8. Motor Pathway

Question 1

Explain the functional segregation of the motor system

Answer 1

Organised into different areas that control different aspects of movement

Question 2

Describe the hierarchial organisation of the motor system.

Answer 2

• High order areas are involved in complex tasks (programme + decisions on movements, coordinate muscle activity)
• Lower levels perform lower level tasks (execution of movement)

Question 3

Describe the pyramidal system.

Answer 3

1. The primary motor cortex receives information from all the sensory cortices (sight, hearing, taste, smell) –> processed in the thalamus
2. Sends instructions to the spinal cord (via brainstem) and alpha motor neurones
3. Goes to musculature

Question 4

Describe the extrapyramidal system.

Answer 4

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

Question 5

What do the nuclei in the brainstem supply.

Answer 5

The nerves of the face.

Question 6

Locate the primary motor cortex and define its function

Answer 6

• 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

Question 7

What are the descending motor pathways?

Answer 7

Lateral corticospinal tract and anterior corticospinal tract

Question 8

Describe the lateral corticospinal tract.

Answer 8

1. Motor neurone send axons down through subcortical structures – fibre pathway called internal capsule
2. Internal capsule becomes cerebral peduncles
3. Pass through pons
4. At base of medulla, 95% of fibres cross over at pyramids –> descend in lateral corticospinal tract. Decussation forms basis of contralateral motor control
5. At appropriate level, synapse with alpha-motor neurones –> go out ventral root –> spinal nerve –> effector

Question 9

Describe the Anterior Corticospinal Tract.

Answer 9

1. Motor neurone send axons down through subcortical structures – fibre pathway called internal capsule
2. Internal capsule becomes cerebral peduncles
3. Pass through pons
4. At base of medulla, 5% of fibres don’t decussate at pyramids
5. Carry on down to form anterior corticospinal tract
6. These fibres support axial musculature
7. When it reaches the appropriate level, decussation occurs in spinal cord

Question 10

Describe the corticobulbar pathways.

Answer 10

Same but related to motor nuclei in brainstem

M1 projections going to brainstem structures e.g. hypoglossal nucleus –> innervate tongue muscles

Question 11

Describe the location and function of the premotor cortex

Answer 11

• 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)

Question 12

Describe the Location and function of the supplementary motor area.

Answer 12

• 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

Question 13

Describe the Association Cortex

Answer 13

• 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

Question 14

Define Lower Motor Neuron

Answer 14

(spinal cord + brainstem) = the neurone found in ventral horn and its processes going out to musculature; also found in brainstem e.g. hypoglossal nucleus

Question 15

Define upper motor neuron

Answer 15

found in M1 = fibres go down Corticospinal + corticobulbar tracts to next motor neurones in chain

Question 16

Define pyramidal

Answer 16

defines lateral corticospinal tract

Question 17

Define extrapyramidal.

Answer 17

relate to basal ganglia + cerebellum, rather than primary motor tract

Question 18

What are the signs of upper motor neuron lesions?

Answer 18

• Negative signs = Loss of function:
  
  1. Paresis: graded weakness of movements
  2. Paralysis (plegia): complete loss of activity of muscle
• Positive signs = increased motor function due to loss of inhibitory descending inputs:
  
  1. Spasticity: increased muscle tone
  2. Hyper-reflexia: exaggerated reflexes
  3. 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

Question 19

What are the signs of lower motor neuron lesions?

Answer 19

• 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

Question 20

Describe Motor Neurone Disease (MND).

Answer 20

• 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

Question 21

What are the components of the Basal Ganglia

Answer 21

• 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

Question 22

What is the function of the basal ganglia?

Answer 22

• 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

Question 23

What happends to the circuitry of basal ganglia in

• Parkinsons Disease
• Huntingtons Disease
• Ballistic Movement

Answer 23

• 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

Question 24

Describe Parkinson’s Disease.

Answer 24

• 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

Question 25

Describe Huntington’s Disease

Answer 25

• Massive atrophy of caudate nucleus first à then possible putamen atrophy
• Genetic neurodegenerative disorder
  
  • HTT gene on Chr 4, autosomal dominant à toxic huntingtin protein
  • CAG repeat (cut-off is 35 repeats)
• Degeneration of GABAergic inhibitory neurons in striatum, caudate + putamen
• Motor signs:
  
  • Choreic movements (Chorea = dance) = rapid jerky involuntary movement; hands and face affected first à then legs + rest of body
  • Speech impairment
  • Difficulty swallowing
  • Unsteady gait
  • Later stages, cognitive decline and dementia

Question 26

What are the three pathways to the cerebellum?

Answer 26

Pathways via cerebellar peduncles:

• Inferior = input from spinal cord
• Middle = largest, transverse fibres connect 2 halves of cerebellum
• Superior = main output to basal ganglia + thalamus

Question 27

Describe the trilaminar structure of the cerebellum.

Answer 27

• Trilaminar structure (3 layers of grey matter and underlying white matter):
  
  • 1^st layer = molecular layer – very few neurones and lots of glial cells
  • 2^nd layer = piriform layer – contains Purkinje cells (main processing cells of the cerebellum)
  • 3^rd layer = granular cell (neuronal) layer – small neurones packed tightly
  • Inputs = inferior olivary nucleus (and spinal cord) projects to Purkinje cells via climbing fibres – terminate in molecular layer where dendritic tree of Purkinje fibres are found
  • All other input to granule cells via mossy fibres –> go onwards to parallel fibres which innervate Purkinje cells
  • Output = All output from Purkinje cells via deep nuclei which then project out.

Question 28

What are the divisions of cerebellum?

Answer 28

• Vestibulocerebellum: oldest part
  
  1. Regulation of gait, posture, and equilibrium
  2. Coordination of head + eye movements
• Spinocerebellum:
  
  1. Coordination of speech
  2. Adjustment of muscle tone
  3. Coordination of limb movements
• Cerebrocerebellum: most recently developed part – involved in motor learning
  
  1. Coordination of skilled movements
  2. Cognitive function, attention
  3. Processing of language
  4. Emotional control

Question 29

Describe cerebellar dysfunctions.

Answer 29

• Vestibulocerebellar Syndrome = damage (tumour) causes vestibular-disease-like syndrome –> gait ataxia, tendency to fall (even when patient sitting even with the eyes open)
• Spinocerebellar syndrome = damage (degeneration + atrophy associated with chronic alcoholism) affects mainly legs –> abnormal gait/wide-based stance
• Cerebrocerebellar or Lateral Cerebellar Syndrome = damage affects mainly arms/skilled movements (tremor) + speech

Question 30

What are the motor signs of cerebellar problems.

Answer 30

Deficits apparent only upon movement

1. Ataxia: impairments in movement coordination + accuracy. Affects posture + gait: wide-based, staggering (“drunken”) gait
2. Dysmetria: Inappropriate force + distance for target-directed movements (knocking over a cup rather than grabbing it)
3. Intention tremor (when thinking about action): Increasingly oscillatory tremor in a target-directed movement (nose-finger tracking – when asked to think about putting finger or nose, the thought of doing this would cause a tremour)
4. Dysdiadochokinesia: Inability to rapidly alternate movements (rapidly pronating and supinating hands and forearms)
5. Scanning speech: staccato, due to impaired coordination of speech muscles