Motor system

Question 1

Describe the distribution of motor neurones between CNS and PNS. (5)

Answer 1

All of the upper motor neurone exists in the CNS, with its cell body in the primary motor cortex.
The cell body of the lower motor neurone also exists in the CNS, in the ventral horn or brainstem. The axon of the LMN projects into the PNS and ends up on a skeletal muscle.

Question 2

Describe the distribution of the cranial nerve nuclei. (8)

Answer 2

III + IV - midbrain
V + VI - pons
(IX, X + XI) + XII - medulla

Question 3

Describe the medial longitudinal fasiculus. (4)

Answer 3

Connects the trochlear, Abducens and occulomotor neuclei so the eyes can point in the same direction. It lies in the lateral wall of the third ventricle, meaning if the cerebral aqueduct is blocked, it gets squished and eye movements are not co-ordinated.

Question 4

Describe an example of a monosynaptic reflex of LMNs. (2)

Answer 4

L3 knee jerk reflex.

Inhibitory interneurones switch off the lower motor neurones of the hamstrings so they relax.

Question 5

Describe and explain signs of a lower motor neurone lesion. (8)

Answer 5

Wastage - denervation atrophy due to loss of tropic factors.
Weakness of muscle
Hypotonia
Arreflexia or hyporeflexia
These three are all caused by the loss of impulses to the muscle.
Fasiculations - upregualtion of nAChR to boost response to the minimal amount of ACh released from damaged neurones.

Question 6

Describe and explain signs of upper motor neurone damage. (9)

Answer 6

Weakness - voluntary action of LMN lost
Hypertonia - rigidity due to loss of UMN inhibition on LMNs. Has two types: spasticity (most powerful muscle group wins when hypertonia equal) and clasp knife reflex (resistance to a point until it gives way).
Hyperreflexia - overactivity of LMN without UMN inhibition
Extensor plantar reflexes like seen in babies.

Question 7

Describe Babinski’s Reflex. (4)

Explain why it can be seen in Alzheimer’s Disease. (2)

Answer 7

UMNs inhibit LMNs through inhibitory interneurones. In an adult, mature interneurones mean that when the sole of the foot is stimulated, the toes curl under.
However, in a baby, these are not yet mature, so stimulating the bottom of the foot causes toes to be extended back.
It can be seen In Alzheimer’s Disease because the disease process involves a de-maturation of these interneurones, so infantile reflexes reappear.

Question 8

Explain why initially upper motor neurone lesions can present as lower motor neurone lesions. (4)

Answer 8

Spinal shock is a phenomenon that occurs in the days after UMN lesions. Initially there is flaccid paralysis and arreflexia (like LMN lesions) which slowly develops into hypertonia and hyperreflexia. Mechanism is unclear.

Question 9

Describe the corona radiata. (4)

Answer 9

It is the “crown shape” of UMN axons as the flow from the motor cortex to the brainstem, condensing between the thalamus and the lentiform nucleus to form the white matter path of the internal capsule.

Question 10

Describe the path of an UMN that supplies a distal muscle. (9)

Answer 10

Corona radiata 
Internal capsule
Cerebral peduncle of the midbrain
Pons 
Medullary pyramids where it decussates
Lateral corticospinal tract 
Ventral horn where it synapses onto a LMN

Question 11

Describe the path of an UMN that supplies a postural muscle. (9)

Answer 11

Corona radiata 
Internal capsule
Cerebral peduncle of the midbrain
Pons 
Medullary pyramids
Ventral corticospinal tract
Decussation at spinal level 
Ventral horn where it synapses onto a LMN

Question 12

Describe the organisation of fibres in the lateral corticospinal tract. (3)

Answer 12

Arm medially, trunk centrally, leg laterally.

Question 13

Explain the differences between a motor cortex lesion and Bell’s Palsy. (3)

Answer 13

Bell’s palsy is not forehead sparing. Motor cortex lesion is forehead sparing.
Top half of the face has innervation from bilateral motor cortexes that converge in the motor nuclei of the facial nerve.

Question 14

List the parts of the basal ganglia. (7)

Answer 14

Caudate nucleus
Putamen
Globus pallidus (internal and external segments)
Subthalamic nuclei
Substantia nigra (pars compacta and pars reticulata).

Question 15

Describe the basal ganglia. (3)

Answer 15

A collection of grey matter structures found deep in the cerebral hemispheres that communicates with the primary motor cortex through the thalamus so increased thalamic activity leads to increased cortical activity.

Question 16

Describe the striatum. (2)

Answer 16

Caudate nucleus and putamun.

Question 17

Describe the lentiform nucleus. (2)

Answer 17

Putamen and globus pallidus.

Question 18

What are the important things to remember when looking at the that diagram. (8)

Answer 18

Dopamine excites the direct pathway through D1 receptors.
Dopamine inhibits the indirect pathway through D2 receptors.
However, because two negatives make a positive, inhibiting the indirect path has the same result as exciting the direct path: dopamine reduces the inhibition on the thalamus so increase motor cortex action, so increases movement.

Question 19

Describe and explain the results of a unilateral basal ganglia lesion. (2)

Answer 19

Ipsilateral motor cortex damage but contralateral body signs due to decussation of corticospinal tracts.

Question 20

Describe the pathophysiology of Parkinson’s Disease. (2)

Answer 20

Degeneration of dopaminergic neurones in SNc so dopamine-drive facilitation through direct and indirect pathway lost.

Question 21

Describe and explain signs and symptoms of Parkinson’s disease. (10)

Answer 21

Tremour - unknown
Rigidity - unknown
Bradykinesia - slow movements due to loss of cortical stimulation.
Hypophonia, mask-like facies and micrographia - bradykinesia related.
Dementia - forms Lewy Bodies
Depression - basal ganglia has a role in higher mental functions.

Question 22

Describe the pathophysiology of Huntington’s Disease. (2)

Answer 22

Autosomal dominate, progressive disorder that presents commonly between 30-50.

Question 23

Describe and explain the signs and symptoms of Huntington’s Disease. (9)

Answer 23

Early hyperkinesia - loss of inhibitory projections from striatum to GPe.
Chorea - dance like movements caused by increased motor cortex activity.
Dystonia - uncontrolled muscle contraction in which the strongest group wins.
Loss of co-ordination
Cognitive decline and behavioural disturbances - basal ganglia involved in higher mental function.

Question 24

Describe the pathophysiology and the main sign of hemiballismus. (3)

Answer 24

A rare disorder caused by sub-cortical strokes or damage to the subthalamic nucleus (normally inhibits the thalamus).
Characterised by unilateral “ballistic” movements.

Question 25

Describe the anatomical location of the cerebellum. (2)

Answer 25

Posterior cranial fossa. Sits above the fourth ventricle.

Question 26

Describe the parts of the body that different areas of the cerebellum influence. (2)

Answer 26

Midline vermis deals with the trunk, lateral hemispheres deal with ipsilateral limbs.

Question 27

Describe how the cerebellum communicates with the rest of the CNS. (3)

Answer 27

Via the cerebellar peduncles.
Superior cerebellar peduncle - midbrain
Middle cerebellar peduncle - pons
Inferior cerebellar peduncle - medulla.

Question 28

Describe the functions of the cerebellum. (2)

Answer 28

Sequences movements within the basal ganglia.

Communicate with the contralateral sensory and motor cortices, so has ipsilateral body control.

Question 29

Describe signs of cerebellar disease. (12)

Answer 29

Dysdiadochokinesia - difficulty with rapidly alternating movements.
Ataxia - unsteady gait due to loss of proprioception and difficulty sequencing leg muscle movements.
Nystagmus - flickering eye movements due out malcoordination of extraocular muscles.
Intention tremour - a tremour that gets worse when they approach the target.
Slurred speech (dysarthria) - malcoordination of laryngeal and tongue muscles.
Hypotonia - unclear.