UMN Weakness Flashcards

1
Q

responsible for voluntary control of movement

A

pyramidal tract

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2
Q

responsible for involuntary pathways for co-ordination of movement

A

extrapyramidal tracts

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3
Q

components of the pyramidal tract

A

corticobulbar and spinal

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4
Q

injury to the pyramidal tract results in…

A

UMN syndrome

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5
Q

what is the UMN?

A

located in brain or brainstem – spinal chord – innervates ventral horn

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6
Q

what is the LMN?

A

ventral horn to periphery

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7
Q

see homunculus

A
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8
Q

CTBs routes

A

CBTs arise lateral aspect of motor cortex → synapse on cranial nerves (CN 5,7,9,10,11,12) to control muscles of face + neck (face, jaw, swallow, tongue movts)

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9
Q

what does corticobulbar supply and what does the mean for symptoms if lesion?

A

Bilateral CN nuclei - unilateral CBT lesion gives mild muscle weakness

EXCEPT
CN 7 = paralysis of contralateral Lower face - UMN lesion

CN 12 = UMN lesion → paralysis of contralateral genioglossus → deviation of the tongue towards contralateral side

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10
Q

how to clinically assess a weak patient?

A
  1. MRC grading
  2. doing what they say, movement and maintaining posture e.g. outstretched arms
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11
Q

Spasticity

A

velocity-dependent increase in a muscle’s resistance to a passive stretch. Slow passive movements of the arms or legs will not elicit the increased resistance. Brisk stretches of muscles will cause an abrupt increase in tone followed by a decrease in muscular resistance with continued stretch. This phenomenon is called clasp-knife rigidity. The antigravity muscles of the arms and legs are most affected. These include the flexors of the arms and the extensors of the leg. Because of the decreased modulation of spinal reflexes in UMN syndrome, patients will often exhibit flexor and extensor spasms.

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12
Q

Clonus

A

Clonus is a sequence of rhythmic, involuntary muscle contractions. These contractions occur at a frequency of 5 to 7 Hz and are a response to abruptly applied stretch stimuli. Clonus is most easily elicited at the ankle with brisk dorsiflexion and plantar-flexion movements. Clonus can also be observed during voluntary movement or through cutaneous stimulation.

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13
Q

Reflexes

A

Hyperreflexia of deep tendon reflexes
Patients can be seen to have abnormally brisk reflexes which are due to decreased modulation by descending inhibitory pathways. Radiation of reflexes is a regular observation with the hyperreflexia of UMN lesions. For example, tapping of the supra-patellar tendon would elicit a knee-jerk reflex.
Hyporeflexia of superficial reflexes
The superficial abdominal reflex and the cremasteric reflex are seen to be decreased or abolished following UMN lesions. The superficial abdominal reflex is the tensing of abdominal by stroking the overlying skin while the cremasteric reflex is the elevation of the scrotum in response to stroking the medial thigh.

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14
Q

Pseudo-bulbar palsy

A

As previously stated, most cranial nerves have bilateral innervation from the brain with the exception of CN VII and CN XII. The muscles of cranial nerves with bilateral innervation include the eyes, jaw, pharynx, upper face, larynx, and neck. These muscles would only show deficits with bilateral UMN lesions. Bilateral damage of UMN’s to cranial nerves is known as a pseudobulbar palsy. Slurred speech is often the first presenting symptom. Other characteristic deficits include dysphagia, dysarthria, brisk jaw jerk, spastic tongue, and pseudobulbar affect.

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15
Q

Spinal shock

A

Spinal shock refers to the period of acute flaccid paralysis following spinal cord injury.

Hypotonia and hyporeflexia are the most characteristic symptoms.

The paralysis is most evident in the arms and legs with preservation of truncal musculature.

The duration can range from a few days to weeks after which spasticity and hyperreflexia replace the prior symptoms.

The symptoms of spinal shock are most pronounced with lesions of the spinal cord versus cerebral lesions.

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16
Q

once assessed as weak then what?

A

what type of weakness

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17
Q

Disuse atrophy
increased tone / spasticity
increased reflexes
clonus
plantar response

A

UMN lesion

18
Q

atrophy
fasiculations
normal or reduced reflexes
absent clonus
decreased plantar

A

LMN lesion

19
Q

pattern that is confined to nerve to root and bilateral proximal muscles

A

LMN pattern

20
Q

pattern that extensors of arm and flexors of leg and anti-gravity muscles

A

UMN pattern

21
Q

PATTERN PICS

22
Q

Clinical assessment of the weak patient

A
  1. are they weak
  2. type of weakness
  3. pattern of distribution
  4. additional neuro signs
  5. causes + Ddx
23
Q

localised cognitive functions

A
  • language
  • reading
  • writing
  • calc
  • visuospatial
24
Q

distributed cognitive functions

A
  • arousal
  • memory
  • personality
  • behaviour
25
visiospatial presents as...
Right - non dominant
26
aphasia presents as ...
left hemisphere - dominant
27
rule of 4
There are 4 structures in the 'midline' beginning with M. There are 4 structures to the side beginning with S. There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain).
28
posterior lateral CST function
sensory - vibration, sense, fine touch, JPS
29
anterolateral STT
sensory - pain, temp and crude touch
30
where is the lesion: differential weakness: F/A>>L, or L>>F/A hemianopia, aphasia, hemineglect cortical or primary sensory loss cognitive dysfunction
cortex
31
where is the lesion : differential weakness: F/A>>L, or L>>F/A primary sensory loss
Corona radiata
32
where is the lesion:dense weakness F=A=L
dense weakness F=A=L internal capsule
33
where is the lesion: dense weakness A=L cranial nerve signs (eyes/bulbar) esp crossed cerebellar signs
brainstem
34
where is the lesionno face involvement spastic para/quadraparesis sensory level sphincter involvement
spinal
35
motor or sensory deficit only
lacunar
36
PACS criteria - partial anterior
> motor or sensory deficit > higher cortical dys > hemianopia ( must have 2 )
37
TACS criteria
> motor or sensory > cortical > hemianopia
38
POCS criteria
> isolated hemianopia > brainstem signs > cerebellar signs
39
Pure motor stroke Pure sensory stroke Sensori-motor stroke Ataxic hemiparesis Dysarthria-clumsy hand Must not have higher cortical function loss - dysphasia or neglect
Lacunar
40
Higher cerebral dysfunction (e.g. dysphasia) Homonymous visual field defect Ipsilateral motor and/or sensory deficit of at least two areas (out of face, arm and leg). Or dysphasia/neglect alone Or a motor/sensory deficit smaller than a LACI (e.g. confined to one limb)
PACS
41
Must have 3 of 3 of Higher cerebral dysfunction (e.g. dysphasia) Homonymous visual field defect Ipsilateral motor and/or sensory deficit of at least two areas (out of face, arm and leg).
TACS
42
Any of: Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit Bilateral motor and/or sensory deficit Disorder of conjugate eye movement Cerebellar dysfunction Isolated homonymous visual field defect.
POCS