Motor Tracts Flashcards
Upper motor neurons
Arise and contained within cerebral cortex or brain stem
Axons travel in descending trapes
Synapse with LMN or interneurons
-Corticospinal/corticobulbar tract
Lower motor nuerons
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
Corticospinal tract
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
Pathway of corticospinal tract
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
Voluntary motor control
Primary motor cortex initiates voluntary movement via corticospinal tract
Right side controls left side of body, visa versa
Vascular supply to internal capsule
Lenticulostriate arteries
What supplies corticospinal tract in midbrain
P1 branch of posterior cerebellar
What supplies corticospinal tract in the pons
Paramedian branches of the basilar artery
What supplies corticospinal tract in medulla
Anterior spinal artery
What supplies corticospinal tract in spinal cord
Legs supplied by posterior spinal artery
Arms supplied by anterior spinal artery
Orientation of hands vs legs in midbrain/pons/medulla
Legs are lateral, hands are medial (opposite of brain)
Corticobulbar tract
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
Corticobulbar tract pathway
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
Corticobulbar inputs to each nuclei
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
Lesion to corticobulbar tract above the pons- effects to mastication, forehead, lower face, palate muscles, tongue
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
LMN organization
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
Lateral UMN tract indirect pathways
Rubrospinal
Lateral reticulospinal
Medial UMN tract indirect pathways
Tectospinal
Medial reticulospinal
Lateral vestibulospinal
Medial vestibulospinal
Medial LMNs are receive input from which tracts which are located where
Located in anterior funiculus Tectospinal tract Medial vestibulospinal Medial reticulospinal Medial corticospinal Lateral vestibulospinal
Lateral LMNs receive input from which tracts which are located where
Located in
Rubrospinal
Lateral reticulospinal
Lateral corticospinal (know location of these in SC)
How much detail do we need to know on these tracts
Not a ton, but know where they start and where they are going
Lateral vestibulospinal tract
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
Medial vestibulospinal tract
Starts in medial vestibular nucleus in medulla
Goes to cervical and thoracic levels- neck/shoulder muscles
Interprets what head movements and relation to gravity
Medial reticulospinal tract
Starts in pontine reticular formation
Goes to ipsilateral LMN innervating postural muscles and limb extensors
Lateral reticulospinal tract
Starts in medullary reticular formation in medulla
Facilitates flexor motor neurons and inhibits extensor motor neurons
Rubrospinal tract
Starts in the red nucleus in midbrain
Innervates upper limb flexors
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
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!!**
UMN syndrome
Combination of the loss of corticospinal tract and the loss of regulation from the indirect brainstem motor control pathways
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)
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)
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)
Spinal cord lesions give UMN/LMN signs where
UMN signs below level of the lesion
LMN signs at the level of the lesion
UMN contralateral vs ipsilateral
Lesion above lower medulla- clinical signs will be CL
Lesion in spinal cord- clinical signs are ipsilateral
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
Decerebrate posture/rigidity
Lesion below red nucleus, but above reticulospinal/vestibulospinal nuclei
UE in pronation and extension and the LE in extension
Lesion in what location will give you contralateral UMN probems (spasticity/hyper reflexia) and contralateral face droop
Cortex
Internal capsule
Cerebral peduncles
Damage above pyramidal decussation will give what signs/symptoms
Contralateral UMN signs
What issue will mask other problems
LMN problem will mask other problems because its the final pathway
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
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
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
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
Central cord syndrome
Syringomyelia is an example of central cord syndrome
Can be caused by cervical hyperextension
Same symptoms as syringomyelia
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
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
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
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
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
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
Polyneuropathy
Involvement of sensory, motor and autonomic
Progressing from distal to proximal
Impaired axonal transport
Demyelization may also contribute
