Images ✏️ For MOTOR System Flashcards
Where are LMN cell bodies found?
In the ventral horn
and in cranial nerve motor nuclei
(oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus etc)
Axon then projects into PNs to muscles
What is a LMN?
All voluntary movement relies on spinal lower motor neurons, which innervate skeletal muscle fibers and act as a link between upper motor neurons and muscles. Cranial nerve lower motor neurons control movements of the eyes, face and tongue, and contribute to chewing, swallowing and vocalization.
- they participate in spinal reflexes particularly deep tendon reflexes
How are LMNs typically activated and how are they controlled?
- activated by incoming impulses from sensory neurones that communicate with muscle spindles (stretch receptors) but can also be inhibited
- Controlled by UMNs
Function of UMNs
Responsible for conveying impulses for voluntary motor activity through descending motor pathways
They send fibres to LMNs that exert direct or indirect (through interneurones) supranuclear control over the LMNs of cranial and spinal nerves
Give examples of primitive spinal reflexes that exist in babies, why do these disappear as the baby grows? What could they indicate if they are persistent in adults?
Upgoing planter (Babinski’s sign in adults) - stimulate sole of foot with blunt instrument then big toe goes up and other toes fan out (should all curl down) if remains shows disease of CNS
Moro reflex - hold head and shoulders off mat with arms flexed, then let go -> arms should extend and abduct before returning to midline with thumb and index finger forming a C (if it remains longer than 6 months could indicate cerebral palsy)
Palmar grasp (if in adults could show frontal lobe damage or anterior cerebral artery syndrome)
Should Disappear as baby grows due to maturation of descending ulcer motor neurone pathways (through inhibitory interneurones)
What signs are seen in muscles if their LMNs are damaged?
- weakness (denervation)
- a reflex is (denervation)
- wasting (in Myotomes, loss of trophic factors to muscle)
- hypotonia (loss muscle activation)
- fasciculation (up regulation of muscle nAChRs to try compensate for denervation)
Where are UMNs cell bodies found and where do they synapse onto LMNs?
Found in the primary motor cortex (precentral gyrus) whole neurone in CNS only and synapse onto LMNs directly or indirectly in the ventral horn or cranial nerve motor nuclei
What is the next effect of UMNs on LMNs?
Inhibition of muscle contraction (=relaxation)
Describe the structures the majority of UMNs axons descend through from the motor cortex to reach their LMN
Corona radiata
Internal capsule (between lentiform nucleus and thalamus)
Cerebral peduncle (midbrain)
Pons
Medullary pyramids
Decussation of pyramids (caudal medulla)
Lateral corticospinal tracts (in lateral funiculus) fine motor control primarily distal musculature 85%*
Ventral horn
Synapse directly (but usually indirectly via inhibitory interneurones) on LMNs
*15% stay on ipsilateral side through ventral corticospinal tract until at Same level as LMN (important for posture e.g. spinal muscle/ gluteals)
What do UMNs that supply facial structures (innervated by cranial nerves not spinal) descend through?
Corona radiata
Internal capsule
Leave the pathway at the Brainstem
Form corticobulbar (aka corticonuclear) tract
Innervate LMNs in cranial nerve motor nuclei (e.g. facial motor nucleus)
Describe how the facial motor nucleus for CN 7 is innervated and what it supplies. What does this arrangement mean for UMN lesions involving the face/ stroke of middle cerebral artery?
Facial motor nucleus is a special case of CN motor nuclei that is split in two halves superior half (which contains LMN cell bodies that supply the upper half of the face I.e forehead mostly occipitofrontalis) and inferior half (lower half of the face, most remaining muscles of facial expression)
The superior half receives UMNs from both hemispheres whereas the inferior half only receives contralateral UMN input
So if there’s an UMN lesion involving the face the forehead will be spared (bilateral innervation) as opposed to true facial nerve palsies which affect all muscles of facial expression
Slide 4
What signs are evident in parts of the body supplied by damaged UMNs? When wouldn’t these signs be present?
- weakness (loss of direct excitatory inputs onto LMNs)
- hypertonia (loss of descending inhibition - spasticity flexed position upper limbs, extended lower limbs)
- clasp- knife rigidity (pull and eventually rigidity gives way as Golgi tendons turns off hyperreactive neurones)
- hyperreflexia (overactive reflex arc due to loss of descending inhibition)
- extensor plantar reflexes (loss of descending modulation of spinal reflexes)
Wouldn’t be present initially due to spinal shock - ACuTe flaccid paralysis (before hypertonia)
And also wouldn’t be present if LMN damaged too bc loss of descending inhibition would have no effect
What is spinal shock?
A phenomenon that occurs in days following UMN lesion - initially flaccid paralysis with areflexia then tone increases (hypertonia) and reflexes become exaggerated (hyperreflexia) mechanism is unclear but related to neuroplasticity in spinal cord
In the lateral corticospinal tract (that 85% UMNs take) how does the upper body add on?
Upper body adds medially e.g. higher up the body part the more medial its axons are found in the tract
What could a central cord lesion affect?
A central cord lesion can affect dorsal column, spinothalmic and lateral corticospinal tracts differentially
