motor control

Question 1

What is hierarchical organisation?

Answer 1

Higher order areas of hierarchy are involved in more complex motor tasks than lower order areas

Question 2

What is functional segregation?

Answer 2

Different parts of the brain are involved in different parts of movement

Question 3

What are the major descending tracts?

Answer 3

Corticospinal and corticobulbar tracts

Question 4

What are pyramidal tracts? UMN and LMN where? Names? What do they do?

Answer 4

Pyramidal tracts pass through the pyramids of the medulla. UMN in primary motor cortex and LMN in spinal cord or brain stem nuclei. Corticospinal & corticobulbar tracts. They control fine, discrete voluntary movement. Send singals in order toe execute voluntary movements of the body & face.

Question 5

What are extrapyramidal tracts? UMN and LMN? Examples? Uses?

Answer 5

Extrapyramidal tracts do not pass through the pyramids of the medulla. Have UMN in primary motor cortex and LMN in brainstem nuclei. Examples: vestibulospinal tract, tectospinal, reticulospinal, rubrospinal. Autonomic control of movement and posture.

Question 6

Where is primary motor cortex? What does it do?

Answer 6

In pre-central gyrus in front of central sulcus. Sends descending signals to execute fine, discrete voluntary movements.

Question 7

Where is pre-motor area and what is it involved in?

Answer 7

pre-motor area is anterior to the primary motor cortex. Involved in planning externally cued movements (picking up an object)

Question 8

Where is supplementary motor area and what is it involved in? when does it become active?

Answer 8

Supplementary motor area is anterior and medial to primary motor cortex. Involved in planning complex internally cued movements such as speech. Becomes active prior to voluntary movement.

Question 9

Corticospinal tract? UMN & LMN? Path of tract and types - what is each responsible for?

Answer 9

Corticospinal tract for fine, discrete movement of the body. UMN in primary motor cortex, LMN in spinal cord. Most fibres decussate at the medulla to go to the other side and form the lateral corticospinal tract which provides voluntary motor innervation to the limbs. The fibres that do not decussate at medulla form the anterior corticospinal tract which provides motor innervation to the trunk muscles.

Question 10

What is somatotopic represention? What is seen motor cortex medially?

Answer 10

Different parts of body are represented in the brain in relation to where they are in the body, eg. Lower limbs more medial in the motor cortex, and as we go more laterally we get the upper limbs and the face.

Question 11

Corticobulbar tract functions? Where do they synapse?

Answer 11

Corticobulbar tracts synapse at brainstem nuclei and innervate face and neck mostly.

Question 12

Where do extrapyramidal tracts have LMN? What are they responsible for?

Answer 12

Extrapyramidal tracts have LMN in brainstem nuclei. They are responsible for autonomic movement and postural stability.

Question 13

Functions of vestibulospinal tract? Where LMN?

Answer 13

vestibulospinal tract has LMN in vestibular nuclei. Functions include stabilising head when body is moving, postural stability, coordinating head with eye movements.

Question 14

Functions of reticulospinal tract? What type of tract and location?

Answer 14

Reticulospinal tract is primitive desceding tract - from medulla and pons. Postural stability and changes in muscle tone.

Question 15

Functions of tectospinal tract? Location?

Answer 15

Superior colliculus of midbrain. Functions include orientation of head and neck during eye movements

Question 16

Functions of rubrospinal tract? Location?

Answer 16

Red nucleus of midbrain. Mostly replaced by corticospinal tract now. Innervates the LMN of the flexors of the upper limb.

Question 17

What are negative signs of a UMN lesion + definitions?

Answer 17

Loss of voluntary movement, paresis (graded weakness of movement), paralysis (complete loss of voluntary movement)

Question 18

What are positive signs of a UMN lesion and why do they happen?

Answer 18

Positive signs happen due to loss of inhibitory descending signals causing increased abnormal movement. 1. spasticity (increased tone). 2. hyperreflexia (increased reflexes). 3. clonus (oscillatory muscle contractions) 4. babiinski’s sign

Question 19

What is apraxia? Where lesion for apraxia? Common causes?

Answer 19

Apraxia is when they cannot perform certain skilled movements. Not paretic but lack information on how to perform skilled movement. Lesion in inferior pareietal lobe or frontal lobe. Most commonly due to stroke or dementia.

Question 20

LMN lesion signs? Definitions?

Answer 20

Hypotonia (decreased tone), hyporeflexia (decreased reflexes), muscle atrophy, fasciculations (spontaneous action potnetials seen with the naked eye), fibrillations (spontnaoeus muscle twitches not seen with naked eye), weakness of voluntary movements.

Question 21

Difference between fasciulations and fibrillations?

Answer 21

Fasciculations are spontaneous action potentials that are visible. Fibrillations are spontanoeus twitches of muscle fibres that are not visible - recorded in electromyography)

Question 22

What is motor neurone disease and what does it affect? Leads to death by what?

Answer 22

ALS is a neurodegenrative conditions affecting UMN and LMN neurones and the brainstem (therefore leading to death by loss of control of respiratory muscles)

Question 23

What are UMN signs of ALS? LMN signs ALS?

Answer 23

UMN: dysarthria (difficulty speaking), dysphagia (difficulty swallowing), spasticity, brisk limbs and jaw, loss of dexterity, babinski’s sign. LMN: dysphagia, muscle atrophy, weakness of movement, tongue fasciculations and wasting,

Question 24

What are structures of the basal ganglia?

Answer 24

Caudate, putamen, nucleus accumbens, globus pallidus, thalamus, amygdala

Question 25

Function of the basal ganglia?

Answer 25

Inntention of movement. Associated movements. Supressing unwanted movements. Performing movements in order.

Question 26

What diseases cause dysfunction of basal ganglia?

Answer 26

PD, huntingtons

Question 27

What is parkisnons disease? What does it affect? What are symptoms of PD + definitions?

Answer 27

PD causes neurodegeneration of the dopaminergic neurones in the substantia nigra of the brain which project to the striatum. It affects the intention of movement and the fluidity of movement. Affects ability to make small dextrous movements. 1. bradykinesia (slowing of small movements) 2. hypomimic face (expressionless face), 3. akinesia (difficulty initiating movements) 4. rigidity (increased tone) 5. tremor at rest which then becomes pin-rolling tremor

Question 28

What is huntingtons disease? In what areas of the brain? Signs? What is it caused by?

Answer 28

Loss of GABAergic neurones in striatum (caudate + putamen). Causes choreic movements (rapid jerky movements starting at face and then at limbs), dysphagia, unsteady gate, later on cognitive decline and dementia. Causesd by autosomal dominant CAG repeat

Question 29

What is ballism due to? What does it cause?

Answer 29

usually by stroke affecting subthalamic nucleus. Uncontrollable flinging of extremities (contrallaterally)

Question 30

Where is cerebellum and what separates it from cerbrum? What is its function?

Answer 30

Cerebellum is in posterior cranial fossa. Tentorium cerebelli. Function in coordinating movement and predicting movement to make it fluid.

Question 31

What is the function of the verstibulocerebellum? Damage causes what?

Answer 31

Vestibulocerebellum for posture, gait and coordination of head movmenets with eye movements. Damage causes similar presentation to vestibular disease, gait ataxia and tendency to fall.

Question 32

Function of spinocerebellum? What does damage cause and what can cause atrophy of spinocerebellum?

Answer 32

Coordination of speech, limb movements and muscle tone. Atrophy can happen due to alcoholsm. Damage causes wide-based stance and gait, affects mostly legs

Question 33

Function of cerebrocerellum? What can damage cause?

Answer 33

Emotions, speech, executive function, skilled movments language. Damage affects skilled movement mostly and speech.

Question 34

What are the main signs of cerebellar dysfunction and the definitions?

Answer 34

1. ataxia (uncoordinated movement - abnromal stance & gait) 2. dysmetria (abnormal force for movement) 3. dysdiadochokinesia (inability to perform rapidly alternating movements) 4. intention tremor (tremor when doing a target directed movement), 5. scanning speech (stacatto of speech, non-fluid speech due to loss of coordination of speech muscles)

Question 35

What are extrafusal muscle fibres and intrafusal muscle fibres?

Answer 35

Extrafusal muscle fibres are those that are contractile and produce movement. Intrafusal muscle fibres contian the sensory organs that respond to stretch/tension.

Question 36

What are alpha motor neurones? Where are they located? What do they do?

Answer 36

Alpha motor neurones are LMN that innervate the extrafusal muscle fibres to bring on muscular contraction. They are located in the ventral/anterior horn of the spinal cord and when stimulated bring on muscular contraction.

Question 37

What is a motor neuron pool?

Answer 37

All alpha neurones inervating a specific muscle

Question 38

What is a motor unit? Difference in motor neurones at birth and during development? What happens if u stimulate one motor unit?

Answer 38

A motor unit is a motor neurone and all the muscle fibres it innervates. At birth there may be overlap between different motor neurones and the fibres they innervate but during development one motor neurone wins and innevates this msucle fibre. If you stimulate a motor unit u get contraction of all its muscle fibres.

Question 39

What does a small innervation ratio of a motor unit show?

Answer 39

for more precise movement.

Question 40

What are the types of motor units? What are their characteristics?

Answer 40

Type I - slow twitch -> small cell bodies, small dendritic trees, thin axons. Type Iia - fast fatigue resistant - big cell bodies, large dentritic trees, thick axons. Type Iib - fast fatiguable - same as fatigue resistant

Question 41

How do motor units differ in terms of force and duration?

Answer 41

Slow produce little force but for a very long time. Fast fatiguable produce the most force but not for a long time. Fast fatigue resistant produce a little less force but for more time

Question 42

What muscle units for muscles of posutral stability?

Answer 42

slow twitch

Question 43

How does the CNS regulate muscle force (2 priniciples)?

Answer 43

Recruitment and rate coding

Question 44

What is recruitment?

Answer 44

Motor units are recruited in terms of how much force is needed. If little force is needed slow twitch recruited first, and as more force needed fast recruited later. Derecruited in opposite order

Question 45

What is rate-coding? What is summation?

Answer 45

Rate-coding is the ability of the CNS to change firing intensities of the motor units recruited to fit the needs of the force needed. Summation happens when the motor unit is firing at a rate too high to allow relaxation of the muscle fibre between AP.

Question 46

What are neurotrophic factors?

Answer 46

Growth factors that are neuroprotective and allow neuronal growth after injury.

Question 47

What effect does motor neurone have on the muscle fibres it innervates?

Answer 47

Muscles fibres will take on the characterstics of the motor neurone innervating it (can become fast, slow)

Question 48

What plasticity is possible between motor units and under what conditions?

Answer 48

Can go from fast fatiguable to resistant with training. Can go from type I to II with severe spinal deconditioning and in space travel. In old age and atrophy can go from fast to slow.

Question 49

What is a reflex? Can it be stopped? What affects magnitude and timing of stimulus?

Answer 49

A reflex is a an automatic response to a stimulus which involves a receptor being activated and sending a senosry neruone tospinal cord in order to have a motor neurone cause afferent effect (contraction). Magnitude and timing affected nby intensity and onset of stimulus

Question 50

Describe a monosynaptic stretch reflex?

Answer 50

Tendon hammer causes stretch of the muscle so activation of the sensory organ, sening sensory neurones to spinal cord, and activating motor neurone to ellciit contraction and another motor neurone to inhibit antagonistic muscle

Question 51

What is desceding supraspinal control of reflexes? What can you do to make reflex bigger and what is this called?

Answer 51

Clenching teeth, making a fist or pulling against locked fingers during tap will make reflex larger - jendrassik manoevre

Question 52

What do higher centres of CNS do to regulate stretch reflexes? Damage to UMN causes what?

Answer 52

Higher centres of CNS can exert inhibitory and excitatory regulation, with inhibitory singals dominateing. Decerebration casues loss of these inhibitory descending signals (UMN lesions) and thus increased muscle tone in forms of spasticity and rigiditiy seen

Question 53

What do gamma motor neurones do?

Answer 53

Gamma motor neurones alter the sensitivity of sensory organs in muscles so that they remain sensitive at different lengths

Question 54

What is hyper-reflexia and cause?

Answer 54

veractive reflexes due to loss of descedning inhibition - UMN

Question 55

What is clonus?

Answer 55

involuntary rhythmic muscle contraction due to UMN

Question 56

What is babinski’s sign? Cause?

Answer 56

When sole sitmulates with blunt isntrument toes should curl down if up babinksi but curl up normally in infants

Question 57

What is hyporeflexia? Cause?

Answer 57

Below normal or absent reflexes due to LMN lesion