Session 5: Motor system, basal ganglia, cerebelleum Flashcards
properties of upper motor neurones including their action on lower motor neurones
include:
Cell body, axon, targets,
· Cell body – in CNS, motor cortex (pre-central gyrus) [NOT IN THE BASAL GANGLIA, CEREBELLUM,)
· Axon – in CNS, projects down the spinal cord
· Target – cell body of lower motor neurone/ cell body of inhibitory interneurones
action of UMN on LMN
UMN r ALWAYS excitatory upon the neurones that they exert their action upon.
- However, when all charges add up (see pic)>> the net effect of UPN on LMN is inhibitory.
§ Must excite LMN to tell them what to do (occure lesser extent)
§ Can inhibit LMN by exciting inhibitory interneurones (this occurs to a greater extent)
function of basal ganglia and cerebellum on LMN?
they regulate their activity but do NOT participate in them!
Basal ganglia functions
malfunction of the basal ganglia are implicated in neurological illnesses such as:
- Motor function
- Psychological function:
- **- Emotion
- Cognition***
- Behaviour
- Parkinson’s disease
- **- Wilson’s disease
- Huntington’s disease***
UMN disease?
is a clinical term used to denote interruption of the corticospinal tract somewhere along its course
early and late signs of UMN lesion
EARLY SIGNS:
· Weakness – interrupted path of impulses from cortex to LMN
LATE SIGNS (days to wks):
· Hypertonia – increased muscle tone (eg. Try to move someone’s muscle but cannot because too rigid). This is because the net effect of the UMN on the LMN is inhibitory. Therefore, loss of descending inhibition leads to increased activity of the LMN.
· Hyperreflexia – enhanced reflexes.
· Extensor plantar reflex :=”Babinski sign” –
Is it easier to elicit a reflex on a healthy or a person w/ stroke?
- In a healthy patient, it is usually quite difficult to elicit a reflex.
- In a patient with a stroke, it is easier to elicit reflexes due to increased activity of the LMN
remember UMN effect on LMN is inhbitory, in ppl w/ stroke this inhibiton is lost and u get hyperreflexia
properties of lower motor neurones and their involvement in the spinal reflex arc
include:
Cell body, axon, targets,
· Cell body – in CNS, ventral horn of spinal cord/brainstem motor nuclei
· Axon– in PNS, project with peripheral nerves to muscles
· Target – skeletal muscle
· Features
o ‘Point of no return’ – once stimulated, there will be contraction of skeletal muscle
o Involved in reflex arcs
· Damage – can be damaged by CNS lesions (cell body) or PNS lesions (axon)
look at some specific reflex arcs
ex: babinski and patella tendon
babinski reflex
adults vs babies
in babies it always positive, bc their CNS is unmyelinated!
consider the effects of lower motor neurone lesions
look at the pathways through which UMN project to LMN
signs of LMN lesion
· Weakness – interrupted the path of impulses from neurone to muscle
· Areflexia – absence of reflexes as the last part of the reflex arc is damaged
· Wasting – lower motor neurone provides the muscle with trophic factors (growth factors)that cross the synapse and interact with the muscle membrane so these are absent. This takes some time to develop so will be a delayed sign
· Fasciculation – uncoordinated muscle contractions
- fibrillation
· Hypotonia – decreased muscle tone due to interruption of the path of impulses from neurone to muscle leading to lack of constant low level stimulation and contraction (eg. Muscle tone of a baby)
what r fasciculations vs fibrillation? why do they arise?
which are visible twitches of small groups of muscle fibres in the early stage of wasting.
They arise from spontaneous discharge of motor neurons with activation of motor units
most common form of MND? (motor neuron disease)
amyotrophic sclerosis (ALS)
ALS is characterised by a combination of upper and lower motor neuron signs; there are rarer, pure lower (progressive muscular atrophy) or upper (progressive lateral sclerosis) motor neuron variants of MND.