Motor function and dysfunction Flashcards

1
Q

Upper motor neurones can be excitatory or inhibitory of lower motor neurones (via inhibitory inter neurones), what is the net effect of UMN on LMNs?

A

Net effect is inhibitory

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2
Q

Describe the path of motor neurones from motor homunculus to muscle

A
  • fibres come together at corona radiata and converge and go through internal capsule (between thalamus and lenticulate nucleus)
  • fibres pass though cerebral peduncle of midbrain (mickey mouses ears)
  • fibres decussate at medullary pyramids
  • fibres travel down lateral corticospinal tract
  • UMN Fibres synapse with LMN in the ventral horn
  • LMN fibres exit the ventral root and enter the spinal nerve and go to the muscle
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3
Q

What is the function of the pontine reticulospinal tract, rubrospinal tract , lateral vestibulospinal and ventral corticospinal tracts?

A

potine reticulospinal= paralysis in sleep
rubrospinal= not functional in adults, only animals and babys
ventral corticospinal= undecussated fibred involved in posture & trunk muscles
lateral vestibulospinal tract= postual control, balance etc

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4
Q

give 5 features of LMN lesions

A
  • weakness
  • areflexia
  • muscle wasting (normally LMN provide trophic factors (growth factors), also loss of use)
  • fasciculation (uncoordinated contractions, dont need to know why)
  • hypotonia (floppy)
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5
Q

Give and explain 5 features of UMN lesions

A
  • weakness (no excitation of LMN)
  • hypertonia (net effect of UMN is inhibition, loss of UMN= more excitation= more rigid muscles)
  • hyperreflexia (loss of descending inhibition= muscle spindles can excite LMN more easily)
  • extensor- planter reflex (and increased flexor activity as these muscles are generally more powerful)
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6
Q

Describe the path of motor neurones for cranial nerves

A

From homunculus, down to relevant cranial nerve nucleus via corticotubular tract- found next to internal capsule

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7
Q

Why do lesions of UMN to facial nerves (eg strokes) tend to be forehead sparing?

A

Because UMN fibres to the upperface split and go to both ipsilateral and contralateral CNVII nucleus, whereas UMN fibres to the lower face only go to the contralateral nucleus. This means in a right sided stroke, the left upper face can still get innervated by the left side of the brain, but the lower face cannot.

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8
Q

Which parts of the cerebellum control which parts of the body?

A

Vermis regulates trunk musculature
Hemisphere regulate limbs
Tracts are ipsilateral in cerebellum.

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9
Q

Why may cerebellar tumours lead to hydroencephalus?

A

The 4th ventricle is just infront of the cerebellum, behind the pons. Blockage of this= CSF build up

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10
Q

Give 6 signs of cerebellar pathology?

A
  • Disdidochokinesis
  • Ataxia
  • Intention tremour
  • slurred speech
  • Hypotonia
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11
Q

What is the role of the basal ganglia and of the cerebellum?

A

Basal ganglia takes an idea/ motor plan from prefrontal cortex and determines the most appropriate set of movements, also kick starts and and fine tunes movement by stimulating appropriate (direct pathway)and inhibiting inappropriate movements (indirect pathway) .
Cerebellum looks at current position of limbs and determines appropriate sequence. It is also involved in muscle memory.

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12
Q

What structures make up the basal ganglia? (5)

A
  • lentiform nucleus (putamen, globus pallidus interna and externa)
  • striatum (putamen, caudate nucleus)
  • substantia nigra
  • subthalamic nucleus
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13
Q

What is the general effect of the direct and indirect pathway?

A
Direct= stimulatory (stimulate putamen, more  inhibit GPi, less inhibits thalamus, more stimulate cortex)
Indirect= inhibitory (inhibit GPe, less inhibit STN, more stimulate GPi,  more inhibits thalamus, less stimulate cortex)
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14
Q

Why does dopamine release lead to more stimulation of cortex? (2)

A

dopamine stimulates putamen to activate direct pathway and also inhibits the indirect pathway

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15
Q

Does the basal ganglia communicate with the ipsi or contralateral cortex?

A

ipsilateral cortex, so coordinates contralateral movement

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16
Q

What is the pathophysiology behind parkinsons disease?

A

Destruction of substantia nigra and so less dopamine release, so less inhibition of indirect pathway and less activation of indirect pathway

17
Q

What are the 3 cardinal signs of parkinsons?

A
  • resting tremour
  • bradykinesia
  • hypertonia
18
Q

Give 3 non cardinal signs (but still signs) of parkinsons?

A
  • hypophonia
  • reduced facial expression
  • micrographia
  • dementia
  • depression
  • shuffling gait
19
Q

What is the pathophysiology behind huntingons?

A

loss of cells within the striatum so loss of indirect pathway so less inhibition so more movement

20
Q

Give 3 symptoms of huntingdons?

A
  • chorea (involuntary jerky movements)
  • dystonia (sustained repetitive muscle contractions resulting in twisting and repetitive movements)
  • poor coordination
  • cognitive decline and behaviour dificulties
21
Q

What is hemiballismus?

A

Subthamic nucleus damage, so less excitation of GPi by indirect pathway so less inhibition of the thalamus. This means more movement

22
Q

How can hemiballismus present?

A

unilateral, explosive, involuntary movements often secondary to subcortical stroke

23
Q

What is motor neurone disease? how will it present?

A

Destruction of motor neurones- both upper and lower. They will present with weakness, poor coordination, fasiculation, hypo or hypertonia areflexia, hyperreflexia- they may have upper and lower motor neurone signs. the SOD genes have been implicated.

24
Q

Which parts of the internal capsule correspond to which structures?

A
Genu= face (corticobulbar tract)
posterior limb, from medial to lateral:
- upper limb
- trunk
- lower limb