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Motor pathways Flashcards

1
Q

Upper and lower motor neurons

A
  • Upper motor neurons (UMN): cell body in motor cortex and subcortical nuclei that synapse on anterior horn cells in the SC, or somatomotor neurons of cranial nerve nuclei
  • For UMNs, the cell body and axon is within the CNS
  • Lower motor neurons (LMN): anterior horn cells of the SC or somatomotor neurons of cranial nerve nuclei that send their axons to terminate on skeletal muscles @ NMJs
  • For LMNs, the cell body is in CNS but the axons travel to the periphery
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2
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Types of LMNs

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  • Somatomotor (alpha) neurons: found in SC and cranial nerve nuclei. Innervate skeletal muscle for voluntary contraction and provide trophic support (via tonic activation) for muscle survival
  • Gamma motor neurons: found in the SC and brain stem, innervates muscle spindle fibers to maintain sensitivity to stretch reflexes
  • Both types of LMNs are activated by UMNs when voluntary activity is initiated
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3
Q

Location of LMNs

A
  • LMNs of the neck, trunk and limbs (not head) are found in the SC
  • LMNs that control proximal muscles are located medially in the ventral horn, while neurons controlling distal muscles are located laterally
  • Cranial nerve nuclei in the brain stem contain that contain LMN to innervate skeletal muscles of the face are: CNs III, IV, V, VI, VII, IX, X, XI, XII (all but I, II, VIII- the ones that are only special senses)
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4
Q

Location of UMNs

A
  • Can be from 2 places: either the motor cortex or subcortical nuclei (red nucleus, reticular formation, vestibular nuclei)
  • Motor cortex neurons can either be in the primary motor cortex or the FEF (frontal eye field), they send out axons that descend through the medullar pyramids (pyramidal tracts) to reach the SC or the cranial nerve
  • Both the corticospinal tracts (for body) and corticobulbar tracts (for head) are pyramidal tracts
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5
Q

Corticospinal tracts

A
  • UMN axons pass through medullar pyramids and enter the SC
  • The axons descend the SC until they reach the LMNs they innervate
  • The LMNs innervate muscles of the neck, trunk, and limbs
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6
Q

Corticobulbar tracts

A
  • UMN axons end in the brainstem (some do travel down the medullar pyramids)
  • They synapse on the somatomotor neurons of cranial nerves that innervate muscles of the head, larynx and pharynx
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7
Q

Motor cortex 1

A
  • Motor association cortices: planning and programming of motor activity, precedes the activation of primary motor cortex (PMC). Occurs in the supplementary motor area (SMA) and premotor area (PMA)
  • Prefrontal cortex (PFC) is responsible for what the action will be, sends info to the SMA and PMA. PFC is anterior to motor association cortices and is not part of them
  • In addition to the motor association cortices and PMC, motor contributions can come from the general sensory cortex and sensory association areas of the parietal lobe
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8
Q

Motor cortex 2

A
  • Primary motor cortex (PMC) gives origin to the corticospinal (CST) and corticobulbar (CBT) tracts
  • Neurons of origin of CST and CBT are mostly found in the precentral gyrus (PCG) and paracentral lobule
  • In the PMC there is somatotopic representation of the body parts (homunculus) with the feet and legs in the paracentral lobule (near longitudinal fissure) and hands and face at the lateral part of the precentral gyrus near the lateral sulcus
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9
Q

Vascular supply to PMC

A
  • The more medial part of the PMC (near the longitudinal fissure, controls the lower limbs) is supplied by the anterior cerebral arteries (ACA)
  • The more lateral parts of the PMC (controlling the upper limbs and face) is supplied by the middle cerebral arteries (MCA)
  • Areas of the PMC that represent different body parts are proportionate to the complexity of motor functions of that body part (i.e. the thumb/hand and muscles for speech take an exceptionally large amount of PMC)
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10
Q

Corticospinal tract (CST) 1

A
  • Axons of cortical neurons come together to form the corona radiata
  • Below the corona the tract condenses into the posterior limb of the internal capsule
  • Somatotopic arrangement in the posterior limb of the internal capsule for CST are fibers destined for the face/upper limbs are more medial anterior, while fibers destined for the leg/lower body are more lateral posterior
  • Important: motor axons in internal capsule run with sensory (superior internal capsule) and run w/o sensory (inferior internal capsule)
  • Therefore lacunar infarcts of internal capsule may affect just motor (inferior) or both sensory and motor (superior)
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11
Q

Corticospinal tract (CST) 2

A
  • The CST then descends through the middle 3/5ths of the crus cerebri in the midbrain. In the crus cerebri the upper limb fibers are medial to the lower limb fibers
  • The CST descends to the pons where it traverses the ventral part of the pons. There is no clear somatotopic localization
  • In the upper medulla the CST axons gather at the pyramid. 75-90% of CST axons decussate in the medullary pyramid, at the medullary-SC junction
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12
Q

Corticospinal tract (CST) 3

A
  • After decussating, the axons form and descend in the lateral corticospinal tract in the lateral funiculus (region of white matter just lateral to the dorsal horns)
  • This is the split btwn the lateral (crossed) vs anterior (uncrossed) CST
  • The anterior CST are the remaining fibers that descend the SC in the medial part of the ventral funiculus: just anterior to the white commissure and medial/anterior to the ventral horns (most medial and anterior part of the SC)
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13
Q

Lateral CST

A
  • LCST is located in lateral funiculus of SC, axons leave the tract at all levels and synapse on LMNs in the anterior horn on the same side (contralateral to side of origin)
  • The LMNs innervated by axons in LCST usually then innervate muscles in the distal parts of the limbs
  • At any level below the decussation (i.e. the SC), damage to the LCST will affect the LMNs and skeletal muscles on the same side of the lesion
  • Above the pyramidal decussation, damage to this pathway will affect LMNs and skeletal muscles on the contralateral side of the lesion
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14
Q

Anterior CST

A
  • Found only in the cervical and upper thoracic levels
  • Axons may end contralateral to the side of origin, by crossing thru the white commissure to synapse on the medial group of LMNs in the anterior horn of the other side of the SC
  • Many axons do not cross thru the white commissure, and synapse on medial group of LMNs in the ipsilateral anterior horn
  • Therefore the tract ends bilaterally
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15
Q

Corticobulbar tract (CBT) 1

A
  • Axons originate from neurons in the PMC (regions that represent the face and head), close to the lateral sulcus
  • They descend in the corona radiate and intermingle w/ CST
  • In the internal capsule the CBT and CST are still intermingled. The CBT lies at the genu (flexure) of the posterior limb of the internal capsule, posterior and medial to the CST fibers
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16
Q

Corticobulbar tract (CBT) 2

A
  • In the midbrain the CBT fibers are medial to the CST fibers, as they flow through the crus cerebri
  • In the basal part of the pons and the pyramid, the CST and CBT are intermingled and indistinguishable
  • Axons in the CBT leave the tract at the level of the cranial motor nuclei (in the brainstem) they will innervate
  • These cranial motor nuclei are at many different levels, and the CBT does not extend much below the medulla except to innervate the nucleus of XI in the upper cervical regions (C2-5)
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17
Q

Locations of cranial nerve motor nuclei

A
  • Midbrain: nucleus of III (move eye) in upper midbrain, nucleus of IV (move eye) in lower midbrain
  • Pons: nucleus of V (mastication) in midpons, nucleus of VI (move eye) in lower pons, nucleus of VII (facial expression) in lower pons
  • Medulla: nucleus of IX and X (nucleus ambiguous, muscles of larynx and pharynx) in upper medulla, nucleus of XII (muscles of the tongue) in the upper medulla
  • Cervical SC: nucleus of XI (SCM and trapizious) in C2-5
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18
Q

Terminations of CBTs for bilateral innervation of muscles

A
  • CBTs for CN V, IX, X and XI end bilaterally on cranial motor nerve nuclei (to innervate the jaw, larynx, pharyngeal, and palatine muscles)
  • This means that the left CBT for V will synapse on both the left and right CN V motor nuclei (and the right CBT for V will do the same)
  • Axons destined for each pair of nuclei leave the tract immediately above the nuclei
  • Because of the bilateral innervaiton pattern, unilateral UMN lesions of the CBT may not show clinical deficits in CN V, IX, X, and XI
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19
Q

Terminations of CBTs for contralateral innervation of muscles (XII)

A
  • The CBT for CN XII ends bilaterally, but the contralateral input on the cranial motor neurons of the hypoglossal nucleus predominates
  • Axons destined for XII nuclei leave CBT immediately above the nuclei
  • In the upper medulla the CBT for CN XII decussate and end on motor neurons of the hypoglassal nucleus (in upper medulla)
  • Unilateral UMN lesions of the CN XII CBT results in contralateral tongue weakness (tongue points away from lesion- toward side of muscle innervation loss)
  • Unilateral LMN lesions of CN XII results in ipsilateral tongue weakness (tongue points toward lesion- toward side of muscle innervation loss)
20
Q

Terminations of CBTs for bi and contralateral innervation of muscles (VII) 1

A
  • Innervation of motor nucleus of VII is partly bilateral and partly contralateral
  • Facial nucleus (lower pons) is divided into 2 parts: upper and lower groups
  • Upper group of neurons innervates upper facial muscles (frontalis and obicularis oculi)
  • LMNs that innervate the upper face receive bilateral innervation from CBT of VII
21
Q

Terminations of CBTs for bi and contralateral innervation of muscles (VII) 2

A
  • Lower group of neurons innervates orbicularis oris and lower facial muscles
  • LMNs that innervate the lower face receive contralateral input from the CBT of VII
  • Thus, the upper face (forehead) is dually controlled by both right and left motor cortex (will not be damaged by unilateral lesions of CBT)
  • Whereas the lower face (muscles below the eye) is dependent on the contralateral CBT and is vulnerable to unilateral lesions of CBT
22
Q

Terminations of CBTs for bi and contralateral innervation of muscles (VII) 1

A
  • Innervation of motor nucleus of VII is partly bilateral and partly contralateral
  • Facial nucleus (lower pons) is divided into 2 parts: upper and lower groups
  • Upper group of neurons innervates upper facial muscles (frontalis and obicularis oculi)
  • LMNs that innervate the upper face receive bilateral innervation form CBT of VII
23
Q

Terminations of CBTs for bi and contralateral innervation of muscles (VII) 2

A
  • Lower group of neurons innervates orbicularis oris and lower facial muscles
  • LMNs that innervate the lower face receive contralateral input from the CBT of VII
  • Thus, the upper face (forehead) is dually controlled by both right and left motor cortex (will not be damaged by unilateral lesions of CBT)
  • Whereas the lower face (muscles below the eye) is dependent on the contralateral CBT and is vulnerable to unilateral lesions of CBT
24
Q

Lesions to the CBT of VII or CN VII

A
  • Unilateral UMN lesion anywhere along the CBT for VII will result in bilateral sparing of the upper face
  • The lower face, however, will be paralyzed in the contralateral side of the lesion, and the symptoms will show UMN lesion
  • UMN lesions affect anywhere from the cortex to the mid pons
  • If there is a unilateral LMN lesion (like in bell’s palsy), due to lesion in facial nucleus, or compression of CN VII before or after it leaves the stylomastoid foramen, the subsequent paralysis will involve the entire ipsilateral half of the face and have LMN symptoms
25
Q

Conjugate eye movements

A
  • Voluntary eye movements that are controlled by III, IV, and VI. There are 2 major types
  • Saccades: rapid movements that redirect gaze to place object on fovea
  • Smooth pursuit movements that track moving objects to place them on fovea
26
Q

Principles for saccades in horizontal plane

A
  • This process involves the eye muscles medial rectus (MR) and lateral rectus (LR)
  • Medial rectus muscle is required for adduction (CN III) and the lateral rectus is required for abduction (CN VI)
  • Normally eyes move in a conjugate fashion: for both to look right, the right eye must abduct (LR, VI) and the left eye must adduct (MR, III)
27
Q

Pathways for saccades in horizontal plane 1

A
  • The motor commands for UMNs sending info to CNs III and VI begin in the FEF (frontal eye fields) in the posterior part of the middle frontal gyrus
  • The axons do not run thru the CBT
  • They descend to the pons (pathway ill-defined), and then cross and end on the opposite side in the PPRF (paramedic pontine reticular formation), located near the VI nucleus
  • The PPRF is the “center for horizontal gaze”, and it sends axons to synapse on the VI nucleus on the ipsilateral side to activate the LR muscle of that side
  • The axons from the VI nucleus then go out to innervate the LR to abduct the eye
28
Q

Pathways for saccades in horizontal plane 2

A
  • Some axons from the VI cross back over to the contralateral side (ipsilateral to the origin from the FEF) and enter the medial longitudinal fasciculus (MLF) to reach III nucleus
  • This results in the activation of the MR in the other eye, causing it to adduct and thus both eyes achieve the same position
  • Therefore, activation of FEF on one side results in contractions of LR and abduction of the eye on the opposite side (by VI), and in contractions of the MR and adduction of the eye on the same side (by III). This results in horizontal deviation of both eyes to the opposite side
29
Q

Pathology of horizontal conjugate gaze

A
  • Any pathology that destroys the FEF of one side results in the inability to move both eyes to the opposite side due to lack of stimulation from the FEF
  • Unopposed activity from the intact FEF results in spontaneous deviation of eyes towards the side of the lesion
  • A unilateral brain stem lesion at the level of the pons that involves the PPRF and the VI nucleus results in an inability to move the eyes to the side of the lesion (opposite of the KO’d FEF pathway)
  • Lesion at branch of VI communicating to III nucleus (before it re-decussates) leads to ability to abduct ipsilateral eye (VI OK), but inability to adduct contralateral eye (communication to III nuc from VI is gone). Therefore only one eye will move (it abducts)
30
Q

Signs of UMN lesions

A
  • UMN lesions deprive the LMNs of the control normally exerted by the UMNs
  • There will be weakness and paralysis in the affected muscles (contralateral or ipsilateral depending on location of lesion)
  • Small lesions can affect many UMNs, b/c they are so close together, resulting in half the body paralyzed (hemiplegia), both lower limbs (paraplegia), or one limb (monoplegia)
  • Paralysis often affects the distal parts of the extremities, whereas the larger proximal limbs are spared or recover
  • There will be increased tone (hypertonia) of the affected limbs, leading to the state called spasticity (due to heightened sensitivity of DTRs from lack of cortical input)
  • Hyperreflexia: exagerated DTRs
  • Absence of profound muscular atrophy (except in disuse)
  • Absence of fasciculations
  • Abnormal babinski sign (toes go up)
31
Q

Signs of LMN lesion

A
  • LMN lesions lead to muscle paralysis limited to the muscles innervated my the lesioned nerves, almost always ipsilateral
  • LMN lesions may involve anterior horn cells, brain stem cranial nerve motor nuclei, ventral roots of spinal nerves, dorsal or ventral rami, peripheral or cranial nerves
  • Signs include paralysis (complete LOF) or paresis (reduced function)
  • Tends not to be widely distributed like hemiplegia, but is likely to affect one limb or parts of a limb
  • Flaccidity (hypotonia): paralyzed muscles have no resting state of partial contraction and thus a complete loss of tone
  • Loss of DTRs
  • Muscle atrophy: since the muscles depend on LMNs to survive the denervated muscle will degenerate and be replaced by connective tissue (irreversible)
  • Fasciculations: abnormal muscle twitches due to spontaneous activity of muscle
32
Q

UMN lesions vs LMN lesions

A
  • UMN lesions show: weakness or paralysis, no atrophy, no fasciculations, increased reflexes, and increased tone
  • LMN lesions show: weakness or paralysis, atrophy, fasciculations, decreased reflexes and decreased tone
33
Q

Locations of cranial nerve motor nuclei at various levels 1

A
  • From most superior to most inferior
  • In the upper midbrain (at the level of the superior colliculi and red nucleus), the nucleus for CN III is immediately posterior-medial to the red nuclei (anterior-medial border of the 4th vent)
  • In the lower midbrain (level of inferior colliculi and decussation of superior cerebellar peduncles), the nucleus for CN IV lies on the posterior-medial border of the decussation of superior cerebellar peduncles
34
Q

Locations of cranial nerve motor nuclei at various levels 2

A
  • In the upper pons (level of non-decussating superior cerebellar peduncles), the nucleus for CN V is directly posterior to the middle part of the ML
  • In the mid-lower pons (level of middle cerebellar peduncles), the nucleus for VI is on the anterior border of the 4th ventricle (near midline)
  • Also in the mid-lower pons, the nucleus for VII is immediately posterior to the ML on the ML’s most lateral part
35
Q

Locations of cranial nerve motor nuclei at various levels 3

A
  • In the upper medulla (level of nucleus/tractus solitarius and medullar olives), the nuclei for CNs IX and X (in the same area) are just medial to the ascending STT tracts
  • In the same level of the upper medulla, the nucleus for CN XII is the large bump of grey matter that is the most medial-anterior border of the 4th ventricle (medial to tractus/nucleus solitarius)
  • In the upper spinal cord (C2-C5), nucleus for CN XI is in the most anterior-lateral edge of the anterior horn
  • In general CN nuclei tend to be in the medial and posterior parts of the CNS (many lining the 4th ventricle)
36
Q

Exiting of CNs from the brainstem

A
  • CNs III, VI, and XII all leave the brainstem in regions to the corticospinal tract, and thus damage to the CST will cause loss of those CNs on the side of damage
  • CNs IX and X leave the medulla just medial to the STT, and thus ipsilateral tongue weakness and horseness would accompany loss of the STT
  • The CBT runs with the CST all throughout the internal capsule, midbrain, and pons
  • This means that lesions to CBT in these regions will also KO CN inputs from the CBT for all CNs at and below the level of damage (except for VI which does not run in the CBT)
37
Q

Lesions of the CST in upper midbrain (Weber’s syndrome) 1

A
  • In the upper midbrain if there are lesions to the PCA and top of the basilar artery, the blood supply to the CST/CBT will be lost
  • Since CN III exits the midbrain just medial to the CST/CBT (crus cerebri), CN III on the side of the lesion will also be lost
  • Results in contralateral hemiparesis/hemiparalysis of body muscles, with increased DTRs on contralateral side (loss of CST; UMN)
  • Loss of CBT to contralateral VII nucleus (but due to bilateral VII upper-nucleus innervation, only the mouth- lower-nucleus of VII- will be affected: contralaterally b/c VII has not yet decussated)
38
Q

Lesions of the CST in upper midbrain (Weber’s syndrome) 2

A
  • Ipsilateral loss of MR and other eye/eye muscle functions (III), like ptosis (loss of sympathetic innervation to superior tarsal from III or loss of SM to levator palpebrae also from III), loss of para/symp to sphincter pupilae muscles from III (dilated pupil), and loss of cilliary muscles
  • Loss of innervation to MR on the ipsilateral side means that the ipsilateral eye cannot adduct
  • There will not be loss of CN XII input from CBT b/c each XII nucleus is bilaterally innervated, even though the contralateral innervation predominates
  • Important to note that since VI does not run in the CBT abduction of the contralateral eye is intact
39
Q

Lesions in the medulla (medial medullary syndrome)

A
  • In the upper medulla, lesions of the paramedian branches of vertebral artery and the anterior spinal artery leads to infarction of the anterior-medial part of the medulla
  • This includes the medullary pyramids containing CST, the ML carrying info from contralateral side, CN XII as it exits the medulla near the CST
  • Clinically, KOing of the CST here results in contralateral hemiparesis/hemiparalysis (CST not yet decussated), with increased contralateral DTRs (UMN lesion)
  • Losing ML here results in loss of light touch, vibration, proprioception to contralateral side of body
  • Loss of CN XII (LMN) leads to ipsilateral tongue weakness; tongue will point toward the side of lost muscle innervation (which is ipsilateral to lesion)
40
Q

Lesions in the medulla (lateral medullary syndrome) 1

A
  • In the upper medulla, lesions of the paramedian branches of the vertebral artery and posterior inferior cerebellar artery (PICA) leads to infarction of the posterior-lateral part of the medulla
  • This includes the STT, nuclei and CNs of IX and X, descending hypothalamospinal tract (carrying sym/pre), and descending spinal tract of V
  • While this area also includes the TTT it does not ever seem to be affected (but spinal tract of V is)
  • This region also includes the nucleus tractus solitaries (NTS: carrying taste to CNS from VII), however unilateral loss of this does not result of loss of taste b/c the other nucleus/tractus will give bilateral innervation to the thalamus
  • Just next to the NTS is the descending hypothalamospinal tract, which will be destroyed, and thus prevents the CNS from communicating w/ the sym/pre cells on the ipsilateral side
41
Q

Lesions in the medulla (lateral medullary syndrome) 2

A
  • Clinical manifestations of lateral medullary syndrome include contralateral loss of pain/temp (STT)
  • Also ipsilateral loss of IX and X leading to difficulty swallowing and hoarseness
  • Horner’s syndrome (little ptosis) of droopy ipsilateral eye due to loss of the descending hypothalamospinal tract (carrying sym/pre that would eventually reach the superior tarsal thru III)
  • Horner’s syndrome is also characterized by miosis of eye (constriction) and facial anhydrosis, both due to lack of SNS innervation from the destroyed HTST
  • Ipsilateral loss of pain and temp to face due to loss of descending tract of V
42
Q

Lesions in the mid-lower pons 1

A
  • Lesions in the mid-lower pons that destroys the CST/CBT will also destroy the CN VI for the same side since it exits the pons directly through the CST/CBT
  • Unilateral lesions of CN VI (and/or PPRF) result in loss of ipsilateral eye abduction and contralateral eye adduction, since the CN VI also crosses back over thru MLF (medial longitudinal fasciculus) to innervate the contralateral CN III nucleus
  • Therefore, if someone has hemiparalysis/hemiparesis on contralateral side, weakness of tongue on contralateral side (tongue points away from lesion- UMN- due to loss from CBT), and eyes drifting away from lesion (due to loss of VI/III) they have a lesion of the CBT/CST/VI in mid-lower pons
43
Q

Lesions in the mid-lower pons vs lesions in FEF

A
  • How to distinguish loss of CN VI/PPRF (and thus III loss indirectly, LMN) from FEF loss (UMN): in FEF loss the eyes will drift toward the side of the lesion (contralateral loss of VI so no contralateral eye abduction, and ipsilateral loss of III so no ipsilateral eye adduction)
  • In CN VI/PPRF loss (and thus III loss) you get eyes drifting away from side of lesion, since you have loss of ipsilateral eye abduction and loss of contralateral eye adduction
44
Q

Decorticate posturing

A
  • Posture when lying down in which the arms are placed on chest, stiff, and legs are held out straight. Muscles are rigid
  • Occurs with higher lesions (corticate= cortex) above the red nucleus
  • Better prognosis
  • Causes: intracranial hemorrhage, brain tumor, stroke, head injury, increase intracranial pressure
45
Q

Decerebrate posturing

A
  • When lying down posture is arms down to the side, wrists flexed down, and those are pointed downward (plantar flexed). Muscles are also rigid
  • Occurs with lower lesions (cerebrate= cerebrum below cortex) at and below the red nucleus
  • Worse prognosis
  • Causes (same as decorticate): intracranial hemorrhage, brain tumor, stroke, head injury, increase intracranial pressure

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