Jacewicz - Control of Eye Flashcards
30-y/o woman with sudden onset of worst headache in her life. Double vision, stiff neck, and has vomited twice.
Which of the following is the most likely dx in this woman?
- Partial 3rd N paresis 2o to PCOM aneurysm
- NOTE: a nuclear lesion would show complete ptosis, and damage to all mm innervated by CN III
55-y/o woman presents to ED with one week of mild headache, double vision, and drooping eyelid on the right. She has a 20-yr hx of DM. Left and right pupils are 3mm, round, and react to both direct and consensual light.
What right eye muscle is likely to be functioning normally in this woman?
- Superior oblique
- Lateral rectus
- Tarsal muscle (Muller’s muscle)
- Pupil constrictor and dilator mm
55-y/o woman presents to ED with one week of mild headache, double vision, and drooping eyelid on the right. She has a 20-yr hx of DM. Left and right pupils are 3mm, round, and react to both direct and consensual light.
Where would you localize the lesion in this woman? What is the most likely dx?
- 3rd N on the right
- Partial 3rd N paresis due to diabetes
1. There is a dual supply to every N: peripheral and penetrating -> most infarction is in penetrating vessels with diabetes, but not a complete paresis due to second blood supply via peripheral vessel
48-y/o woman w/3-4-wk hx of droopy left eyelid. Has smoked 2 PPD since teens. Non-productive cough for 1 year, and has lost 10 pounds over last few months w/o dieting. Left eyelid partially covers left pupil. In dim light, right pupil is 7-8mm, round and reactive to direct and consensual light. In same dim light, left pupil is 3-4mm, round and reactive to consensual light. Both eyes fully abduct, adduct, elevate, and depress.
What eye muscle is NOT functioning normally in this woman’s eye mvmt/pupillary deficits? Most likely dx?
- Tarsal muscle/pupil dilator mm damaged
- No CN paresis
Identify the four LMN nuclei involved in eye mvmt and pupil control.
- Dorsal view of brainstem
- All 4 nuclei lie near midline, and are located dorsally, i.e., closer to 4th ventricle in the brainstem
- CN’s III and IV are in midbrain, just ventral to superior and inferior colliculi, respectively (aka, quadrigeminal plate)
- CN VI in caudal 1/2 of pons
Which nuclei innervate each of the eye muscles?
- Dorsal nuclei = inferior rectus
- Medial nuclei = superior rectus
- Central caudaul nuclei = levator palpebrae superioris
- Ventral nuclei = medial rectus
- Intermediate nucleus = inferior oblique
- NOTE: while Edinger-Westphal nucleus (PARA supply to constrictor mm of iris) is closely assoc w/CN III, it is considered a separate nucleus
Describe the laterality of the CN III nuclei. What does this mean clinically?
- BILATERAL INPUT: Edinger-Westphal and caudal nucleus
- IPSILATERAL: ventral, dorsal, intermediate
- CONTRALETERAL: medial nucleus (lateral rectus)
- CLINICAL SIGNIFICANCE: inconsequential bc CN III complex is small, and near midline, and only in rarest of conditions does it suffer lesion localized only to L or R half of the complex
1. Fascicles (axons from subnuclei) join together quickly and lateralize, so lateralized lesions of midbrain can produce unilateral eye mvmt and pupillary abnormalities, as do lesions of CN III as it leaves the brainstem - NOTE: CN VII sends its axons over top of CN VI, creating facial colliculus; raised bump in 4th floor of ventricle, immediately above CN VI
Which two cranial nerve nuclei controlling eye movement serve contralateral eye muscles?
Trochlear nucleus and the medial nucleus of CN III
Which nerves are these? Describe where they exit the brainstem.
- Ventral view of brainstem
- CN III: exits ventrally at junction of midbrain and pons
- CN IV: exits dorsally -> only CN that exits brainstem dorsally (just caudal to inferior colliculus)
1. Crosses over to innervate contralateral superior oblique - CN VI: exits at pontomedullary junction
How would a lesion of the oculomotor nucleus on one side affect upgaze?
- An oculomotor nucleus lesion on ONE side would disrupt upgaze in BOTH eyes
- Loss of the nucleus would remove source of fibers supplying superior rectus on the opposite side, and would also destroy crossed fibers from the opposite intact nucleus affecting the ipsilateral superior rectus
- Neither superior rectus muscle would receive nerve impulses to contract the muscles -> this is a primary characteristic of a dorsal midbrain stroke
- NOTE: axons from medial nucleus immediately cross over and join contralateral fascicle, so there is no error in figure regarding CN III fascicle within the brainstem
How is CN III related spatially to cranial vasculature? What does this mean clinically?
- CN III, IV, and VI proximal to cerebral blood vessels
- Of particular importance, is route of CN III as it passes b/t superior cerebellar artery and posterior cerebral artery, then alongside PCOM and underneath the internal carotid artery
1. Juxtaposition of CN III w/these intracranial aa subjects it to compression/injury from vascular outpouchings (aneurysms) that devo in aa branch points at base of the brain -> CN III passes near several of these - NOTE: see attached cross-section through midbrain
Identify the structures outlined in red here.
- Mickey Mouse face:
1. Ears = cerebral peduncles and substantia nigra
2. Eyes = red nuclei
3. Nose = PAG and cerebral aqueduct of Sylvius; EW nucleus just above this
4. Chin = superior colliculi
What is the cavernous sinus? What structures pass through it?
- Maze of venous sinusoids lateral to the pituitary and sphenoid sinus -> drains blood from the eyes and cortical veins to empty into jugular vein
- CN III, IV, VI, V1, V2 + ICA (carotid siphon = hairpin turn of ICA before entering subarachnoid space)
- SYM fibers traveling w/ICA on their way to dilator mm of pupil also travel through sinus
- NOTE: attached image is a coronal section through cavernous sinus at level of the pituitary
What is cavernous sinus syndrome? What might cause this?
- Hemorrhage from a ruptured ICA aneurysm, tumors, infections, and inflammatory diseases such as Tolosa-Hunt syndrome may cause cavernous sinus syndrome
- Lesions of cavernous sinus may produce symptoms and signs affecting all or just some of the structures passing through the sinus
1. CN III, IV, VI, V1, V2, ICA, SYM fibers to pupil dilator mm
What is the autonomic innervation of the eye?
- PARA: pupillary constrictors and ciliary mm
1. Ciliary muscle: produces changes in lens shape as eyes converge on target moving toward them; resulting pupillary constriction produces ACCOMODATION REFLEX - SYM: tarsal mm (elevation of eyelid not subject to voluntary control) + pupil dilator mm
How are the two oblique eye mm innervated, and what mvmts do they produce?
- SUPERIOR oblique: intorsion (and depression) of the eye
- INFERIOR oblique: extorsion (and elevation) of the eye
How should the patient’s eye be oriented to test the function only of the superior/inferior oblique? Superior/inferior rectus?
ADDUCTION
- Superior oblique: adducted -> ask pt to look down
- Inferior oblique: adducted -> ask pt to look up
ABDUCTION
- Superior rectus: abducted -> ask pt to look up
- Inferior rectus: abducted -> ask pt to look down
When examining the pt’s right eye, which mvmts will test which muscles?
When examining the pt’s left eye, which mvmts will test which muscles?
When examining both eyes, which mvmts will test which muscles?
Describe the pathway of SYM innervation of the pupil and tarsal muscle.
- 1o neurons originate in hypothalamus, travel through lateral brainstem, and synapse w/2o neurons in intermediolateral gray area of spinal cord, C8-T2
- 2o neurons send axons out ventral roots to para-vertebral SYM ganglia chain, and travel up to synapse in superior cervical ganglion
- 3o neurons in superior cervical ganglion send fibers along ICA in carotid sheath, and enter calvarium w/ICA
- Intracranially, SYM fibers join Nasociliary N to innervate superior TARSAL muscle, and Long/Short Ciliary NN to innervate DILATOR muscle of pupil
Describe the pathway/mech of the pupillary light reflex. What are the clinical consequences of this?
- Bright light flashed in front of L eye sends afferent signals via CN II through optic chiasm and tract to synapse in L and R pretectal nuclei in midbrain, under superior colliculi
- 2o neurons in pretectal nuclei send bilateral axons to EW nucleus (single, midline nucleus that project bilaterally to both pupils) -> light from either eye will stimulate EW nucleus neurons to send signals to both L and R pupillary constrictor mm
- PARA fibers travel from EW nucleus to pupil constrictors via CN III (and ciliary ganglia)
- CLINICALLY: light shown in 1 eye will produce constriction of BOTH eyes -> ipsilateral = direct, and contralateral = consensual
1. Testing both afferent and efferent pathways
How are the PARA fibers organized in CN III? How can this organization help you distinguish b/t the 2 neuro syndromes that can affect this N?
- Darker band lying along dorsal medial surface of the nerve = PARA fibers from EW nucleus
- ANEURYSMS (at aa branch pts, esp. PCOM): when they compress CN III, peripherally located PARA pupillary constrictors affected first -> unilateral pupil dilation may be clue of enlarging aneurysm
1. As it enlarges, entire CN III may be injured, producing unilateral paresis of extraocular mm innervated by this N -> neuro emergency bc rupture of cerebral aneurysm carries 30-40% incidence of death or permanent disability - OCCLUSION of SM ARTERIES: supplying center of CN III -> more common, and less dangerous devo of oculomotor paresis (occurs w/o enlargement of pupil)
1. Small vessel disease as a result of DM or other vasculopathy
2. Superficial placement of PARA fibers + super-ficial blood vessels (less prone to diabetic involvement/occlusion) protects PARA fibers from central ischemia of CN III - NOTE: about 1/20 cases of pupil-sparing oculomotor paresis caused by aneurysm, so these pts must have urgent vascular imaging w/CT angiography or MRI angiography (MRA) to exclude possibility of aneurysm
What is the accommodation reflex? Describe its pathway/mech.
- Accommodation reflex = convergence of eyes + PARA-mediated constriction of pupil and thickening of lens to allow for near vision
- Initiated by combo of cortical areas, incl. prefrontal eye fields and occipital-parietal fields -> cause pretectal activation that triggers PARA output via EW nucleus to produce pupil constriction and lens thickening in conjunction w/activation of CN III bilaterally to produce eye convergence
1. Contraction of ciliary m. causes suspensory ligaments attached to lens to relax, INC diameter to allow for near vision - Activation of CN III nuclei for this reflex independent of medial longitudinal fasciculus (MLF) pathway connecting contralateral abducens to CN III nuclei -> bilateral activation of CN III allows eyes to still converge in the face of a lesion of MLF
Describe the function, nerves, and neuron/muscles of the eye (table).
- Voluntary = green
- SYM = light blue
- PARA = yellow
How do the PPRF and MLF mediate horizontal mvmt of the eyes?
- Fibers from CN VI nucleus (to initiate abduction of ipsilateral eye) immediately cross midline and travel rostrally via MLF to synapse on ventral nucleus of CN III to cause adduction of contralateral eye
- Any failure of conjugate mvmt, called dysconjugate gaze, will misalign eyes & produce DIPLOPIA (double vision) since the 2 eyes will present visual cortex with slightly or markedly displaced images
- Phasic firing of conjugate link b/t abducens and contralateral ventral nucleus of CN III regulated by paramedian pontine reticular formation (PPRF), aka horizontal gaze center and parabducens nucleus
1. Activation of left PPRF triggers left abducens nucleus to simultaneously activate contraction of L lateral rectus and R oculomotor nucleus to activate R medial rectus m. - NOTE: frontal eye field in Brodmann’s area 8 (not the area suggested in the attached image)
Where is the lesion (left = leftward gaze; right = rightward gaze)?
- Right abducens nerve (CN IV palsy)
- Lesion 1 in the attached image
Where is the frontal eye field?
- Brodmann’s area 8 (see attached image)
Where is the lesion (left = leftward gaze; right = rightward gaze)?
- Right abducens nucleus or right PPRF = right lateral gaze palsy (right PPRF should trigger the right abducens, but damaged here)
1. Often clinically indistinguishable, and both may be affected - Lesion 2 or 3 in attached image
Where is the lesion (left = leftward gaze; right = rightward gaze)?
- Left MLF (left INO = internuclear ophthalmoplegia)
- Lesion 4 in attached image
- Test convergence in this pt, and it will be fine; this can help you rule out CN III damage (remember that convergence innervation via pretectal/EW nuclei is bilateral)
1. If this is an older person with DM or HTN, this could be due to a unilateral infarction
2. Nystagmus is going to be the earliest sign
3. These lesions typically are reversible
Where is the lesion (left = leftward gaze; right = rightward gaze)?
- Left MLF and left abducens nucleus = 11/2 syndrome
- Lesion 5 on attached image
Describe the mechanism/pathway of the vestibulo-ocular reflex (VOR).
- Rotation of head to R in horizontal plane stimulates R horizontal semicircular canal, prompting vestibular apparatus to signal R medial vestibular nucleus via R vestibular N
- R vestibular nucleus activates contralateral PPRF, which activates L abducens nucleus and R ventral nucleus of CN III to move eyes left
- Consequence of turning head suddenly to R is a compensatory reflex movement of eyes to L so person can maintain visual fixation on an object of interest
What is the clinical use of the VOR? Name and describe func and non-func response.
- In comatose pts, can use this reflex to test the structural integrity of the midbrain to the pons
- If integrity is preserved, eyes will move conjugately in opposite direction of rotation when head is quickly turned R or L
- Called OCULOCEPHALIC MANEUVER (aka, Doll’s eyes maneuver)
- Absence of eye movement indicates the nuclei and tracts mediating the VOR are not functioning, either due to a severe metabolic derangement or due to a structural lesion such as infarction or hemorrhage
- NOTE: this is the third type of slow conjugate mvmt
Describe the mech/pathway of saccadic eye mvmt. Provide some examples.
- Can be voluntarily triggered or reflexive
- Saccadic pathway from frontal eye field (FEF) contralateral to gaze travels w/ipsilateral corticobulbar fibers through internal capsule to ipsilateral superior colliculus and on to the CONTRALATERAL PPRF
- Right FEF activates left PPRF, which activates L abducens nucleus and R ventral nucleus of CN III, causing eyes to conjugately look L
- EXAMPLES: voluntary - hold head still and look with only eyes from one corner of room to the other; reflexive - bug crawling in corner causes you to reflexively look at it (collicular vision)
What part of the brain is in control of the slow pursuit eye mvmts? Provide an example.
- Under control of POT area; in contrast to the FEF, the POT directs eye mvmt in the ipsilateral direction
- Contralateral cerebellum and vestibular nuclei participate in this control mechanism
- EXAMPLE: hold finger in front of face, and move hand from right to left, keeping eyes fixed on finger
1. As eyes track finger to L, L POT controls mvmt
Describe the use of the optokinetic strip.
- Used to test the integrity of the saccadic and smooth pursuit eye mvmts
1. Cloth w/alternating vertical stripes held in front of pt’s eyes and moved from R to L, then L to R
2. Pt asked to fix on stripes, and as strip moves, eyes will transiently pursue 1 stripe, then snap back to midline to pick-up next stripe - Initial slow pursuit mvmt controlled by ipsilateral POT area, and quick snap back (saccade) controlled by ipsilateral FEF (contralateral PPRF) -> lesions in either of these areas will impair one or other component of OKN test
1. As striped bars are moving in visual field from right to left, L POT tracks w/slow pursuit and L FEF causes eyes to saccade back toward the right for the next stripe (OKN nystagmus shows fast component (saccadic) beating to the R)
Describe the lesions responsible for A and B.
- A: eyes away from paresis (frontal cortex lesion) -> lesion of L frontal lobe produces R hemiparesis and loss of input to R PPRF, allowing combo of R FEF and L PPRF to drive eyes to L, i.e., away from paresis
- B: eyes toward paresis (pontine lesion) -> lesion of L pons produces R hemiparesis and LOF of L PPRF, allowing R PPRF to drive eyes to R, i.e., towards the paresis
