S5) The Motor System Flashcards
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
Where is a lower motor neurone found?
A lower motor neurone is located in either the ventral horn of the spinal cord or the cranial nerve nuclei of the brainstem. Cell body in the CNS and its axon spreads to the PNS sending impulses to the rest of the body
What do lower motor neurones do?
LMNs participate in spinal reflexes, particularly the deep tendon reflexes
what are deep tendon reflexes
are involuntary reflexes that occur when a muscle is stretched. These reflexes are mediated by the spinal cord and are used to test the integrity of the nervous system.
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 (upper motor neurones) that communicate with muscle spindles (muscle stretch reflex)
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
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
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 in the CNS
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)
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), UPNs mainly inhibit LMNs
Describe the 8 structures which the descending axons of UMNs pass through in the lateral cortical spinal tract
⇒ Corona radiata
⇒ Internal capsule
⇒ Cerebral peduncle (connects cerebral hemisphere to the brainstem) in the midbrain
⇒ Pons
⇒ Medullary pyramids
⇒ Decussation of the pyramids (in the caudal medulla → lateral direction = lateral CST)
⇒ 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 leave the pathway in the brainstem and form the corticobulbar tract (aka corticonuclear tract) which innervates LMNs in the cranial nerve motor nuclei
found in the primary motor cortex (pre central gyrus) and synapse onto the LMN in the ventral horn or 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 (upper spares Upper)
- 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 (However, in individuals with certain neurological conditions or injuries, the stimulation of the sole of the foot can cause the toes to fan out and the big toe to extend upwards. This is called an extensor response, or a positive Babinski sign.)
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, following by hypertonia and thereafter hyporeflexia, so these are seen initially with an UMN lesion
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?
- bidirectional white matter pathway connecting cerebral hemisphere to the CNS
- corona radiata → internal capsule → cerebral peduncle
- primarily contains descending UMN and some 3rd order sensory neurones ascending
what three things does the internal capsule split into?
- anterior limb: axons connecting motor cortex with the cerebellum
- Genu: bend containing axons of UMN supplying face
- posterior limb: axons of UMN supplying upper limb, contains 3rd order sensory axons connecting thalamus to post central gyrus supplies most of the body
what is the posterior limb of the internal capsule supplied by?
lenticulostriate arteries (branches of the MCA)
what is the anatomy of the spinal cord at cervical end?
→ wide due to presence of brachial plexus
→ many LMN cell bodies and second order sensory neurones cell bodies to supply upper limbs
what is the anatomy of the spinal cord at the thoracic level?
→ narrow
→ few cell bodies due to few dermatomes and myotomes
→ contains the lateral horn (sympathetic preganglionic nerve fibres)
what is the the anatomy of the spinal cord at lumbosacral level?
→ wide
→ lumbosacral plexus
→ lots of LMN and second order sensory neurones to supply lower limbs
what is the anatomy of the spinal cord at the sacral level? (conus medullaris)
→ narrow
→ few muscles that need suppling in this level
→ S2-S4 contain parasympathetic preganglionic cell bodies and cell bodies of the LMN
how does the level of white matter vary at the different spinal cord levels?
→ C1 = maximum amount as it contains UMN axons
→ descend UMN → LMN in grey matter so white matter reduces
→ if you ascend up cord there is a gradual increase in white matter
what horns does the grey matter contain?
→ dorsal and ventral horns
→ most lateral In ventral horns are LMNs supplying distal muscles
→ most medial in ventral horns are LMNs supplying proximal muscles
what are the two types of rigidity?
- Lead pipe (seen in Parkinson’s) → constantly ridge
- Clasp Knife → pull on limb until the limb gives way. Caused by the Golgi apparatus
what is spinal shock
→ phenomenon that occurs in the days immediately following a UMN lesion, temporary as the spinal cord can regenerate:
→ flaccid paralysis with areflexia (absence of deep tendon reflexes)
→ tone then increases (hypertonia)
→ reflexes become exaggerated (hyperreflexia)
what is the role of the medial longitudinal fasiculus?
→ coordinates eye movements to maintain
→ provides connections between all the nuclei for conjugate eye movements
what is the area shaded called?
cerebral peduncles
what is the area shaded called?
red nucleus
what is the yellow area shaded called?
substantia nigra
what is the pink area shaded called?
→ spinothalamic fibres
→ medial lemniscus
(sensory fibres)
what is the white area in the middle called
cerebral aqueduct
what is the area shaded in squiggles in pink called
periaqueductal grey matter
what is the shaded area of green in the middle called
it is the nucleus if the oculomotor nerve and the nuclei of the edinger westphal that contains parasympathetic motor nerve fibres
what do the two curves at the bottom show?
superior colliculus
