8/26 Upper Motor Neurons - Glendinning Flashcards
“path” to a movement
role of upper motor neurons
idea → find stored motor memories → develop the plan → pull the trigger → send commands to spinal cord → use spinal cord patterns → CONTRACT MUSCLES
UMNs are the neurons that send commands to spinal cord in this chain
origin of a movement
IDEAS re: voluntary movement - frontal lobe
- frontal lobe is all about planning, motivation [also inhibitions re: stuff you shouldn’t do]
ORGANIZATION OF MOVEMENT (i.e. movement planning) - premotor cortical areas (supplementary motor area + premotor cortex)
INFO RE: SPATIAL RELATIONSHIPS - posterior parietal cortex (primary somatosensory cortex + parietal association cortex)
- primary somatosensory cortex: where is the body?
- parietal association cortex: where are objects in the environment?
EXECUTION of the planned and organized action (with the input from the sensory parts) : activation of LMNs in brainstem/spinal cord
apraxia
difficulty in using a body part to perform complex voluntary actions
test: ask patients to grasp a pencil, button a button despite obvious weakness/paralysis/altered tone
result of lesions to premotor cortex OR posterior parietal cortex (organization/planning of skilled movements!)
2 major descending pathway groups
how they interact with alpha/gamma/interneurons
- lateral white matter (axons from motor cortex)
- medial white matter (axons from brainstem)
both project to diff regions of the ventral horn → project to spinal cord & brainstem alpha motor neurons and interneurons
REMEMBER: alpha motor neurons are arranged somatotopically!!! therefore…
- medial pathways → proximal motor neurons
- lateral pathways → distal motor neurons
upper motor neuron overview
UMNs are descending motor neurons from:
1. cerebral cortex
- CROSS MIDLINE
- hit lateral white matter of spinal cord → LMN in lateral ventral horn : distal limb muscles (skilled movements)
2. brainstem
- CROSS MIDLINE
- hit anterior-medial white matter of spinal cord → LMN in medial ventral horn : axial and proximal limb muscles (posture and balance)
corticospinal tract pathway
primary pathway for goal-directed movements
majority of CST originates in primary motor cortex
- minority originate in premotor and somatosensory cortex too
primary motor cortex (precentral gyrus) → decussates in medullary pyramids → down spinal cord → onto LMN
- ONLY descending pathway to project directly to alpha motor neurons of distal muscles
- ONLY pathway that generates fine movements of fingers
what does the motor cortex “encode”/execute?
motor cortex keys
NOT specific muscles
codes entire movements
therefore…motor cortex lesions affect several muscles!
keys:
- stimulation to one site elicits completely diff sets of muscle patterns depending on start position BUT those varied muscle patterns get you to the same endpoint (from the diff start positions)
- motor cortex cells don’t code for indivd muscles - code for endpoints (goals) of movements
anatomy of corticospinal tract
aka pyramidal tract
nerves move from site of origin down through posterior limb of internal capsule → cerebral peduncles in midbrain → ventral pons → ventral medulla (medullary pyramids!)
- within posterior limb, lower limb stuff more posterior, upper limb stuff more anterior
at inferior portion of med pyramids, MAJOR DECUSSATION: approx 80-90% of pathway crosses midline and enters opp lateral (crossed) corticospinal tract
- rest of it stays ipsilateral in anterior (direct) CST
LCST vs ACST
lateral corticospinal tract
- projects directly and indirectly to motor neurons and motor interneurons in lateral ventral horn (distal muscles/extremities)
anterior corticospinal tract
- projects bilaterally to motor neurons and interneurons in medial ventral horn (proximal and trunk muscles)
functions of CST
deficits with CST lesions
- which side?
- major pathway for voluntary movements of lumbs
- ONLY pathway for fine finger movementss
almost NEVER affected by itself!
deficits:
- voluntary motor weakness (distal > proximal) on one side of body
- Babinski sign
how do you know which side you’ll see deficits on?
- lesions above spinal cord = contralateral deficits
- lesions of spinal cord = ipsilateral deficits
*deficits ALWAYS below level of lesion!
Babinski sign
extensor plantar response
“release” phenomenon [seen in babies before CST is myelinated
- stroke lateral plantar surface (sole) of foot
- observe response
- normal : toes flex
- Babiski : toes extend upwards
brainstem centers for responsing to stimuli or errors in movement
control posture/tone
midbrain centers
- red nucleus
- tectum
pontine centers
- reticular formation
medullary centers
- reticular formation
- vestibular nuclei
reticulospinal tracts
- project mainly ipsilaterally (some bilateral) to medial alpha motor neurons throughout length of spinal cord
- contribute to posture, gait-related movements, muscle tone
feed-forward, preparatory muscle activation
ex. guy being told to pull on something on command; BEFORE the biceps begin pulling, the gastrocs prep to stabilize
lateral and medial vestibulospinal tracts
elaborate sensory system in inner ear comprising specialized receptors that monitor head position, movement, acceleration
lateral vestibular nuclei
- to entire spinal cord
- projects ipsilaterally to medial LMNs to proximal muscles
- esp facilitates extensor muscles in response to deviations from stable balance and upright balance
medial vestibular nuclei
- only to cervical
- projects bilaterally to conrol/restore head position in response to acceleration
- “vestibulocervical reflex”
both pathways project to medial-ventral horn
tectospinal tract
originates in superior colliculus and crosses in midbrain
part of medial motor system → only goes to cervical region
- generates orienting movements of the head to visual or auditory stimuli
- helps coordinate eyes and head
rubrospinal tract
originates in red nucleus of midbrain, then crosses in the midbrain → travels to LCST, extends to cervical spinal cord
- role unclear in humans…we think it facilitates flexor muscles > extensors in the arms
- receives inputs from cerebellum
summary of tracts
tabular summary of tracts/descriptions
UMN lesions
initial shutdown of spinal circuits that lasts several days
- most extreme/longest duration : spinal shock after SC injury
followed by:
- weakness for voluntary movements (paresis)
* due to loss of voluntary drive to motor neurons - increased reflexes (hyperreflexia)
* due to change in descending influences and neuroplastic changes - hypertonia
* due to hyperreflexia - posturing
* due to imbalanced activity in muscle groups
2+3+4 = spasticity
why does spasticity occur?
- UMN damage disturbs balanced modulation of spinal cord interneurons and motor neurons by descending pathways (+ and -)
* removing any of these inputs changes the balance of excitability of motor neurons and reflexes - loss of inputs to motor neurons → neuroplastic changes in motor neurons
* denervation supersensitivity and sprouting from local interneurons - reduced muscle extensibility due to muscle contracture → increased muscle spindle activation
hypertonia in UMN lesions
velocity-dependent: less resistance to slow movement (compared to fast)
clasp-knife response: initial resistance followed by inhibition of muscle (poss due to Golgi tendon organ response)
posturing in spasticity
many muscle groups are affected by weakness and hypertonia
postures are produced by imbalanced tone
decorticate posture in lesions above midbrain:
upper limb: flexors > extensors
lower limb: extensors > flexors
decerebrate posture in lesions below midbrain (below red nucleus):
all limbs extended
features of UMN syndrome
- spreading of movements
* movement of one part of body produces movements in other parts of body (maybe mirroring, maybe flexion in hand/flexion in foot type of association with children) - decreased ability to isolate movement
Hoffman’s sign
hold finger loosely, flick fingernail downwards
- finger will rebound into extension
- IF THUMB FLEXES/ADDUCTS → positive Hoffman’s sign!
comparison of UMN and LMN lesions
weakness
atrophy
fascibulations
reflexes
tone
corticobulbar tract
UMNs for head
comprise several CNs originating in brainstem with motor neuron components
- CN III, IV, VI; V; IX, X, XI; VII, XII - name functions!
mostly bilateral innervation
- exception: lower VII (contralateral motor neurons to lower face)
- exception: XII (mostly contralateral motor neurons to tongue)
- midbrain: III, IV (both ipsilateral and contralateral)
-
pons: VI, V, VII upper, VII lower
- VI, V, and VII upper (ispi and contralat)
- VII lower (contralat only)
- medulla: XII; IX/X/XI (ipsi and contralat)
what is the normal innervation pattern of the corticobulbar tract?
what are the exceptions?
what signs will you see with corticobulbar tract lesion?
normal: bilteral!
* exceptions for VII lower (lower face) and mostly for XII (tongue) : contralateral innervation
therefore, lesions to one corticobulbar tract produce…
- paralysis to contralateral lower face
- some paralysis to opposite tongue, difficulty swallowing (dysphagia)
how would you test CN VII?
test in 2 parts: upper and lower
- upper: close eye or raise eyebrow
- lower: retract mouth (smile)
if CN VII lesion, see Bell’s palsy : LMN paralysis of half of face (both upper and lower affected one one side)
causes of UMN syndrome
- trauma
- stroke (sudden onset)
- multiple sclerosis (sx separated in time and space)
- ALS (fasciculations, weakness, spasticity; rapid progression - death in 2 or 3 yr)
cerebral palsy
what is it?
causes
presentation
incidence
variety of non-progressive neurological disorders appearing in infancy or early childhood → permanently affect body movement, muscle coordination
causes
- ischemia at birth
- hypoperfusion
- trauma
presentation
- spasticity
- dystonias
- intellectual disability
- abnormal motor control
incidence: 2/1000 live births, higher in preterms
how do you localize lesions?
keys
- what is the pattern of weakness?
- are chars upper or lower motor neuron?
- which pathways?
- additional sx? (somatosensory, cognitive, visual, etc)
- where woudl ONE lesion produce this pattern???
