Motor function

Question 1

What are the 6 different types of movement?

Answer 1

Simple reflexes - mediated at level of spinal cord
Posture and postural change e.g. standing, balancing
Locomotion e.g. walking
Sensory orientation e.g. head turning, eye fixation
Species specific action patterns e.g. ingestion, courtship, grooming
Acquired skills e.g. speech, dressing, driving

Question 2

What is the Pyramidal System?

Answer 2

(corticospinal tract) is a descending tract originated from pyramidal cells of motor cortex. Is the pathway concerned with voluntary, discrete, skilled movements (especially at distal part of limbs). It predominantly promotes the activity of flexors of the legs and extensors of the arms.
Motor cortex - main motor output, projects through pyramidal tracts to spinal cord where synapses with peripheral motor neurons
Supplementary motor cortex - conception and initiation of movement (lesions cause deficits in voluntary movement/speech)
Premotor cortex - motor coordination (lesions = impairment in stability of stance, gait and hand coordination)

Question 3

What is the extrapyramidal system?

Answer 3

Other pathways that run parallel from the cortex, basal ganglia and cerebellum via the brainstem and spinal cord, running outside of the pyramidal tract

Question 4

What are the four main tracts of the extrapyramidal system?

Answer 4

Tectospinal tract - coordinating head and eye movements as part of optic reflexes, originates in various regions of brainstem e.g. superior colliculus
Vestibulospinal tract - Influences postural muscles, originating from vestibular nuclei (pons and medulla)
Reticulospinal tract - Projects from reticular formation (brainstem), inhibition or facilitation of movement
Rubrospinal tract - origin in red nucleus of midbrain, subconscious regulation of upper limb muscle tone and movement

Question 5

How do the basal ganglia and the cerebellum contribute to the control of movement?

Answer 5

Cerebellum - controls neural “programs” for the execution of skilled movements, learning of skills mostly occurs here; receives inputs from both the visual and somatosensory cortex
Basal ganglia - group of subcortical forebrain nuclei (caudate nucleus, putamen, globus pallidus, subthalamic nucleus) responsible for modulating patterns of motor activity; signals sent via the motor nuclei of the thalamus to the key regions of the pyramidal system

Question 6

What can damage motor neurons –> paralysis?

Answer 6

Viral e.g. poliomyelinitis which destroys spinal motor neurones (and cranial motor neurones in more severe cases) –> muscles atrophy
Toxins/hereditary e.g. amyotrophic lateral sclerosis which leads to degeneration of motor neurons in brainstem and spinal cord –> target muscles waste away –> gradually worsening paralysis
Injury - severing of spinal cord (permanent paralysis) or bruising/compression (transient if pressure relieved before neurones die from oxygen starvation)

Question 7

What happens when the primary motor cortex itself is damaged?

Answer 7

Paralysis or partial paralysis of voluntary movement on contralateral side of body to side of damage
Extent of paralysis depends on extent of damage, and is often also accompanied by spasticity and abnormal reflexes (muscles not receiving normal inhibitory inputs)
Disturbance usually greatest in distal muscles such as hands

Question 8

What is apraxia?

Answer 8

Inability to carry out movement in response to commands
No paralysis, loss of comprehension or motivation
May be due to disconnection of PMC from supplementary motor areas and motor association cortex (illustrates importance of the role played by these in forming a motor pattern upon being asked to do something)

Question 9

What can result if there is damage to the premotor cortex?

Answer 9

1) Apraxia - acuired inability to carry out skilled actions that could previously be performed (but without paralysis)
2) Deficits in contralateral fine motor control, such as the performance of complex serial movements
3) Difficulty in using sensory feedback for the control and performance of movements.

Question 10

What is meant by “decomposition of movement”?

Answer 10

Inability to perform motor patterns e.g. walking
Motor patterns are broken up into individual segments instead of being executed smoothly, and movements now require thought for execution rather than being “automatic”
Often due to cerebellar damage (cerebellum key for putting motor patterns together, especially for learned skills)

Question 11

What are the main symptoms of Parkinson’s?

Answer 11

Symptoms start mild and unilateral but progress to bilateral
Resting tremor in limbs (disappears on movement/during sleep)
Muscle rigidity
Jerky (cogwheel) movement
Akinesia (general paucity of movement)
Stooped posture
Shuffling gait (all of the above are deficits in movements controlled by extrapyramidal pathways)
Excessive sweating and salivation
Micrographia
Altered cognitive function, depression, dementia

Question 12

What causes Parkinson’s?

Answer 12

Degeneration of the nigro-striatal pathway, leading to depletion of striatal dopamine (some degeneration of other dopamine pathways too)
See lost pigmentation in areas affected

Question 13

How can Parkinson’s be treated?

Answer 13

Drugs which increase dopamine - dopamine itself cannot cross the blood-brain barrier so use L-Dopa which can cross and is converted into dopamine once in the brain
Can cause severe side effects e.g. dyskinetic movements and psychoticism caused by L-Dopa that doesn’t cross the barrier
Neuron loss in the substantia nigra continues, however, and eventually too few dopamine neurons remain and L-DOPA stops being effective
Surgical interventions and neural transplantation are possible alternatives being explored

Question 14

What are the key features of Huntington’s disease?

Answer 14

It is a PROGRESSIVE disease causing involuntary muscle jerks which ultimately affects the whole body
Also causes intellectual deterioration, depression and occasional psychoticism (which can appear before motor symptoms), with symptoms beginning around 30-45 yrs
Single dominant gene causes degeneration of output neurons from the striatum, reducing inhibitory modulation of motor function usually performed via GABA –> excessive movement
This condition highlights the vital role of inhibition in normal motor control

Question 15

How can Huntington’s be treated?

Answer 15

There is no effective treatment - some relief can come from GABA replacement or dopamine antagonists, but there is currently no way to halt the disease progression

Question 16

What do somatic motor pathways involve?

Answer 16

At least 2 motor neurons - upper motor with cell body in CNS and lower motor with cell body in brainstem (cranial nerves) or spinal cord (peripheral nerves)
Activity in upper can facilitate or inhibit lower, and it is activation of the lower that triggers contraction in the innervated muscle

Question 17

What happens if there is damage/destruction of the axon of a lower motor neuron

Answer 17

It is only these axons that actually extent outside of the CNS, and we see eliminated voluntary and reflex control over the innervated motor unit

Question 18

How can descending motor pathways be divided?

Answer 18

Into lateral and medial motor systems based on location in spinal cord

Question 19

What are the lateral motor pathways?

Answer 19

Lateral corticospinal and rubrospinal tracts (descend contralateral to extremities innervated)

Question 20

What are the medial motor pathways?

Answer 20

Anterior corticospinal, vestibulospinal, reticulospinal and tectospinal - control proximal axial and girdle muscles for postural tone, balance, head/neck orientation etc
Descend ipsilateral or bilateral (unilateral damage produces no obvious deficits)

Question 21

What are the features of the motor homunculus?

Answer 21

Mapped at the primary motor cortex - the number of motor neurons feeding an area determine the scale, and positioning depends on where within the motor cortex neurons leave to go to the periphery
Source of pyramidal tract neurones

Question 22

What do the supplementary and premotor areas do?

Answer 22

responsible for formation of motor patterns that are then sent out via the primary motor cortex
Lesions in association areas –> apraxia

Question 23

How does the premotor cortex differ from the supplementary motor area?

Answer 23

PMC is activated when motor sequences are guided externally by stimuli, rather than generated internally

Question 24

What is the basal ganglia involved with?

Answer 24

Subconscious control of skeletal muscle tone and coordination of learned movement patterns - not responsible for initiating movement but once movement has started they provide the general rhythm
Each structure receives wide input from cerebral cortex and sends much of its output back to cortex via thalamus (loop

Question 25

What are the cerebellar feedback loops like?

Answer 25

Involved in fine tuning of movements controlled at both conscious and subconscious levels - compare motor commands to proprioceptive info and make adjustments to ensure smooth movement
All circuitry guides movement by INHIBITING neurones
Damage produces ataxia i.e. disturbance of muscle coordination

Question 26

What is the key role of the basal ganglia?

Answer 26

Determining amplitude and direction of movement and movement initiation - much function is through modulation of other brain circuits such as the cortical motor pathways

Question 27

What are the 4 stages of a spinal reflex?

Answer 27

1) Afferent fibres carry information about a stretch to a muscle
2) Afferents connect monosynaptically to motor neurons that control the stretched muscle
3) Motor neurons stimulate the muscle to oppose the stretch
4) Simple negative feedback that restores the limb to its desired position

Question 28

What is the significance of the medulla to the pyramidal system?

Answer 28

Pyramidal tract is seen most clearly where it passes through the floor of the medulla, and it is here that crossover occurs such that the cortex innervates muscles on the contralateral side of the body

Question 29

How do most pyramidal-tract neurones influence spinal motor neurones?

Answer 29

Through polysynaptic routes, sharing control with other descending influences (likely aiding coordination of movements which involve multiple muscles)

Question 30

What is meant by Flaccid Paralysis?

Answer 30

when spinal cord completely severed and reflexes below level of injury are lost
Alternatively, in cases with minimal widespread tissue destruction, reflexes below damage may actually become abnormally strong as lack dampening effect from brain inhibition

Question 31

What are the 2 main types of apraxia?

Answer 31

Ideomotor - inability to carry out simple motor activities either in response to verbal commands or by copying gestures, although identical action possible when spontaneous
Ideational - impairment in carrying out a SEQUENCE of actions, but each individual step can be done correctly in isolation

Question 32

What is the spinocerebellum?

Answer 32

Uppermost part of cerebellum which receives sensory info about spatial location of body and anticipates movements - damage produces a characteristic gait and posture esp ataxia of legs
Can be caused by long term alcoholism

Question 33

What is the cerebrocerebellum?

Answer 33

Lowest part of cerebellum, implicated in planning complex movements - damage causes diverse motor problems inc decomposition of movement
Also see cognitive deficits as area involved in higher level processing

Question 34

What is the vestibulocerebellum?

Answer 34

Closely connected to vestibular nucleus, receives info about body orientation and outputs help maintain posture and appropriate orientation
Damage = gaze errors and difficulty tracking moving objects

Question 35

What are the muscular dystrophies?

Answer 35

Group of diseases characterised by general muscle wastage - appear to involve biochemical abnormalities which lead to structural changes in muscle cells

Question 36

What is Duchenne’s muscular dystrophy?

Answer 36

Most common, wasting of muscles caused by single recessive X-linked gene (so affects males most)
Dystrophin not produced properly, normally involved in regulation of intracellular calcium

Question 37

Why are females only ever carriers?

Answer 37

Onset of symptoms at around 6 years and death in 10, prior to reproductive age so impossible for affected male to pass on the gene

Question 38

What is myasthenia Gravis?

Answer 38

Profound weakening of skeletal muscle due to reduced numbers of ACh receptors at NMJs due to autoimmune destruction of NMJs (similar symptoms from Bungarotoxin in snake venom)
Reduced transmission of signals activating muscles due to antibodies attacking ACh receptors or affecting other proteins associated with the receptors
Often first affects muscles of the head, suffocation if breathing muscles affected

Question 39

How can myasthenia gravis be treated?

Answer 39

removal of the thymus gland where immune cells are made, and drugs which suppress immune system

Question 40

What are some of the symptoms of MS?

Answer 40

Loss of sensation
Difficulty moving/balancing 
Muscle weakness
Visual problems 
Fatigue
Chronic pain
Cognitive impairment

Question 41

What causes MS?

Answer 41

Breakdown of myelin sheath surrounding axons –> compromised axonal transmission
Thought to be autoimmune - can be transient due to inflamed sheath or permanent due to actual breakdown
Damages and scars the sheath, and potentially the underlying nerves, meaning that messages travelling along the nerves become slowed or disrupted.

Question 42

How can MS be treated?

Answer 42

No treatments to reverse the process but interferon can slow it down
Primarily treat symptoms e.g. with corticosteroids