S5) The Motor System

Question 1

What are the primary components of the somatic motor system?

Answer 1

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

Question 2

What is a lower motor neurone?

Answer 2

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

Question 3

What controls LMNs?

Answer 3

They are controlled by upper motor neurones, which descend through the cord or brainstem
and synapse on LMNs

Question 4

Where is the cell bodies of a lower motor neurone found?

Answer 4

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)

Question 5

What do lower motor neurones do?

Answer 5

LMNs participate in spinal reflexes, particularly the deep tendon reflexes

Question 6

What are primitive spinal reflexes and when are they seen?

Answer 6

Primitive spinal reflexes are reflexes which exist in babies but disappear as a baby grows due to maturation of descending upper motor neurone pathways

Question 7

LMNs can be activated and inhibited.

Describe how they are activated

Answer 7

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)

Question 8

When LMN are damaged, identify 5 signs that can be seen.

Answer 8

• 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)

Question 9

Describe the role of the interneuron in the reflex arc at the knee

Answer 9

• Inhibitory interneuron inhibits the contraction of the flexor hamstring muscles
• Stimulatory interneuron stimulates the contraction of the extensor muscles - quadriceps muscles

Question 10

Spinal reflexes - modulation and coordination

Answer 10

Question 11

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?

Answer 11

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

Question 12

What are the five principle features of LMN damage?

Answer 12

• Fasciculations
• Muscle atrophy
• Hyporeflexia/ areflexia
• Hypotonia/ atonia
• Flaccid muscle weakness or paralysis

Question 13

Explain the pathophysiology of the fasciculations seen in LMN damage

Answer 13

Fasciculations caused by uncoordinated muscle contractions due to up-regulation of muscle nAChRs to try to compensate for damaged motor neurones (denervation)

Question 14

Explain the pathophysiology of the muscle atrophy seen in LMN damage

Answer 14

Muscle atrophy is caused by the loss of neurotrophic growth factors from the α-motor neuron to the muscle membrane (across neuromuscular junction)

Question 15

Explain the pathophysiology of the hyporeflexia seen in LMN damage

Answer 15

Hyporeflexia/areflexia caused by disruption of the efferent portion of the reflex arc leading to decreased/absent reflexes

Question 16

Explain the pathophysiology of the hypotonia seen in LMN damage

Answer 16

Hypotonia / atonia caused by loss of muscle activation due to loss of α-motor neurons

Question 17

Explain the pathophysiology of the muscle weakness seen in LMN damage

Answer 17

Flaccid muscle weakness due to α-motor neuron damage, muscles receive a weakened/absent signal to contract

Question 18

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

Answer 18

Question 19

What is an upper motor neurone?

Answer 19

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

Question 20

Where is an upper motor neurone found?

Answer 20

An upper motor neuron originates either in the primary motor cortex (pre-central gyrus) / in the brain stem (CNS)

Question 21

UMNs synapse onto …

Answer 21

They synapse onto LMNs directly (or indirectly) in the ventral horn or cranial nerve motor nuclei

Question 22

Where in the CNS are upper motor neurones absent?

Answer 22

• Basal ganglia
• Cerebellum

Hence, damage to these structures does not cause an UMN syndrome

Question 23

What effect do UMNs have on LMNs?

Answer 23

The net effect of UMNs on LMNs is inhibitory (inhibition > stimulation) .: explains most of the features of UMN lesions.

Question 24

Describe the 8 structures which the descending axons of UMNs pass through

Answer 24

⇒ 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

Question 25

What is the role of the lateral corticospinal tract?

Answer 25

The **lateral corticospinal tract** is involved with f**ine motor control in the limbs**, primarily the **distal extremities** (but all of limb can be affected by a UMN lesion)

Question 26

Describe the anatomical course of UMNs that innervate facial structures (i.e. structures innervated by cranial nerves not spinal nerves)

Answer 26

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

Question 27

Explain how the facial motor nucleus differs from a usual cranial nerve motor nucleus

Answer 27

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)

Question 28

Explain how the facial motor nucleus functions

Answer 28

- 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**

Question 29

Explain how UMN lesions differ from true facial nerve palsies

Answer 29

- **UMN lesions** involving the **face will spare the forehead** - **True facial nerve palsies** will affect all of the muscles of facial expression

Question 30

What are the four principle features of UMN damage?

Answer 30

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**

Question 31

Explain the pathophysiology of the weakness seen in UMN damage

Answer 31

**Weakness** due to loss of direct excitatory inputs onto LMNs from UMNs

Question 32

Explain the pathophysiology of the hypertonia seen in UMN damage

Answer 32

**Hypertonia** due to loss of descending inhibition (net effect of UMNs on LMNs is inhibition)

Question 33

Explain the pathophysiology of the hyperreflexia seen in UMN damage

Answer 33

**Hyperreflexia** due to loss of descending inhibition (an overactive reflex arc)

Question 34

Explain the pathophysiology of the extensor plantar reflexes seen in UMN damage

Answer 34

**Extensor plantar reflexes** due to the loss of the descending modulation of spinal reflexes (reversion to the situation in a baby)

Question 35

What is spinal shock?

Answer 35

- **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.

Question 36

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

Answer 36

Question 37

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

Answer 37

Question 38

What is the internal capsule?

Answer 38

A **bidirectional white matter pathway connecting** the **cerebral hemisphere with the rest of the CNS**

Question 39

The internal capsule is superiorly and inferiorly continuous of which structures?

Answer 39

**Superiorly** continuous with the **corona radiata** **Inferiorly** continuous with the **cerebral peduncle of the midbrain**

Question 40

What does the internal capsule primarily contain?

Answer 40

Primarily contains **descending axons of upper motor neurones** but **also has ascending axons of third order sensory neurones**

Question 41

What does the internal capsule primarily contain?

Answer 41

Primarily contains **descending axons of upper motor neurones** but **also has ascending axons of third order sensory neurones**

Question 42

The internal capsule has 3 anatomical divisions visible on a transverse section. What are they?

Answer 42

1. Anterior limb 2. Genu 3. Posterior limb

Question 43

The anterior limb is found between which two structures.

Answer 43

Anterior limb is found between: lentiform nucleus and the caudate nucleus.

Question 44

What is the purpose of the anterior limb?

Answer 44

* **Relatively unimportant** for your purposes * Contains **axons connecting** the **motor cortex with the cerebellum**

Question 45

What is the purpose of Genu?

Answer 45

* The **‘bend’** in the internal capsule * Contains **axons of upper motor neurones** **supplying the face**

Question 46

The posterior limb is found between which two structures?

Answer 46

It is found between the lentiform nucleus and the thalamus

Question 47

What is the purpose of the posterior limb of the internal capsule?

Answer 47

* 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

Question 48

What is the corticofugal fibres?

Answer 48

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

Question 49

What is the internal capsule supplied by and why is the supply clinically important?

Answer 49

Supplied by the **lenticulostriate arteries** (**branches of the MCA**) .: very important structure when it comes to **lacunar strokes**

Question 50

The lateral CST supplies ..

Answer 50

Distal muscles

Question 51

At the decussation of the pyramids, around **85%** of axons decussate to form the **lateral CST**. The **remaining 15%** remain to form …

Answer 51

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**

Question 52

In the lateral CST, what does it supply from medial to lateral?

Answer 52

Question 53

What does the ventral CST supply?

Answer 53

The ventral CST supplies **proximal and trunk muscles**

Question 54

The cord is wide at the cervical enlargement (lower half of cervical segments). What does this correlate with?

Answer 54

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**

Question 55

At the thoracic levels, the spinal cord is narrow. This is a relatively boring section of the cord. Why is it narrow?

Answer 55

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**)

Question 56

The spinal cord is wide at the lumbosacral enlargement (lower lumbar segments and upper sacral). What does this correlate with?

Answer 56

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.**

Question 57

The spinal cord is narrow at the lower sacral levels (aka the conus medullaris). Why?

Answer 57

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.

Question 58

Describe the trends in the **amount of white matter** at **different cord levels.**

Answer 58

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**

Question 59

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.

Answer 59

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**

Question 60

The trajectories of axons in spinal cord injuries …

Answer 60

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

Question 61

Corticonuclear projections: Describe the innervation to trigeminal nucleus, facial nucleus and nucleus ambiguus.

Answer 61

Question 62

Identify the labels of the midbrain

Answer 62

Question 63

Normally, LMNs are held in a state of. …

Answer 63

**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!

Question 64

If you damage the CST pathway/ UMN pathway, what occurs?

Answer 64

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 ton**e 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**

Question 65

Compare the LMN lesion vs UMN lesion in terms of power, tone, rigid/flaccid, reflexes, fasciculation/ fibrillation and atrophy.

Answer 65

Question 66

Pathophysiology of hypertonia and spasticity (manifestation of hypertonia)

Answer 66

Question 67

When hypertonia occurs, why does the upper limb assume a flexed posture?

Answer 67

**All muscles are equally affected** - both flexors and extensors but in the upper limb, the f**lexors 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

Question 68

Fancy images ….

Answer 68

Question 69

Fancy images 2 …

Answer 69

Question 70

The lentiform nucleus is made of 2 structures. What are they?

Answer 70

1. Putamen (Darker) - found laterally 2. Globus pallidus (paler) - found medially - the globus pallidus has 2 further segments: the external and internal segments

Question 71

What is the fundamental relationship between motor and sensory systems?

Answer 71