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Flashcards in Jacewicz - Control of Eye Deck (40)
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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 



Contraction of which two eye muscles moves the eye globe in such a way that there is no intorsion or extorsion?

- Medial rectus (CN III; ventral nucleus)

- Lateral rectus (CN VI)


How should the patient's eye be oriented to test the function only of the superior/inferior oblique? Superior/inferior rectus?


- Superior oblique: adducted -> ask pt to look down

- Inferior oblique: adducted -> ask pt to look up


- 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?


How do partial and complete lesions of CN III vary in their clinical presentation?

- PARTIAL lesion = paresis (weakened or incomplete mvmt) of CN III muscles, and eyelid only partially closed 

- COMPLETE lesion = complete paralysis of all CN III muscles, incl levator palpebrae superioris, w/resultant eye closure


Describe the pathway of SYM innervation of the pupil and tarsal muscle.

- 1o neurons originate in hypothalamus, travel through lateral brainstem, and synapse w/2neurons 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 

- 2neurons 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)