Motor Tracts Flashcards

(51 cards)

1
Q

Upper motor neurons

A

Arise and contained within cerebral cortex or brain stem
Axons travel in descending trapes
Synapse with LMN or interneurons
-Corticospinal/corticobulbar tract

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2
Q

Lower motor nuerons

A

Directly innervate skeletal muscle
Cell body in spinal cord or brain stem
Gamma motor neuron- medium sized, myelinated, project to intrafusal fibers in spindle
Alpha motor neuron- large cell bodies and myelinated, project to extrafusal skeletal muscle
-Peripheral nerves and cranial nerves

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3
Q

Corticospinal tract

A

UMN arise in cortex and synapse with LMN
Medial corticospinal tract- postural muscles- not clinically significant
Lateral corticospinal tract- limb muscles, fractionation (ability to move fingers precisely)
Send collaterals to indirect pathway

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4
Q

Pathway of corticospinal tract

A

Descends from cortex through posterior limb of internal capsule
Passes through cerebral peduncles, anterior pons, pyramids in medulla, fibers cross in the pyramids/lower medulla
Descends in lateral column, synapse with LMN

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5
Q

Voluntary motor control

A

Primary motor cortex initiates voluntary movement via corticospinal tract
Right side controls left side of body, visa versa

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6
Q

Vascular supply to internal capsule

A

Lenticulostriate arteries

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7
Q

What supplies corticospinal tract in midbrain

A

P1 branch of posterior cerebellar

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8
Q

What supplies corticospinal tract in the pons

A

Paramedian branches of the basilar artery

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9
Q

What supplies corticospinal tract in medulla

A

Anterior spinal artery

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10
Q

What supplies corticospinal tract in spinal cord

A

Legs supplied by posterior spinal artery

Arms supplied by anterior spinal artery

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11
Q

Orientation of hands vs legs in midbrain/pons/medulla

A

Legs are lateral, hands are medial (opposite of brain)

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12
Q

Corticobulbar tract

A

Arises from ventral part of cortical area 4
Comprised of UMN
Descends into brain stem and influences muscles innervated by CN V, VII, IX, X, XI, XII- does not move eyes

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13
Q

Corticobulbar tract pathway

A

Same as corticospinal tract except when descending it travels through the genu of the internal capsule instead of posterior limb
Stops at specific motor nuclei of CNs it works with

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14
Q

Corticobulbar inputs to each nuclei

A

In pons, it gives bilateral input to both trigeminal motor nuclei (each nuclei receives input from both sides of brain)
For facial nucleus in lower pons- it gives bilateral input for areas of forehead, but contralateral input for lower face areas
In medulla- hypoglossal and nucleus ambiguous (CN IX/X) receive bilateral input, but muscles of palate and tongue muscles seem to receive contralateral input in clinical assessment
For spinal accessory- receives ipsilateral input

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15
Q

Lesion to corticobulbar tract above the pons- effects to mastication, forehead, lower face, palate muscles, tongue

A

No difference to muscles of mastication because of bilateral input
Forehead will have no change because of bilateral input
Lower face will have contralateral drooping
Contralateral palate muscles weak, uvula deviates to side of lesion
Tongue deviates to contralateral side because contralateral muscles are weakened

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16
Q

LMN organization

A

Found in anterior horn
Medial LMN project to axial muscles (biceps)
Lateral LMN project to limb muscles (forearm/hand)
LMNs innervating extensors lie ventrally
LMNs innervating flexors lie dorsally

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17
Q

Lateral UMN tract indirect pathways

A

Rubrospinal

Lateral reticulospinal

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18
Q

Medial UMN tract indirect pathways

A

Tectospinal
Medial reticulospinal
Lateral vestibulospinal
Medial vestibulospinal

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19
Q

Medial LMNs are receive input from which tracts which are located where

A
Located in anterior funiculus
Tectospinal tract
Medial vestibulospinal
Medial reticulospinal
Medial corticospinal
Lateral vestibulospinal
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20
Q

Lateral LMNs receive input from which tracts which are located where

A

Located in
Rubrospinal
Lateral reticulospinal
Lateral corticospinal (know location of these in SC)

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21
Q

How much detail do we need to know on these tracts

A

Not a ton, but know where they start and where they are going

22
Q

Lateral vestibulospinal tract

A

Starts in lateral vestibular nucleus in medulla
Projects to ipsilateral LMNs innervating postural muscles and limb extensors
Gets info about your body and gravity to influence its muscle actions

23
Q

Medial vestibulospinal tract

A

Starts in medial vestibular nucleus in medulla
Goes to cervical and thoracic levels- neck/shoulder muscles
Interprets what head movements and relation to gravity

24
Q

Medial reticulospinal tract

A

Starts in pontine reticular formation

Goes to ipsilateral LMN innervating postural muscles and limb extensors

25
Lateral reticulospinal tract
Starts in medullary reticular formation in medulla | Facilitates flexor motor neurons and inhibits extensor motor neurons
26
Rubrospinal tract
Starts in the red nucleus in midbrain | Innervates upper limb flexors
27
Tectospinal tract
Starts in superior colliculus in midbrain Innervates neck muscles If you hear something, tectospinal will help you turn head to look at stimulus
28
Lower motor neuron lesion
Flaccid paralysis Wasting or atrophy Hyporeflexia or areflexia due to denervation Hypotonia- decreased muscle tone Denervation or hypersensitivity seen as fasciculations (random contractions) ALL IPSILATERAL!!**
29
UMN syndrome
Combination of the loss of corticospinal tract and the loss of regulation from the indirect brainstem motor control pathways
30
Direct pathway/corticospinal tract effects of UMN syndrome** important
``` Loss of distal extremity strength/dexterity Babinski sign (inverted plantar reflex) Pronator drift (not sure if this is direct or indirect path) ```
31
Indirect tract effects of UMN syndrome** important
Hypertonia- collapse of resistance at the end of range of motion Rigidity- basal ganglia disease- shows constant resistance throughout full PROM Hyperreflexia- may be seen as clonus Clasp-knife phenomenon (faster you try to move patients arm, more resistance you get. At end of PROM resistance suddenly gives out) and spasticity (spastic paralysis)
32
Spinal level in relation to where the dysfunction is- C5-C8, T1, L2-L5, S1
``` C5 shoulder extension C6 arm flexion C7 arm extension C8 wrist extensors T1 hand grasp L2 hip flexion L3 knee extension L4 knee flexion L5 ankle dorsiflexion S1 ankle plantarflexion (these are not perfect but will get you close to the level) ```
33
Spinal cord lesions give UMN/LMN signs where
UMN signs below level of the lesion | LMN signs at the level of the lesion
34
UMN contralateral vs ipsilateral
Lesion above lower medulla- clinical signs will be CL | Lesion in spinal cord- clinical signs are ipsilateral
35
Decorticate posture/rigidity
Lesion is above the level of the red nucleus Thumb tucked under flexed fingers in fixed position, pronation of forearm, flexion at elbow with the lower extremity in extension with foot inversion
36
Decerebrate posture/rigidity
Lesion below red nucleus, but above reticulospinal/vestibulospinal nuclei UE in pronation and extension and the LE in extension
37
Lesion in what location will give you contralateral UMN probems (spasticity/hyper reflexia) and contralateral face droop
Cortex Internal capsule Cerebral peduncles
38
Damage above pyramidal decussation will give what signs/symptoms
Contralateral UMN signs
39
What issue will mask other problems
LMN problem will mask other problems because its the final pathway
40
Complete SC transection
All sensation lost 1 or 2 levels below lesion Bladder/bowel control lost Spinal shock- lost of tendon reflexes- looks like LMN issue UMN signs at levels below lesion about 6 weeks post accident LMN signs at level of lesion
41
Hemisection of spinal cord
Pain and temp from contralateral side 2 levels below lesion Discriminative touch and conscious proprioception ipsilaterally LMN signs at level of lesion UMN signs on ipsilateral side This pattern of loss is called Brown-Sequards syndrome
42
Syringomyelia
Formation of cysts within spinal cord Pain and temp first affected- Anterior white commissure Resulting pattern is cape distribution May have LMN signs if ventral horns affected May have UMN signs if lateral corticospinal tract is affected Syringomyelia is highly correlated with Chiari type I
43
Anterior cord syndrome
Compression/damage to anterior spinal cord Usually due to spinal cord infarction, intervertebral disc herniation, and radiation myelopathy, anterior spinal artery blockage ALS Corticospinal LMN signs at level of lesion UMN signs below level Everything bilateral
44
Central cord syndrome
Syringomyelia is an example of central cord syndrome Can be caused by cervical hyperextension Same symptoms as syringomyelia
45
Medial medullary syndrome
Anterior spinal artery is cause Hypoglossal nucleus Medial lemniscus Contralateral UMN signs from pyramid damage Contralateral loss of proprioception/vibratory sense Tongue deviation toward side of lesion
46
Lateral medullary syndrome
PICA is cause ALS- loss pain and temp contralaterally Spinal trigeminal nucleus/tract- loss of pain/temp to ipsilateral face (If you see these two symptoms- you know the lesion is in the medulla or lower pons. You can tell b/w pons or medulla because nucleus ambiguous is in medulla and damage will cause hoarseness. CN VI and VII nuclei are in pons) Vestibular nuclei- vertigo/nausea/nystagmus Restiform body- ataxia, wide gait, pt looks drunk Hypothalamospinal tract- Ipsilateral horners syndrome
47
Corticobulbar tract lesion
Central seven palsy Lesion of corticobulbar tract involving CN VII Contralateral face droop To distinguish b/w bells palsy and CN VII issue just look and see if patient can wrinkle forehead
48
Weber syndrome
P1 segment of posterior cerebral artery Corticospinal tract- CL hemiplegia, CL UMN signs Corticobulbar tract- CL face droop CN III- down and out, ptosis, dilated pupil
49
Spastic cerebral palsy
Abnormal supraspinal influences Failure of normal neuronal selection- failure to reach developmental milestones Consequent aberrant muscle development Paresis/weakness Abnormal tonic stretch reflexes at rest and during movement Reflex radiation Lack of postural preparation prior to movement Abnormal cocontraction of muscles Inverted legs, scissor walk, up on the toes
50
Amyotrophic lateral sclerosis ALS
Destroys only somatic motor neurons - UMN and LMN Leads to paresis, myoplastic hyperstiffness, hyperreflexia, babinskis sign, atrophy, fasciculations CN involvement leads to difficulty breathing, swallowing and speaking
51
Polyneuropathy
Involvement of sensory, motor and autonomic Progressing from distal to proximal Impaired axonal transport Demyelization may also contribute