Neuro10 - Disorders of the Motor System

Question 1

4 anatomical features of the basal ganglia

Substantia Nigra Pars Compacta (SNc)
Striatum
Lentiform Nucleus
Subthalamic Nucleus (STN)

Answer 1

1. ) Substantia Nigra Pars Compacta (SNc)
   - source of dopamine in the midbrain
   - dopamine acts to stimulate the motor cortex
2. ) Striatum - receives input from SNc and cortex
   - made up of the putamen and caudate nucleus
   - caudate is C-shaped, lining the lateral ventricle
3. ) Lentiform Nucleus - putamen + globus pallidus
   - globus pallidus contains internal and external segment
   - putamen and globus pallidus are anatomically but not functionally related
4. ) Subthalamic Nucleus (STN)
   - small area sitting beneath the thalamus

Question 2

5 functional features of the basal ganglia

Inputs x2
Outputs x2
Direct Pathway
Indirect Pathway
Lateralisation

Answer 2

1. ) Inputs - from the cortex and the midbrain (SNc)
   - cortex –> basal ganglia: corticostriatal pathway
   - midbrain (SNc) –> basal ganglia: nigrostriatal pathway
2. ) Outputs - to the PMC via the thalamus
   - basal ganglia –> thalamus: pallidothalamic tract
   - thalamus –> PMC: thalamocortical tract
   - ↑thalamic activity –> ↑cortical activity
3. ) Direct Pathway - reinforces appropriate movements
   - normal function: excitatory to the motor cortex
   - dopamine stimulates excitatory D1 receptors on striatal neurones, exciting the motor cortex
4. ) Indirect Pathway - edits out inappropriate movements
   - normal function: inhibitory to the motor cortex
   - dopamine stimulates inhibitory D2 receptors on striatal neurones, inhibiting the motor cortex
5. ) Lateralisation - lesions produce contralateral signs
   - basal ganglia communicates w/ ipsilateral PMC
   - PMC communicates w/ contralateral body part
   - however, the SNc is near the midline of the midbrain so is often affected bilaterally –> bilateral symptoms

Question 3

2 general features of Parkinson’s disease

Pathophysiology
Mechanism

Answer 3

1. ) Pathophysiology - degeneration of dopaminergic neurones in the SNc
   - lose dopamine-driven facilitation of movement via the direct and indirect pathway
2. ) Mechanism - more inhibition of thalamus from GPi
   - direct pathway: ↓dopamine –>↓putamen excitation which leads to less inhibition of the direct pathway
   - indirect pathway: ↓dopamine –> ↓putamen inhibition which leads to ↑inhibition of the indirect pathway

Question 4

8 clinical signs of Parkinson’s disease

Answer 4

1. ) Bradykinesia - slow movement
   - due to loss of cortical excitation
   - reduced amplitude, non-rhythmic
2. ) Hypophonia - quiet speech
   - due to bradykinesia of the larynx and the tongue
3. ) Micrographia - small handwriting
   - due to bradykinesia in the hands
4. ) Resting Tremor - dysfunction of indirect pathway
   - no inhibition of inappropriate movements
   - pin rolling tremor abolished by movement
5. ) Lead-Pipe Rigidity - sustained resistance to passive movement throughout the whole range of motion
   - ↓co-ordination between agonists and antagonists

6.) Dementia - due to progression of causative agent (e.g. protein aggregates)

7. ) Depression
   - basal ganglia has a role in cognition and mood
8. ) Glabellar Tap Sign - primitive reflex elicited by repetitively tapping the forehead
   - positive when patient continues to blink

Question 5

3 general features of Huntington’s chorea

Onset
Pathophysiology
Mechanism

Answer 5

1. ) Onset - early onset at around 30-50 years old
   - autosomal dominant, progressive disorder

2.) Pathophysiology - loss of inhibitory projections from striatum (putamen) to GPe leads to hyperkinetic features

3. ) Mechanism - less inhibition of the thalamus from GPi
   - ↓GPe inhibition –> ↓STN inhibition –> ↑GPi excitation

Question 6

4 clinical signs of Huntington’s chorea

Answer 6

1.) Loss of Coordination

2. ) Dystonia - uncontrollabe muscle contrations
   - loss of coordination between agonist and antagonist muscle circuits leading to odd postures
3. ) Chorea - dance-like movements
   - due to increased motor cortex activation
4. ) Cognitive Decline and Behavioural Disturbances
   - due to to role of basal ganglia in higher mental functions

Question 7

3 features of hemiballismus

Pathophysiology
Mechanism
Clinical Sign

Answer 7

1. ) Pathophysiology - damage to subthalamic nucleus
   - can be caused by a sub-cortical stroke (lacunar infarct)
2. ) Mechanism - less inhibition of the thalamus from GPi
   - due to ↓GPi excitation from the subthalamic nucleus

3.) Clinical Sign - unilateral explosive movements

Question 8

3 anatomical features of the cerebellum

Location
Vermis and Hemispheres
Cerebellar Peduncles x3

Answer 8

1. ) Location - sits above the 4th ventricle
   - therefore cerebellar lesions can cause hydrocephalus
2. ) Vermis and Hemispheres - cerebellum is made up of a midline vermis and 2 laterally placed hemispheres
   - vermis deals with the trunk whilst the hemispheres deal with the ipsilateral side of the body
3. ) Cerebellar Peduncles - communicates w/ brainstem
   - superior cerebellar peduncles –> midbrain
   - middle cerebellar peduncles –> pons
   - inferior cerebellar peduncles –> medulla

Question 9

3 phylogenetic subdivisions of the cerebellum

Anterior Lobe
Posterior Lobe
Flocculonodular Lobe

Answer 9

1. ) Anterior Lobe - aka paleocerebellum
   - receives fibres from the spinocerebellar tract
   - function: maintainence of gait
2. ) Posterior Lobe - aka neocerebellum
   - communicates w/ PMC and basal ganglia
   - function: postural tone and modulation of motor skills
3. ) Flocculonodular Lobe - aka archicerebellum
   - receives fibres from the vestibular system
   - function: maintenance of balance

Question 10

4 functional features of the cerebellum

Sequencing and Coordination of Movements
Inputs x2
Output
Lateralisation

Answer 10

1. ) Sequencing and Coordination of Movements
   - basal ganglia decides most appropriate movements
   - cerebellum correctly sequences those movements w/ info about where the body is in already (proprioception)
2. ) Inputs - contralateral motor cortex (via the pontine nucleus) and the ipsilateral spinal cord
   - PMC –> pontine nucleus: corticopontine pathway
   - pontine nucleus –> cerebellum: pontocerebellar
   - spinal cord –> cerebellum: spinocerebellar tract
3. ) Output - contralateral motor cortex (via the thalamus)
   - cerebellum –> thalamus: cerebellothalamic tract
   - thalamus –> PMC: thalamocortical tract
4. ) Lateralisation - lesions lead to ipsilateral signs
   - cerebellum communicates w/ contralateral PMC
   - PMC communicates w/ contralateral body part

Question 12

6 signs of cerebellar disease

D
A
N
I
S
H

Answer 12

1. ) Dysdiadochokinesia - difficulty rapidly alternating movements e.g pronation and supination
   - maybe due to a problem with sequencing
2. ) Ataxia - unsteady (ataxic) gait
   - difficulty sequencing lower limb muscle contractions and loss of unconscious proprioception of lower limb
3. ) Nystagmus - flickering eye movements
   - due to malcoordination of extraocular muscles

4.) Intention Tremor - worsens as a target is approached

5. ) Slurred Speech - dysarthria
   - malcoordination of laryngeal and tongue musculature

6.) Hypotonia - unclear mechanism

Question 12

The brain, basal ganglia, and cerebellum in layman’s terms

PMC Function
Corticostriatal Tract and Cortico-Ponto-Cerebellar Tract

Basal Ganglia Function
Pallido-Thalamo-Cortical Tract (direct and indirect pathway)

Cerebellum Function
Spinocerebellar Tract, Cerebello-Thalamo-Cortical Tract

Corticospinal Tract

Answer 12

1. ) The brain decides what it wants the body to do
   - it then sends that information to the basal ganglia and the cerebellum

2a. ) The basal ganglia determines the most appropriate set of movements to carry out the brain’s plan
- the appropriate movements are reinforced by the direct pathway whilst the inappropriate movements are edited out by the indirect pathway

2b. ) The cerebellum receives information about what position the body already is in (proprioception)
- it then decides what order the movements should be done in relation to where the body already is
- it then sends that information back to the brain

3.) The brain then sends the information to the body to carry out those movements