NEURO-OPHTHALMOLOGY

Abstract

A. Components 1. Retina, retinal nerve fiber layer, optic nerves, opticchiasm, optic tracts, lateral geniculate bodies, optic radiations, and visual cortices (Fig. 3-1)B. Retina 1. Extends from ora serrata to optic nerve (Fig. 3-2) 2. Divided into four quadrants by the maculaa. Vertical meridian: separates superior and inferior retina b. Horizontal meridian: separates nasal and temporal retina3. Retina layers (Fig. 3-3) a. Retinal pigment epithelium1) Deepest layer of retina 2) Forms outer blood-retinal barrier and supportsphotoreceptors physiologically b. Photoreceptor layer1) First neural elements in the retina to react to light 2) Rod and cone cells contain light-sensitive pigmentrhodopsin 3) Photoreceptors hyperpolarize (membrane potentialbecomes more negative) in presence of light 4) Rod cells are sensitive to low levels of lighta) Minimal role in color vision (except blue spectrum) b) Rods are concentrated in peripheral retina c) No rods within the macula5) Cone cells respond to color a) Red, green, and blue b) Cones are densely concentrated in the maculac. Outer nuclear layer: contains cell bodies of photoreceptorsd. Outer plexiform layer: contains synapses between photoreceptors and bipolar and horizontal cellse. Inner nuclear layer 1) Amacrine cells are horizontally oriented, dopaminer-gic cells that modulate and convey photoreceptor information to ganglion cells2) Bipolar cells convey photoreceptor information to ganglion cells3) Horizontal cells provide antagonistic surround signals to bipolar cellsf. Inner plexiform layer: contains synapses between bipolar and amacrine cells and ganglion cellsg. Ganglion cell layer 1) Most superficial retinal layer 2) Ganglion cells divided into M and P cells 3) M and P cell axons project to superior colliculus orlateral geniculate nucleus 4) M cells lack color information, but have high contrastsensitivity, fast temporal resolution, low spatial resolution5) M cell axons project to magnocellular neurons in layers 1 and 2 of lateral geniculate nucleus, and these neurons project to layer IVC alpha neurons in cortical area 176) P cells have color opponency, low contrast sensitivity, and high spatial resolution7) P cell axons project to parvocellular neurons in layers 3, 4, 5, and 6 of lateral geniculate nucleus, and these neurons project to layer IVC alpha neurons in cortical area 178) Two types of signal processing a) ON center, OFF surroundi) ON center: activated when light hits center of the receptive fieldii) OFF surround: deactivated when light hits periphery of the receptive fieldb) OFF center, ON surround: center receptive field stimulation is OFF, and peripheral stimulation is ONc) ON-OFF signal processing helps establish sharp boundaries of objects in visual field9) Ganglion cell axons traveling to the optic nerve form the retinal nerve fiber layerC. Retinal Nerve Fiber Layer 1. Papillomacular bundle: nerve fibers extending frommacula to optic nerve 2. Temporal nerve fibers arch around papillomacular bun-dle to reach optic disc 3. Optic nerve creates a physiologic blind spot on visualfield testing (temporal) 4. Scotomas (“blind spots”): areas of poor or absentvision within the visual field 5. Specific scotoma and visual field abnormalities mayoccur from optic nerve and retinal lesions based on arrangement of retinal nerve fiber layer a. Arcuate scotoma or defects: arch-shaped, characteristicof nerve fiber bundle defects (e.g., glaucoma) (Fig. 3-4)b. Central scotoma (macular type of defect): a blind spot in the visual field represented by the macula (e.g., macular degeneration) (Fig. 3-5 left)c. Centrocecal scotoma (optic nerve type of defect): affects the visual field in region of the macula and papillomacular bundle (Fig. 3-5 right)d. Paracentral scotoma: affects retina and visual field just outside the macula (Fig. 3-6 left)e. Ring scotoma: from combined superior and inferior retina and arcuate scotoma (Fig. 3-6 right)f. Ring scotoma with a horizontal step: typically indicates retinal or nerve fiber layer lesion as opposed to ringMonocular scotoma and noncongruous visual field abnormalities (especially monocular) occur from optic nerve and retinal lesions based on arrangement of retinal nerve fiber layerscotoma with a vertical step, which may indicate lesion in occipital lobe near calcarine fissureg. Enlargement of blind spot (e.g., optic disc swelling) (Fig. 3-7)h. Altitudinal defects: blind spots with a horizontal step; typically appear as an abrupt, monocular loss of superior or inferior visual fieldi. Sector scotoma or defects: typically caused by retinal lesion (e.g., retinal detachment) (Fig. 3-8)j. Noncongruous visual field defects: dissimilar monocular visual field patternsD. Optic Nerve 1. Segmentsa. Intraocular segment (optic nerve head) b. Intraorbital segment c. Intracanalicular (optic canal) segment d. Intracranial segment2. Topographic arrangement of nerve fiber layer within optic nerve a. Similar to topology of nerve fiber layer before entry intooptic nerve b. Macular fibers (papillomacular bundle) are locatedperipherally (temporal aspect of the optic nerve) in the portion of optic nerve closest to the globec. Macular fibers become more centrally located in more distal portion of optic nerve closest to the chiasmd. Peripheral retinal fibers travel peripherally 3. Monocular vision loss is usually due to disease of reti-na, optic disc, or optic nerve: anterior to optic chiasm a. Central field defects are caused by lesions that affect opticnerve, macula, or papillomacular bundle 1) Unilateral central scotomas, for example, optic neu-ropathy, optic neuritis, or macular degeneration 2) Bilateral central or centrocecal defects, for example,suggestive of bilateral optic neuropathies (hereditary, compressive, nutritional, inflammatory) or bilateral occipital lesionsb. Unilateral temporal defects 1) Lesion of nasal retina, optic nerve, or nasal optic nervefibers at anterior optic chiasm (e.g., junctional scotoma of Traquair, see below)2) Monocular temporal crescent: retinal disease or lesion of anterior occipital lobec. Altitudinal defects: characteristic of disease of the central retinal artery, with macular sparing (cilioretinal arteries) or posterior ciliary artery (anterior ischemic optic neuropathy)E. Optic Chiasm 1. Nasal retinal nerve fibers: cross to contralateral optictract at level of the optic chiasm (constitute about half of optic nerve fibers)2. Inferior nasal fibers of one optic nerve cross ventrally into contralateral optic nerve proximally and are known as Wilbrand’s knee (Fig. 3-1), (the existence of this anatomic entity has been questioned)3. Temporal retinal nerve fibers remain ipsilateral in optic chiasm and optic tracts4. Posterior to optic chiasm: pituitary stalk 5. Optic chiasm lesions: bitemporal field defects, almostnever complete bitemporal field defects and exact field defect depends on localization of the compressive lesion a. Anterior chiasm (Fig 3-1)1) Compressive lesion anterior to optic chiasm generally causes bitemporal field defects involving the upper quadrants early on (may eventually evolve to more extensive bitemporal field defects)2) Junctional syndrome of Traquair a) Monocular superior temporal field defect in eyecontralateral to the lesion b) Often due to early, anterior chiasmal compressivelesion limited to crossing fibers from inferonasal retina of contralateral eye (Wilbrand’s knee), situated anterior to the ipsilateral inferonasal fibers (Fig. 3-1, left lower inset, C)3) Junctional syndrome a) Ipsilateral central scotoma with contralateral supe-rior temporal defect b) Due to compression of Wilbrand’s knee and ipsi-lateral optic nerve (Fig. 3-1, defect 4, Fig. 3-9)4) Bilateral superior temporal field defects due to early anterior compression of both inferonasal crossing fibersb. Body of the chiasm syndrome: typically bitemporal visual field defects (often incomplete, may be limited to central fields, peripheral fields, or both)c. Posterior chiasm syndrome 1) Compressive lesion posterior to optic chiasm general-ly causes bitemporal field defects involving lower quadrants early on (may eventually evolve to more extensive bitemporal field defects)2) Bilateral temporal scotomas (involving central vision, peripheral fields spared)3) Bitemporal field defects primarily affecting inferior temporal fields due to early compressive lesionsF. Optic Tracts 1. Optic chiasmal fibers leading to lateral geniculatenucleus 2. Visual field defect related to lesion involving optic tracta. Complete (macular-splitting) homonymous hemianopia b. Wallerian degeneration and dying-back axonal loss caus-ing ganglion cell fiber atrophy of contralateral nasal macula and nasal retina and ipsilateral temporal retinac. Contralateral relative afferent pupillary defect: optic tract lesion on one side may cause the contralateral eye to have a relative afferent pupillary defect (i.e., greater number of crossed vs. uncrossed fibers in chiasm, 53:47) and a temporal visual field defectd. This is the last post-chiasmal site for a relative afferent pupillary defect other than an asymmetric posterior midbrain lesionG. Lateral Geniculate Nucleus 1. Has six layers (Fig. 3-1, bottom right inset) 2. Superior retinal fibers lie superomedial in the nucleusJunctional syndrome: an anterior chiasm lesion causes a central scotoma in one eye and a superior temporal visual field defect in the other eye (Fig. 3-9)Bitemporal visual field defects are typical of a lesion affecting the body of the optic chiasmNasal retinal fibers cross in the optic chiasm and temporal retinal fibers remain ipsilateralInferior nasal fibers of one optic nerve cross ventrally into the contralateral optic nerve proximally and are known as Wilbrand’s kneeAn isolated monocular temporal field defect affecting the contralateral optic nerve or Wilbrand’s knee is called a junctional scotoma of Traquair3. Inferior retinal fibers lie lateral in the nucleus 4. Anterior choroidal artery occlusion causes a quadruplesectoranopia: homonymous defect affecting superior and inferior quadrants, with sparing of the horizontal sectors (Fig. 3-10 A)5. Posterior lateral choroidal artery occlusion causes a horizontal homonymous sector defect: a homonymous defect of horizontal sectors (wedge-or triangle-shaped) (Fig. 3-10 B)H. Optic Radiations 1. Optic radiations exit the lateral geniculate nucleus inthree bundles, which course around the lateral ventricle through white matter to reach calcarine cortex (cortical area 17)2. Three optic radiation bundles a. Upper bundle1) Originates from medial part of lateral geniculate nucleus2) Represents superior retina3) Passes deep in parietal white matter and ends in superior lip of the calcarine fissureb. Central bundle 1) Originates from medial part of lateral geniculatenucleus 2) Represents macular region 3) Traverses posterior temporal and occipital white mat-ter and ends on both lips of posterior part of the calcarine fissurec. Lower bundle 1) Originates from lateral part of lateral geniculate nucleus 2) Represents inferior retina 3) Courses anteriorly from lateral geniculate nucleus andthen turns around temporal horn of lateral ventricle (Meyer’s loop) to end on inferior lip of the calcarine fissure3. Superior homonymous quadrantic (“pie in the sky”) defects may result from lesion of Meyer’s loop (i.e., optic radiations that pass through temporal lobe to occipital lobe inferior to the calcarine fissure)4. Inferior homonymous quadrantic (“pie on the floor”) defects result from lesion of optic radiations that passSuperior retinal nerve fiber information travels in the superior optic radiations to the superior lip of the calcarine fissureInferior retinal nerve fiber information travels in the inferior optic radiations to the inferior lip of the calcarine fissureComplete homonymous hemianopias indicate retrochiasmal disease (e.g., lateral geniculate nucleus, optic radiations, occipital cortex)Visual field defects become more congruous (i.e., similar pattern in both eyes) from the lateral geniculate body toward the occipital lobeA superior homonymous quadrantic (“pie in the sky”) defect may result from a lesion of Meyer’s loop in the temporal lobe or inferior occipital cortexAn inferior homonymous quadrantic (“pie on the floor”) defect results from a lesion of the optic radiations traveling through the parietal lobe or superior occipital cortexthrough parietal lobe to occipital lobe superior to the calcarine fissureI. Visual Cortex (Fig. 3-11) 1. Striate cortex, or primary visual cortex, is Brodmann’sarea 17: located along superior and inferior banks of calcarine fissure2. Central 10 to 15 degrees of vision represent a disproportionate amount of surface area (50%-60%) of occipital cortex3. Homonymous quadrantic defects can occur from unilateral occipital lobe lesions; the visual field defects typically have a sharp horizontal edge4. Medial occipital lesions cause congruous homonymous hemianopias, typically with macular sparing and are usually due to infarcts in territory of the posterior cerebral artery (absolute congruence in comparison with lesions of optic tracts or optic radiations, which are not as congruent)5. Macular sparing is believed to be due to dual arterial supply (both posterior and middle cerebral arteries supplying the occipital pole responsible for macular vision) and also a larger cortical representation of the macular region6. Striate cortex lesion localization a. Anterior lesion: causes a temporal crescent or half moonsyndrome in contralateral eye (Fig. 3-1, defect 11); the only retrochiasmal lesion that can cause a unilateral visual field defectb. Intermediate lesion: affects from 10 to 60 degrees in contralateral hemifieldc. Posterior lesion: affects macular vision (central 10 degrees in contralateral visual field)7. Cortical blindness: complete blindness or keyhole vision that may result from bilateral occipital lobe disease8. Anton’s syndrome: cortical blindness with denial of neurologic impairmentA. Introduction 1. Purpose of efferent visual system: direct and maintainthe fovea toward target of interest 2. Efferent visual system has both slow and rapid visualtracking systems, with voluntary and reflex mechanisms 3. Efferent visual system: supranuclear, nuclear, infranu-clear and internuclear neurons; neuromuscular junc-tion; ocular motor muscles 4. “Ocular motor” refers to cranial nerves (CNs) III, IV,and VI as a group 5. “Oculomotor” refers to CN III onlyB. Ocular Muscles (Fig. 3-12 and Table 3-1): six muscles for each eye1. Four rectus muscles (superior, inferior, medial and lateral)2. Two oblique muscles (inferior and superior)C. Cranial Nerve III (oculomotor nerve) 1. Neuroanatomya. Oculomotor nuclear complex: located in midbrain at level of the superior colliculus; two unpaired and four paired columns of nuclei within the nuclear complexWith lesions affecting the optic nerve or chiasm, patients may have decreased visual acuity, a relative afferent pupillary defect, and visual field defectsophthalmoscopic findings are usually presentWith unilateral retrochiasmal lesions, patients typically have retained visual acuity, no relative afferent pupillary defect, a visual field defect, and usually normal ophthalmoscopic findings-an exception is an optic tract lesion1) Single caudal central nucleus (unpaired): innervates left and right levator palpebrae superioris muscles2) Single visceral Edinger-Westphal nucleus (unpaired): most dorsal localization, provides parasympathic innervation of pupil (pupillary constrictors and ciliary muscle)3) Medial nuclei (paired): each innervates superior rectus muscle ipsilaterally and sends decussating fibers (through contralateral medial nucleus) to contralateral superior rectus muscle (ablative lesion in one medial nucleus causes weakness in superior recti bilaterally); paired nuclei with decussating axons4) Intermediate nuclei (paired): each innervates ipsilateral inferior oblique muscle5) Dorsal nuclei (paired): each innervates ipsilateral inferior rectus muscle6) Ventral nuclei (paired): each innervates ipsilateral medial rectus muscleb. Fascicular arrangement is maintained similar to nucleartopology c. Oculomotor fascicles travel ventrally, exit the interpe-duncular fossa as the oculomotor nerve in the subarachnoid spaced. Subarachnoid space: oculomotor nerve passes between posterior cerebral and superior cerebellar arteries; near the uncus of temporal lobe (and in proximity to posterior communicating artery), it penetrates the dura mater into cavernous sinus (Fig. 3-13)e. Cavernous sinus: oculomotor nerve is superior and lateral in cavernous sinus and exits the sinus to enter superior orbital fissure (Fig. 3-14)f. Superior orbital fissure: after entering this fissure, oculomotor nerve divides into superior (innervates superior rectus and levator palpebrae superioris) and inferior (innervates medial and inferior recti and inferior oblique) divisions and provides parasympathetic input to ciliary ganglionOcular muscle innervation mnemonic: “SO4 LR6” SO = superior oblique innervated by cranial nerve IVLR = lateral rectus, innervated by cranial nerve VIOther ocular muscles are innervated by cranial nerve IIISuperior muscles intort or “SIN” mnemonic: the superior oblique (SO) and superior rectus (SR) muscles are intorters of the eyeTable 3-1. Summary of the Extraocular Muscles, Innervation, and ActionPrimary Innervation Muscle action Secondary (cranial nerve)g. Orbit: oculomotor nerve divisions (superior and inferior)2. Localization of third nerve palsy a. Nuclear lesions: ipsilateral complete pupil-involved thirdnerve palsy (including ptosis), contralateral eyelid ptosis, and superior rectus palsy 1) Subnuclear lesions: rare, but can cause isolated mus-cle paresis (e.g, inferior oblique) or bilateral eyelid ptosis2) Nuclear lesions may spare Edinger-Westphal nucleus (pupil-sparing lesion)3) Differential diagnosis: focal hemorrhage, infarct, or mass (neoplastic, vascular malformation)b. Fascicular lesions 1) Plus-minus syndrome (within midbrain): example offascicular lesion causing ipsilateral ptosis and contralateral eyelid retraction (occurs with midbrain lesions involving fascicles supplying ipsilateral levator palpebrae and inhibitory projections to opposite subnucleus for contralateral levator palpebrae)2) Differential diagnosis: infarction, hemorrhage, mass, demyelination, infection3) Ipsilateral syndromes a) Weber’s syndrome: ipsilateral third nerve palsywith contralateral hemiparesis due to involvement of CN III and cerebral peduncleb) Nothnagel’s syndrome: ipsilateral third nerve palsy with ipsilateral ataxia (superior cerebellar lesion)c) Claude’s syndrome: ipsilateral third nerve palsy and contralateral ataxia, due to involvement of the tegmentum, red nucleus, and CN IIId) Benedikt’s syndrome: clinical features of Claude’s syndrome plus contralateral hemiparesis, latter due to involvement of cerebral pedunclec. Subarachnoid space lesions 1) Posterior communicating artery aneurysm: usuallyinvolves pupils 2) Uncal herniation 3) Tumors and other mass lesions, arachnoid cysts 4) Meningeal (inflammatory or infectious) disease (e.g.,sarcoidosis, tuberculosis) 5) Small-vessel ischemia in setting of diabetes mellitus(often pupil sparing, painful) or vasculitis d. Cavernous sinus lesions (Fig. 3-14)1) Third nerve palsy with or without pain 2) Third nerve palsy with some combination of othercavernous sinus constituents: CNs IV, VI, ophthalmic division of V (V1) (and sometimes maxillary division of V [V2] anatomy variable)3) Third nerve palsy and Horner’s syndrome (sympathetic fibers along carotid artery)4) Masses of cavernous sinus may cause aberrant regeneration of CN III5) Differential diagnosis a) Compressive lesions: pituitary adenoma and otherneoplastic compressive lesions, carotid-cavernous fistulas, pituitary apoplexy, aneurysm of intracavernous portion of internal carotid artery, cavernous sinus thrombosisb) Cavernous sinus infection with Mucor or Aspergillus, usually in setting of diabetes or immunosuppressionc) Inflammatory (e.g., Tolosa-Hunt syndrome) e. Superior orbital fissure lesions1) Third nerve palsy with possible palsies of CN IV, VI, V12) Differential diagnosis (similar to the cavernous sinus lesions): inflammatory (Tolosa-Hunt syndrome,granulomatous disease often affecting superior orbital fissure), compressive lesions such as tumors (e.g., meningioma, metastatic tumor)f. Orbital lesions 1) Divisional third nerve palsy, optic neuropathy, prop-tosis, orbital injection, chemosis 2) Differential diagnosisa) Compressive lesions (neoplastic, including meningioma and metastatic tumors, and vascular malformations)b) Trauma (orbital fractures) c) Inflammatory (idiopathic orbital pseudotumor)g. Disorders of neuromuscular transmission 1) Myasthenia gravis 2) Lambert-Eaton myasthenic syndromeh. Disorders of muscle 1) Graves’ ophthalmopathy (most often affecting inferi-or rectus muscle) 2) Dystrophic myopathies (e.g., oculopharyngealdystrophy) 3) Ocular neuromyotonia: rare, episodic diplopia in set-ting of previous radiotherapy, usually in sellar or parasellar regionsi. Other nonlocalizing causes 1) Miller Fisher variant of Guillain-Barré syndrome 2) Ophthalmoplegic migraine: most frequently involv-ing the oculomotor nerve and, commonly, the pupillary response and accommodation3) Lyme disease with meningeal involvement 3. Pupillary involvement (“the rule of the pupil”)a. Pupillomotor fibers are located superficially (peripherally) in CN III and tend to be spared by ischemic insults (which primarily affect deep fibers)b. Pupil-sparing third nerve palsy occurs with nerve infarction in setting of diabetes, giant cell arteritis, or systemic lupus erythematosusc. Compressive lesions generally tend to affect pupils (may be delayed)d. Exceptions to “the rule of the pupil”: partial third nerve palsy or partial pupillary involvement 1) Some ischemic lesions due to diabetes may produceminimal anisocoria 2) Aneurysms presenting with partial oculomotor palsiesmay have minimal involvement of pupillomotor fibers (relative pupillary sparing)3) Certain cavernous sinus or subarachnoid partial compressive lesions involving only portions of CN III carrying no pupillary fibers4) The pupillary function is also spared by a) Some slow-growing tumors sparing pupillary fibersthat tend to be more pressure-resistant than underlying oculomotor fibersb) Acute stage of a rapidly expanding mass (becomes more obvious later)D. Cranial Nerve IV (trochlear nerve) 1. Neuroanatomy (Fig. 3-15)a. Nucleus: trochlear nucleus is at level of inferior colliculusb. Fascicles: travel posteriorly around cerebral aqueduct, decussate, and exit brainstem under the inferior colliculic. Subarachnoid space 1) CN IV: only cranial nerve to exit dorsally 2) CN IV and CN III innervation of contralateral supe-rior rectus muscle: only cranial nerves with axons that decussate3) CN IV travels through quadrageminal, ambient, crural, and pontomesencephalic cisterns4) CN IV travels in proximity to tentorium cerebellum: entrapment may occur at edge of the tentoriumd. Cavernous sinus: CN IV enters cavernous sinus inferior to CN III, the lateral aspect of the clivus, and lies within lateral wall of cavernous sinus (Fig. 3-14)e. Superior orbital fissure: CN IV exits cavernous sinus and enters superior orbital fissuref. Orbit: within the orbit, CN IV innervates superior oblique muscle2. Localization of fourth nerve palsy (differential diagnosis similar to third nerve palsy) a. Nuclear and fascicular lesions1) Contralateral fourth nerve palsy2) Anterior medullary velum lesions: bilateral fourth nerve palsies (common cause in children is medulloblastoma)b. Subarachnoid space (CN IV): ipsilateral fourth nerve palsyc. Cavernous sinus: ipsilateral fourth nerve palsy with combination of deficits involving cavernous sinus constituents (CN III, VI, V1, sympathetic innervation of orbit [Horner’s syndrome])d. Superior orbital fissure and orbit: ipsilateral fourth nerve palsy with possible combination of CN III, VI, or V1E. Cranial Nerve VI (abducens nerve) 1. Neuroanatomy (Fig. 3-16)a. Nucleus: abducens nucleus is in pons and adjacent to floor of fourth ventricleb. Fascicles: abducens fascicles travel ventrally through pons and emerge at pontomedullary junctionc. Subarachnoid space 1) Long intracranial upward course: CN VI travelsthrough prepontine cistern subarachnoid space, enters Dorello’s canal beneath petrosphenoidal ligament of Gruber to enter cavernous sinus2) Lesion can cause “false localizing sign” (see below)d. Cavernous sinus: CN VI lies inside cavernous sinus (Fig. 3-14)e. Superior orbital fissure and orbit: CN VI exits cavernous sinus, passes through superior orbital fissure into orbit to innervate lateral rectus muscle2. Localization of sixth nerve palsy (differential diagnosis similar to third nerve palsy) a. Pons (nucleus and fascicles)1) Ipsilateral sixth nerve palsy for discrete lesion 2) Foville’s syndrome (see also Chapter 4)a) Ipsilateral lower motor neuron facial paralysis b) Ipsilateral gaze paralysis (abducens nucleus lesion) c) Contralateral hemiparesis3) Millard-Gubler syndrome (see also Chapter 4) a) Ipsilateral lower motor neuron facial paralysis b) Ipsilateral abducens paralysis c) Contralateral hemiparesisb. Subarachnoid space 1) Ipsilateral sixth nerve palsy 2) Gradenigo’s syndrome (lesion of petrous apex orDorello’s canal) a) Ipsilateral sixth nerve palsy: CN VI may bestretched over the petrous ridge b) Ipsilateral facial painc) Ipsilateral deafnesss (CN VIII) d) Due to compressive neoplastic or vascular malfor-mation, inferior sinus thrombosis 3) False localizing sign in setting of increased intracranialpressure (e.g., hydrocephalus, pseudotumor cerebri)—CN VI has longest intracranial course of all cranial nerves and is more predisposed to stretch-induced injury, especially with shearing over the petrous ridgec. Cavernous sinus: ipsilateral sixth nerve palsy for discrete lesion with possible involvement of CN III, IV, V1 or Horner’s syndromed. Superior orbital fissure and orbit: similar to cavernous sinus but may have orbital signs (e.g., proptosis, injection, chemosis)F. Smooth Pursuit (Fig. 3-17) 1. Keeps an image on the fovea during slow movement ofan object, such as a line moving slowly across an optokinetic drum2. Cannot be created voluntarily 3. Must be slower than 5 degrees per second to maintainvision with high resolution and high visual acuity 4. Visual targets moving faster than 50 degrees per secondinduce voluntary fast saccades 5. Stimuli for smooth pursuits may be visual or nonvisuala. Example of a nonvisual stimulus: proprioceptive input guiding the subject to make pursuit eye movements that follow movements of the limbs in the dark (or with eyes closed)6. Temporary volitional anticipatory (predictive) pursuit movements also occur in response to predictable target motion, based on previously learned experience a. Examples: predictive movements of the eyes in anticipa-tion of onset of movement of the visual target (even in the absence of movement of the target) or predictive acceleration of the eye movements when the visual target actually movesb. These depend on memory for previous tracking experiences7. Afferent visual information is conveyed to striate cortex and then to occipitotemporal region called medial temporal (MT) and medial superior temporal (MST) areas8. From MT/MST, information on speed and direction of moving target is conveyed ipsilaterally via arcuate fiber bundles to posterior parietal cortex and contralaterally through corpus callosum to contralateral MT/MST9. Posterior parietal cortex: directs attention to moving visual stimuli10. Frontal eye fields and supplementary eye fields a. Have reciprocal connections with posterior parietalcortex and MT/MST b. Both fields are responsible for predictive pursuitmovements 11. Pursuit pathways: descend to dorsolateral and lateralpontine nuclei via internal capsule and cerebral peduncles12. Nucleus of the optic tract a. Pretectal localization in brachium of the superiorcolliculus b. Receives retinal input from superior colliculus and corti-cal input from MT/MST and striate cortex c. Projects to pontine nuclei and superior colliculus:important for initiating pursuit movements 13. Cerebellar flocculus and paraflocculus: important rolein executing smooth pursuit eye movements and in gaze-holding14. ImpairmentBilateral dysfunction of smooth pursuit system has many nonspecific causes (fatigue, medications, old age, dementia, bilateral smooth pursuit pathway lesions)Smooth pursuit deficit toward one side usually indicates unilateral lesion(s)a. With impairment of pursuit eye movements, compensatory catch-up saccades are produced, causing saccadic pursuit eye movementsb. Symmetric saccadic pursuit movements are nonspecific and may occur in several degenerative and toxic or metabolic conditionsc. Asymmetric or unilateral abnormalities of pursuit eye movements may indicate unilateral lesion somewhere in the pathwayd. Unilateral cerebral hemisphere lesions 1) May cause abnormal pursuit and/or impaired trackingof objects to the side of the lesion 2) Often may cause contralateral visual neglect after anacute lesionG. Saccades 1. Fast (300-700 degrees per second) eye movements thatbring visual images of interest onto the fovea 2. Types of saccadesa. Intentional saccades: bring an item quickly into vision b. Antisaccades: intentional saccades made to look awayfrom an object; requires suppression of saccade toward a novel stimulus and generation of a saccade away from the stimulus (frontal eye fields and prefrontal cortex are probably largely responsible)c. Reflexive saccades: in response to sudden movement or soundd. Spontaneous saccades: occur spontaneously at rest or with speech3. Two mathematical eleme