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Block 3 > Motor > Flashcards

Motor Flashcards

0
Q

What is a myotome?

A

Muscle fibres innervated by a single spinal nerve

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1
Q

What is a motor unit?

A

A motor neuron and the extrafusal muscle fibres it innervates

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2
Q

What is the general function of the lateral corticospinal tract?

A

Motor supply to body

Speed, direction and agility of movements involved in rapid skilled fine movement

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3
Q

What is the general function of the rubrospinal tract?

A

Control of flexor muscle tone

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4
Q

What is the general function of the lateral vestibulospinal tract?

A

Control of extensor muscle tone

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5
Q

What is the general function of the ventral corticospinal tract?

A

Motor supply to body

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6
Q

How many spinal arteries are there?

A

2 posterior supply 1/3

1 anterior supply 2/3

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7
Q

What can be causes of infarction of spinal arteries?

A 
Embolus
Atheroma
AAA
Tumour 
Trauma
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8
Q

What are alpha motor neurons?

A

Innervate extrafusal muscle fibres

Large myelinated axons

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9
Q

What are gamma motor neurons?

A

Innervate intrafusal muscle fibres of the muscle spindle

Smaller diameter neurons

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10
Q

Which corticospinal tract decussates at the medullary pyramids?

A

Lateral corticospinal tract

The ventral tract decussates at the level of the lower motor neuron synapse

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11
Q

What does an upper motor neuron lesion cause?

A

Spastic paralysis
Hyper-reflexia
No muscle wasting or fasiculations
Extensor plantar response present

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12
Q

What symptoms does a lower motor neuron lesion cause?

A

Flaccid paralysis
Hypo-reflexia
Muscle wasting (atrophy)
Fasciculations

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13
Q

What is Babinski sign?

A

Normal adult response is digit plantarflexion - flexor plantar response
Extensor-plantar response occurs following upper motor neuron lesions
Great (big) toe extension & digit splaying
Present in newborn-2 years old and adults with UMN lesions

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14
Q

Corticospinal (pyramidal) tract lesions are associated with what signs and symptoms?

A

Loss of fine-skilled voluntary movements
Absent superficial abdominal reflexes
Cremasteric reflex absent
Clonus (rhythmic involuntary oscillation of a joint)
Extensor plantar response (Babinski)

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15
Q

Where can upper motor neuron symptoms occur?

A 
Cortex 
Internal capsule 
Corona radiata 
Descending tracts 
Brainstem 
Spinal cord
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16
Q

Where can lower motor neuron lesions occur?

A

Spinal cord (at level of LMN cell body)
Spinal nerve
Cauda equina
Peripheral nerve damage e.g. radial nerve

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17
Q

What can cause motor neuron lesions?

A 
Stroke 
Motor neuron disease
Multiple sclerosis 
CNS Tumour 
Meningeal tumour 
Spinal tumour 
Trauma 
Penetrating injury 
Fracture 
Dislocation 
Stenosis 
IV disc prolapse
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18
Q

What symptoms will a spinal cord hemisection cause?

A

Upper and lower motor neuron signs in different parts of the body
LMN at level of injury, UMN below injury Ipsilateral
Brown-Sequard syndrome
Ipsilateral loss of fine touch and proprioception below
Contralateral loss of pain and temperature below

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19
Q

Describe cortical connections to cranial nerve motor brainstem nuclei

A

Bilateral supply from cortex
Innervation comes from corticobulbar/corticonuclear neurons
Main UMN innervation comes from contralateral cortex
MAIN EXCEPTION = Unilateral supply to CN VII to the lower face

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20
Q

What motor losses are associated with a brainstem lesion?

A

Ipsilateral face

Contralateral body

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21
Q

Describe the rubrospinal tract

A

From red nucleus in midbrain, decussates here
Descends contralaterally
Mainly to proximal upper limb & trunk muscles
Excite flexor LMN, Inhibit extensor LMN

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22
Q

Describe the vestibulospinal tract

A

Lateral vestibular nucleus in brainstem - pons/medulla border
Descends ipsilaterally
Antigravity (upright posture & balance)
Excites extensor LMN, Inhibits flexor LMN

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23
Q

What do reticulospinal tract neurons do?

A

Modulate lower motor neuron activity, locomotion and posture
Inhibit or excite lower motor neurons (α and γ)
Modulate sympathetic activity
Mostly originate from brainstem nuclei mesh
Fibres mostly run ipsilaterally
Modulate muscle activity/tone – especially in antigravity muscles
Control emotional movement of muscles of facial expression

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24
Q

Lesion to which tract results in spasticity seen in upper motor neuron lesions?

A

Reticulospinal tract, Net loss of lower motor neuron inhibition
Reticulospinal neurons excite inhibitory Renshaw cells to modulate muscle tone. Loss of the medullary reticular pathways in spinal cord injury contributes to spasticity and over-activity in α-motor neurons

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25
Q

Why can cervical cord damage lead to Horners syndrome?

A

Ventrolateral medullary nucleus helps control the sympathetic system Neurons in tract innervate preganglionic sympathetic fibres in lateral grey horn

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26
Q

What is Lou Gehrig’s disease?

A 
Amyotrophic lateral sclerosis
Degeneration of corticospinal tracts 
Degeneration of ventral horn 
Descending autonomic fibres interrupted 
Start in lower limbs, progresses to trunk & upper limbs
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27
Q

Describe the myotatic reflex

A

Passive muscle stretch sensed by muscle spindle
Reflex arc stimulates contraction of stretched muscle
Reflex arc inhibits antagonist muscle - reciprocal inhibition

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28
Q

Describe the inverse myotatic reflex

A

Golgi tendon organ detect stretch in tendons, initiate a protective reflex
1b afferent neurons carry sensation from tendon organ
Reflex arc inhibits agonist muscle and stimulates contraction of antagonist muscle

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29
Q

Describe the flexor withdrawal reflex

A

Withdrawal of a limb from a painful or noxious stimulus mediated by free nerve endings
Synaptic connections span several spinal cord levels
Stimulates ipsilateral flexors of limb
Inhibits ipsilateral extensors of limb

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30
Q

Describe the crossed extensor reflex

A

Ipsilateral flexor withdrawal and contralateral extensor activation

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31
Q

What are the supplementary and pre motor area for?

A 
Motor pattern selection 
Generate intention to move 
Convert intention into movement 
Movement plan selection 
Area 4 words, Area 6 phrases/sentences
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32
Q

To move in an accurate meaningful we way require…?

A 
Somatosensory inputs 
Visual inputs 
Proprioceptive inputs 
In order to create a mental body image 
Integrated in posterior parietal cortex (area 5,7) which receive  extensive inputs from sensory cortex
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33
Q

What can damage to SMA/PMA lead to?

A

Apraxia: inability to carry out complex movements

34
Q

Which area of the cortex will light up on fMRI when a motor movement is simply mentally rehearsed, no action?

A

PMA

35
Q

What re entrant loops are involved in motor control?

A

Both cerebellum and basal ganglia receive inputs from the cerebral cortex and project to motor areas of the cortex via the thalamus
also influence brain stem and spinal mechanisms

36
Q

What are the major cerebellar tracts?

A

Spinocerebellar (muscle spindle/ tendon organ) connecting the spinal cord and cerebellum (mossy fibres)
Vestibulospinal:semicircular canals and cerebellum, vestibular nuclei -spinal cord
Olivocerebellar tract: Inferior olivary nucleus (climbing fibres)
Cortex, spinal cord to olive - carry error signal

37
Q

What are the major output cells of the cerebellum?

A

Purkinje cells

GABAergic

38
Q

What is the Corticopontocerebellar tract?

A

Biggest tract in brain

Connects the cerebral cortex via the pons to the cerebellum

39
Q

What is the Dentatorubrothalamic tract?

A

Connects the dentate nucleus of cerebellum, the red nucleus and the thalamus outputs: via deep cerebellar nuclei

40
Q

What are unconscious motor functions?

A

Maintenance of balance
Muscle tone and posture
Muscle co-ordination trajectory, speed and force
Eye movements (Vestibular-ocular reflex)
Planning movements and evaluating sensory information
Learning of motor skills

41
Q

What is the function of the cerebellum?

A

Muscle co-ordination trajectory, speed and force
Evaluates disparities between intention and action by adjusting the operation of motor centres while a movement is in progress
Motor learning: Efficiency of movements enhanced, Learn through trial and error, Once learned, performed automatically

42
Q

What three parts of cerebellum anatomy underlie function?

A

Extensive inputs: Spinal cord proprioception/sensory feedback, Vestibular (semicircular canals), Superior Colliculi, Cerebral cortex (via Corticopontocerebellar pathway)
Outputs focus on premotor and motor systems
Synaptic transmission within circuit is plastic - long term depression

43
Q

What is cerebellar ataxia?

A

Symptoms - depend on area of lesion
Ataxia - uncoordinated voluntary movements
Intention tremor
Dysmetria - overshoot
Dysdiadochokineasia - inability to produce simple repetitive movement
Slurred speech
Nystagmus - involuntary movements of eyes

44
Q

What are the 4 subcortical nuclei that make up the basal ganglia?

A

Striatum (caudate nucleus, putamen, nucleus accumbens)
Globus pallidus (Gp)
Substantia nigra
Subthalamic nucleus

45
Q

Describe the basal ganglia feedback loop

A

Primary input: cerebral cortex
Output: brain stem and via the thalamus to prefrontal, premotor and motor cortices
No direct output to spinal cord

46
Q

What is the role of the basal ganglia?

A

Damage disrupts movements, cause deficits in cognition, perception
Facilitate movement and/or suppress movement
Act to reinforce a selected motor pattern and suppress potentially conflicting motor patterns
Balance between direct and in-direct pathways
Primarily function through disinhibition

47
Q

Describe the direct pathway of the basal ganglia

A

Cortex excites the striatum
Striatum inhibits Globus palidus interna which in turn disinhibits the thalamus
Thalamus is then able to excite the cortex and therefore facilitate movement
Meanwhile the striatum acts via the substantia nigra to activate D1 receptors in the striatum and in turn facilitate the pathway

48
Q

Describe the indirect pathway of the basal ganglia

A

Cortex excites striatum
Striatum inhibits Globus palidus externa which in turn disinhibits the Subthalamic nucleus which is then more able to excite the Globus palidus interna. This in turn inhibits the thalamus to reduce movements.
Meanwhile, the striatum acts via the substantia nigra to activate D2 receptors which act to inhibit the striatum and therefore reduce the indirect pathway

49
Q

What are types of hypokinesia?

A

Akinesia
Bradykinesia
Rigidity (Increased muscle tone) Cog-wheel rigidity
Tremor at rest

50
Q

Describe the effect of Parkinson’s disease on the direct and indirect pathways of the basal ganglia

A

Degradation of the substantia nigra disrupts balance between direct pathway excitation of cortex and indirect pathway inhibition of cortex.
Tipped in favor of the indirect pathway, with a subsequent pathological global inhibition of motor cortex areas

51
Q

Describe the nigrostriatal pathway

A

Direct pathway striatal neurons have D1 dopamine receptors, which depolarize the cell in response to dopamine
Indirect pathway striatal neurons have D2 dopamine receptors, which hyperpolarize the cell in response to dopamine
Dual effect of exciting the direct pathway and inhibiting the indirect pathway
Excitation of the nigrostriatal pathway has the net effect of exciting cortex by two routes, by exciting the direct pathway and inhibiting the indirect pathway (thereby disinhibiting the net inhibitory effect of the indirect pathway on cortex)

52
Q

What is hyperkinesia (Huntingtons chorea)?

A

Violent involuntary movement of limbs chorea (dance like movements)
An inherited autosomal dominant disorder associated with a trinucleotide expansion in the gene coding f or the protein Huntingtin on chromosome 4
Effects Cerebral cortex (particularly frontal lobes) and basal ganglia (particularly caudate nucleus)
Presents typically in midlife with a progressive dementia and abnormal movements
Tips balance towards direct pathway

53
Q

What are symptoms of Parkinson’s disease?

A 
Bradykinesia
Resting tremor (pill rolling)
Rigidity
Festinating gait
Lack of facial expression
Micrographia 
No weakness
Normal reflexes
54
Q

What are symptoms of Huntingtons disease?

A 
Choreiform 
Clumsy
Unsteady gait
Difficulty with speech and swallowing
Cognitive changes
55
Q

What are symptoms of hemiballismus?

A

Unilateral large flinging involuntary movements of proximal limbs
Caused by neurodegeneration of subthalamic nuclei
Treated as for Chorea
Intravenous diazepam and oral haloperidol

56
Q

What are dystonias?

A

Lasting, twisting muscle spasms or altered posture
Often focal eg writers cramp
Primary (genetic) and secondary (acquired)

57
Q

What is athetosis?

A

Snake like writhing movements

58
Q

What are symptoms of Wilson’s disease?

A

Choreoathetotic - involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing)
Dementia and liver cirrhosis

59
Q

Which subcortical nuclei is affected in Huntingtons? And which neurotransmitter?

A

Striatum

GABA

60
Q

Which subcortical nuclei is affected in Hemiballismus?

A

Subthalamic nuclei

61
Q

What is Parkinsonism?

A

Group of disorders exhibiting similar signs and symptoms
Divided into three main groups:
Pure Parkinsonism: Idiopathic – Parkinson’s disease, Iatrogenic - drug induced, Post-encephalitic
Parkinsonism plus: Multiple systems atrophy (3-types: A, -P, -C), Progressive supranuclear palsy
Pseudoparkinsonism: Wilson’s disease, Benign Essential Tremor, Trauma and vascular-related

62
Q

What are the 4 cardinal features of Parkinson’s?

A 
TRAP
Tremor 
Rigidity
Akinesia/Bradykinesia 
Postural instability
63
Q

What are additional features of Parkinson’s?

A

Micrographia - small writing
Mask-like face
Sleep disturbances
Aprosodia - monotonous voice

64
Q

What causes Parkinson’s disease?

A

Loss of ~80-90% of dopamine neurons in the substantia nigra

Lewy body formation and presence of abnormal levels of parkin and synuclein proteins

65
Q

What are the 4 dopamine pathways?

A

Nigrostriatal
Mesolimbic - changes in memory, mood and emotion
Mesocortical - higher functions
Tubero-hypophyseal - between pituitary and hypothalamus, prolactin involvement

66
Q

Describe the use of dopamine agonists and name 3 examples

A

Synthetic agonists replace dopamine loss acting on dopamine receptors (primarily D2)
Useful in younger patients and initial treatment of PD
Fewer motor complications long-term, but less improvement overall More psychiatric side-effects
May be combined with Levodopa at later stages
Includes: Pramipexole Ropinirole Rotigotine

67
Q

Why must Levodopa be used in conjunction with other drugs?

A

Metabolised quickly to dopamine. Use metabolism inhibitors to prevent breakdown until in the brain

68
Q

Which drugs are used in combination therapy with Levodopa?

A

Dopa-decarboxylase inhibitors: Benserazide, Carbidopa
Often combined with Levodopa: Co-beneldopa, Co-careldopa
Catechol-O-methyltransferase (COMT) Inhibitors: entacapone, Tolcapone
Monoamine oxidase inhibitors (MAOI-B):Selegiline, Rasagiline

69
Q

What are side effects associated with dopamine based treatments?

A 
Peripheral effects commonly cause nausea and vomiting 
Anorexia 
Drowsiness 
Hypomania 
Psychosis 
Sudden onset sleep 
Hypotension 
Tachycardia 
Arrythmias 
Later stages ‘on-off’ effects likely (>2 years treatment, 50-90% cases)
70
Q

What drugs can be used to fill in gaps when on off effects occur in Parkinson’s disease?

A

Apomorphine
Domperidone: always administered prophylactically before apomorphine use
Combination therapies and use of controlled release drugs may reduce onset of on-off effects (both co-beneldopa and co-careldopa available)

71
Q

Describe anticholinergic use in Parkinson’s disease therapy and name 3 drugs

A

Decrease in dopamine leads to an increase in acetylcholine concentration
Anticholinergics (antimuscarinics) to redress the balance
Only have mild anti-Parkinsonism effects (tremor) and may reduce absorption of Levodopa
Useful for iatrogenic (drug-induced) Parkinsonism
Includes: Orphenadrine, Procyclidine, Trihexphenidyl

72
Q

What is the link between caffeine and basal ganglia disorders?

A

Adenosine Antagonists may interact with glutamatergic transmission
Adenosine2A antagonists decrease receptor sensitivity
Possible neuro-protectant role
Currently licences in Japan
Includes: Caffeine (A1/A2 antagonist)

73
Q

What is essential tremor?

A

A familial progressive disorder characterised by intention tremor, not present at rest
Rhythmic tremor 4-12Hz frequency
Essential tremor generally first appears in the arms, spreading to other regions of the body, particularly the head, neck, jaw and voice
Head tremor (titubation) is more common in women
Treatment: β-Blocker – Propanolol, AED – Primidone, Botox – head and voice, 1-2 units of alcohol

74
Q

What is Huntingtons disease?

A

Inherited neurodegenerative disorder – autosomal dominant

Degeneration of cholinergic cells in the striatum, particularly the caudate nucleus

75
Q

What are treatment options for Huntingtons?

A

Dopamine depleting drugs: Tetrabenazine - prevents monoamine transport to vesicles (VMAT-2), reduces the amount released at the
terminal, reducing involuntary movement
Antipsychotics: risperidone, quetiapine and haloperidol, reduce chorea and tics; help control delusions, hallucinations and violent outbursts
Benzodiazepines: clonazepam and diazepam, general relaxants
Depression and Mood disorders associated with HD are treated with SSRIs/TCAs

76
Q

What is Wilson’s disease?

A

Hepatolenticular Degeneration caused by copper accumulation

Three forms: Dystonic, Pseudoparkinsonism, Cerebellar (pseudosclerotic)

77
Q

What are treatments for Wilson’s disease?

A

Copper chelators: Penicillamine or Trientine, cause excess copper
to be excreted. Administered at maintenance doses following
clearance of initial build-up of copper
Zinc: blocks copper absorbtion in the gut, preventing further build-up. Has fewer side effects that alternative therapeutics

78
Q

What are tics?

A

Small involuntary movement
Most commonly associated with Tourettes, which presents with a combination of vocal and motor tics
Tics are also seen in Wilson’s disease and Huntington’s disease

79
Q

What are treatments for tics?

A

Patient education and CBT
Atypical antipsychotics
Typical antipsychotics

80
Q

What are treatments for dystonias?

A

Botulinum toxin injections (botox) is used to relax excessive muscle contraction, with injections given every three months
Trihexyphenidyl and procyclidine - Anticholinergics
Baclofen, GABA agonist, is an anti-spasm medication
Diazepam, BDZ GABA co-agonist, a good muscle relaxant
Physiotherapy
Deep brain stimulation
Denervation

81
Q

What is chorea?

A

Chorea describes involuntary, irregular, random and dance-like, flowing movements which flit from one part of the body to another
Primary - inherited, e.g. Huntington’s, benign hereditary chorea Secondary - acquired, e.g. Many drugs and toxins, including antipsychotics, AEDs, CO, cyanide

82
Q

What are treatments of chorea?

A

Dopaminergic antagonists – antipsychotics
Use is limited by side-effects, e.g. tardive dyskinesia and Parkinsonism
Dopamine-depleting drugs
GABAergic drugs, e.g. anti-epileptics, gabapentin and benzodiazepines
Post-surgical Chorea may to respond to steroids

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