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Motor Flashcards

1
Q

What is a myotome?

A

Muscle fibres innervated by a single spinal nerve

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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
Why can cervical cord damage lead to Horners syndrome?
Ventrolateral medullary nucleus helps control the sympathetic system Neurons in tract innervate preganglionic sympathetic fibres in lateral grey horn
26
What is Lou Gehrig's disease?
``` Amyotrophic lateral sclerosis Degeneration of corticospinal tracts Degeneration of ventral horn Descending autonomic fibres interrupted Start in lower limbs, progresses to trunk & upper limbs ```
27
Describe the myotatic reflex
Passive muscle stretch sensed by muscle spindle Reflex arc stimulates contraction of stretched muscle Reflex arc inhibits antagonist muscle - reciprocal inhibition
28
Describe the inverse myotatic reflex
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
29
Describe the flexor withdrawal reflex
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
30
Describe the crossed extensor reflex
Ipsilateral flexor withdrawal and contralateral extensor activation
31
What are the supplementary and pre motor area for?
``` Motor pattern selection Generate intention to move Convert intention into movement Movement plan selection Area 4 words, Area 6 phrases/sentences ```
32
To move in an accurate meaningful we way require...?
``` 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 ```
33
What can damage to SMA/PMA lead to?
Apraxia: inability to carry out complex movements
34
Which area of the cortex will light up on fMRI when a motor movement is simply mentally rehearsed, no action?
PMA
35
What re entrant loops are involved in motor control?
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
What are the major cerebellar tracts?
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
What are the major output cells of the cerebellum?
Purkinje cells | GABAergic
38
What is the Corticopontocerebellar tract?
Biggest tract in brain | Connects the cerebral cortex via the pons to the cerebellum
39
What is the Dentatorubrothalamic tract?
Connects the dentate nucleus of cerebellum, the red nucleus and the thalamus outputs: via deep cerebellar nuclei
40
What are unconscious motor functions?
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
What is the function of the cerebellum?
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
What three parts of cerebellum anatomy underlie function?
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
What is cerebellar ataxia?
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
What are the 4 subcortical nuclei that make up the basal ganglia?
Striatum (caudate nucleus, putamen, nucleus accumbens) Globus pallidus (Gp) Substantia nigra Subthalamic nucleus
45
Describe the basal ganglia feedback loop
Primary input: cerebral cortex Output: brain stem and via the thalamus to prefrontal, premotor and motor cortices No direct output to spinal cord
46
What is the role of the basal ganglia?
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
Describe the direct pathway of the basal ganglia
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
Describe the indirect pathway of the basal ganglia
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
What are types of hypokinesia?
Akinesia Bradykinesia Rigidity (Increased muscle tone) Cog-wheel rigidity Tremor at rest
50
Describe the effect of Parkinson's disease on the direct and indirect pathways of the basal ganglia
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
Describe the nigrostriatal pathway
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
What is hyperkinesia (Huntingtons chorea)?
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
What are symptoms of Parkinson's disease?
``` Bradykinesia Resting tremor (pill rolling) Rigidity Festinating gait Lack of facial expression Micrographia No weakness Normal reflexes ```
54
What are symptoms of Huntingtons disease?
``` Choreiform Clumsy Unsteady gait Difficulty with speech and swallowing Cognitive changes ```
55
What are symptoms of hemiballismus?
Unilateral large flinging involuntary movements of proximal limbs Caused by neurodegeneration of subthalamic nuclei Treated as for Chorea Intravenous diazepam and oral haloperidol
56
What are dystonias?
Lasting, twisting muscle spasms or altered posture Often focal eg writers cramp Primary (genetic) and secondary (acquired)
57
What is athetosis?
Snake like writhing movements
58
What are symptoms of Wilson's disease?
Choreoathetotic - involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing) Dementia and liver cirrhosis
59
Which subcortical nuclei is affected in Huntingtons? And which neurotransmitter?
Striatum | GABA
60
Which subcortical nuclei is affected in Hemiballismus?
Subthalamic nuclei
61
What is Parkinsonism?
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
What are the 4 cardinal features of Parkinson's?
``` TRAP Tremor Rigidity Akinesia/Bradykinesia Postural instability ```
63
What are additional features of Parkinson's?
Micrographia - small writing Mask-like face Sleep disturbances Aprosodia - monotonous voice
64
What causes Parkinson's disease?
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
What are the 4 dopamine pathways?
Nigrostriatal Mesolimbic - changes in memory, mood and emotion Mesocortical - higher functions Tubero-hypophyseal - between pituitary and hypothalamus, prolactin involvement
66
Describe the use of dopamine agonists and name 3 examples
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
Why must Levodopa be used in conjunction with other drugs?
Metabolised quickly to dopamine. Use metabolism inhibitors to prevent breakdown until in the brain
68
Which drugs are used in combination therapy with Levodopa?
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
What are side effects associated with dopamine based treatments?
``` 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
What drugs can be used to fill in gaps when on off effects occur in Parkinson's disease?
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
Describe anticholinergic use in Parkinson's disease therapy and name 3 drugs
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
What is the link between caffeine and basal ganglia disorders?
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
What is essential tremor?
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
What is Huntingtons disease?
Inherited neurodegenerative disorder – autosomal dominant | Degeneration of cholinergic cells in the striatum, particularly the caudate nucleus
75
What are treatment options for Huntingtons?
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
What is Wilson’s disease?
Hepatolenticular Degeneration caused by copper accumulation | Three forms: Dystonic, Pseudoparkinsonism, Cerebellar (pseudosclerotic)
77
What are treatments for Wilson’s disease?
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
What are tics?
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
What are treatments for tics?
Patient education and CBT Atypical antipsychotics Typical antipsychotics
80
What are treatments for dystonias?
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
What is chorea?
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
What are treatments of chorea?
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
83
What is a motor unit?
A motor neuron and the extrafusal muscle fibres it innervates

Block 3 AR (8 decks)

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