sole leads to extension and fanning of the toes.
In human infants, corticospinal pathways are not complete matured, so a similar response occurs – evidence for incomplete upper motor neuron control of the alpha motor neuron circuitry.
