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Brain and Behaviour Year 2 > Motor System II > Flashcards

Motor System II Flashcards

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1
Q

What regions of the cortex are involved in motor control

A
  • all regions of the frontal lobe

- the more anatomically anterior the cortical region the more complex or abstract its role in movement is

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2
Q

what broadmann area is the primary motor cortex

A
  • This is broadmann area 4
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3
Q

Where is the primary motor cortex

A
  • It is immediate anterior to central sulcus
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4
Q

where is the primary motor cortex involved in the motor hierarchy

A
  • Lowest level of motor ‘hierarchy’
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5
Q

what do the lesions of the primary motor cortex involve

A
  • Local lesions causes initial paralysis or paresis of specific muscle groups. However some recovery of function may occur due to cortical plasticity
  • With larger lesions more muscle groups are involved and recovery less likely
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6
Q

describe what recovery is like in stroke

A
  • These tend to take out large areas of the cortex therefore recovery is much less limited
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7
Q

what does strokes tend to effect

A

Never affect just one anatomical area of cortex like the primary motor cortex-they always involve multiple cortical areas

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8
Q

What is effected when there is a stroke involving the middle cerebral artery

A
  • Strokes involving occlusion of the middle cerebral artery affect almost all of one side of the frontal lobe and produce severe motor disability in all parts of the contralateral body except the lower limb as this region of motor cortex is supplied by anterior cerebral artery.
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9
Q

what happens if there is infarction to the proximal segment of the middle cerebral artery

A
  • Infarction of the proximal (M1) segment of the MCA will affect the blood supply to the basal ganglia via the lenticulostriate arteries as well as the blood supply to the motor cortex.
  • This is much more disabling than a stroke that affects the motor cortex(M3 segment) alone
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10
Q

What broadmann areas are Premotor cortex and supplementary motor cortex

A

broadmann areas 6 and 8

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11
Q

what happens when there is damage to the premotor and supplementary motor cortex

A
  • damage to areas 6 and 8 either medial or lateral lead to the clinical syndrome of motor apraxia
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12
Q

what do patients with apraxia have

A
  • normal reflexes and normal muscle strenght but have difficulty performing complex motor tasks such as typing or tying a shoelace
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13
Q

what happens if there is damage to only one side of the premotor cortex and supplementary motor cortex

A
  • Damage to one side side(as in stroke) may however produce only minimal symptoms as the contralateral area may be able to take over some functions of the damaged tissue.
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14
Q

what broadmann area is the posterior parietal cortex

A

Posterior parietal cortex broadman areas 7 and 19

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15
Q

what does damage to the posterior parietal cortex do

A
  • Damage to the posterior parietal cortex can lead to the clinical syndrome of sensory apraxia
  • Patients with sensory apraxia have difficulty performing complex motor tasks when these are triggered by sensory input for example when asked verbally to do something
  • This kind of apraxia is not strictly speaking a motor deficit rather a difficulty in linking a sensory input to the motor system
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16
Q

what are the frontal eye fields and brocas area and what are they involved in

A
  • These are two specialised cortical areas adjacent to the premotor area that are dedicated to motor control of two special motor systems
    • the extraocular eye muscles and the muscles regulating speech
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17
Q

what can damage to brocas area lead to

A

motor aphasia

- where a patient has difficulty generating speech motor outputs, and linking word strings into complex sentences.

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18
Q

what is oculomotor aphasia

A
  • this is a condition where patients have difficultly moving their eyes horizontally and moving them quickly
  • for example when trying to follow a moving object or when tryign to read a line of text on a screen
  • patients may have to turn there head in order to compensate for the lack of eye movement in order to follow an object or see objects in their peripheral vision - they often move their head too far and have to move several times to get there desired object effect on their fovea
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19
Q

what causes oculomotor apraxia

A

bilateral lesions of the frontal eye fields (FEF)

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20
Q

what is oculomotor apraxia always a bilateral condition

A
  • Always bilateral lesions this may be due to the idea that contralateral eye fields can compensate for the unilateral damage therefore only shows up in bilateral conditions
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21
Q

what is the parietal lobe involved in

A
  • it is involved in motor control
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22
Q

what is causes sensory apraxia

A
  • Damage to connections from the posterior parietal lobe to the premotor cortex are associated with sensory apraxia
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23
Q

what arises from the anterior parietal lobe

A
  • About 40% arise from the corticobulbopsinal tract axons arise from the anterior parietal lobe e.g. the somatosensory cortex (area 1, 2 and 3)
  • These axons send commands down the spinal cord that modulate sensory input – they can modulate spinal reflexes (e.g. suppression nociceptive reflexes)
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24
Q

what broadmann area is the somatosensory cortex

A

1,2 and 3

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25
Q

What broadmann area is the dorsolateral prefrontal cortex

A

areas 9 and 10

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26
Q

what is the doroslateral prefrontal cortex involved in

A
  • planning of movement
  • it evaluates different possible future actions and decides which one is the best
  • problem solving and judgement
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27
Q

what are executive functions

A
  • planning of movement
  • it evaluates different possible future actions and decides which one is the best
  • problem solving and judgement
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28
Q

what happens if you have a lesion in the dorosolateral prefrontal cortex

A
  • apathy
  • personality changes
  • lack of ability to plan or to sequence actions of tasts
  • poor working memory for verbal information (if the left hemisphere has a lesion ) or spatial information (if the right hemisphere has a lesion)
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29
Q

What is a common test for dorsolateral prefrontal cortex damage

A
  • Wisconsin card sorting tests

- this tests for the inability to switch behaviour appropriately

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30
Q

what commonly causes damage to the dorsolateral prefrontal cortex

A

MRI studies have shown that the frontal cortex may easily be damaged by impact with the frontal bone for example if a road traffic accident or blow tot he head that causes contusions (brain bruising)

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31
Q

what broadmann area is the orbitofrontal cortex in

A

broadman area 11

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32
Q

what does the orbitofrontal cortex do

A
  • control inhibition of motor responses associated with the limbic system
  • These include responses to hunger, thirst, sexual drives etc
33
Q

What happens if you have damage to the orbitofrontal cortex

A
  • Disinhibition of these drives after orbital damage leads to pseudopsychopathic behaviour
  • This can be defined as impulsiveness, puerility, a jocular attitude, sexual disinhibition, and complete lack of concern for others.
  • Patients with such acquired sociopathy, or pseudopsychopathic disorder, are said to have an orbital personality
34
Q

describe the motor hierarchy in the frontal lobe

A

areas 11 (orbital cortex - control of drives) and areas 9 and 10 (dorsal prefrontal cortex - future movements (highest level) project into areas 6 and 8 (premotor area and supplementary motor area - integration of information from frontal lobes, formation and rehearsal of motor programs)

  • the frontal eye fields, broca’s area and areas 6 and 8(premotor area - execution of motor functions and supplementary motor area - sensory feedback from muscles and joints) all project into area 4 ( primary motor cortex)
  • area 4 (primary motor cortex) and areas 1,2 and 3(somatosensory cortex) all feed into the corticobulbospinal tract
  • the corticobulbospinal tract then goes into the motor neurones in the spinal cord
35
Q

describe where the corticospinal tract travels

A
  • Travels through the internal capsule and runs between the caudate and the putamen in the frontal lobe and then goes down into the midbrain where it forms two large wedges of fibres on the anterior surface of the midbrain
  • From here still anterior it passes into the medullary pyramids
  • It them decussates at the top of the spinal cord where it from the lateral and anterior corticospinal tract
36
Q

where does the corticospinal tract decussate and what does it turn into

A
  • top of the spinal cord, upper spinal cord (C1-C5)

- forms the lateral and anterior corticospinal tracts

37
Q

where does the corticobulbar component of the tract terminate on

A
  • This terminates on various cranial nerve nuclei V and VII for cortical control of the muscles of the head and oculomotor nuceli (III, IV and VI for control of eye movements.
  • It also terminates on cells of the pontine nuclei, the reticular formation and the red nucleus.
38
Q

What is the red nucleus

A

The red nucleus is a large nucleus in the midbrain (next to the oculomotor nuclei).

39
Q

where does the corticospinal part of the corticobulbar tract decussate

A
  • The corticospinal component of the tract continues on to the lower medulla where it crosses (decussates) to the opposite side to form the large lateral corticospinal tract and the small medial corticospinal tract
40
Q

what happens if there is injury to the corticospinal tract

A
  • . If the brain is injured ABOVE the spinal cord/medulla junction, the motor deficit is on the opposite side.
  • If the injury is in the spinal cord is injured, the motor deficit is on the same side
41
Q

where do the lateral cotricospinal tract and anterior cotricospinal tract run

A

Lateral corticospinal tract runs in the dorsolateral cord

Anterior corticospinal tract in medial ventral cord (only present in the cervical cord)

42
Q

what type of synapse connections does the corticospinal tract have

A
  • has monosynaptic connections only with moto neurones of the thumb and digits
43
Q

How are motor actions initiated in other muscles be the corticospinal tract

A

The motor actions initiated in other muscles by the CST are mediated by actions of the CST on spinal interneurones. The CST drives interneurones which modulate spinal reflexes.

44
Q

where does the small anterior corticospinal tract terminate and control

A
  • There is a small anterior (or ventral) corticospinal tract (also crossed). This ventral corticospinal tract terminates in the cervical cord.
  • It controls voluntary movements of the neck.
45
Q

what does damage to the corticospinal tract in the spinal cord do

A

Damage to the corticospinal tract in the spinal cord causes loss of control of hands and fingers, but NOT normally loss of posture or locomotion and gait. (at least not in the long term)

46
Q

what control motor functions of posture, locomotion and gait

A
  • other descending motor tracts known as extra-pyramidal system
47
Q

where do the extrapyramidal system originate

A
  • they all originate from groups of cell bodies in the brainstem
48
Q

what are the main components of extrapyramidal system

A

Lateral vestibulospinal tract and reticulospinal tracts.

49
Q

describe the lateral vestibulospinal tract

  • origin
  • where the nucleus projects
  • what does it control
A
  • Origins: vestibular nuclei in upper medulla/lower pons
  • Nucleus projects ipsilaterally to antigravity muscles
  • Tonically active during upright posture
  • Controls posture and balance
50
Q

describe the reticulospinal tract

  • origin
  • where the nucleus projects
  • what does it control
A
  • Arises in reticular formation of pons and medulla
  • Projects diffusely (bilaterally) down spinal cord
  • Responsible for autonomic control (drives sympathetic preganglionic neurones) also drive to respiration (phrenic nerve)
  • General ‘arousal’ of spinal cord
51
Q

describe the rubrospinal tract

  • origin
  • what does it do
A
  • origin is the red nuclues in brainstem
  • carries cerebellar commands to the spinal tract
  • probably plays a role in control of movement velocity and transmitting motor commands from the cerebellum to the musculature
52
Q

where does the red nuclues receive its main input from

A

cerebellum

53
Q

name some minor extrapyramidal pathways

A
  • tectospinal tract

- medial vestibulospinal tract

54
Q

describe what the tectospianl tract do and where does it originate

A
  • a pathway that cooridnates voluntary head and eye movement, it activates reflex movements of the head in response to visual and auditory stimuli
  • originates in the superior collicus and projects to the contralteral cervical spinal cord to terminate in lamine VI, VII, VIII
55
Q

What is the medial vestibulospinal tract a continuation of

A
  • medial longitudinal fasiculus
56
Q

what does the medial vestibulospinal tract do

A
  • it mediates reflex co-ordination of the head and neck muscles with the extraocular eye muscles to maintain objects in view despite movement of the body
57
Q

what an the major descending motor tracts act on

A
  • the major descending motor tracts can act on interneurones in the cord to modulate the strength and activity of reflex pathways within the spinal cord
58
Q

what is the only upper motor neurones that act directly on lower motor neurones

A

The only upper motor neurones that act directly on lower motor neurones in the spinal cord are those driving the muscles of the thumb and fingers (and the lips and tongue)

59
Q

what is spasticity

A
  • can be defined simply as as abnormally increased muscle tone.
  • Spastic muscles often have increased tendon reflexes.
  • Spasticity is a characteristic of upper motoneurone lesions, i.e. damage to the motor cortex or any of the descending tracts.
60
Q

what is clonus

A

Is a series of (jerky) contractions of a particular muscle following sudden stretching of the muscle

61
Q

What is hyperreflexia

A

This where is an abnormally (pathologically) brisk tendon reflex is seen in one or more muscles.

62
Q

What are the two more severe signs of motor system damage

A

Decorticate posturing

Decerebrate posturing

63
Q

What is the decorticate posturing and what does it indicate

A
  • Arms are adducted and flexed
  • With the writs and fingers flexed on the chest, the legs may be intenrally rotated and stiffy extended with plantar flexion of the feet
  • Decorticate posture indicates damage to the corticospinal tract in the midbrain
64
Q

What is the decerebrate posturing

A
  • Arms are adducted and extended with the wrists pronated and the fingers flexed
  • The legs may be internally rotated and stiffly extended with plantar flexion of the feet
  • decerebrate posturing indicates a severe injury to the brain at the level of the brainstem, including damage to cotricospinal and rubrospinal tracts.
  • More severe form
65
Q

describe the mechanism of action that causes decorticate posture

A
  • indicated amage predominantly to the corticospinal tract
  • usually more favourable that the decerebrate posture
  • usually seen in the unconscious patients
  • may progress to the decerebrate posture or two may alternate
  • may occur on one or both sides of the body
66
Q

describe the decerebrate posture

A
  • This posture is thought to be due to excessive activity (disinhibition) in the extrapyramidal system, particularly the vestibulospinal tract.
  • Normally the vestibulospinal tract is under tonic inhibition by the corticobulbospinal tract and the red nucleus
  • . If the red nucleus is damaged by a severe midbrain injury then decerebrate posturing may develop.
  • It is only seen in unconscious patients
67
Q

what do discrete acute lesions lead to

A
  • Discrete acute lesions lead to initial paralysis followed by variable degree of recovery.
  • during recovery there is weakness, clumsiness and fatigue of movements
68
Q

Why does recovery occur

A
  • Recovery occurs because of plasticity in the cortex.
  • After a lesion to the face area face muscles may become driven by cells from different part of cortex- the homonculus is changed the areas that are not damage expand .
69
Q

what do large lesions lead to

A
  • slower recovery and permanent loss of certain movement

- weakness, clumsiness and fatigue are greatly increased

70
Q

describe chronic effects of lesion of motor cortex

A
  • If the lesion is small there may eventually be good recovery of motor skills but motor weakness and quick fatigue will always be present.
  • If there is persisting spasticity following a lesion of the motor cortex, the spasticity is invariably combined with a profound motor weakness.
  • This often leads to a persistent flexion of arms and extension of the legs; this is “HEMIPLEGIC DYSTONIA”.
  • The clasp-knife reflex is particularly characteristic of chronic cerebral motor lesions.
71
Q

What is hemiplegic dystonia

A

persistent flexion of arms and extension of the legs

72
Q

what are the effects of lesions of motor tracts in the cord

A

Spinal shock is a clinical condition that occurs after acute (eg traumatic) damage to the spinal cord that includes damage to any of the descending tracts.

73
Q

how long can spinal shock last

A

Spinal shock can last for days, weeks or months depending on the severity of the injury.

74
Q

describe what happens if lesions are in the spinal cord

A
  • there is paralysis or paresis and reduced reflex responses in all muscles below the region of the injry
  • in the severest form after total transection of the cord all reflexes at all levels of the cord below the lesion are inactive
75
Q

describe the chronic effects of damage to the spinal cord

A
  • Eventually spinal shock wears off and weak monosynaptic reflexes reappear Crossed extensor reflexes may also recover.
  • In severe injury these reflexes are not controlled by the brain and may become exaggerated and hyperactive (hyperreflexia) after time.
  • Clonus may be present. A Babinski sign will be normally be present
76
Q

name the tract that is responsible

  • paralysis/weakness of voluntary movement
  • loss of bladder/bowel control
  • loss of ability to stand upright and or balance properly
  • poor gait
  • loss of temperature regulation
  • loss of blood pressure regulation
  • hyperactive tendon reflexes
A
  • paralysis/weakness of voluntary movement - corticospinal tract
  • loss of bladder/bowel control - reticulospinal tract
  • loss of ability to stand upright and or balance properly - vestibulospinal tract
  • poor gait - reticulospinal tracts and vestibulospinal tracts
  • loss of temperature regulation - reticulospinal tracts
  • loss of blood pressure regulation - reticulospinal tracts
  • hyperactive tendon reflexes - corticospinal tracts
77
Q

describe upper motor neurones

  • possible location
  • common causes
  • structures involved
  • distribution
  • voluntary movements
  • muscle tone
  • myotactic reflexes
  • cutaneous relfexes
  • muscle bulk
  • classical description
A
  • possible location - CNS only
  • common causes - CVA, trauma, MS, ALS, infectious disease
  • structures involved - Motor cortex or corticospinal tract
  • distribution- never individual muscles, always group of muscles
  • voluntary movements - paralysis or paresis especially of skilled movements
  • muscle tone -increased, particularly in antigravity muscles
  • myotactic reflexes - hyperactive or exaggerated
  • cutaneous relfexes - some abnormalities e.g. positive babinski sign
  • muscle bulk - may be slight atrophy
  • classical description - spastic paralysis
78
Q

describe lower motor neurone lesion

  • possible location
  • common causes
  • structures involved
  • distribution
  • voluntary movements
  • muscle tone
  • myotactic reflexes
  • cutaneous reflexes
  • muscle bulk
  • classical description
A
  • possible location - CNS or PNS
  • common causes- CVA, polio, tumour, trauma, alcoholism, diabetes
  • structures involved - spinal or brainstem - motor neurones or peripheral motor axons
  • distribution - segmental - limited to muscles innervated by damaged motoneurons or their axons
  • voluntary movements - paralysis
  • muscle tone - decreased
  • myotactic reflexes - decreased or absent
  • cutaneous reflexes - decreased or absent
  • muscle bulk - pronounced atrophy
  • classical description - flaccid paralysis

Brain and Behaviour Year 2 (36 decks)

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