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MBBS II HNNS > L18 - Motor system 1 > Flashcards

L18 - Motor system 1 Flashcards

1
Q

Origin, tract and end-point of Upper motor neuron?

A 
Origin = cerebrum 
Tract = +/- inter-neurons in brain stem & spinal cord 
End = spinal cord
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2
Q

Origin, tract and end-point of Lower motor neuron?

A 
Origin = cranial nerve nuclei or anterior horn cells of spinal cord 
Tract = spinal cord 
End = Muscles
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3
Q

Compare the overall role of UMN and LMN.

A

UMN = Command and modulate movement

LMN = efferent component of reflex arc/ activate muscles

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4
Q

Purpose of higher and lower levels of motor control?

A

 Feedback loops, reflexes, memory, purposes, planning

 Parallel, non-binary, non-hierarchical processing

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5
Q

What are the cortical motor regions?

A
  • Primary motor cortex (Brodmann’s Area 4; M1; precentral gyrus)
  • Premotor area (PMA) (area 6)
  • Supplementary motor area (SMA) (area 6)
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6
Q

Functions of the main cortical motor regions?

A
  • Primary motor area (M1): main generator of projecting signals to spinal cord
  • Supplementary motor area (SMA): planning, sequence of movement
  • Premotor area (PMA): sensory guidance
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7
Q

Overall function of brodmann area 6?

A

Pre and supplementary motor areas included:

• Identify targets in space, choose the type of action, and programming of movements.

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8
Q

Overall function of brodmann area 4?

A

Primary motor cortex

main generator of projecting signals to spinal cord

Executes commands via brain stem / spinal cord

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9
Q

How does cerebral blood flow correspond to metabloc demands and activities?

A

Different degrees and patterns of involvement, depending on the nature of motor movement

More complex =larger area of activation

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10
Q

Difference in outcome between more medial or lateral lesions in the primary motor area?

A

Medial = Lower limb affected

Lateral = Upper limb + head muscles affected i.e. aphasia

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11
Q

Symptoms of SMA syndrome?

A

Supplementary Motor Area (SMA) Syndrome

• SMA injured&raquo_space; affected planning, initiating sequence of movement

NO ACTUAL PARALYSIS

  • Reduced spontaneous & voluntary movements
  • M1 & UMN intact, good recovery
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12
Q

What tracts does the pyramidal tract consist of? Origin?

A
  • Pyramidal tract mainly from Layer V of M1 cortex
  • Consists of:
  1. Corticobulbar tract - to cranial nerve nuclei
  2. Corticospinal tract - to spinal motor neurons
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13
Q

Sequence of structures passed through by pyramidal tract?

A

1) M1 cortex layer V
2) Internal capsule of cerebrum
3) Cerebral peduncle of midbrain
4) Ventral pons
5) Decussate at pyramids of medulla oblongata
6) Interact with stem nuclei
7) Corticospinal tracts
8) Activate and modulate LMNs: anterior horn cells, spinal, cranial nerves

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14
Q

How is M1 connected to internal capsule? Functional division of internal capsule?

A

Corona radiata:
- twist of fibers when going down to pass through internal capsule

3 parts:

  • Upper limb and face control @ anterior limb of internal capsule
  • Lower limb control @ posterior limb of internal capsule
  • Genu
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15
Q

All the fibers descending from cortex to internal capsule are corticospinal tract. True or False

A

False

 Only 10-20% of descending fibres from cortex = corticospinal tract

 Rest = cortico-pontine fibres (connect with brainstem, cerebellum)

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16
Q

Corticospinal tract is divided into what tracts? Each tract’s function?

A
  • Majority (80%) = lateral corticospinal tract: contralateral, crossed fibres serving limb muscles
  • Minority (20%) = ventral corticospinal tract: ipsilateral, uncrossed fibres serving paraxial muscles (more primitive)
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17
Q

Function and downstream innervation of Corticobulbar tract?

A
  • Control motor function of NON-OCULAR cranial nerves
  • LMN Innervated bilaterally:
    1) Motor trigeminal nucleus (V)
    2) Facial nucleus (VII)** except for lower face with contralateral innervation **
    3) Ambiguus nucleus (CN IX, X, XI)
    4) Hypoglossal n. (XII) **except genioglossus muscle with contralateral innervation **
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18
Q

Which cranial nerves do not receive bilateral innervation by the corticobulbar tract?

A

Facial (VII) - lower muscles

Hypoglossal (XII) - genioglossus muscles

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19
Q

List some causes of UMN lesions.

A
  • MCA infarction
  • Tumour in corona radiata
  • Infarction of posterior limb of internal capsule
  • Pontine/ brainstem infarction
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20
Q

Which arteries supplying the internal capsule is prone to cause stroke?

A

Lentico-striate arteries = common site of stroke:

End artery prone to Occlusion/rupture&raquo_space; Intracerebral infarction / haemorrhage

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21
Q

Compare the effects of UMN lesions and LMN lesions in CN with bilateral innervations?

A

 Lesion in upper motor neuron = no symptoms on either side (bilateral innervations)

 Lesion in lower motor neuron = symptoms in lesion side

22
Q

Compare the effects of UMN lesions and LMN lesions in CN with contralateral innervations?

A
  • Facial nerve lower face muscles + Hypoglossal nerve genioglossus

 Lesion in UMN = symptoms on contralateral side

 Lesion in LMN = symptoms on lesion side

23
Q

Compare the effects of UMN lesion on the face muscles controlled by facial nerve.

A 
Facial nerve (VII):
 Upper facial nerve nuclei receive bilateral UMN input = function is preserved in all UMN lesions

 Lower facial nerve nuclei receive UMN only from contralateral cortex = function is lost in contralateral UMN lesion (paralyzed)

24
Q

Compare the effects of LMN lesion on the face muscles controlled by facial nerve.

A

ipsilateral upper and lower faces are affected.

25
Q

Compare the effects of UMN lesions and LMN lesion on the genioglossus muscle?

A

Hypoglossal nerve: genioglossus muscle is innervated contralaterally
- Weakness of the left genioglossus muscle (tongue protrusion) resulting in unopposed protrusion by right genioglossus

  • UMN lesion = contralateral genioglossus weakness, tongue deviate away from the lesion side
  • LMN lesion = tongue deviates towards the lesion side
26
Q

Patient has tongue deviation to the left, with marked muscle atrophy. Dx? What if there was no atrophy?

A

Muscle atrophy is unique to left LMN CN XII lesion
Deviation to the left due to unopposed right genioglossus muscle

No atrophy: then right UMN lesion paralyzing the left genioglossus m.

27
Q

List the key structure of the basal ganglia?

A 
Caudate nucleus, 
(Putamen+ Globus pallidus = Lentiform nucleus)
Striatum, 
Subthalamic nucleus, 
substantia nigra
28
Q

Function of basal ganglia?

A
  • Help cerebral cortex, brainstem motor regions to generate, modulate movements (coordinate precision)
  • Does not directly activate muscles
29
Q

Lentiform nucleus is separated from the head of caudate nucleus by?

A

lentiform nucleus that is separated from the head of the caudate nucleus and the thalamus by the internal capsule

30
Q

Location of Caudate nucleus?

A

head and a body that sit in the frontal lobe; its tail sits at the temporal lobe

31
Q

Results of diseases of the basal ganglion?

A

abnormalities in the initiation, pattern, speed, rhythm etc. of movement,

but not muscle weakness/paralysis

32
Q

Sequence of activation between areas of the basal ganglia? (start with signal from cortex)

A

Input from Thalamus and Cortex
» Striatum
» Caudate and Putamen (Corpus striatum)
» Globus pallidus:
a) External globus pallidus to subthalamic nucleus to internal globus pallidus
b) Directly to internal globus pallidus

> > output to thalamus and cortex

33
Q

Individual roles of striatum and pallidum?

A

Striatum = store programmes and initiate movement

Pallidum = project to premotor cortex via subthalamic and thalamic nuclei

34
Q

List examples of negative signs of basal ganglia pathway.

A

Patient wants to perform but cannot (e.g. bradykinesia, hesitancy, abnormal posture)

35
Q

List examples of positive signs of basal ganglia pathway.

A

patients cannot prevent movement (e.g. rigidity, dyskinesia, chorea, athetosis, ballismus)

36
Q

Which part of the basal ganglia circuit is affected in Parkinson’s.

A

Loss of dopaminergic activities in substantia nigra compacta:
 Loss of inhibitory signals to D2
 Loss of excitatory signals to D1

 Overall: imbalance between activation, inhibition at various points: over-inhibition = less signal to cortex = bradykinesia

37
Q

Which part of the basal ganglia circuit is affected in Huntington’s.

A

 Loss of inhibition from D2 to lateral part of globus pallidus

 Overall: uncoordinated overdrive from thalamus to cortex

38
Q

3 Function of cerebellum?

A
  • Does not directly activate muscles*
    1) Updates motor commands by comparing descending control signals with sensory feedback of the movement – fine tuning
    2) Uses vestibular inputs to control posture
    3) Involved with planning and initiation of movements via projections to the primary motor cortex
39
Q

Anatomical and functional division of the cerebellum?

A

Anterior lobe = Spinal cerebellum
Posterior lobe = Cerebral cerebellum
Flocculonodular lobe = Vestibular cerebellum

40
Q

Functions of the 3 divisions of the cerebellum?

A

Anterior lobe =
a) Input from mechanoreceptors via spinocerebellar tracts
b) output to limb via brainstem nuclei
» for walking and gait stability

Posterior lobe =
a) Input from cortex via middle peduncle
b) output to thalamus and cortex
» Coordination of voluntary movement

Flocculonodular lobe =
a) Input from vestibular apparatus
b) output to axial muscles
» for truncal balance

41
Q

Connections between cerebellum and brainstem?

A

via Superior, Middle and Inferior Cerebellar Peduncles

42
Q

List the tracts that go through the superior cerebellar peduncle.

A

Mainly output to midbrain:
 Dentate (= main nucleus) &raquo_space; thalamus

 Interposed nuclei&raquo_space; red nucleus

 Fastigial nuclei» vestibular nuclei

43
Q

List the tracts that go through the middle cerebellar peduncle.

A

Middle cerebellar peduncle
 Mainly input from pons

 E.g. corticopontine projections = pontine mossy fibers***

44
Q

List the tracts that go through the inferior cerebellar peduncle.

A

 Mainly input from medulla

 Climbing fibers from inferior olive

 Proprioceptive information from DORSAL spinocerebellar tract (mossy fibers)

45
Q

Clinical manifestation of cerebellar haemorrhage?

A

ipsilateral intentional tremor, dysmetria, Dysdiadochokinesia, etc.

46
Q

Clinical manifestation of Medulloblastoma in cerebellum?

A

affecting vermis, truncal ataxia (cannot sit / stand still)

47
Q

List the various brain nuclei in the reticular formation?

A
  • Vestibular nuclei
  • Red nuclei
  • Reticular nuclei
48
Q

Input, output and function of Vestibular nuclei.

A

Vestibular nuclei (in medulla oblongata)

  • Input from vestibular apparatus
  • Output to limb & trunk muscles
  • Equilibrium & balance: Extensor predominant
49
Q

Input, output and function of Red nuclei.

A

Red nucleus (in midbrain)
• Input from cerebral cortex and cerebellum
• Output through rubrospinal tract
• UL flexor predominant

50
Q

Input, output and function of Reticular nuclei.

A 
Reticular nuclei (in medulla & pons) 
• Pontine – extensor output predom. 
• Medullary - flexor output predom.
51
Q

4 Function of the brainstem in motor control?

A

• Processes information from

(i) higher level special senses (smell, visual, auditory etc.)
(ii) the spinal cord (peripheral mechanoreceptors)

• Modulate activities of:
– Corticobulbar tract to cranial nerves nuclei
– Corticospinal tract to spinal nerve nuclei

  • Send descending fibres in addition to the pyramidal tracts (i.e., extrapyramidal tracts) to further modulate motor activities
  • Critical for postural adjustments and control of axial and proximal musculature

MBBS II HNNS (57 decks)

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