1.BYABDELRAHMAN AHMAD. MSc.

2. AGENDA Short notes about Anatomy & physiologyI. EyeII. VisionIII. reflexes Evaluation and examination of the eye 3. AnatomyA.Eyelids Three muscles control lid position1. Levator palpebrae superioris2. Mullers muscle3. Orbicularis oculi 4. AnatomyB. Ocular muscles 5. AnatomyC. Nervous control of eye movement1. Oculomotor nerve.2. Trochlear nerve.3. Abducens nerve. 6. Extraocular Muscles 7. Types of Eye Movements1. Saccades: Quick, (darting = jumping), conjugate movements which direct the eyes to a new target.2. Smooth pursuit: A slower conjugate movement which allows for tracking of a moving object, or of a stationary object while we are moving.3. Convergence: A dysconjugate movement of both eyes toward the midline to allow for focusing on a near object by adjusting the angle between the eyes. 8. Anatomy eye muscles control gaze by1. Occulomotor system2. Optokinetic response 9. Occulomotor system1. Vestibulo-ocular response systemThree semicircular canals, Resting firing rate increased byacceleration/rotation of the head .Canal function is initiated by head rotation toward it Generate compensatory eye movements in the directionopposite the head motion to keep the eye stable2-OtolithsAlso component of the vestibular systemSaccule and utricle, Detect linear accelerations of the head 10. Optokinetic Reflex Combination of saccades andsmooth pursuit that allow tracking oftargets in turn (e.g. counting sheepas they jump over a fence). smoothly follow one target, thensaccade in the opposite direction topick up the next target parieto-temporal junction (smoothpursuit area) projects down toipsilateral vestibular nucleus,inhibits it allowing ipsilateralsmooth pursuit then, the FEF of the samehemisphere generates a saccade backto the next target 11. Saccadic pathway 12. Pursuit pathway 13. AnatomyD. Pupillary anatomy1. Parasympatheticpathway2. Sympathetic pathway 14. AnatomyParasympathatic supplya. Muscles innervatedi. Iris sphincter: for pupillary constrictionii. Ciliary muscle: for accommodationb. CN IIIi. Innervation of intraocular musclesii. Pupillomotor fibers are located on the outside (susceptible to compression)iii. Within the orbit, the parasympathetic fibers synapse in the ciliary ganglion and postganglionic parasympathetic fibers proceed anteriorly as short ciliary nerves to innervate the iris sphincter and ciliary muscles 15. Anatomy Sympathetic pathway First-order neurons: originate in the posterolateralhypothalamus and synapse within the intermediolateralgray matter column of the lower cervical and upperthoracic spinal cord Second-order neurons: arise from the ciliospinal centerand exit the spinal cord through the ventral roots of C8T2 to synapse in the superior cervical ganglion Third-order (postganglionic) neurons: originate from thesuperior cervical ganglion and travel as a plexus along theinternal carotid artery 16. AnatomyE. Retina:light first enters the innermost layer of the retina throughthe ganglion cell layer Rods: use rhodopsin pigment; mediate light perception Cones: use iodopsin pigment; mediate color vision 17. Anatomy The medial longitudinal fasciculus (MLF) is a pair of crossed fiber tracts, one on each side of the brainstem, situated near the midline and are composed of both ascending and descending fibers 18. Anatomy The Medial Longitudinal Fasciculus carries informationabout the direction that the eyes should move. It connect the cranial nerve nuclei III , IV and, VI together, andintegrates movements directed by the gaze centers (frontal eyefield) and information about head movement (from cranialnerve VIII, Vestibulocochlear nerve). It also carries the descending tectospinal tract and medialvestibulospinal tracts into the cervical spinal cord, andinnervates some muscles of the neck and upper limbs 19. Anatomy Input of MLB1.the 8th cranial nerve about head movements,2. from the flocculus of the cerebellum,3. head and neck propioce- ptors and foot and ankle muscle spindle, via the fastigial nucleus 20. Important reflexesLight reflex 21. Anatomy Accomodation reflex 22. II. Clinical Assessment1. Oculara. Loss of vision in one eye vs. both eyesb. Homonymous hemianopia may be misinterpreted by patient as monocular vision loss2. Retro-oculara. Hemianopia vs. quadrantanopiab. Peripheral visual fields vs. central visual field 23. II. Clinical Assessment3. Timea. Duration: transient vs. permanentb. Time of onset (acute, subacute, chronic)c. Prior events4. Associated phenomenologya. Positive (hallucinations, scotoma, diplopia, etc.)b. Negative (vision loss with darkness; complete vs. partial)c. Associated symptomatology (eye pain, headache, focal weakness) 24. EYE EXAMINATIONa. Eyelidsb. Conjunctivac. Visual acuity:d. Visual fieldse. Extra ocular movementf. Pupillary reactivityg. Ophthalmoscopic examination 25. EYE LED EXAMINATION Periorbital edemaa. Ocular inflammationb. Cavernous sinus diseasec. Thyroid ophthalmopathyd. Renal impairement 26. EYE LED EXAMINATION Ptosis CN III palsy Horners syndrome Neuromuscular junction (MG, botulism) Myopathic (occulopharyngeal myopathy) Congenital Progressive external ophthalmoplegia Endocrine (thyroid) Trauma 27. EYE LED EXAMINATION Blepharospasma. Abnormally low and upper lid position that results from excessive contraction of the orbicularis oculi 28. EYE LED EXAMINATION CAUSES OF BELPHAROSPASMi. Isolatedii. Associated with other facial dystonias: Meiges syndromeiii. Part of a generalized dystoniaiv. Occurs with parkinsonian syndromesv. Medications (levodopa or the neuroleptics)vi. Focal brain stem or basal ganglia lesions 29. Conjunctiva EXAMINATIONi. Transparent with only a few visible blood vesselsii. Tortuous conjunctival vesselscarotid cavernous fistulaiii. Halo of redness at the limbusuveitis or acute glaucomaiv. Palpebral rednesskeratopathy or dry eye syndromev. Diffuse eye injectionviral conjunctivitis 30. Visual acuity examination Snellen visual acuity testPseudoisochromatic color plates assessment of colordiscrimination 31. Visual field examination Visual field testing: confrontation methodscomparisons between hemifields and quadrants; Goldmann perimetry standardized visual field testing 32. PART II 33. Eye movement examination1- myopathic disordera. Congenital myopathy (Myotubular ,Central core )b. Muscular dystrophy ( Oculopharyngeal dystrophy)c. Myotonic disorders ( Paramyotonia congenita , Hyperkalemic and hypokalemic periodic paralyses)d. Mitochondrial myopathyi. Progressive external ophthalmoplegia/Kearns- Sayre syndromeii. MELASe. Metabolic myopathy: abetalipoproteinemia 34. Eye movement examinationf. Endocrine myopathyi. Thyroid (Graves) ophthalmopathy: characteristic feature is lid retractionii. Steroid myopathy 35. Eye movement examination 2-Neuromuscular disordersa. MGi. Symptoms more likely as day progresses or with significant motor activityii. Ptosis that increases throughout the day, ptosis that worsens with repeated eye openingiv. Diplopia with extraocular muscle involvementb. Lambert-Eaton myasthenic syndrome: ocular signs are rarec. Toxinsi. Organophosphate insecticidesii. Botulismiii. Venom (cobras, kraits, coral snakes, and sea snakes) 36. Eye movement examination3. Neuropathic disorders Etiologiesi. Ischemic (atherosclerotic, diabetes mellitus)ii. Hemorrhagiciii. Increase ICT (tumor, aneurysm)iv. Traumav. Acute inflammatory demyelinating polyradiculopathy (Miller-Fisher variant)vi. Cavernous sinus problem 37. Eye movement examination Oculomotor (CN III) palsy Idiopathic (3035%)Vascular (25%) Trauma (15%) Tumor (10%) Inflammatory/infectious (510%) 38. Eye movement examination Clinical Diplopia Ptosis Blurred near visionComplete CN III palsy Eye in primary position is down and out Cannot elevate or adduct Full abduction Ptosis is severe Accommodation impaired Pupil is large and does not constrict to light or on convergence(C) Pupil rule pupil involved in >90% in PCA Aneurysm 39. In nuclear occulomotor lesion there is Ophthalmoplegai with bilateral ptosis and contralateralsuperior rectus palsy 40. Eye movement examination Trochlear (CN IV) palsy Trauma (30%) Idiopathic (2025%) Ischemic (15%) Congenital (10%) Tumor (510%) 41. Eye movement examinationClinical Compensatory lateral head tilt away from the side of thelesion to minimize diplopia It is impossible to differentiate clinically betweentrochlear lesion and nuclear lesion 42. Eye movement examinationDifferential diagnosis of vertical diplopia(1) Ocular MG(2) Thyroid ophthalmoplegia(3) Orbital lesion (i.e., tumor)(4) CN III palsy(5) CN IV palsy 43. Eye movement examinationAbducens (CN VI) palsyIdiopathic (25%)Tumor (20%)Trauma (15%) Ischemia (15%) 44. Eye movement examination Clinical Horizontal diplopia that is uncrossed, meaning that theipsilateral image belongs to the ipsilateral eye and is morenoticeable for distant targets 45. Rules for Evaluation for Diplopia Head tilt: When the weak extraocular muscle is unableto move the eye, the head moves the eye. Therefore, thehead tilts or turns, or both, in the direction of action ofthe weak muscle The image from the nonfixating eye is the false imageand is displaced in the direction opposite the deviation;thus, when the patient fixates with the nonparetic eye,the false image is displaced in the direction of action ofthe paretic muscle 46. The false image is the most peripheral image and is displaced in the direction of action of the weak muscle, except when the patient fixes with the paretic eye. When the lateral rectus is paralyzed, the eyes are esotropic (crossed), but the images are uncrossed. The diplopia is worse at a distance and on looking to the side of the weak muscle. When the medial rectus is paralyzed, the eyes are exotropic ,but the images are crossed . The diplopia is worse at near and on looking to the opposite side. 47. The images are most widely separated when an attempt ismade to look in the direction of the paretic muscle. Secondary deviation (the angle of ocular misalignment whenthe paretic eye is fixating) is always greater than primarydeviation (when the good eye is fixating). Patients whofixate with the paretic eye may appear to have intracranialdisease. Comitance: With a comitant strabismus, the angle of ocularmisalignment is relatively constant in all directions of gaze.With a noncomitant (paralytic) strabismus, the angle ofmisalignment varies with the direction of gaze. 48. Eye movement examinationCavernous sinus syndromesEtiologies Tumors (70%) Nasopharyngeal carcinoma (most common cause) Pituitary Adenoma Meningioma Craniopharyngioma Chondroma Metastatic (breast, lung, and prostate) carcinoma Aneurysms (20%) Infection 49. Eye movement examinationTolosa-Hunt syndrome idiopathic noncaseating granulomatous inflammation in the cavernous sinus Diagnosis of exclusion Clinical Acute painful ophthalmoplegia Progression over days to weeks Most commonly, CNs III and VI involved CN IV and CN V-1 in one-third of cases Optic nerve is affected in 20% CN V-2 sensory loss in 10% Horners syndrome, CN V-3 sensory loss, and CN VII palsy are unusual May have elevated erythrocyte sedimentation rate and positive systemiclupus erythematosus preparation May have recurring attacks over months to years 50. 35-year-old woman with Tolosa-Hunt syndrome presenting with painfulophthalmoplegia. Extension of enhancing tissue into left orbital apex(arrow) is seen on contrast-enhanced axial T1-weighted image. 51. Eye movement examination Pituitary apoplexya. Multiple oculomotor palsiesb. Severe headachec. Bilateral vision loss 52. Eye movement examination Internuclear ophthalmoplegiaEtiologiesa. Lesion of the medial longitudinal i. Brain stem ischemia (usuallyfasciculus (MLF) blocks informationunilateral)from the contralateral ii. MS (usually bilateral)CN VI to the ipsilateral CN IIIiii. Brain stem encephalitisb. Internuclear ophthalmoplegia namediv. Behcets diseaseafter ipsilateral MLF lesion v. Cryptococcosisc. Clinicalvi. Guillain-Barr syndromei. Impaired adduction during conjugategaze away from the side of the MLFlesionii. Nystagmus of the abducting duringconjugate version movementsiii. Slowed adducting saccades with lag inthe adducting eye compared with theabducting eye 53. Eye movement examination One-and-a-half syndromea. Combined damage toi. ipsilateral paramedian pontine reticular formationii. MLF and ipsilateral CN VI nucleusb. Clinicalcharacterized by "a conjugate horizontal gaze palsy in one direction and an internuclear ophthalmoplegia in the other 54. Nystagmus Nystagmus is an involuntary biphasic rhythmic ocularoscillation in which one or both phases are slow . The slow phase of jerk nystagmus is responsible for theinitiation and generation of the nystagmus, whereas thefast (saccadic) phase is a corrective movement bringingthe fovea back on target. 55. Nystagmus may result from dysfunction of the vestibularend organ, vestibular nerve, brainstem, cerebellum, orcerebral centers for ocular pursuit Pendular nystagmus is central (brainstem or cerebellum)in origin Jerk nystagmus with a linear slow phase is caused byperipheral vestibular dysfunction. 56. Nystagmus syndromesLOCALIZATIONDownbeat nystagmusBilateral cervicomedullary junction (flocculus)Floor of the fourth ventricleNUSTAGMUS SYNDROMESPeriodic alternating nystagmusCervicomedullary junctionUpbeat nystagmusBilateral pontomesencephalic junctionBilateral pontomedullary junctionCerebellar vermisPendular nystagmusDeep cerebellar (fastigial) nucleiSeesaw nystagmusMesodiencephalic junction, chiasm,disorders that disrupt central visionHemi-jerk SSN Unilateral mesodiencephalic (upper polesof the eyes jerk toward side of lesion)Lateral medullary lesions (upper poles ofthe eyes jerk away from side of lesionAlternating hemi-SSN with vertical gaze Middle cerebellar peduncle 57. Optokinetic nystagmus Normal physiologic response to a series of objects movingin the same direction across the visual field. It is a reflex phenomenon depends on the integrity of thecortical visual pathways. May be absent with deep parietal lesions. 58. Physiologic nystagmus It is jerk nystagmus. Appear on extreme gaze; lateral or upward. Distinuished from pathological nystagmus: Neurological features Occurs with gaze angle less than 30 59. Eye movement examinationNystagmus Pendular nystagmusDue toi. MS (most common)ii. Strokesiii. Encephalitisiv. Brain stem vascular 60. Nystagmus Spasmus nutansa. Disorder of young children, with age at onset usually 6 12 months and resolves by age 3 yearsb. Clinical triadi. Ocular oscillationsii. Head noddingiii. Head turn 61. Nystagmus Seesaw nystagmus Present in all gaze positions Etiologiesi. TumorPituitary adenoma, Craniopharyngiomaii. Stroke Pontomedullary infarct, Midbrain/thalamic infarctiii. Traumaiv. Congenitalv. Vision loss 62. Nystagmus 63. nystagmus Downbeat nystagmusi. Clinical(A) Associated signs/symptoms(1) Ataxia(2) Blurred vision(3) Oscillopsiaii. Etiologies(A) Arnold-Chiari syndrome (2025%)(B) Idiopathic (20%)(C) Spinocerebellar degeneration (20%)(D) Brain stem stroke (10%)(E) MS (510%)(F) Tumor(G) Medication (lithium, antiepileptic drugs)/alcohol(H) Trauma 64. Nystagmus Mechanism: Interruption of the posterior semicircular canal projections,which are responsible for the downward vestibulo-ocularreflex. Impaired cerebellar inhibition of the vestibular circuits forupward eye movements. 65. Nystagmus 66. nystagmus Upbeat nystagmusi. Associated with(A) Oscillopsia(B) Ataxiaii. Etiologies(A) Spinocerebellar degeneration (2025%)(B) Brain stem stroke/vascular malformation (20%)(C) MS/inflammatory (1015%)(D) Tumor (10%)(E) Infection(F) Medication/alcohol(G) Trauma 67. Nystagmus 68. nystagmus Torsional nystagmusUsually attributed to dysfunction of vertical semicircular canalinputs ,The fast phase changes with direction; Toward the side of the lesion on downward gaze Away from the side of the lesion on upward gaze Etiologies(A) Stroke(B) MS(C) Vascular malformation(D) Arnold-Chiari syndrome(E) Tumor(F) Encephalitis(G) Trauma 69. Gaze-evoked nystagmusa. Most common nystagmusb. Dysfunction of cerebellar flocculus in conjunction with the lateral medulla for horizontal gaze and the midbrain for vertical gazec. Differential diagnosis/etiologiesi. Medications(A) Antiepileptic agents(B) Sedative hypnotics, alcoholii. Bilateral brain stem lesioniii. Cerebellar lesioniv. MG 70. Vestibular nystagmus The most common form of jerk nystagmus, mostly rotatory. Result from damage of the labyrinth, vestibular nerve,vestibular nucei, or their connections in the brainstem orcerebellum also, in Meniere disease. No change in intensity with removal of fixation (using Frenzelgoggles). Central or peripheral: Peripheral type is associated with vertigo, nausea and vomiting. While in the central type it is less common but associated with neurological findings. 71. Vestibular nystagmus Normally occurs with: Caloric irrigation Galvanic stimulation of the labyrinth or vestibular nerve. 72. Bruns Nystagmus It is bilateral and asymmetrical. It occurs in: large cerebellopontine angle tumors. AICA territory stroke. It is of large-amplitude and low frequency on gaze towardthe side of the lesion but small-amplitude, high-frequencyon gaze to the other side. 73. Ictal Nystagmus It may accompanies adversive seizures. Rarely is the only motor manifestation of a seizure. Nystagmus in comatose patients may be a manifestationof a seizure. 74. Periodic Alternating Nystagmus It is a jerk nystagmus. Its fast phase beats in one direction and then damps or stops fora few seconds before changing direction to the opposite side. A complete cycle takes approximately 1 - 3 minutes. Causes: Congenital Craniocervical junction lesion e.g. MS, Chiari malformations Creutzfeldt-Jakob disease. 75. Monocular nystagmus Causes: Monocular blindness (in blind eye) Amblyopia Spasmus nutans Brainstem infarction Internuclear ophthalmoplegia Multiple sclerosis 76. Opsoclonus1. Pathophysiology: dentate nucleus lesion2. Clinicala. Involuntary bursts of spontaneous saccades in all directionsb. Classic triad i. Opsoclonus ii. Myoclonus iii. Ataxia (trunk and gait)3. Etiologiesa. Neuroblastoma (childhood)b. Infection (young adults)i. Enterovirusii. Coxsackie virus B3, B2iii. St. Louis encephalitis 77. Opsoclonusiv. Rickettsiav. Salmonellavi. Rubellavii. Epstein-Barr virusviii. Mumpsc. Paraneoplastici. Breastii. Lungiii. Uterine/ovariand. Brain stem strokee. Head traumaf. MSg. Midbrain tumor 78. Ocular bobbing1. Clinical: rapid downward jerk with slow return to primary gaze2. Causesa. Pontine lesionb. Subarachnoid hemorrhagec. Head traumad. Leigh diseasee. Cerebellar hemorrhage 79. Oculogyric crisis1. Temporary period of frequent spasms of eye deviation, often upward, Lasts for seconds to hours2. Etiologya. Medicationi. Neurolepticsii. Carbamazepineiii. Tetrabenazineiv. Lithium toxicityb. Brain stem encephalitisc. Retts syndromed. Tourettes syndrome 80. Disorders of the visualsystem and pathways 1. Optic disc edemaCauses of optic disc edemai. Papilledema (elevated intracranial pressure)ii. Optic neuritisiii. Anterior ischemic optic neuropathy (AION)iv. Giant cell arteritisv. Diabetic papillitis 81. Disorders of the visualsystem and pathways 1-Optic neuritisa. inflammation of the optic nerveb. Pain in the involved eye worsened with eye movement followed by monocular vision lossc. Usually young adultsd. 5 females:1 malee. Visual acuity is usually affected with central scotoma as the classic findingf. Relative afferent pupillary defect may persist even after the visual function improvesg. Visual-evoked potential: prolonged P100 82. Disorders of the visualsystem and pathways2-AIONa. Pathophysiology: ischemic infarct of the optic disc due to atherosclerotic disease (nonarteritic AION), or from vasculitis, most commonly giant cell arteritis (arteritic AION)b. Clinicali. NB: Sudden painless vision loss associated with unilateral optic disc swellingii. Usually >45 y/o 83. Disorders of the visualsystem and pathways 3-Papilledemaa. Associated with bilateral optic disc edema due to elevatedintracranial pressureb. Secondarily, compression of the venous structures within the nervehead that causes venous engorgement and tortuosity, capillarydilation, and splinter hemorrhagec. Etiologiesi. Intracranial mass lesionii. Pseudotumor cerebriiii. Hydrocephalusiv. Intracranial hemorrhagev. Venous thrombosis/obstructionvi. Meningitis 84. Disorders of the visualsystem and pathways4-Tumors affecting the anterior visual system, asOptic nerve sheath meningiomas , gliomas 85. Disorders of the visualsystem and pathways5-Toxic/nutritional optic neuropathiesa. Nutritional deficienciesi. Pyridoxineii. B12iii. Folateiv. Niacinv. Riboflavinvi. Thiamine b. Toxici. Ethambutolii. Ethanol with tobaccoiii. Methanoliv. Ethylene glycolv. Amiodaronevi. Isoniazidvii. Chloramphenicolviii. Chemotherapy c. Toxic amblyopiai. Typically affects heavy drinkers and pipe smokers 86. Disorders of the visualsystem and pathways6-Hereditary optic neuropathies Lebers optic neuropathyi. Pathophysiology: maternal mitochondrial DNA point mutationii. Clinical(A) Optic neuropathy: upper limb, acute, painless optic neuritis(B) Asymptomatic cardiac anomalies including accessory cardiac atrioventricular conduction pathways (Wolff-Parkinson-White)(C) Adolescent males 87. Disorders associated with the opticchiasm1. Clinical: classic pattern is bitemporal visual field defects2. Etiologiesa. Sella tumorsi. Pituitary macroadenomas (may have associated endocrineabnormalities): pituitaryapoplexyacute enlargement of a pituitary adenoma due to necrotichemorrhageor postpartum (Sheehans syndrome)ii. Craniopharyngiomasiii. Gliomasb. MSc. Aneurysmd. Trauma 88. Anterior chiasm lesion(Willebrands knee)a. Nasal retinal fibers cross anterior in the chiasm before joining the contralateral temporal fibersb. Signs/symptomsi. Ipsilateral monocular central scotomaii. Contralateral upper temporal field cut 89. Retrochiasmal visual pathways Disorders of the optic tract Disorders involving the lateral geniculate nucleus Optic radiations Occipital lobeMost common causesStroke, SOL 90. Disorders of pupillaryfunction Pupil should be Regular ,Rounded, Equal in sizeTopical cholinergic agents that influence pupil sizea. Cholinergic agonists that produce miosisi. Pilocarpine , Carbachol , Methacholine , Physostigmine , Organophosphate insecticidesb. Cholinergic antagonists that produce mydriasisi. Atropineii. Scopolamine 91. Disorders of pupillaryfunctionAdrenergic agonists that produce mydriasisEpinephrine , Phenylephrine, Cocaine,Hydroxyamphetamine Ephedrine,b. Adrenergic antagonists that produce miosisGuanethidineReserpineThymoxamin 92. Disorders of pupillaryfunction(Marcus Gunn pupil)a. Diagnosis via swinging flashlight testb. Etiologiesi. Amblyopiaii. Retinopathiesiii. Maculopathiesiv. Optic neuropathiesv. Optic chiasm lesionsvi. Optic tract lesionsvii. Midbrain lesion involving the pretectal nucleus or the brachium of the superior colliculusviii. Lateral geniculate nucleus 93. Disorders of pupillaryfunction Large and poorly reactive pupili. Unilateral(A) Adies tonic pupil(B) Pharmacologic (anticholinergic agent, jimson weed, adrenergic agonist)(C) Trauma/surgery(D) Ischemia (carotid artery insufficiency, giant cell arteritis, carotid cavernous fistula)(E) Iridocyclitis(F) Complication of infection (e.g., herpes zoster)(G) CN III palsy(H) Tonic pupil associated with peripheral neuropathy or systemic dysautonomia 94. Disorders of pupillaryfunctionBilateral(A) Adies tonic pupils(B) Pharmacologic (anticholinergic agent, jimson weed, adrenergic agonist)(C) Parinaud syndrome(D) Argyll-Robertson pupils(E) CN III palsy(F) Carcinomatous meningitis(G) Chronic basilar meningitis(H) Guillain-Barr syndrome(I) Eaton-Lambert syndrome(J) Botulism 95. Disorders of pupillaryfunctionArgyll-Robertson syndrome Miotic irregular pupilsLight-near dissociation(A) Absence of light response associated with normal anterior visual pathway function(B) Brisk pupillary constriction to near objectiii. Normal visual acuityiv. Diminished pupillary dilatation, particularly in darkv. Usually bilateral 96. Disorders of pupillaryfunctionEtiologyi. Neurosyphilisii. Muscular dystrophyiii. MSiv. Chronic alcoholismv. Sarcoidosis 97. Disorders of pupillaryfunctionHorners syndromei. Miosisii. Ptosis (denervation of Mllers muscle)iii. Anhidrosis (ipsilateral facial) 98. Disorders of pupillaryfunction(A) Brain stem (Wallenbergs) or thalamic stroke(B) Intra-axial tumor involving the thalamus, brain stem, orcervical spinal cord(C) Demyelination or inflammatory process involving thebrain stem or cervicalspinal cord(D) Syringomyelia(E) Neck trauma 99. Disorders of pupillaryfunction(A) Tumors involving the pulmonary apex, mediastinum,cervical paravertebralregion, or C8T2 nerve roots(B) Lower brachial plexus injury(C) Subclavian or internal jugular vein catheter placement(D) Stellate or superior cervical ganglion blocks(E) Carotid dissection below the superior cervical ganglion 100. Disorders of pupillaryfunction(A) Internal carotid artery dissection(B) Cluster headache(C) Skull base or orbital trauma or tumors(D) Intracavernous carotid artery aneurysm(E) Carotid endarterectomy(F) Herpes zoster ophthalmicus(G) Complicated otitis media 101. Disorders of pupillaryfunction Opiate overdosea. Bilateral pinpoint pupilsb. Also seen in pontine dysfunction 102. Fundus examinationAdjust the diopter dial to bring the retina into focus.*Find a blood vessel and follow it to the optic disc.*Inspect outward from the optic disk in at least four quadrantsand note any abnormalities.* Move nasally from the disk to observe the macula 103. Normal fundus 104. Why it is performed Fundus examination is one of the most valuable testsconducted during an eye examination because it can detectsome signs and physiological effects of various circulatory,metabolic and neurological disorders. Fundus examination is routinely used to assess anddiagnose vitro-retinal diseases (such as diabetic retinopathy,retinal tear and detachment, macular hole, retinalhaemorrhage, retinal artery and vein occlusion, choroidaltumor, or macular edema), optic nerve defects, andhereditary diseases 105. StagesEarly papilledema I Earliest change is disc hyperemia and dilated capillaries. Blurring of disc margins, Spontaneous venous pulsation is absent Splinter hemorrhages at or just off the disc-margin. 106. . An optic nerve with mild swelling (papilledema).Note the pathologic"C"-shaped halo of edema surrounding the optic disk (Grade I papilledema). 107. stageIIEstablished papilledema: Disc margins become indistinct and centralcup is obliterated.Disc surface is elevated above the retinal plane (more than + 3D (1mm) with direct ophthalmoscope). Peripapillary oedema. Venous engorgement . Flame-shaped hemorrhages and cotton-wool spots around the disc. Hard exudates in radiating pattern around the macula, [macular star] 108. Grade II papilledema. The halo of edema now surrounds the optic disc 109. Stage IIIChronic papilledema or Vintage papilledema: Disc edema resolves, but margins are blurred Hemorrhagic and exudative components gradually resolve. Optic disc appears pale like a champagne cork. 110. Stage IVAtrophic papilledema Peripapillary retinal vessels are attenuated and heathed.Dirty-white appearance of the optic disc, due to reactive gliosis leading to secondary optic atrophy. 111. Grade IV papillededema. With more severe swelling in addition to a circumferential halo, the edemacovers major blood vessels as they leave the optic disk (grade III) and vessels on the disk (grade IV).