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COM Neuroendocrine > Motor Tracts > Flashcards

Motor Tracts Flashcards

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
Q

Lateral reticulospinal tract

A

Starts in medullary reticular formation in medulla

Facilitates flexor motor neurons and inhibits extensor motor neurons

26
Q

Rubrospinal tract

A

Starts in the red nucleus in midbrain

Innervates upper limb flexors

27
Q

Tectospinal tract

A

Starts in superior colliculus in midbrain
Innervates neck muscles
If you hear something, tectospinal will help you turn head to look at stimulus

28
Q

Lower motor neuron lesion

A

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
Q

UMN syndrome

A

Combination of the loss of corticospinal tract and the loss of regulation from the indirect brainstem motor control pathways

30
Q

Direct pathway/corticospinal tract effects of UMN syndrome** important

A 
Loss of distal extremity strength/dexterity
Babinski sign (inverted plantar reflex)
Pronator drift (not sure if this is direct or indirect path)
31
Q

Indirect tract effects of UMN syndrome** important

A

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
Q

Spinal level in relation to where the dysfunction is- C5-C8, T1, L2-L5, S1

A 
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
Q

Spinal cord lesions give UMN/LMN signs where

A

UMN signs below level of the lesion

LMN signs at the level of the lesion

34
Q

UMN contralateral vs ipsilateral

A

Lesion above lower medulla- clinical signs will be CL

Lesion in spinal cord- clinical signs are ipsilateral

35
Q

Decorticate posture/rigidity

A

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
Q

Decerebrate posture/rigidity

A

Lesion below red nucleus, but above reticulospinal/vestibulospinal nuclei
UE in pronation and extension and the LE in extension

37
Q

Lesion in what location will give you contralateral UMN probems (spasticity/hyper reflexia) and contralateral face droop

A

Cortex
Internal capsule
Cerebral peduncles

38
Q

Damage above pyramidal decussation will give what signs/symptoms

A

Contralateral UMN signs

39
Q

What issue will mask other problems

A

LMN problem will mask other problems because its the final pathway

40
Q

Complete SC transection

A

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
Q

Hemisection of spinal cord

A

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
Q

Syringomyelia

A

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
Q

Anterior cord syndrome

A

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
Q

Central cord syndrome

A

Syringomyelia is an example of central cord syndrome
Can be caused by cervical hyperextension
Same symptoms as syringomyelia

45
Q

Medial medullary syndrome

A

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
Q

Lateral medullary syndrome

A

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
Q

Corticobulbar tract lesion

A

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
Q

Weber syndrome

A

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
Q

Spastic cerebral palsy

A

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
Q

Amyotrophic lateral sclerosis ALS

A

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
Q

Polyneuropathy

A

Involvement of sensory, motor and autonomic
Progressing from distal to proximal
Impaired axonal transport
Demyelization may also contribute

COM Neuroendocrine (46 decks)

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