Motor System Flashcards
What are lower motor nerones
• They are the ‘final common path’, and when activated will cause muscle contraction
• They are controlled by upper motor neurones, which descend through the cord or brainstem
and synapse on LMNs
• They participate in spinal reflexes, particularly the deep tendon reflexes (highly clinically
relevant)
Whee are the cell bodies of lower motor neurones located
NC motor nuclei in the brainstem (which is like an upward extension of the cord), and the venal horn of the cord. The ventral horn has the majority of lmns in the cns
Describe the descending influences on lmns
Vast majority of descending influences on lmns are inhibitory.
There is net inhibition of lmns by umns vis inhihibitory interneurones
Most umn signs due to damage so no inhibition leading to hyperactity of lmn
• They are typically activated by incoming impulses from sensory neurones that communicate
with muscle spindles (muscle stretch reflex), but are also inhibited (best example is inhibition of antagonist muscles such as hamstrings following patellar reflex activation)
Describe the maturation of inhibitory reflex’s in babies
• ‘Primitive’ spinal reflexes exist in babies:
- Plantar reflex- in babies toes extend, in adults flex when sole stimulated
- Moro reflex - drop baby slightly - arms extend and then flex
- Palmar grasp reflex
But these reflexes disappear as a baby grows due to maturation of descending upper motor neurone pathways
Maturation of inhibitory influences means babies have some reflex that adults dont - lose about the time at which they learn to walk.
What are the signs of lmn lesions
Signs of lmn lesion
• weakness
• Wasting
• Loss of trophic factors (muscle constantly receives growth factors from lmn to keep it alive - if you destroy it, it can no longer supply these, hence wasting)
• Hypertonia (normal tone - not much resistance moving a relaxed joint. Babies are hypotonic. Damage to lmn - no constant low level of big activity - muscles go limp bc lost their wiring)
• Areflexia (if lmn broken - lost spinal reflex)
• Fibrillations Fasiculations ? ( involuntary contractions of skeletal muscle. Thought to be of upregulation of nachrs in muscle. - increased amounts of receptors
What are umns
• They synapse onto LMNs directly (or indirectly) in the ventral horn or cranial nerve motor
nuclei
1. Hence, neurones in the basal ganglia and cerebellum are NOT upper motor
neurones (damage to these structures does not cause an UMN syndrome, but
something completely different)
• The net effect of UMNs on LMNs is inhibition – this explains most of the features of UMN
lesions
Where are umn call bodies located
Primary motor cortex
What is the corona radiata
White matter sheet - both ascending and descending axons to and from the cerebral cortex
What is the internal capsule
White matter located between letiform nucleus and thalamus. Axons coalesce here. Cortex-body interactions. It also encapsulates the thalamus
Describe 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)
M1 -> corona radiata -> internal capsule -> cerebral peduncle -> through brainstem -> decussate a caudal medulla - decussation of the pyramids -> descend down cor -> synapse on lmns -> lmn -> distal muscle
Describe the corticobulbar tract
Aka corticonuclaear
• 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 (aka the corticonuclear) tract, which innervates LMNs in the cranial nerve motor nuclei
M1 -> corona radiata -> internal capsule -> peduncle -> brainstem -> cn motor nuclei -> lmn ->facial structures
Corticobulbar - some decussate - dont need to know details except facial nerve
Describe the ventral/anterior cst
M1 -> corona radiata -> internal capsule -> peduncle -> brainstem -> decussate at level of lmn -> lmn -> proximal postural muscle
Describe umn lesions involving the face
- The facial motor nucleus is a special case of a cranial nerve motor nucleus, in that it is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)
- The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres, whereas the part that supplies the lower face only receives a contralateral UMN input
- Hence UMN lesions involving the face will spare the forehead (as opposed to true facial nerve palsies which affect all of the muscles of facial expression)
What are umn lesion signs
UMn signs
• weakness (umn damaged, lost influence on lmn
• Hypertonia - spasticity (hypertonia in muscles - equal in flexors and extensors - in upperlimb flexors more powerful so limb flexed. Lower limb reverse so lower limb extended) clasp knife reflex - applying force to leased limb - resistance but suddenly gives way
Get this bc overactivity in lmns
• Hyperreflexia - (remove descending inhibition - overexaggesrated reflexed)
• Extensor plantar reflexes (complex reflexes messed up.. interrupted descending projections
When doing plantar - dont tough big toe bc big toe response to touch is dorsiflextion
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) but then tone increases (becoming hypertonia) and reflexes become exaggerated (hyperreflexia). The mechanism of this is unclear, but is related to neuroplasticity in the spinal cord
Immediately after an upper motor neurone lesion, lower motor neurones actually decrease their level of activity. This means that in the early phase of a stroke for example, a patient will actually have hypotonia and hyporeflexia. Only after a few days to weeks will this then convert into the classic UMN syndrome.
