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Neuroscience (Yeo) > Motor Control - Disorders of Movement > Flashcards

Motor Control - Disorders of Movement Flashcards

1
Q

What motor disturbances can be seen in disease?

(give 6)

A
  • Weakness
  • Spasticity
  • Rigidity
  • Ataxia
  • Akinesia
  • Apraxia

(usually a patient will show more than one of these symptoms)

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2
Q

What is meant by ‘weakness’?

A
  • This is not the same as having weak force production in muscles
  • Inability to produce forceful movements under voluntary control
  • It can be a weak but active muscle response
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3
Q

What is meant by spasticity?

A
  • Too much tonic (basal) drive to the muscles
  • This causes unwanted contractions
  • Therefore causing joints to be fully flexed/extended
  • It can apply to both agonists & antagonists
  • It causes co-contraction spasticity –> making joints very rigid –> giving spastic rigidity
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4
Q

What is ataxia?

A
  • Cerebellum Damage
  • Loss of Coordination
  • The sequence of muscle activation/contraction is messed up –> thus the cooperation between agonist & antagonist is faulty
  • There is a decomposition of movement
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5
Q

What is meant by akinesia?

A
  • Absence of Movement

(little/no movement)

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6
Q

What is bradykinesia?

A

Low Level of Movement

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7
Q

What is apraxia?

A
  • Inability to produce purposeful movements (e.g. can move arms but with no purpose)
    (i. e. cannot make a specific grasp)
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8
Q

What is praxia?

A

Movement with purpose

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9
Q

In terms of time, what effect will a vascular occlusion or haemohrrage have?

A
  • Immediate Paralysis
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10
Q

In terms of time, what effect will a tumour have?

A
  • Slowly progressive symptoms & signs
  • Tumour progresses slowly so motor deficit will be slowly progressive
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11
Q

What is the confusion caused with small ministrokes?

A
  • Their effects can accumulate
  • They are more difficult to establish
  • Usually though there is one major event which is critical that causes a major loss which is obvious
    *
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12
Q

In terms of time, how do neurodegenerative losses (e.g. Parkinson’s) present?

A
  • Slow & progressive symptoms
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13
Q

Where are flexors & extensors generally located in the spinal cord?

A
  • Flexors –> near the centre (central canal)
  • Extensors –> further out (edges)
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14
Q

Image showing Rexed Laminas.

A
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15
Q

What four tracts does the cerebellum access & influence?

A
  • Corticospinal Tract
  • Rubrospinal Tract
  • Reticulospinal Tract
  • Vestibulospinal Tract
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16
Q

What does the basal ganglia mainly influence?

A
  • Corticospinal / Pyramidal Tract
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17
Q

What is the vestibulospinal tract important for?

A
  • Balance Control
  • Posture Control

(Pathologies here will cause problems with posture & balance)

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18
Q

What is the reticulospinal tract important for?

A

Locomotion

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19
Q

What is an important point to note in general about the signals between neurones in the NS?

A
  • There is always a basal/tonic firing rate/drive
  • Signals are simply modulated on top to increase/decrease activity with excitatory/inhibitory flow
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20
Q

Why is it important there is always a tonic drive to the muscles?

A
  • So small motor units can contract –> all the time
  • Giving the muscle tone
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21
Q

Why do big neurones not fire in the background at basal/tonic levels?

A
  • Size Principal
  • Bigger drive needed to stimulate them as they have low resistance
  • Tonic levels only sufficient for small motor units which have high resistance
  • More drive can cause the bigger ones to contract
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22
Q

What are the two functionally distinct divisions in nervous system pathology?

A
  • Lower Motoneurone (LMN)
  • Upper Motoneurone (UMN)

They produce entirely different symptoms & consequences

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23
Q

What is a lower motoneurone lesion usually caused by?

A
  • Alpha Motor Neurone Damage
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24
Q

What is an upper motoneurone lesion usually caused by?

A
  • Motor Cortex
  • Corticospinal Tract
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25
Q

What damage corresponds (can cause) a Lower Motoneurone Lesion?

A
  • Alpha motoneurones (usually this)
  • Muscle Spindle
  • Primary Afferents (1a afferents)
  • Type II Afferents (for sustained movement)
  • Myelination of the Efferent/Afferent Signals
  • Spinal Cord
  • Alpha-Motoneurons
  • Motoneuron axons
  • Neuromuscular junction
  • Muscle (itself)

(think of the whole reflex arc and anything involved in it)

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26
Q

What are the effects of a lower motor neurone lesion (LMN)?

A
  • Strength of Muscle Stretch Reflex Decrease (or even absent)
  • Weak Voluntary Movements (cannot move limbs)
  • Muscle weakness

All the components of the reflex arc can cause LMNL thus can cause these symptoms

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27
Q

In terms of afferent signals, what are you testing with a muscle jerk reflex?

A
  • 1a Afferents
  • NOT the Type II Afferents –> as these measure sustained movements
  • The tendon reflex is dynamic therefore it is testing the 1a afferents & not Type II
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28
Q

What happens if a muscle loses its innervation?

A

Muscle Atrophy

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29
Q

What needs to happen next after you have determined a LMNL?

A
  • Further tests to assess which part of reflex arc has the problem
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30
Q

Give 5 causes of a LMN Lesion, which have been indicated with weak Muscle Stretch Reflex.

A
  • Peripheral Neuropathies
  • Injury in Dorsal/Ventral Root (e.g. herniated vertebral disc)
  • Poliomyelitis (virus kills motoneurons)
  • Myasthenia Gravis (decreased neuromuscular transmission)
  • Muscular Dystrophy (primary muscle disease)
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31
Q

What is peripheral neuropathy?

A
  • Damage to Nerve in the Periphery
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32
Q

What occurs in Myasthenia Gravis?

A

Decreased neuromuscular transmission (due to reduced post-synaptic AChRs)

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33
Q

What is a common cause of LMNL?

A
  • Injury to Dorsal/Ventral Root
  • This is usually caused by a herniated vertebral disc
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34
Q

What is a common phrase used by those with an Upper Motoneurone Lesion (UMNL)?

A
  • ‘I cannot move’
  • ‘I am too tired to move’
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35
Q

What occurs in an Upper Motoneurone Lesion?

A
  • System that tries to generate movements voluntarily (primarily the corticospinal tract but maybe reticulospinal tract) –> causes weak movements which are tiring to produce
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36
Q

What occurs when you perform a Knee Jerk Reflex on someone with an UMNL?

A

Unusually brisk reflex (rapid & strong)

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37
Q

Why does the reflex jerk on UMNL do what it does?

A
  • Voluntary Control via Corticospinal Tract is Lost
  • It cannot generate voluntary movement
  • However reflex system works better (no descending inhibition)
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38
Q

Describe the pathway of the corticospinal tract.

A
  • Excitatory axons from Motor Cortex
  • Come down the spinal cord –> synapse with motor neurones & interneurones which control movements
  • These are turned off –> so no voluntary movements
  • Causes a decrease of excitatory movements –> thus less likely to depolarise
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39
Q

Why does the reflex get stronger in UMNL?

A
  • Reflex circuits have a lot of inhibitory interneurones which synapse onto it (renshaw cells 1a & 1b)
  • There are more inhibitory motoneurones than excitatory motoneurones
  • These all get their drive from the motor cortex
  • Therefore, the motor cortex sends tonic instructions to excitatory & inhibitory interneurones –> excitation of motoneurones based on net sum balance
  • If both stop (due to more inhibitory stopping) –> there is a net gain in excitation –> thus motoneurones more excitable –> closer to threshold –> thus brisk reflex
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40
Q

Generally, why does UMNL cause a brisk reflex?

A
  • Due to overall disinhibitory effect of loss the descending command
  • Causing a net loss of inhibitory commands –> thus increased excitability
  • This raises excitability + changes property of some intrinsic spinal reflexes
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41
Q

Does muscle wasting take place in UMNL?

A
  • No
  • There is no denervation –> thus no atrophy
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42
Q

What are the effects of an UMN lesion?

A
  • (Spastic) Weakness
  • Voluntary Movements are weak & tiring to produce
  • Unusually brisk (exaggerated) muscle stretch reflexes - spasticity
  • No signs of muscle denervation (no wasting) - Normal Tone
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43
Q

What does UMN lesions do in terms of FRA-driven reflexes?

A

Reverse some FRA-driven reflexes

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44
Q

Where can damage take place to cause an Upper Motoneurone Lesion?

A

Involves the:

  • Corticospinal Tract (always)
  • (with or without) the rubrospinal tract
  • (with or without) the reticulospinal tract

Damage may be in:

  • Motor Cortex
  • Any part of the descending corticospinal tract
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45
Q

How does an UMNL affect muscle?

A
  • Does not affect individual muscles
  • Muscles affected as groups

This can involve whole limbs or whole sides of the body

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46
Q

Which places do not produce the same pattern of deficits as an UMNL?

A

Other parts of the motor system that do not produce the UMNL pattern of deficit:

  • Basal Ganglia
  • Cerebellum
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47
Q

Why is an UMNL non-specific?

A
  • Affecrs anywhere below the level of the lesion in the corticospinal tract (or even M1)
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48
Q

Clinical signs of an UMNL.

A
  • Spastic Weakness
  • Normal Muscle Tone (no/little atrophy)
  • Not entirely rigid
  • Vigirous activation of 1a afferents (very quick - part of dynamic system)
  • Exaggerated dynamic stretch reflex
  • Joint is not rigid (weakness not co-contraction)

(If patient’s arm is pulled back there is a jerk pull back reflex as arm is extended - this is an exaggerated dynamic stretch reflex - spastic weakness0

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49
Q

What is spasticity of gait formally called?

A

Scissor Walking

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50
Q

What does scissor walking involve (spasticity of gait)?

A
  • Flexed hips & knees (patient leans forwards)
  • Plantar flexed ankles
  • Tone increases in agonists & antagonists leads to limb stiffness
  • Inward rotation of each lower limb
  • Walking by circumduction at the hip (giving swivelling movement)
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51
Q

What is important when making a normal locomotory gait?

A
  • Hip flexion
  • Ankle flexion
  • Knee flexion
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52
Q

Why do they use scissor walking pattern?

A
  • Point on Point rotation of the legs
  • Limitations in walking trajectory
  • Solution is to swivel with trunk movements with relatively stiff legs
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53
Q

What causes scissor walking?

A
  • Spastic Rigidity
  • Due to Upper Motor Neurone Lesion of the Lower Limb
54
Q

What is the babinski sign?

A
  • Reflex associated with vigorous stimulation/irritation of the sole of the foot
55
Q

In which cohort of patients do we see a positive babinski sign?

A
  • Babies before 6 months
  • UMN Lesion Patients
56
Q

What do babies or UMNL adults when you perform the babinski test do?

A
  • Dorsiflex
57
Q

What do healthy adults when you perform the babinski test do?

A
  • Plantarflex

(stand up on their toes)

58
Q

Why is there a positive babinski reflex for 6-12 months in babies?

A
  • Due to demyelination of the corticospinal tract
  • It takes around 6-12 months
59
Q

How is the babinski reflex suppressed in healthy adults?

A
  • Suppressed in healthy adults by corticospinal tract
  • This tract activated by the interneurone pool where some are inhibitory
  • These inhibitory neurons reverse direction of the reflex
  • They cause plantarflexion (healthy adults)
60
Q

Why do babies below 12 months not need to plantarflex?

A
  • They are not walking yet
  • Do not need to step on toes to avoid irritatant
  • Replaced by plantarflexion reflex when they begin to walk (around 1)
61
Q

What is the Bing Sign?

A
  • Reflex which applies to any high level stimulation (not just nociception)
62
Q

What is the Bing Sign used for?

A
  • UMN Lesion
63
Q

Describe the Bing Sign?

A
  • Repeated pin prick which eventually causes dorsiflexion
  • Unusual as the foot moves towards the stimulus
  • Same reflex as babinski reflex
  • It is not specific to a particular place on the foot –> thus prick on dorsal side will cause dorsiflexion
64
Q

What is the Babinski & Bing sign diagnostic for?

A
  • Upper Motor Neurone Lesions in the Lower Limb
65
Q

Why use these reflexes and why lower limb?

A
  • These will always be present if there is an UMNL –> as even if the lesion is lower down it should stil be included

(Foot etc. is a good place to start when looking for an UMNL as the insult is always above or the same level as the one you are testing - work your way up)

66
Q

What are the symptoms of a complete spinal cord lesion (UMN)?

A
  • Loss of Voluntary Movements (reported weakness - cannot move)
  • Total Anaesthesia
  • Temporary Loss of Reflexes (spinal shock)
  • Followed by Hyper-Reflexia
67
Q

What does a cervical transection cause?

A
  • Quadriplegia
68
Q

What is quadriplegia?

A

Paralysis of all four limbs

69
Q

What effect does a transection below the cervical enlargement produce?

A
  • Paraplegia
70
Q

What is paraplegia?

A

​Paralysis of the legs and lower body

71
Q

Why cant you make a diagnosis shortly after an UMNL onset?

A
  • Spinal Shock
  • May not see exaggerated reflex (may see no reflex at all)
  • Need a period of hours/days/weeks for system to rebalance itself for excitability
  • Then hyperreflexia takes place (variable)
72
Q

What does a brainstem lesion produce?

A
  • UMN deficits on the contralateral side of the body
  • Often LMN deficits for cranial nerve nuclei

(depends if above or below decussation of course)

73
Q

Why does a lesion in the brainstem cause a LMN deficits for cranial nerve nuclei?

A
  • Corticospinal tract in pons & midbrain sections
  • These are very close (proximal) to cranial motor neurones (e.g. facial nucleus which controls facial muscles + oculomotor neurons which control eye movements)
  • Therefore a lesion in corticospinal tract –> will often also directly damage motor neurones

(due to cut/damaged fibres which will do local damage at the levels of the motoneurones themselves of the cranial nuclei + combined effect for motoneurones down the body)

74
Q

If there is a lesion in the brainstem, what are the general signs?

A
  • LMN Lesion on Ipsilateral Side of Face & Neck (e.g. facial/trigeminal/oculomotor nuclei)
  • UMN Lesion on the Contralateral Side of the Body
75
Q

Damage to the internal capsule & cerebral cortex is often due to cerebrovascular disease (i.e. stroke). What are the 3 main causes?

A
  • Thrombosis (clot)
  • Embolism (bubble)
  • Haemorrhage (bleed)
76
Q

What arteries supply the internal capsule?

A
  • Lateral Striate Arteries
77
Q

What is important to note about the Lateral Striate Arteries?

A
  • Supply Internal Capsule
  • Very fine & vulnerable
  • Sensory & motor fibres are separated at internal capsule
78
Q

How can capsular strokes be presented?

A

Sensory & motor fibres are separated at internal capsule (blood supply can be blocked to parts or all)

Therefore lesion can be:

  • Motor
  • Sensory Mixed
79
Q

What happens if there is a full stroke of one-side of the internal capsule?

A
  • Hemiplegia
80
Q

What is a hemiplegia?

A
  • Analgesia on whole contralateral side of the body
81
Q

What are the possible effects of a cerebral cortex lesion?

A
  • Apraxia

Therefore:

  • Inability to conceptualise
  • Inability to plan movement

(you cannot execute movements)

82
Q

What is apraxia?

A
  • Ability to make purposeful movement
83
Q

How are diseases of the basal ganglia & cerebellum presented?

A
  • Unique & Particular Symptoms
  • They cannot be characterised using the LMN & UMN concepts
84
Q

What do basal ganglia diseases cause generally?

A
  • Dyskinesia (bad movement)
  • No Weakness
  • No Apraxia (movements can be conceptualised)
85
Q

What are the two sub-divisions of dyskinesia?

A
  • Hyperkinesia
  • Hypokinesia
86
Q

What is hyperkinesia?

A
  • Excess & involuntary spontaneous movement
87
Q

What is hypokinesia?

A
  • Lack of spontaneous movement
  • Slowing of voluntary movement
88
Q

Name 3 types of basal ganglia diseases.

A
  1. Parkinson’s disease
  2. Huntington’s disease
  3. Ballism (hemiballism)

They are characterised by dyskinesia (i.e. hyperkinesia or hypokinesia)

89
Q

What do basal ganglia diseases not present?

A
  • Weakness (there is no weakness)
  • Apraxia (they show clear intent & motor plan & conceptualise movements)

(problem lies with executing the motor plan)

90
Q

What are the different hyperkinetic movements?

(name 5)

A
  1. Chorea
  2. Athetosis
  3. Dystonia
  4. Ballismus
  5. Tics
91
Q

What is chorea?

A
  • Continuing series of rapid, jerky movements
  • They are fragments of purposeful movements
92
Q

What is athetosis?

A
  • Continual uncontrolled writing

(takes place especially after drug treatment)

93
Q

What is dystonia?

A
  • Extreme contractions forcing unusual movements

(extreme forceful co-contractions can cause strong postural problems)

94
Q

What is ballismus?

A
  • Jumping about
95
Q

What are tics?

A
  • Repeats, stereotyped fragments of movement

(segments of movements that have been fractionated out –> usually stereotypical movements which are difficult to control)

96
Q

What does huntington’s disease exhibit in terms of hyperkinetic movements?

A
  • Chorea
97
Q

What can basal ganglia diseases affect?

A

Direct Pathways and/or Indirect Pathway

98
Q

What is dopamine overall?

A
  • Pro-Movement

Inhibits indirect pathway

Excites direct pathway

99
Q

What is the striatum made up of?

A
  • Putamen
  • Caudate
100
Q

What are the 2 receptors found on the striatum?

A
  • D1 Receptors
  • D2 Receptors
101
Q

What do the D1 receptors on the striatum do?

A
  • When dopamine binds –> they cause stimulation of movement –> via the direct pathway
102
Q

What do the D2 receptors on the striatum do?

A
  • When dopamine binds –> they cause stimulation of movement –> via the inhibiting the indirect pathway
103
Q

Name two basal ganglia diseases with hyperkinetic symptoms?

A
  • Ballismus
  • Huntington’s Disease
104
Q

Why do these problems occur in basal ganglia diseases?

A
  • System is finely balanced between excitation & inhibition
  • Disturbance of balance –> causes either hyperkinesia or hypokinesia
105
Q

What is ballism?

A
  • Degeneration of the Subthalamic Nucleus
  • Leads to disinhibition of movement via the indirect pathway
106
Q

What is huntington’s disease?

A
  • Degeneration of the caudate/putamen (striatum)
  • Causes choreiform movements
  • Striatal spiny neurones that inhibit the indirect pathway are the most affected initially
107
Q

What is hemiballism?

A
  • Degeneration of the Subthalamic Nucleus on only (1) Side
108
Q

What does the subthalamic nucleus do?

A
  • Involved in Indirect Pathway
  • It excites the Globus Pallidus Internal Segment –> which increases inhibition of the Thalamus
  • This causes a broken indirect pathway
  • Disinhibition of GPi –> means decreased inhibition of thalamus –> increasing thalamic activity –> large amplitude involuntary limb movements
109
Q

What are the symptoms of ballism & hemiballism?

A
  • Large Amplitude & Involuntary limb movements
110
Q

What is Huntington’s Disease?

A
  • Progressive degenerative condition
  • Initial Loss –> are the D2 expressing neurones in the striatum which go to the GP external segment (involved in indirect pathway)
  • Therefore it is GPe is disinhibited
  • Movement is not supressed as much
  • Increased inhibition of the subthalamic nucleus
  • Therefore less excitation of the GPi by the subthalamic nucleus
  • Less inhibition of the thalamus

This causes increased movements –> thus brief involuntary movements

111
Q

What happens in a lost/broken indirect pathway?

A
  • Too much movement
112
Q

What are the signs of Huntington’s disease?

A
  • Sudden and brief involuntary twitches
  • Occurs to all parts of the body
  • Voluntary movements are slowed
113
Q

Name a basal ganglia disease with hypokinetic symptoms?

A
  • Parkinson’s Disease
114
Q

What is Parkinson’s disease?

A
  • Degeneration of dopamine producing neurons in the Substantia Nigra pars compacta
  • Low dopamine input to the striatum
  • Therefore cannot energise movements through the direct & indirect pathways

(not enough dopamine drive on D1 & D2 receptors thus decreased effect on direct & indirect pathways –> thus hypokinesia)

115
Q

What are the three symptoms of Parkinson’s Disease?

A
  1. Bradykinesia (slow movement)
    * *Resting Tremor**
  2. Rigidity (including cog-wheel rigidity)
  3. Postural Instability
116
Q

What are the different drug therapies available?

A
  • Levadopa (L-DOPA)
  • Dopamine Agonists
  • Monoamine Oxidase-B Inhibitors
117
Q

What surgical treatments are available for Parkinson’s Disease?

A
  • Deep Brain Stimulation (DBS)
  • Electrodes implanted close to basal ganglia circuitry –> can restore thalamic excitability & restore movements

Placed in the thalamic / subthalamic nucleus area –> to increase excitability (or turn down activation from GPi) –> thus to boost activity

(complex treatment & may not be available to all)

118
Q

When can L-DOPA be administered?

A
  • When the substantia nigra pars compacta is not all lost
  • L-DOPA is fed into the system
  • Increases the amount of DOPA released by the existing substantia nigra that remains
  • Best drive out of remaining neurones
119
Q

When do you stop using L-DOPA and start using dopamine agonist?

A
  • Neurons in existing SNpc are so low (or gone)
  • L-DOPA is no longer helpful

Need to give Dopamine Agonist + MOB –> to drive movement up

120
Q

What is the cerebellar control of movement like?

Where does it control?

A
  • Ipsilateral

Damage to the right side impaired movements on the same side

(usually damaged by infarcts to arteries to cerebellum)

It controls the contralateral side of the cerebral cortex which controls the contralateral side of it (thus cancel out –> ispilateral)

121
Q

What does the flocculo-nodular lobe control?

A
  • Balance
  • Eye Movements
122
Q

What does the vermis & pars intermedia adjust?

A
  • Ongoing movement of the whole body
123
Q

What does the cerebellar hemispheres help coordinate?

Where do they project to?

A
  • Planning of movement (especially limbs)

(they project to PM cortex in particular)

124
Q

How does the cerebellum exert its influence?

A
  • No private output pathways

Acceses the:

  • Corticospinal Tract
  • Rubrospinal Tract
  • Vestibulospinal Tract
125
Q

Where does a major output from the lateral parts of the cerebellum go to?

A
  • Thalamus
  • Motor Cortex
126
Q

Where does an important output from the medial parts of the cerebellum go to?

A
  • Vestibular Nuclei
127
Q

Where does a smaller output from the intermediate parts of the cerebellum go to?

A
  • Red Nucleus
128
Q

What are the different effects of cerebellar lesion? (ranked by importance)

A
  1. Ataxia (loss of co-ordination)
  2. Dysmetria (movement distance deficiency)
  3. Asynergia (loss of co-ordination between muscle groups)
  4. Postural Abnormalities
  5. Gait Ataxia (trunk and legs)
  6. Intention Tremor (loss of smooth muscle movement)
  7. Hypotonus (loss of muscle tone - spindles?)
  8. Dydiadochokinesia (loss of force & rhythm)
129
Q

What effect does a cerebellar lesion potentially have on walking?

A
  • Ataxia of Gait

(uncoordinated walking)

(Not because of problem flexing or extending joints but due to agonist-antagonist relationship breakdown)

Movement has to be done entirely consciously (rather than automatically)

130
Q

Why does ataxia of gait occur in cerebellum patients?

A
  • Propioceptive information cannot be coordinated with vestibular information
  • Agonist-Antagonist relationship breaks down
  • Balance is impaired
  • Patient adopts a wide stance –> to increase stability
131
Q

Which part of the cerebellum usually leads to gait ataxia?

A

Anterior Lobe

132
Q

Why is someone with anterior lobe cerebellum lesion very wobbly?

A
  • Vestibular Loss + Poor Balance Control
  • Controls vestibular aspects –> meaning problems with good sequence of flexor-extensor activation at the knee & ankle –> which are key during walking

Need to make movements entirely conscious as there is a breakdown of communication between agonist & antagonist pairs

Neuroscience (Yeo) (8 decks)

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