UMN Flashcards

1
Q

How would UMN lesion causing facial weakness present?

A

Unilateral lesion: Contralateral lower face weakness - can’t smile etc but can still raise eyebrows. Little effect on speech

Bilateral lesion: all muscles paralysed. Preserved emotional expression. Major difficulty producing labial and labiodental sounds

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2
Q

How would LMN lesion causing facial weakness present and what is this condition called?

A

Bell’s palsy

IPSILATERAL weakness of upper and lower face

loss taste ant 2/3 tongue, hyperacusis, decreased or absent lacrimation, positive synkinesis test (voluntary muscle movement causes simultaneous involuntary contraction of other muscles)

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3
Q

Name 11 anatomical levels/sites at which a UMN lesion may occur.

A
  1. Motor cortex
  2. Corona radiata
  3. Internal capsule
  4. Midbrain
  5. Pons
  6. Medulla
  7. Spinal cord
  8. Bulbar tract
  9. Lower motorneuron tract
  10. Corticospinal tract
  11. Corticobulbar tract to brainstem.
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4
Q

Where is the lesion if dense hemiplegia of acute onset involving arm, leg, face

A

UMN
Most probably lesion of posterior limb of internal capsule (secondary to occlusion of deep penetrating lat lenticulo-striate aa for eg)
Or basal pons (eg occlusion of paramedic penetrating aa)

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5
Q

What are the 2 most prevalent pathologies in the internal capsule?

A
Lacunar infarcts (<15 mm size, secondary to lipohyalinosis of penetrating a)
Haemorrhages
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6
Q

Hemiplegia is pathopneumonic for which lesion?

A

UMN

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7
Q

Hemiparesis of acute onset with arm weaker than legs favours which lesion?

A

UMN- middle cerebral artery

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8
Q

Hemiparesis of acute onset with leg weaker than arm - where is lesion?

A

Anterior cerebral artery (umn)

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9
Q

Dense hemiplegia with hemisensory deficit and homonymous hemianopia- where is lesion?

A

Internal capsule

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10
Q

Monoparesis - where is lesion

A

Localised to motor cortex (umn)

Cortical branch occlusion syndrome secondary to cerebral a embolism affecting a distal cerebral a branch.

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11
Q

Spastic paraparesis- where is lesion?

A

Spinal cord at thoracic/cervical level

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12
Q

What is cortical paraplegia

A

Bilateral medial motor cortex lesions, with confusion or other cerebral symptoms

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13
Q

6 causes of cortical paraplegia

A
  1. CP
  2. Parafalx meningioma
  3. Butterfly astrocytoma of corpus callosum
  4. Sagittal sinus thrombosis
  5. Anterior Communicans artery aneurysm with spasm of both ant cerebral arteries
  6. Prox ant cerebral a stem occlusion
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14
Q

Where is lesion in spastic quadriplegia usually

A

Cervical spinal cord

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15
Q

What is crossed hemiplegia

A

Ipsilateral UMN signs arm, contralateral leg

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16
Q

How do lesions at lower level of medulla oblongata (cranio-cervical junction) (at crossing of corticospinal tracts) typically present? (2)

A

Crossed hemiplegia

Characteristic pattern of progression of umn weakness eg ipsilat arm then leg weak, then contralat arm then leg weak.

17
Q

What is Brown Sequard syndrome

A

Hemi-section of spinal cord

18
Q

How does Brown Sequard syndrome present? (3)

A

Umn weakness ipsilat - corticospinal
Dorsal column signs ipsilat (proprioception, vibration, fine touch)
Spinothalamic signs contralat below lesion (pain and temp )

= hemisection

19
Q

What is Weber syndrome? (3)

A

Caused by a lesion (stroke circumferential a) in 1/2 midbrain medial aspect cerebral peduncle,
resulting in ipsilat CNIII palsy and contralat hemiplegia

20
Q

What is Millard- Gübler syndrome?

A
Lesion (stroke circumferential a) of basal lower 1/3 medial pons causing 
contralat hemiplegia (corticospinal tract), ipsilat CN VI, VII! palsy
21
Q

What is locked-in syndrome? (7)

A

Bilat infarction ventral central pons with or without medulla involve, causing quadriplegic paralysis and mute but still conscious (intact brainstem RF) . Pts can often move eyes vertical (not horiz) due to CN III and IV sparing in midbrain.
May be pseudobulbar palsy. Bilat facial weak
Secondary to pontine myelinolysis, glioma, tuberculoma

22
Q

How does lesion of medulla oblongata present? (2)

A
Contralateral hemiplegia (crossing of corticospinal tract occurs caudally)
Ipsilat CN xii paralysis may be found in Hughlings- Jackson syndrome
23
Q

How would acute stroke in mid pons present? (2)

A

Ipsilat CN V motor paralysis

Contralat hemiplegia

24
Q

Name 5 features UMN lesson

A
  • No wasting, maybe minimal disuse atrophy or contractures
  • increased tone
  • “pyramidal” pattern of weakness (extensors weaker than flexors in arms, flexors weaker than extensors in legs)
  • increased reflexes, clonus
  • babinski sign (extensor plantar response)
25
Q

Name 2 alternatives to babinski reflex

A
  • Chaddock reflex: stroke from lateral malleoulus to small toe
  • oppenheim: anterior tibia
26
Q

Name 6 causes rigidity

A
  • Parkinson’s
  • Catatonia
  • extrapyramidal symptoms of antipsychotics (haloperidol)
  • neuroleptic malignant syndrome
  • tetanus
  • tardive dyskinesia
27
Q

Name 5 causes spasticity

A
  • Cortical lesion: stroke
  • spinal injury: myelopathies, trauma
  • multiple sclerosis
  • cerebral palsy
  • neurogenerative disease affecting UMN, pyramidal and extrapyramidal pathways
28
Q

Name 3 broad causes of stroke in young people

A
  • Embolic causes eg afib
  • vessel wall disease eg HIV
  • hypercoagulability eg antiphospholipid antibody syndrome