Lec 8 Flashcards
What are upper motor neuron lesions
How do you identify the location of the lesion?
injury or disease affecting:
UMN nuclei or motor cortex
axons that descend through brain, brainstem, or spinal cord
ID location based off side of lesion.
what are the symptoms of upper motor neuron lesion (4)
muscle weakness
hyper-reflexia (inc reflexes)
Hypertonicity (inc tone)
positive Babinski sign
How does muscle weakness differ in UMN lesions vs LMN lesions
UMN lesions have spastic motor weakness (r8 and force dependant, includes clasped knife syndrome)
The corona radiata and internal capsule both consist of what type of brain fibres
projection fibres
what are the 7 tracts.
Lateral corticospinal tract
Anterior corticospinal tract - axial muscles, control muscles bilaterally
Cortico-bulbar tract
Rubrospinal tract
Reticulospinal tracts (2)
Vestibulospinal tracts (2)
Tectospinal tract
Anterior corticospinal tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where decussate
where terminate
- Axial muscles (neck and trunk), control muscles bilaterally.
Originate at cortex
Not decussate
Terminate at cervical and upper thoracic (T1-T6)
Lateral corticospinal tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
Hands and feet (control contralateral side)
Originate in cortex
Terminate in cervical and lumbrosacral enlargements
decussate in pyramid just before spinal cord
Cortico-bulbar tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
control facial muscles Upper face receives input from both brain hemispheres, lower, receives contralateral.
- therefore, if upper side of face is preserved, likely upper motor neuron damage. Lower motor neuron damage if whole face or both brain sides affected.
Origin - Motor cortex
Terminates in the brainstem where it connects to facial nerve
Decussate in pons of brainstem.
As a whole, where does the corticospinal tract decussate.
According to lecture slides diagram, decussates at medulla?
Vestibulospinal tracts
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
Medial VST:
- Controls Head and neck position (bilateral)
- Origin - medial and lateral vestibular nuclei (in medulla)
- Terminate - Cervical and upper thoracic cord
Lateral VST:
- Balance (ipsilateral)
- Origin - lateral vestibular nucleus (in pons)
- terminates through entire cord
Reticulospinal tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
Lateral Reticulospinal tract:
- Posture and gait movements (ipsilateral)
- Origin - medulla
- terminate - entire cord
- no decussate
MRT:
- posture and gait (ipsilateral)
- origin - Pons
- terminate - throughout cord
- no decussate
(may be able to simplify into one instead of two tracts for sake of course).
Rubrospinal tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
move contralateral limbs
Origin - red nucleus
Terminate - cervical cord
Decussate in midbrain
Tectospinal tract
What muscles control (also ipsilateral or contralateral control?)
Where originate
where terminate
where decussate
coordinate head and eye movements
Origin - superior colliculus (midbrain)
Termination - cervical cord
Decussation - midbrain
How can tone help ID location of lesion? give examples of different postures and what means
If lesion is above midbrain - de-corticate posture (involve rubrospinal tract)
If lesion below midbrain - De-cerebrate posture (involve vestibulo-spinal influence)
Arms point to location of lesion - arms extended = below midbrain, if arms flexed up = above midbrain lesion
Describe the Babinski reflex
dorsi-flex big toe and fan toes when stroke bottom of foot = pos Babinski sign.
Otherwise most ppl flex toes down and dorsi-flex ankle.
Pos bab = damage to UMN (prob lateral corticospinal tract.
What is primary lateral sclerosis V.S. Amyotrophic lateral sclerosis (ALS)
PLS - degeneration of upper motor neurons = spasticity and weakness. Progressive but non-fatal.
ALS - Degeneration of UMN and LMN. Atrophy and fasciculations, hypertonia and hyperreflexia. Fatal 2-4 years.
No cause known for either. Could be genetic.
