18 - Motor Pathways II Flashcards
1
Q
Brainstem Pathway LMN are…
A
- Cranial Nerve Nuclei
- Ipsilateral to exit from CNS
- So, LMN signs are ipsilateral to damage
2
Q
Corticobulbar UMNs controls which nuclei, and which does it not?
A
- Only fucks with SVE, GSE;
- Controls all SVE + 12
- Does not control any GSE except for 12
- Controls:
- Trigeminal motor nucleus (jaw)
- Facial nucleus (facial expression)
- Nucleus ambiguus (larynx, pharynx, and palate)
- Hypoglossal nucleus
- Accessory nucleus
- DOES NOT CONTROL EYES
- Oculomotor nucleus
- Trochlear nucleus
- Abducens nucleus
3
Q
CN Nuclei with unilateral corticobulbar inputs
A
- Facial nucleus (7)
- Neurons that innervate the lower quadrant of the face only receive unilateral, contralateral input
- Hypoglossal nucleus (12)
- Neurons that innervate tongue only receive unilateral, contralateral input
4
Q
Unilateral corticobulbar lesion effect
A
- Generally do not produce clinical symptoms because most CN nuclei are bilaterally supplied by CBS
- WIll show CN 7 (opposite lower quadrant of face) and CN 12 (opposite half of tongue) paresis
5
Q
Eye movement control UMNs
A
- NOT FROM M1
- Corticopontine fibers from fronal eye field and parietal eye field
- Activate CPGs controlled by superior colliculus
6
Q
Corticobulbar fibers exit where for which cranial nerves?
A
- PONS: 5, 7
- MEDULLA: 9, 10, 12
- FORAMEN MAGNUM (to SC): 11
7
Q
GSE CN Nuclei innervation
A
Paramedian branches
8
Q
CN 12 Function, Innervation, Location, Lesion
A
- GSE nucleus in medulla
- Innervated by ASA paramedians
- Nerve comes out in pre-olivary sulcus
- Functions:
- Extrinsic tongue muscles:
- Geniglossus: protrusion
- Styloglossus: retraction
- Hypoglossus: depression
- Intrinsic tongue muscles control shape
- Extrinsic tongue muscles:
- Lesions:
- Nucleus or nerve = tongue points to side of lesion due to intact genioglossus
- Supranuclear = tongue points to opposite side of lesion
- BE CAREFUL: you can’t tell just from the tongue which side/level is lesioned!
9
Q
Abducens Nucleus Function
A
- Innervates lateral rectus, muscle that abducts the eye on each side
10
Q
Trochlear Nerve Function
A
- Innervates superior oblique of eye CONTRALATERAL to nucleus
- L nerve from R nucleus makes L eye tilt inward and downward
11
Q
Oculomotor Nerve Function
A
- Innervates every other movement besides abduction and inward/downward tilt
12
Q
Eye Muscles, CNs, Directions
A
- To look straight up: superior rectus (to move the eye up), and inferior oblique to counteract torsion
- To look straight down, inferior rectus moves the eye down, superior oblique counteracts torsion
- If eye is abducted (AWAY from nose), you’re fully in line with the rectus, so you don’t use the obliques to counteract anything
- You may also use superior or inferior rectus to look up or down, but still no obliques because there’s no torsional movement introduced
- If eye is looking to midline (converging), you do not use rectus at all; just superior oblique and inferior oblique to control
- You only use the superior oblique when you’re looking down at near objects (trochlear nerve!)
13
Q
Conjugate Gaze vs Intorsion/Extorsion
A
- Elevation of gaze: eyes look upward
- Depression of gaze: eyes look downward
- Horizonal conjugate gaze: both eyes look L or R
- One eye adducts (CN 3), one eye abducts (CN 6)
- Extortion: R eye movement when head tilts L
- Intortion: R eye movement when head tilts R
14
Q
CN VI Palsy
A
- Lesion to actual nerve of CN 6
- Palsy of ipsilateral lateral rectus muscle
- Eye on affected side drifts medially during forward gaze
- Eye on affected side fails to abduct past midline on horiztonal conjugate gaze to the affected side
15
Q
Trochlear Nerve Muscle
A
- Superior oblique
- Critical for binocular vision
- When eye is abducted, SO depresses the eye
- When eye is adducted, SO intorts the eye
16
Q
CN IV Palsy
A
- CN IV nerve lesion results in paralysis of ipsilateral superior oblique muscle
- Pt has diplopia = double vision that’s worse when looking down and medially
- Loss of SO intorsion (so eye extorts)
- Pts typicalkly tilt head forward and to non-lesioned side to comensate
- Lesion to nucleus = contralateral signs (but extremely rare)
- Lesion to nerve = ipsilateral signs
17
Q
Oculomotor Nerve Function, Location
A
- Functions
- Eye movement (GSE)
- Pupil constriction (GSE)
- Eyelid (this is GVE - levator palpebrae superioris, Edinger-Westphal))
- Nuclear complex is in basilar territory in midbrain (posterior to MLF); but nerve goes out laterally (PCh.A) before returning to midline (basilar)
- Peripheral course of nerve runs parallel with PCOM, so is vulnerable to PCOM aneurysms
18
Q
Third Nerve Palsy
A
- CN 3; AKA Down and Out syndrome
- Abducted eye (loss of medial rectus)
- Depressed eye (loss of superior rectus and inferior oblique)
- Complete ptosis (loss of levator palpebrae superioris)
- Ipsilateral mydriasis (dilated pupil) - loss of constrictor pupillae
- Loss of direct, consensual pupillary light reflexes in the ipsilateral eye
19
Q
Internuclear Ophthalmoplegia
A
- Lesion to MLF on one side
- Eye ipsilateral to lesion cannot adduct when looking opposite of lesion
- Contralateral eye shows nystagmus since vestibular signals require MLF
- Oscillatory nystagmus directed at midline for as long as the eye continues to
- Ex: R-sided MLF lesion, asked to look to L.
- R eye cannot adduct, L eye can abduct
- L eye shows nystagmus as long as looking to left
20
Q
Parinaud’s Syndrome
A
- Issue with vertical conjugate gaze (main center is in rostral midbrain)
- Lesions that affect rostral dorsal midbrain lead to paralysis of upward vertical gaze; eyes point downwards
21
Q
Burst Neurons
A
- Goal of burst neurons is to get III, IV, VI to move
- Paramedian Pontine Reticular Formation (PPRF)
- Horizontal saccades
- Near MLF in pons
- Burst neurons for VI nuclei
- Rostral interstitial nucleus of MLF (riMLF)
- Vertical saccades
- Within MLF in upper midbrain
- Burst neurons for III, IV nuclei
22
Q
Neuron Integrators
A
- Activated by burst neuron collaterals to keep eye in eccentric gaze
- Generate step signals
- Nucleus Prepositus Hypoglossi (ppH)
- Horizontal saccades
- Located near MLF in medulla
- Interstitial nucleus of Cajal
- Vertical saccades
- Small nucleus within MLF
23
Q
Frontal vs Parietal Eye Field Inputs
A
- FEF
- Contralateral voluntary saccadic eye movements
- Contralateral smooth pursuit
- Bilateral vergence eye movements
- PEF
- Visual-evoked saccades (Reflexive)
- Smooth pursuit
24
Q
Omnipause Neurons
A
- Clusters of pontine reticular neurons
- Fire continuously (except just prior to and durring saccades)
- Pattern generators for saccadic eye movements
- When eyes are at resting state, omnipause neurons inhibit burst neurons
- PPRF = horizontal
- riMLF = vertical
25
Horizontal Saccade Components
* Burst neuron = Paramedian pontine reticular formation (PPRF)
* Located near MLF in pons
* Neural inegrator = Nucleus prepositus hypolgossi (ppH)
* Located near MLF in medulla
26
Vertical Saccade Components
* Burst neurons = Rostral interstitial nucleus of MLF (riMLF)
* Located in MLF
* Neural integrator = Interstitital nucleus of Cajal
* Located in MLF
27
CN susceptible to PCOM aneurysms
CN 3
28
Horizontal Conjugate Gaze Deficits
VI Nucleus Damage
29
Near Response Cells
* Provide input to CN 3 for vergence
* Drive the **near triad (synkinesis)** sequence by activating GVE Edinger-Westphal nucleus
* Eye convergence (CN 3)
* Lens accomodation (EW)
* Miosis/pupillary constriction (EW)
* Allows for convergence in the setting of MLF damage
30
Synkinesis
* AKA Near triad
* Eye convergence (CN 3)
* Lens accomodation (EW)
* Miosis/pupillary constriction (EW)
* Initiated by near response cells
* Allow for vergence in the absence of MLF
31
CN XI Palsy
* Accessory nucleus = sternocleidomastoid & trap
* Loss of trapezius action
* Winging of the scapula
* Loss of shoulder profile
* Difficulty raising the arm above shoulder level
* Loss of SCM action:
* Pt's head will be permanently turned to the damaged side (Torticollis: "wry-neck")
32
Torticollis
* Symptom of CN XI palsy
* Pt's head permanently turned to damaged side
33
Pre & Post-olivary sulcus CN exits
Pre-olivary sulcus
* CN 12 leaves
Post-olivary sulcus
* CNs 9, 10, 11 leave
34
Gag Test
* Involves only cranial nerves 9 and 10, but uses the spinal nucleus of 5 as an intermediate neuron
* SN5 sends neuron 2 axons containing 9, 10 sensory info to nuclei ambiguus via the VTT
* Promotes gag
35
Facial Nucleus Location, Innervation, Lesion
* Located in pons
* Innervated by AICA
* Axons:
* run dorsally AROUND abducens nucleus (creating a **facial colliculus**)
* Are innervated by basilar paramedians
* Lesions:
* UMN lesion = contralateral lower quadrant palsy (because lower quad of face has unilateral input only)
* Nucleus/nerve = ipsilateral facial hemiplegia (Weakness) & noise sensitivity
36
Eight and a Half Syndrome
* Lesion at the facial colliculus, floor of the 4th ventricle
* 3 structures affected because they're closely associated:
* Abducens nucleus = conjugate gaze
* MLF = internuclear ophthalmoplegia (INO)
* Facial nerve axons = facial muscles
* So, for a right-sided facial colliculus area lesion, pt suffers:
* R Horizontal conjugate gaze palsy (6 nucleus) = 1
* L-sided INO = 1/2
* R Facial nerve 7 palsy (hemiparesis) = 7
* Sums to 8 1/2
37
Corneal Blink Reflex
* THE pontine reflex
* Involves facial nucleus (motor supply to orbicularis oculi) and the rostral spinal trigeminal nucleus (afferent V1)
* Nociception from the cornea is carried by A∂ and C fibers in the long ciliary branches of V1 (ophthalmic) and relayed by trigeminal ganglion neurons
* Spinal nucleus bilaterally signal the facial nucleus
* Facial nucleus (efferent CN 7) causes both eyes to blink
* Reflex is fast (mostly influenced by A∂ fibers)
* Is consensual in that both eyes blink from unilateral stimulation of the cornea
38
Pseudobulbar Palsy
* Bilateral damage to corticobulbar fibers to CN motor nuclei
* Symptoms (UMN weakness):
* Dysarthria: speech problems
* Dysphagia: swallowing problems
* Inappropriate outburst of laughter, crying because emotional inputs to CN motor nuclei from limbic system are intact
* Causes
* Vascular event (bilateral internal capsule infarcts are most common)
* Demyelinating disorders (like multiple sclerosis)
* Amyotrophic lateral sclerosis (ALS)
* High brainstem tumors
* Trauma
39
Locked-In Syndrome
* Damage to basal pons = bilateral cortcibulbar AND corticospinal damage
* Results in complete paralysis of all voluntary muscles = interfering with facial expression, speech, movementSparing of CN III may allow some vertical eye movement and eyelid movement
* But not horizontal eye movement (bc CN 6 is in pons)
* Pt is awake, aware of surroundings because somatosensory pathways and brainstem reticular formation are usually spared
* Causes
* Basilar artery infarct
* Brainstem hemorrhage involving basilar artery
* ALS may also cause this
