8. Motor Pathway Flashcards
Explain the functional segregation of the motor system
Organised into different areas that control different aspects of movement
Describe the hierarchial organisation of the motor system.
- High order areas are involved in complex tasks (programme + decisions on movements, coordinate muscle activity)
- Lower levels perform lower level tasks (execution of movement)
Describe the pyramidal system.
- The primary motor cortex receives information from all the sensory cortices (sight, hearing, taste, smell) –> processed in the thalamus
- Sends instructions to the spinal cord (via brainstem) and alpha motor neurones
- Goes to musculature

Describe the extrapyramidal system.
This is the cerebellum and the ganglia
- These fine tune the instructions from the primary cortex before it goes to the spinal cord
- Cerebellum is important in motor learning and fine movement

What do the nuclei in the brainstem supply.
The nerves of the face.
Locate the primary motor cortex and define its function

- Location: precentral gyrus, anterior to central sulcus
- Primary tract = pyramidal tract
- Function: control fine, discrete, precise voluntary movement
- Provide descending signals to execute movement –> thus, a low-order area
- In layer 5, have large Betz/pyramidal cells to support long axons
- There’s also somatotopic organisation: Penfield’s motor homunculus

What are the descending motor pathways?
Lateral corticospinal tract and anterior corticospinal tract
Describe the lateral corticospinal tract.
- Motor neurone send axons down through subcortical structures – fibre pathway called internal capsule
- Internal capsule becomes cerebral peduncles
- Pass through pons
- At base of medulla, 95% of fibres cross over at pyramids –> descend in lateral corticospinal tract. Decussation forms basis of contralateral motor control
- At appropriate level, synapse with alpha-motor neurones –> go out ventral root –> spinal nerve –> effector

Describe the Anterior Corticospinal Tract.
- Motor neurone send axons down through subcortical structures – fibre pathway called internal capsule
- Internal capsule becomes cerebral peduncles
- Pass through pons
- At base of medulla, 5% of fibres don’t decussate at pyramids
- Carry on down to form anterior corticospinal tract
- These fibres support axial musculature
- When it reaches the appropriate level, decussation occurs in spinal cord
Describe the corticobulbar pathways.
Same but related to motor nuclei in brainstem
M1 projections going to brainstem structures e.g. hypoglossal nucleus –> innervate tongue muscles

Describe the location and function of the premotor cortex

- Location: frontal lobe anterior to M1
- Function: planning of movements = high-order area
- Regulates externally-cued movements e.g. seeing apple + reaching out for it, need to move body part relative to another body part (intra-personal space) AND move body in environment (extra-personal space)

Describe the Location and function of the supplementary motor area.

- Location: frontal lobe anterior to M1, medially
- Function: planning complex movements; programming sequencing of movements
- Regulates internally-driven movements (e.g. speech) – higher order area
- SMA becomes active when thinking about a movement before executing

Describe the Association Cortex

- Not strictly motor areas as their activity doesn’t correlate with motor output/act
- Posterior parietal cortex: ensures movements targeted accurately to external objects
- Prefrontal cortex: selection of appropriate movements for a course of action

Define Lower Motor Neuron
(spinal cord + brainstem) = the neurone found in ventral horn and its processes going out to musculature; also found in brainstem e.g. hypoglossal nucleus
Define upper motor neuron
found in M1 = fibres go down Corticospinal + corticobulbar tracts to next motor neurones in chain
Define pyramidal
defines lateral corticospinal tract
Define extrapyramidal.
relate to basal ganglia + cerebellum, rather than primary motor tract
What are the signs of upper motor neuron lesions?
-
Negative signs = Loss of function:
- Paresis: graded weakness of movements
- Paralysis (plegia): complete loss of activity of muscle
-
Positive signs = increased motor function due to loss of inhibitory descending inputs:
- Spasticity: increased muscle tone
- Hyper-reflexia: exaggerated reflexes
- Clonus: abnormal oscillatory muscle contraction
-
Babinski’s sign (videos in Dr Strutton’s lecture)
- Normally when run pen down sole of foot, foot should point down
- But in Babinski’s sign, foot extends + points upwards
-
Apraxia: disorder of skilled movement –> high-order issue
- NOT paretic, but have lost info about how to perform skilled movements
- Lesion of inferior parietal lobe, frontal lobe (premotor cortex, SMA) –> can cause apraxia, although stroke + dementia are most common causes
What are the signs of lower motor neuron lesions?
- Weakness
- Hypotonia (reduced muscle tone)
- Hyporeflexia (reduced reflexes)
- Muscle atrophy
- Fasciculations/twiches: damaged motor units produce spontaneous APs, visible
- Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination, otherwise can’t see visually
Describe Motor Neurone Disease (MND).
- Progressive neurodegenerative disorder of motor system; several genetic causes (quite rare) – people die about 18-24 months after diagnosis
- Stephen Hawking suffered from this
-
Spectrum of disorders, disease of BOTH upper + lower motor neurones
- E.g. Amyotrophic Lateral Sclerosis (ALS)
- Most people die from respiratory distress – lose control of these muscles
- Upper motor neuron signs
- Increased muscle tone (spasticity of limbs and tongue)
- Brisk limbs and jaw reflexes
- Babinski’s sign
- Loss of dexterity
- Dysarthria (speaking issues)
- Dysphagia
- Lower motor neuron signs
- Weakness
- Muscle wasting (atrophy)
- Tongue fasciculations and wasting
- Nasal speech
- Dysphagia
What are the components of the Basal Ganglia

- Extrapyramidal (not part of main descending tract)
- Supplied by middle cerebral artery
-
Includes:
- Caudate nucleus (tadpole shape)
- Lentiform nucleus (putamen + external Globus pallidus)
- Subthalamic nucleus
- Substantia nigra
- Ventral pallidum, claustrum, nucleus accumbens (reward system), nucleus basalis of Meynert
- STRIATUM = caudate + lentiform nuclei
DIAGRAM
- Anteriorly (D)– caudate nucleus, lateral to the caudate nucleus is the putamen and inferior is the nucleus accumbens
- (C) – Caudate nucleus gets smaller, putamen stays the same and emerge of the globus pallidus (the pale area)
-
(B) – Caudate shrinks even more. Emergence of the thamalus medially (blue structure). Putamen and globus pallidus make a triangular structure - has 3 separate components:
- Most lateral: Putamen
- External Globus Pallidus
- Internal Globus Pallidus
NOTE: The striatum is the lentiform and the caudate
What is the function of the basal ganglia?
- Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
- Moderating + coordinating movement (suppressing unwanted movements)
- Performing movements in order
What happends to the circuitry of basal ganglia in
- Parkinsons Disease
- Huntingtons Disease
- Ballistic Movement
- Parkinsons Disease involves breakdown in communication in nigro-striatal pathway
- Huntingtons Disease affects circuitry + local pathways within striatum
- Ballistic movement = uncontrollable arm movements related to dysfunction in subthalamic nucleus

Describe Parkinson’s Disease.
- See Lewy-bodies in Substantia Niagra (r)
-
Primary pathology involves neurodegeneration of dopaminergic neurons, originating in Substantia Niagra (r) (pars compacta) in midbrain, going to striatum
- Loss of these neurones à movement problems
- Substantia Niagra is usually dark due to accumulation of neuromelanin – breakdown product in DA synthesis
-
Main signs:
- Tremors at rest - 4-7 Hz, starts in 1 hand (“pill-rolling tremor”); with time, spreads to other body parts
- Rigidity- increased muscle tone à resistance to externally imposed joint movements like in clinical examination
- Bradykinesia – slowness of movement
- Hypomimic face – expressionless
- Akinesia – can’t initiate movements b/c can’t initiate movements internally
- Kyphosis in some patients
- Parkinson’s usually starts unilaterally and then progresses


