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100 Cards in this Set

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  • Back
What are the nuclear and infranuclear pathways of the eye?
Involve brainstem nuclei of CN III, IV, VI, peripheral nervise arising from these nuceli, eye movement muscles
What are the supranuclear pathways of the eye?
Brainstem and forebrain circuits that control eye movement through connections with the nuclei of CN III, IV, VI
What do the internal ocular muscles do?
Control pupillary size and lens accommodation
Name the 6 extraoccular muscles and the CNs that innervate them
Lateral rectus (CN VI)
Medial rectus (CN III)
Superior rectus (CN III)
Inferior rectus (CN III)
Superior oblique (CN IV)
Inferior oblique (CN III)
Describe the pathway of the superior and inferior oblique muscles and what action they have on the eye
Superior oblique originates on the sphenoid bone in the posterior medial orbit and passes anteriorly through the trochlea (pulleylike fibrous loop on the medial superior orbital rim). Superior oblique then inserts on the superior surface of the eye to produce INTORSION: movement of upper pole of eye inward.
Inferior oblique originates on anterior medial orbital wall and inserts on the inferior surface of the eye to produce EXTORTION: movement of uppper pole of eye outward.
What movement is caused by the lateral rectus muscles?
Abduction (movement toward the temple)
What movement is caused by the medial rectus muscles?
Adduction (movement toward the nose)
What movement is caused by the superior rectus muscle?
Elevation when abducted, intorsion when adducted
What movement is caused by the inferior rectus muscle?
Depression when abducted, extorsion when adducted
What movement is caused by the superior oblique muscle?
Depression when adducted, intorsion when abducted
What movement does the inferior oblique muscle do?
Elevation when adducted, extortion when abducted
Which 2 muscles does the superior division of CNIII innervate?
superior rectus, levator palpebrae superioris (eyelid elevation)
Which 3 muscles does the inferior division of CNIII innervate?
medial rectus, inferior rectus, inferior oblique
Which cranial nerve controls pupil constriction and ciliary muscles of the lens (for near vision)?
Which nerves constitute the somatic motor column of hte cranial nerve nuclei?
Oculomotor, Trochlear, Abducens, Hypoglossal
Where is CNIII located in the brainstem and where does it exit?
Located in upper midbrain at the level of superior colliculi and red nucleus. CNIII exits the brainstem in the interpeduncular fossa between the posterior cerebral artery and superior cerebellar artery
What aspect of oculomotor function is likely affected by compression from aneurysm of the posterior communicating artery?
Pupil constriction, b/c parasympathetic fibers of CNIII travel in the subarachnoid space near the PCOA.
Trace the path of the oculomotor nerve after it leaves the brainstem
It travels in the subarachnoid space to enter the cavernous sinus and then enters the orbit via the superior orbital fissure.
Can a unilateral lesion of the oculomotor nucleus result in unilateral weakness of the levator palpebrae superior or unilateral pupillary dilation?
No. The oculomotor nucleus innervates these muscles bilaterally.
Indicate whether the oculomotor nuclei innervate these muscles ipsilaterally, contralaterally or bilaterally:
inferior rectus, inferior oblique, medial rectus, pupillary constrictors/lens ciliary muscles, levator palpebrae superior, superior rectus
ipsilateral, ipsilateral, ipsilateral, bilateral, bilateral, contralateral
Where is the trochlear nuclei located in the brainstem and where does it exit?
Located in the lower midbrain at the level of inferior colliculi and decussation of the superior cerebellar peduncle Exits DORSALLY, and the trochlear nerves exit in a completely crossed manner.
Trace the path of the trochlear nerve after it leaves the brainstem
CN IV travels caudally before crossing to the opposite side of the brainstem and exiting at the anterior medullary velum. They travel through the subarachnoid space along the underside of tentorium cerebelli and enter cavernous sinus to reach the orbit via the superior orbital fissure.
Which cranial nerve is particularly vulnerable to shearing injury after a TBI, and what symptom results from injury to this nerve
Trochlear nerve (CN IV) is sensitive b/c it is very thin and it runs along subarachnoid space under the tentorium cerebelli. Trochlear is also sensitive to compression from cerebellar tumors. Symptom is impaired superior oblique muscle (decreased depression when adducted, decreased intorsion when abducted)
Where does the abducens nerve originate in the brainstem, and where does it exit?
Abducens nuclei lies on the floor of the fourth ventricle under the facial colliculi in the mid-to-lower pons. Exits brainstem ventrally at the pontomedullary junction.
Trace the path of the abducens nerve after it leaves the brainstem
Follows a long course through subarachnoid space as it ascends between the pons and clivus. It exits the dura to enter Dorello's canal, running between the dura and the skull. It bends around the petrous tip of the temporal bone to reach the cavernous sinus. It traverses teh cavernous sinus and enters the orbit via the superior orbital fissure.
What cranial nerve is particularly vulnerable to downward traction the is produced by elevated intracranial pressure? What symptom would be noted
Abducens nerve b/c of its long pathway between the dura and skull that bends over the temporal bone. Injury to this nerve results in decreased abduction.
What is the clinical presentation of oculomotor nerve palsey?
"down and out"- eye is abducted and depressed. also may have dilated, non-responsive pupils and ptosis (inability to open eyelid)
What do the terms exotropia, esotropia and hypertropia refer to?
Exotropia = lateral deviation of eye
esotropia = medial deviation of eye
hypertropia = vertical deviation of eye...refers to higher eye
What visual deficit occurs with dyscongugate gaze?
Diplopia (double vision) mild form can just appear blurry. **Image farther toward the direction of the gaze is the one seen by the abnormal eye**
Name 3 causes of 3rd nerve palsey
Head trauma, diabetic neuropathy, intracranial aneurysm at the junction between the posterior communicating artery and the internal carotid artery.
What symptoms are associated with transtentorial uncal herniation (herniation of medial temporal lobe over the edge of the tentorium cerebelli)?
ipsilateral occulomotor palsey, loss of consciousness, hemiplegia
What clinical diagnosis should be considered when a patient presents with painful oculomotor palsy that involves the pupil (oculomotor palsey may be subtle or complete)?
Intracranial aneurysm, likely of the posterior communicating artery.
What clinical diagnosis should be considered with complete oculomotor palsy that spares the pupil?
Diabetes. Partial oculomotor palsy that spares the pupil could be aneurysm
What is the clinical presentation associated with trochlear nerve palsy?
Vertical diplopia (abnormal eye deviates upward because depression of superior oblique is impaired) or hypertropia. Can also have extortion of affected eye due to limits of intorsion of superior oblique, but this is not usally evident when looking at a patient.
How do patients compensate for visual deficits associated with 4th nerve palsy?
Looking up (chin tuck) and turning head away from affected eye can compensate for hypertropia and extorsion
What are the 4 clinical signs that indicate 4th nerve palsy?
1. Hypertropia in affected eye
2. Vertical diplopia worsens when affected eye looks nasally (medially, adducts)
3. Vertical diplopia improves with head tilt away from affected eye
4. Vertical diplopia worsens with downgaze.
What is the most commonly injured cranial nerve in head trauma?
Trochlear nerve b/c it is thin and has long course.
Name three causes of head tilt
Trochlear nerve palsey, cerebellar leasion, meningitis
What is the visual deficit noted with abducens nerve palsy?
Horizontal diplopia
What clinical symptom is evident with 6th nerve palsy? How does it differ from 3rd nerve palsy?
6th nerve palsy results in horizontal diplopia. Double vision is worse when viewing far objects, whereas for 3rd nerve palsy double vision is worse for near objects.
How do you identify diplopia associated with 6th nerve palsy?
The affected eye does not abduct appropriately, and double vision worsens when pt. tries to abduct affected eye. Subtle 6th nerve palsy can be identified by testing bilateral saccades and observing a slight lag in the abduction of affected eye or with cover-uncover test while the affected eye looks laterally.
What disorders should be considered with 6th nerve palsy?
Abducens nerve is susceptible to injury from downward traction from elevated intracranial pressure. It is an early sign of supratentorial or infratentorial tumors, pseudotumor cerebri, hydrocephalus.
Does increased intracranial pressure result in bilateral or unilateral damage to the abducens nerve?
Unilateral or bilateral
Discuss how pontine infarcts and lesions of the abducens nucleus in the pons affect eye movement.
Infarcts in the pontine can cause weakness of the ipsilateral eye abduction. Lesions of the abducens nucleus in the pons can lead to horizontal gaze palsy: abduction of both eyes is weakened. Because the abducens nucleus is close to the facial colliculus, ipsilateral facial weakness is also observed.
Define fascicle, colliculus, nucleus
Fascicle: bundle of nerve fibers.
Nucleus: cell body, CNS structure composed mainly of gray matter that mediates electrical signally for a particular subsystem.
Colliculus: small elevation above the surrounding area
Damage to the Edinger-Westphal nuclei would result in deficits to what clinical function?
pupillary constriction to light
What function is related to the following structures: retinal ganglion cells, optic tracts, extrageniculate pathway, brachium of the superior colliculus, pretectal area, Edinger-Westphal nucleus, posterior commissure, oculomotor nerve, ciliary ganglia, pupillary constrictor muscles
pupillary constriction to light
What structure is involved with the accommodation response that is not involved with pupillary constriction?
Visual cortex
What is the accommodation response?
The response of the eyes when an object moves from far to near. Involves: pupillary constriction, accommodation of the lens ciliary muscle, convergence of eyes
Pupillary constriction to light is innervated by the parasympathetic or sympathetic pathways?
Parasympathetic pathways
Pupillary dilation is directed by parasympatheic or sympathetic pathways?
Sympathetic pathways
What function is governed by the following sympathetic pathway: descending from the hypothalamus along the lateral brainstem and cervical spinal cord to thorasic cord levels T1 and T2 where it activates preganglionic sympathetic neurons in the intermediolateral cell column of thorasic cord and exits via ventral roots T1 and T2. Join paravertebral sympathetic chain and ascend to superior cervical ganglion. Postganglionic sympatheic fibers ascend through carotid plexus along walls of internal carotid artery to what muscle?
Dilating pupils. Pupillary dilatory muscle
What four functions are governed by the sympathetic pathway for the eyes?
Pupilary dilation, elevating eye lid, preventing eye from sinking into the orbit, sweat glands of face and neck
Horner's syndrome consists of ptosis, miosis and anhidrosis. Define these terms
Ptosis: upper eyelid drooping from loss of innervation to Muller's smooth muscle in the upper lid. Miosis: decreased pupillary size from loss of sympathetic innervation of pupillary dilator muscle. Anhidrosis: decreased sweating in the ipsilateral face
What is anisocoria and how does it differ when it is caused by CNIII lesion vs Horner's syndrome?
Anisocoria is pupillary asymmetry. When it is due to a CNIII lesion can have one blown pupil and is more evident in the light vs. dark. When it is due to Horner's syndrome it is more evident in the dark and the pupil may have direct and consensual constricting response to light, but has a dilation lag relative to the normal pupil when light is removed. Can also test anisocoria by testing the ciliospinal reflex where pinch the neck causing sympathetic outflow that causes the normal eye to dilate but not the affected eye.
What causes Horner's syndrome?
Lesions anywhere along the sympathetic pathway: lateral brainstem infarct/hemorrhage, spinal cord damage, long tumor or trauma affecting T1,T2 roots, tumor/trauma affecting sympathetic chain, carotid dissection affecting carotid plexus, damage to cavernous sinus, damage to orbit of eye
What are pontine pupils?
Caused by large bilateral lesions to the pons both pupils are small and reactive to light.
What is the afferent pupillary defect (aka Marcus Gunn Pupil)?
Direct response to light in the affected eye is decreased but the consensual response of the affected eye to light shown to the normal eye is intact. Caused by decreased sensitivity to light in the affected eye.
What causes Marcus Gunn Pupil?
Aka. afferent pupillary defect. The affected eye has decreased response to light but normal consensual reaction to light. Caused by lesions to optic nerve before optic chiasm, retina or eye.
How do you test for Marcus Gunn Pupil?
Swinging flashlight test. Swing light every 2-3 seconds and note that when light is moved from the normal to affected eye the affected eye dilates.
What drugs can mimic pontine pupils (pinpoint) or dilated pupils?
Opiates, barbiturate overdose make pupils constrict. Anticholinergics make pupils dilate.
What do the levator palpebrae superior, Muller's smooth muscle and frontalis muscle of the forehead do and what nerves innervate them?
They cause eye opening. Levator palpebrae superior is innervated by CNIII, Muller's smooth muscle is sympathetic. Frontalis muscle is CNII
What does the orbicularis oculi muscle do?
Eye closure CNVII
What are causes of ptosis?
Unilateral or bilateral ptosis caused by: Horner's syndrome, CNIII palsy, myasthenia gravis. Bilateral ptosis (eye lid closing without LOC) caused by nondominent parietal lobe lesions, dorsal lesions of oculomotor nuclei affecting central caudal nucleus (which controls levator palpebrae superior muscle)
Where is the cavernous sinus located?
It is a collection of venous sinusoids located on either side of the pituitary. Receives venous blood from the eye and superficial cortex and drains to internal jugular vein.
What nerves traverse the carotid sinus?
CNIII, CNIV, CNVI, CNV1. Carotid siphon (part of internal carotid artery) also runs through it and CNVI is closest to artery. CNV2 may also be there. Sympathetic fibers running in the carotid plexus en route to pupillary dilator muscle also traverse cavernous sinus.CNII lies above the cavernous sinus and enters orbital apex via the optic canal.
What is the pathway of CNIII, CNIV, CNVI, CNV1 after cavernous sinus?
They enter ortibal apex through the superior orbital fissure.
What is the orbital apex?
Region where all nerves, arteries and veins of the orbit converge before entering the intracranial cavity via the optic canal and superior orbital fissure.
What clinical syndromes occur with lesions of the cavernous sinus?
Complete lesion results in ophthalmoplegia from disruption of CNIII, IV, VI. Canalso have sensory loss from CNV1 and facial sensory loss from CNV2.
What clinical syndroms occur with lesions of optic apex?
Ophthalmoplegia as seen with cavernous sinus lesions but also vision loss from CNII involvement. Also can have proptosis (bulging of eye) from mass effect in orbit.
What are causes of cavernous sinus syndromes?
metastatic tumors, extension of nasopharyngeal tumors, meningioma, pituitary tumors, aneurysms of intracavernous carotid (usually affects CNVI first), infection of cavernous sinus.
What are the causes of orbital apex syndroms?
metastaic tumors, infection
What does supranuclear control of eye movements refer to?
Refesr to pathways from brainstem and cerebellum to forebrain to output nuclei of CNIII,IV,VI.
What are the 3 types of eye movement affected by supranuclear system?
horizontal eye movement, vertical eye movement, vergence eye movements
What are saccades?
Rapid eye movements that function to bring targets of interest into field of view. Vision is temporarily supressed during saccades. Only type of eye movement that can easily be done voluntarily, but can also be generated by reflexes. Saccades have velocity up to 700 degrees/sec.
What are smooth pursuit eye movements?
Not under voluntary control and allow stable viewing of moving objects. Velocity 100 degrees/sec.
What are vergence eye movements?
Eye movements that allow fused fixation of both eyes as targets move toward or away from viewer. Velocity 20degrees/sec
What are reflex eye movements?
Reflexes include optokinetic nystagmus and vestibulo-ocular reflex.
What is nystagmus?
Nystagmus is a rhythmic form of relfex eye movements composed of slow eye movements in one direction interrupted repeatedly by fast saccade-like eye movements in the opposite direction.
What is the medial longitudinal fasciculus and where is it located?
MLF is the pathway in the brainstem that links nuclei involved in eye movements to each other and the vestibular nuclei. It runs near midline on both sides of the brainstem under the oculomotor and trochlear nuclei in the midbrain and under the floor of 4th ventricle in the pons. Fibers from medial and superior vestibular nucleus ascend in the MLF to the oculomotor, trochlear and abducens nuclei. This pathway mediates the vestibulo-ocular reflex.
What is the vestibulo-ocular reflex?
Eye movements are adjusted for changes in head positioning.
What muscles govern horizontal eye movements?
Lateral rectus (CNVI) and medial rectus (CNIII).
What system allows eye movements to be yoked together allowing conjugate gaze in all directions?
MLF Medial longitudinal fasciculus. For example, with horizontal movements CNIII and CNVI are yoked.
Where is the horizontal gaze center?
Abducens nuclei: ipsilateral innervates lateral rectus, some cross to contralateral CNIII via MLF to activate CNIII medial rectus. Inputs from the cortex direct horizontal gaze via paramedian pontine reticular formation (PPRF) where inputs from cortex synapse to abducens nuclei.
What are the clinical differences between lesions of abducens nerve and lesions of abducens nuclei?
Lesion of CNVI results in ipsilateral impaired eye abduction. Lesion of nuclei results in ipsilateral lateral gaze palsy of both eyes. Lesion of unilateral PPRF also causes ipsilateral lateral gaze palsy.
What is the result of a lesion to the medial longitudinal fasciculus?
Interrupts input to the medial rectus and therfore the eye ipsilateral to the lesion does not adduct fully. There is also nystagmus of the opposite eye. This is called Internuclear Ophthalmoplegia (INO).
What lesions can cause Internuclear Opthalmoplegia (impaired adduction on affected side with nystagmus on unaffected side?)
Side with impaired adduction is the side where MLF was affected. Causes are MS, pontine infarcts, neoplasms of MLF.
What is ONE-AND-A-HALF syndrome?
When have lesion to MLF and adjacent abducens nuclei or PPRF. Have ipsilateral INO (impaired adduction on affected side with nystagmus on contralateral side when trying to adduct) and ipsilateral lateral gaze palsy (inability to abduct toward side of lesion with either eye). So if have left one-and-a-half syndrome this means lesion to left MLF and left abducens nuclei or left PPRF. With leftward gaze have left lateral gaze palsy. With rightward gaze have nystagmus with adduction in right eye and impaired adduction in left eye.
What muscles govern vertical eye movements?
Superior and inferior obliques and superior and inferior rectus (all are CNIII except superior obliques that are CNIV)
What does the rostral midbrain reticular formation and pretectal area govern?
Vertical eye movements. The ventral portion of region mediates downward gaze. The dorsal region (near posterior commissure) mediates upward gaze.
What is the clinical result of a tumor in the ventral portion of the rostral midbrain reticular formation?
Impaired downward gaze.
What is the clinical result of a tumor in the ventral portion of the pretectal area?
Impaired downward gaze.
What is the clinical result of a tumor in the dorsal portion of the rostral midbrain reticular formation?
Impaired upward gaze.
What is the clinical result of a tumor in the dorsal portion of the pretectal area?
Impaired upward gaze.
What eye movement can be spared with locked-in syndrome and why?
Locked-in syndrome can result from large bilateral pontine infarcts that affect bilateral corticospinal tracts and abducens nuclei: resulting in immobility and hoizontal gaze palsy. Vertical eye movements can be spared as the centers are in the midbrain.
What type of eye movements are controlled by the medial recti and lateral recti?
Convergence is controlled by medial recti. Divergence is controlled by lateral recti.
What pathways control vergence?
Descending inputs form the visual pathways in the occipital and parietal cortex. They contribute to the accommodation response.
What is Parinaud's syndrome? Clue: syndrome resulting from lesions compressing the dorsal midbrain and pretectal areas.
4 components of Parinaud's syndrome:
1. Impaired vertical gaze, especially upward
2. Large, irregular pupils that do not react to light but sometimes to near-far accommodation (pathways to Edinger-Westphal nuclei could be affected)
3.Eyelid abnormalities (range from bilateral tucking to bilateral ptosis)
4. Impaired convergence and possible convergence-retraction nystagmus with attempted upward gaze
What are the causes of Parinaud's syndrome?
Reminder: Parinaud's syndrome comes from pressure on dorsal midbrain and pretectal areas. What are the 4 components? Most common causes: pineal region tumors and hydrocephalus (dilation of 3rd ventricle pushes tectum of midbrain).
What is setting-sun sign in children and what is the likely cause?
When eyes are deviated inward from bilateral CNVI palsy and downward from Parinaud's syndrome. From hydrocephalus that results in compressed midbrain and pons.