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Visual Loss Chitsaz A. MD. Professor of Neurology Isfahan University of Medical Sciences, fellowship of Movement Disorders.

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Presentation on theme: "Visual Loss Chitsaz A. MD. Professor of Neurology Isfahan University of Medical Sciences, fellowship of Movement Disorders."— Presentation transcript:

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2 Visual Loss Chitsaz A. MD. Professor of Neurology Isfahan University of Medical Sciences, fellowship of Movement Disorders

3 Visual loss commonly accompanies neurological disease: Ophthalmic causes: Neurological causes pattern of visual loss: central of visual loss peripheral visual loss

4 Temporal profile of visual loss Sudden monocular visual loss Sudden binocular visual loss Without progression, with progression

5 Central visual loss: Scotoma: a defect in visual field surrounded by normal vision Quickly noticed Resulting from lesions of central retina or optic nerve.

6 Peripheral visual loss visual field detect Classified in to three groups Prechisma, chiasmal, retro chiasmal Visual field of one eye: Unilateral prechiasmal lesions Visual fields of both eyes: non homonymous bitemporal: chiasmal lesions Homonymous field defects: retrochiasmal lesions

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8 Transient Monocular visual loss: -Amaurosis fugax Emboli from the carotid or heart to the retinal circulation Attacks are sudden in onset Last from several to 15 minutes Retinal migraine: accompany by headache Closure angle claucoma: attach of eye pain, vomiting, halos around lights, prevent blindness Uhthoff phenomonow: In optic neuritis of MS, increase blurred with body temperature

9 Transient Binocular Visual loss Bilateral optic disc edema Transient dysfunction of visual cortex Migraine aura, visual Cerebral hypoperfusion due to vasospasm, thrombuembolism, systemic hypotension, hyperviscosity, vascular compression

10 Sudden Monooncular Visual Loss Without Progression: AION: Anterior ischemic optic neuropathy Due to loss of blood supply to the optic nerve head Etiology: in younger than 60 year- non arthritic in older than 60 year: giant cell arthritis: urgent, elevated ESR, CRP, giant cells on temporal artery biopsy, treatment with corticosteroids to prevent of blindness

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14 PION: posterior ischemic neuropathy: Perioperative hypotension, spinal surgery, cardiac by pass surgery, hemodynamic shock Central retinal artery occlusion: cause by thrombo embolic events Central retinal veins occlusion: cause by venous thrombosis

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17 Sudden Binocular Visual Loss Without Progression. Result from: Stroke bilateral occipital lobe infarcts cortical blindness

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19 Sudden visual loss with progression Optic neuritis: sudden onset, painful monocular visual loss, worsen, progress over hours to days, stabilizing and than improve: First sign of MS Slow growing compressive lesions: tumors, aneurysm, thyroid ophthalmopathy Careful questioning of patient reveal long- standing deficit that has suddenly been noticed

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21 Progressive visual loss: Is the hallmark of a lesion compressing the afferent visual pathways: pituitary tumors, aneurysms, cranio pharyngiomas, Thyroid orbitopathy: optic nerve compression at orbit apex Hereditary optic neuropathy gradual onset of visual loss Toxic and nutritional: gradual onset visual painless, binocular, vitamin B deficiencies, isoniazide, ethambutol chloroquine

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23 Papilledema: Bilateral optic disc swelling: secondary to IICP Swelling optic disc and elevation, hyperemic of disc, venous dilation of disc, absence of venous pulsation, hemorrhages After weeks to months papilledema becomes chronic result to optic atrophy Causes of papilledema to IICP: brain tumor, cerebral edema due to stroke, ICH, CVT, psedotomor cerebri due to use of vit A, obese women with irregular mense.

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25 Pseudopapilledema Optic disc drusen: calcium deposit within optic nerve head, there is no visual acuity, and visual complain Congenital: optic disc dysplasia.

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27 Pupillary abnormalities Size of pupil parasympathic control: sphincter pupilla. sympathetic control: dilator pupilla. Sphincter located circumferentially around the pupil and constricts the pupil on exposure to light Dilator: is situated radically and dilate the pupil in darkness

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29 Pupillary light reflex On exposure to light, the pupil constricts Afferent limb of light reflex originates in retinal ganglion cells, travel via the optic nerve, chiasma, optic tract, midbrain pretectom, superior collicus, from this neuronal signals are relayed bilaterally to the paired parasympathetic Edinger westphal nuceli of the oculomotor nerve

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32 Efferent limb of light reflex: consists of preganglionic parasympathetic fibers traveling the Edinger-westphal in both oculomotor nerves to the intraorbital cilliary ganglion and postganglionic cilliary nerves caring Parasympathetic to the sphincter muscle.

33 Sympathetic nerves destined for the dilator muscle consist of a chain of three neurons: First order neuron: originate in hypothalamus descend in brain stem and in the intermedio- lateral cell column of the spinal cord to the thoracic level (T2)

34 Second order neurons: After first-neurons synapse in spinal cord second neurons exit to the paravertebral cervical sympathetic chain, ascend near lung apex and them with internal carotid artery reach to superior cervical ganglion in the neck in angle of jaw and synapse with third order neuron.

35 Third-order neurons: From superior cervical ganglion 3th neuron ascend with carotid artery through the skull base and into cavernous sinus, joint with abducent and trigeminal nerves and enter the orbital apex and via long ciliars nerve reach the dilator muscle

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38 Marcus GUNN publics RAPD: Relative afferent pupillary defect or Marcus GUNN pupils a hall mark of optic nerve disease. It is manifestation of unilateral disruption of the afferent limbs of the pupillary light reflex via the optic nerve When light stimulus applied to one eye both pupils constrict as a result of the bilateral connections between protected nuclei and edinger-westphol nuclei.

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41 Evaluate for RAPD by flash light test When the light stimulus is applied to the normal eye, bilateral pupillary construction and when the light stimulus is transferred to the eye with optic neuropathy, loss construction with initial dilation.

42 Anisocoria: unequal pupils Magnification of old photograph Abnormal pupillary size caused visual dysfunction Fixed, dilated pupil fails to protect the retine from increased illumination and causes photophobia and slow dark adaptation. Small, poorly reactive pupils results in poor night vision or dim day time vision.

43 Pupil examination Observation of the resting position of the pupils in the ambient room Degree of anisocoria in light and dark should be evaluated Anisocoria that is more pronounced in the light, suggest that large pupil is abnormal because the small pupil will constrict normally to light Anisocoria that is more pronouced in the dark suggest that the small pupils is pathologic because normal pupil will dilate in the dark.

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45 Next stop in the examination of pupils is evaluation of the direct and consensual pupillary reflexes. Evaluation of pupillary near response: having the patient hold the thum several inches in front the eyes while looking across the room and then shift gaze on the thum.

46 Pharmacological testing: Once abnormal pupils is identified for localization pharmacological testing with eye drop, drop into each eye, 30 minutes later reexamination of pupils. Is there construction to pilocarpin: tonic pupil Is there construction to hydroxy amphetamine Horner syndrome (preganglion and if no post ganglionic Horner syndrome Pilocarpine: will constrict the tonic pupil but no a normal pupil or dilated pupil due to occulomotor palsy or pharmacological toxicity.

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48 Parasympathetic dysfunction: Postganglionic, preganglionic Post ganglionic parasympathetic dysfunction: tonic pupil (Mydriasis): large and react poorly to light and slowly to near stimuli Causes of tonic pupils: damage to cilliary ganglion or short ciliary nerve (herpes zoster, trauma, giant cell arthritis), neuropathy (GBS), botulism.

49 Preganglionic parasympathetic dysfunction: Oculomotor palsy: Mydriasis (pupillary enlargement) Ophthalmoplegia (palsy of inf and sup rectus, inf oblique muscles) Ptosis due to involvement of the levator palpere.

50 Horner syndrome Sympathetic dysfunction, trial: ptosis miosis facial anhidrosis. The lesion may be a where along three neuron sympathetic pathway Causes: Inflammatory Compressive: neoplastic (pancost tumor), carotid dissection.

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52 Eyelid abnormalities The width of palperbial fissure is determined by balance of: orbicularis oculi (VII), levator palparal (III), muler muscle (sympathetic). Eye closure by orbiculoris oculi Eye opening by levator palpebre and muler muscle Resting position of the eyelids: The normal palpepral fissure: mm, upper eyelid normally cover the upper 1 to 2 mm of the iris, upper border of Lowe eyelid just lower border of the iris

53 With upper lid retraction: superior sclera show With lower lid retraction: inferior sclera show Bilateral ptosis: patient effort to elevate the lids have frontalis contraction and eye brow elevation Narrowed palpepral fissures: ptosis Psudoptosis: dermay chalasis of eyelid skin, contralateral lid retraction True ptosis: congenital, myopathies, MG, aging (sensile ptosis), inflammation, trauma Neurogenic etiologies: Horner syndrome, oculomotor palsy.

54 Dynamic eyelid abnormalities: Bepharospasm: uncontrolled bilateral oribicularis oculi contraction causes eyelid closure, focal dystonia Apraxia of lid opening: when asked to patient open their eyes, contract the forehead and elevate brows: cerebral lesion, PD Hemifacial spasm: paroxysmal, in voluntary, synchronous contraction of all muscles innervated by the facial nerve in one side. Idiopathic, MS, CP angle tumor.

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