S5) The Motor System Flashcards
What are the primary components of the somatic motor system?
Upper and lower motor neurones
Somatic motor system = involved in voluntary control .: damage to either upper or lower motor neurone → results in distinctive clinical features
What is a lower motor neurone?
A lower motor neuron (LMN) is a multipolar neuron which connects the upper motor neurone (UMN) to the skeletal muscle it innervates
They are the ‘final common path’, and when activated will cause muscle contraction
What controls LMNs?
They are controlled by upper motor neurones, which descend through the cord or brainstem
and synapse on LMNs
Where is the cell bodies of a lower motor neurone found?
A lower motor neurone’s cell body is located in either the ventral horn of the spinal cord or the cranial nerve nuclei of the brainstem (oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus etc)
What do lower motor neurones do?
LMNs participate in spinal reflexes, particularly the deep tendon reflexes
What are primitive spinal reflexes and when are they seen?
Primitive spinal reflexes are reflexes which exist in babies but disappear as a baby grows due to maturation of descending upper motor neurone pathways
LMNs can be activated and inhibited.
Describe how they are activated
LMNs are activated by incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex)
but can also be inhibited (best example is
inhibition of antagonist muscles such as hamstrings following patellar reflex activation)
When LMN are damaged, identify 5 signs that can be seen.
- Weakness (due to denervation)
- Areflexia (due to denervation)
- Wasting (due to loss of trophic support to the muscle from the LMN across the neuromuscular junction)
- Hypotonia (due to loss of muscle activation)
-
Fasciculation (due to up-regulation of muscle nAChRs to try to compensate for
denervation)
Describe the role of the interneuron in the reflex arc at the knee
- Inhibitory interneuron inhibits the contraction of the flexor hamstring muscles
- Stimulatory interneuron stimulates the contraction of the extensor muscles - quadriceps muscles
Spinal reflexes - modulation and coordination
Often reflexes occur in the absence of supraspinal input. But, inputs descending from the brain have an important modulatory rise upon the way that reflexes manifest themselves.
If patient has a stroke, what can occur?
The descending modulatory sites can be damaged → can result in reflexes manifesting itself in a different way.
e.g. in Babinski reflex - stimulation of the sole of the foot leads to flexion of the toes - normal response
If stroke → due to descending modulatory fibres damaged → can lead to extension of toes instead of flexion
What are the five principle features of LMN damage?
- Fasciculations
- Muscle atrophy
- Hyporeflexia/ areflexia
- Hypotonia/ atonia
- Flaccid muscle weakness or paralysis
Explain the pathophysiology of the fasciculations seen in LMN damage
Fasciculations caused by uncoordinated muscle contractions due to up-regulation of muscle nAChRs to try to compensate for damaged motor neurones (denervation)
Explain the pathophysiology of the muscle atrophy seen in LMN damage
Muscle atrophy is caused by the loss of neurotrophic growth factors from the α-motor neuron to the muscle membrane (across neuromuscular junction)
Explain the pathophysiology of the hyporeflexia seen in LMN damage
Hyporeflexia/areflexia caused by disruption of the efferent portion of the reflex arc leading to decreased/absent reflexes
Explain the pathophysiology of the hypotonia seen in LMN damage
Hypotonia / atonia caused by loss of muscle activation due to loss of α-motor neurons
Explain the pathophysiology of the muscle weakness seen in LMN damage
Flaccid muscle weakness due to α-motor neuron damage, muscles receive a weakened/absent signal to contract
Location of LMN and the cranial nuclei
The concept of:
– Dorsal horn extends up into the brainstem as a series of sensory nuclei
– Ventral horn extends up into the brainstem as a series of motor nuclei
What is an upper motor neurone?
An upper motor neuron is a neuron whose cell body originates in the cerebral cortex or brainstem and terminates within the brainstem or spinal cord
Where is an upper motor neurone found?
An upper motor neuron originates either in the primary motor cortex (pre-central gyrus) / in the brain stem (CNS)
UMNs synapse onto …
They synapse onto LMNs directly (or indirectly) in the ventral horn or cranial nerve motor nuclei
Where in the CNS are upper motor neurones absent?
- Basal ganglia
- Cerebellum
Hence, damage to these structures does not cause an UMN syndrome
What effect do UMNs have on LMNs?
The net effect of UMNs on LMNs is inhibitory (inhibition > stimulation) .: explains most of the features of UMN lesions.
Describe the 8 structures which the descending axons of UMNs pass through
⇒ Corona radiata
⇒ Internal capsule
⇒ Cerebral peduncle in the midbrain
⇒ Pons
⇒ Medullary pyramids
⇒ Decussation of the pyramids (in the caudal medulla)
⇒ Ventral horn
⇒ Synapse (directly/via inhibitory interneurones) on LMNs
What is the role of the lateral corticospinal tract?
The lateral corticospinal tract is involved with fine motor control in the limbs, primarily the distal extremities (but all of limb can be affected by a UMN lesion)
Describe the anatomical course of UMNs that innervate facial structures (i.e. structures innervated by cranial nerves not spinal nerves)
UMNs that supply facial structures (i.e. structures innervated by cranial nerves not spinal
nerves) leave the pathway in the brainstem and form the corticobulbar tract (aka corticonuclear tract) which innervates LMNs in the cranial nerve motor nuclei
Explain how the facial motor nucleus differs from a usual cranial nerve motor nucleus
The facial motor nucleus is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)
Explain how the facial motor nucleus functions
- The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres
- The part of the facial motor nucleus that supplies the lower face only receives a contralateral UMN input
Explain how UMN lesions differ from true facial nerve palsies
- UMN lesions involving the face will spare the forehead
- True facial nerve palsies will affect all of the muscles of facial expression
What are the four principle features of UMN damage?
When UMNs are damaged, the following signs are evident in the parts of the body supplied by the relevant UMNs:
- Weakness
- Hypertonia
- Hyperreflexia
- Extensor plantar reflexes
Explain the pathophysiology of the weakness seen in UMN damage
Weakness due to loss of direct excitatory inputs onto LMNs from UMNs
Explain the pathophysiology of the hypertonia seen in UMN damage
Hypertonia due to loss of descending inhibition (net effect of UMNs on LMNs is inhibition)
Explain the pathophysiology of the hyperreflexia seen in UMN damage
Hyperreflexia due to loss of descending inhibition (an overactive reflex arc)
Explain the pathophysiology of the extensor plantar reflexes seen in UMN damage
Extensor plantar reflexes due to the loss of the descending modulation of spinal reflexes (reversion to the situation in a baby)
What is spinal shock?
- Spinal shock is a phenomenon that occurs in the days immediately following a UMN lesion
- Initially there is flaccid paralysis with areflexia (like in LMN lesions), following by hypertonia (increased tone) and thereafter hyperreflexia
Mechanism of this is unclear, but is related to the neuroplasticity in the spinal cord.
A motor homunculus represents a map of brain areas dedicated to motor processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.
Describe the layout of the motor homunculus
A sensory homunculus represents a map of brain areas dedicated to sensory processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.
Describe the layout of the sensory homunculus
What is the internal capsule?
A bidirectional white matter pathway connecting the cerebral hemisphere with the rest of the CNS
The internal capsule is superiorly and inferiorly continuous of which structures?
Superiorly continuous with the corona radiata
Inferiorly continuous with the cerebral peduncle of the midbrain
What does the internal capsule primarily contain?
Primarily contains descending axons of upper motor neurones but also has ascending axons of third order sensory neurones
What does the internal capsule primarily contain?
Primarily contains descending axons of upper motor neurones but also has ascending axons of third order sensory neurones
The internal capsule has 3 anatomical divisions visible on a transverse section. What are they?
- Anterior limb
- Genu
- Posterior limb
The anterior limb is found between which two structures.
Anterior limb is found between:
lentiform nucleus and the caudate nucleus.
What is the purpose of the anterior limb?
- Relatively unimportant for your purposes
- Contains axons connecting the motor cortex with the cerebellum
What is the purpose of Genu?
- The ‘bend’ in the internal capsule
- Contains axons of upper motor neurones supplying the face
The posterior limb is found between which two structures?
It is found between the lentiform nucleus and the thalamus
What is the purpose of the posterior limb of the internal capsule?
- Contains axons of upper motor neurons supplying upper limb, trunk and lower in that order from anterior to posterior
- Also contains third order sensory axons connecting thalamus to postcentral gyrus
o Like the UMN axons, these fibres run in the order face-arm-trunk-leg from front to back
What is the corticofugal fibres?
Less vital parts of the internal capsule - fibres running from the cerebral cortex downwards - called corticofugal fibres – going from the cortex away from the brain
What is the internal capsule supplied by and why is the supply clinically important?
Supplied by the lenticulostriate arteries (branches of the MCA)
.: very important structure when it comes to lacunar strokes
The lateral CST supplies ..
Distal muscles
At the decussation of the pyramids, around 85% of axons decussate to form the lateral CST. The remaining 15% remain to form …
The remaining 15% remain ipsilateral and descend in the ventral funiculus as the ventral CST
At the level of the target LMN, the ventral CST axons decussate
In the lateral CST, what does it supply from medial to lateral?
What does the ventral CST supply?
The ventral CST supplies proximal and trunk muscles
The cord is wide at the cervical enlargement (lower half of cervical segments). What does this correlate with?
This correlates with the presence of the brachial
plexus at these levels
There are many LMN cell bodies and second order sensory neurone cell bodies at these levels to supply the upper limbs
At the thoracic levels, the spinal cord is narrow. This is a relatively boring section of the cord. Why is it narrow?
Narrow since there are relatively few LMN cell
bodies and second order sensory cell bodies due
to relatively small dermatomes and myotomes at
thoracic levels
However, remember that these levels of the cord (as well as down to about L2) have the lateral horn which contains sympathetic preganglionic cell
bodies)
The spinal cord is wide at the lumbosacral enlargement (lower lumbar segments and upper sacral). What does this correlate with?
This correlates with the presence of the
lumbosacral plexus.
There are many LMN cell bodies and second order sensory neurone cell bodies at these levels to supply the lower limbs.
The spinal cord is narrow at the lower sacral levels (aka the conus medullaris). Why?
Relatively few muscles that need supplying and
small area of skin
However, don’t forget that S2-S4 contains parasympathetic preganglionic cell bodies (in a
region homologous to the lateral horn) as well as
the cell bodies of LMNs that distribute to the perineum in the pudendal nerve.
Describe the trends in the amount of white matter at different cord levels.
the amount of grey matter at each level varies depending upon the presence/absence of limbs.
White matter follows a different pattern:
o At the top of the cord (C1) there is the maximum
amount of white matter since it contains UMN
axons yet to be distributed as well as the
convergence of all sensory axons from levels
below
▪ As we descend the cord the UMN axons are
distributed to LMNs in the cord grey matter (hence as we descend number of UMN
axons decreases)
▪ As we ascend the cord from the bottom
sensory axons are gradually added
▪ The net effect of the above is a gradual increase in total white matter as we ascend the cord
The dorsal and ventral horns can be thought of as cell columns running the length of the cord (they are not tracts!).
Within these columns we have subdivisions containing groups of LMN cell bodies (as well as groups of sensory cell bodies etc)
Describe the LMNs positioned in the ventral horn and what they supply.
o Sitting most laterally in the ventral horn are LMNs supplying distal muscles
▪ This makes sense as they sit closest to the
lateral CST which supplies distal muscles
o Sitting most medially in the ventral horn are LMNs supplying proximal muscles
▪ This makes sense as they sit closest to the
anterior/ventral CST which supplies
proximal muscles
The trajectories of axons in spinal cord injuries …
This is not core material, but I could not very well ignore it since the lesion was sitting right there in the cord!
Interesting to note how the axons go all over the place, which suggests that there might have been some limited regrowth or plasticity of axons after the injury
Corticonuclear projections:
Describe the innervation to trigeminal nucleus, facial nucleus and nucleus ambiguus.
Identify the labels of the midbrain
Normally, LMNs are held in a state of. …
Inhibition.: if you wish to move voluntarily, you need to send strong action potentials via these excitatory pathways and active the LMNs. But during the normal resting behaviour, the net effect of UMNs on LMNs is inhibition!
If you damage the CST pathway/ UMN pathway, what occurs?
Have deprived the LMN of its inhibition but excitatory inputs from the sensory neurons are still present .: activity of LMN also increases hence resulting in increased muscle tone.
However, initially we have immediate decrease in muscle tone due to the ‘spinal shock’ phenomenon - if we acutely deprive LMN of a large number of its inputs → its activity level decreases .: sends fewer impulses to its muscles .: hypotonia. This is the period of spinal shock. Then it wears off and we get hypertonia due to more and more response to the inputs from the muscle spindles and because it no longer has the descending inhibition .: activity increases even further .: this monosynaptic reflex goes into overdrive = hypertonia
Compare the LMN lesion vs UMN lesion in terms of power, tone, rigid/flaccid, reflexes, fasciculation/ fibrillation and atrophy.
Pathophysiology of hypertonia and spasticity (manifestation of hypertonia)
When hypertonia occurs, why does the upper limb assume a flexed posture?
All muscles are equally affected - both flexors and extensors but in the upper limb, the flexors are more powerful.: we get the typical flexed posture in a spastic upper limb (due to overactivity in the mono-synaptic reflex arc due to removal of inhibition on the LMNs)
Hence we get the flexed elbow, wrist and fingers
Fancy images ….
Fancy images 2 …
The lentiform nucleus is made of 2 structures. What are they?
- Putamen (Darker) - found laterally
- Globus pallidus (paler) - found medially - the globus pallidus has 2 further segments: the external and internal segments
What is the fundamental relationship between motor and sensory systems?
