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Neuro-Ophthalmology PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Neuro-ophthalmology” by Marek Michalec, MD.

This medical PowerPoint presentation is about neuro-ophthalmology, a specialized field of medicine that deals with visual problems related to the nervous system. It involves the diagnosis and treatment of eye movement disorders, vision loss, double vision, optic nerve diseases, and other neurologic conditions that affect vision.

Neuro-ophthalmologists are trained to identify and manage conditions that affect the visual system, such as brain tumors, strokes, multiple sclerosis, and other neurological disorders. They work closely with other specialists, including neurologists, neurosurgeons, and ophthalmologists, to provide a comprehensive approach to patient care.

Some of the common conditions that neuro-ophthalmologists treat include optic neuritis, papilledema, nystagmus, diplopia, and visual field defects. They may also use specialized tests, such as visual evoked potentials (VEP) and electroretinograms (ERG), to diagnose and manage these conditions.

Overall, neuro-ophthalmology is an essential field that plays a critical role in maintaining and improving visual health for patients with neurological conditions.

Tags : Neuro-ophthalmology, eye movement disorders, vision loss, double vision, optic nerve diseases, Ophthalmology, Ophthalmology PowerPoint presentation

Published on : Jun 20, 2023 | Views : 1827 | Downloads : 0

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Slide 1-

Neuro-ophthalmology Marek Michalec, MD.
Slide 2-

Neuro-ophthalmology Study integrating ophthalmology and neurology Disorders affecting parts of CNS devoted to vision or eye: Afferent system (visual pathway, incl. optic nerve) Efferent system (ocular motor control, pupillary function)
Slide 3-

Part I Neuro-ophthalmologic Examination
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Examination History Eye examination (visual acuity, tonometry, anterior segment examination, funduscopic examination) Perimetry Color vision, contrast sensitivity, electrophysiology (ERG, VEP) MRI of brain, Neurologic examination
Slide 5-

Visual acuity Each eye separately Distance and near vision Using of corrective lenses, pinhole Using Snellen chart (20 feet) – normal 20/20 Count fingers, hand motion, light perception, no light perception
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Color vision Each eye separately Comparison between eyes Examination: pseudoisochromatic plates (Ishihara) 100 Hue test (Farnsworth-Munsell)
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Farnsworth-Munsell 100 Hue test Ordering the color tiles as patient sees it
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Contrast sensitivity Examining spatial frequency Decreased in some optic nerve disorders (typically optic neuritis)
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Perimetry To assess the quality of visual field Characteristic visual field defect =location of possible intracranial lesions
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Perimetry Automated static perimetry
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Perimetry Goldmann kinetic perimetry
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Electrophysiologic examination ERG = Electroretinography Access possible functional pathology of retina (scotopic, photopic and central part) Flash ERG (activity of bipolar cells as an answer to stimation of photosensitive cells – rods, cones) Pattern ERG (activity of gaglionar cell as a response to stimulation of cones in macula) VEP = Visual evoked potentials (responses) Access the capability of anterior visual pathways –optic nerve Major use: diagnosis/confirm of optic neuritis
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Electrophysiologic examination
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Electroretinography
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Visual evoked potentials
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Multifocal ERG, Multifocal VEP Mostly experimental use, not standard in clinical medical practice here
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Part II Pathology of Afferent system
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Afferent system Retina (cones, rods, bipolar and ganglion cells) Optic nerve Optic chiasm Optic tract Lateral geniculate body Optic radiation Visual cortex (V1 = Brodmann area 17)
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Pathologies of Afferent Visual System Papilledema Optic Neuritis Optic Neuropathy Optic Atrophy
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Papilledema Not a disease - sing secondary due to elevated intracranial pressure (ICP) Unspecific sign Require immediate diagnosis = increased ICP is a life-threatening situation!!! 60% of cases = increased ICP caused by intracranial tumor!!! Other possible causes: hydrocephalus, meningitis, encephalitis, brain abscess...
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Papilledema Clinical picture Early Margins are obscured Optic cup initially preserved Hyperemic disc Acute Elevation of disc Radial hemorrhages Grayish-white exudates Chronic Disc edema Obiterated optic cup
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Optic neuritis Inflammation of the optic nerve Intraocular – within the globe Retrobulbar – posteriot to the globe Usually unilateral Tendency to repeat Etiology Often associated with multiple sclerosis (MS) = demyelinating optic neuritis (20% = first sign of MS) Other possible inflammatory causes: Lyme disease, syphilis, inflammation from orbit, paranasal sinuses...
Slide 23-

Optic neuritis Symptoms Sudden vision loss within several hours (mild blurring/light perception) Central, paracentral scotoma Retrobulbar/parabulbar pain Present afferent pupillary defect Prognosis depends on underlying disorders MS = usually good – significant spontaneous improvement (several weeks) Some permanent disturbances of vision are possible (color vision decreasing, scotoma)
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Anterior Ischemic Optic Neuropathy Etiology Acute disruption of blood supply (due to vascular changes, infarction) Symptoms Sudden unilateral loss of vision Altitudinal or wedge-shaped visual field defect Present afferent pupillary defect Clinical picture Edema of optic disc Segmental obscuration of margins (correlation with visual field defect)
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Anterior ischemic optic neuropathy 2 forms Benign: Nonarteritic AION Malign: Arteritic AION Arteritic AION Association with systemic vasculitis (giant cell arteritis) Diagnosis: sedimentation rate, biopsy of temporal artery High risk of affection of contralateral (fellow) eye within days/ weeks!!! Need for immediate therapy with high dose intravenous corticoids!!!
Slide 26-

AION forms
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Optic Atrophy Irreversible loss of axons as a result to damage of optic nerve Etiology Primary due to trauma, direct pressure by tumor Secondary due to affection of optic nerve (optic neuritis...) Glaucomatous due to glaucomatic damage Pathogenesis Ascending - lesion located anterior to the lamina cribrosa Descending – lesion located posteriot to the lamina cribrosa
Slide 28-

Optic Atrophy Clinical picture Total/partial pale optic disc Well defined / blurred margins Constricted / reduced retinal vessels Etiology Vascular (AION, RAO) Inflammation (optic neuritis, neuroinfections) Compressive (orbital/intracranial mass) Traumatic (avulsion, bone fracture) Toxic (methyl alcohol, various poisons, cytostatics) Congenital/hereditary (LHON, Kjer atrophy) Systemic (hematooncological diseases)
Slide 29-

Part III Pathology of Efferent system
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Efferent system 1) Cranial neuropathies (III, IV, VI) 2) Pupillary abnormalities
Slide 31-

Eye movement Ocular motility – produced by extraocular muscles 4 rectus muscles (lateral, medial, superior, inferior) 2 oblique muscles (superior, inferior)
Slide 32-

Cranial neuropathies Signs Oculomotor nerve palsy Diplopia Multiple muscle paralysis Ptosis Anisocoria Trochlear nerve palsy Vertical diplopia Abnormal head tilt Abducens nerve palsy Horizontal diplopia in the gaze palsy
Slide 33-

Cranial neuropathies Etiology Ischemic (diabetes, hypertension, hyperlipidemia) Demyelinating disease (MS) Compressive (tumor, aneurysm) Elevated ICP Multiple cranial neuropathies = suspect lesion in the posterior orbit or cavenrous sinus region
Slide 34-

Pupil Miosis – parasympathetic nervous system Mydriasis – sympathetic nervous system
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Slide 36-

Sympathetic pathway
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Pupillary abnormalities Anisocoria inequality of pupil size May be physiologic Possible accidental discovery May be isolated / associated with eyelid or ocular motility abnormalities Diagnosis Direct shine at pupil Test near response (miosis with accomodation) Pupil sizes in light and dark
Slide 38-

Horner’s Syndrome Signs Miosis (pupil does not dilate in dark) Ptosis Pseudo-enophthalmus Anhidrosis (diminished sweating) Heterochromia (if congenital) Etiology Trauma, internal carotid artery dissection, brain stem strokes, MS, brain tumor, syringomyelia, apical lung tumor, goiter, thyroid carcinoma...
Slide 39-

Adie’s Pupil Signs No present / slow miosis to light Present miosis to accomodation Pupil is larger with light/near dissociation Etiology Inflammation (viral or bacterial infection) Therapy Pilocarpine drops, thoracic sympathectomy
Slide 40-

Thank you for your attention!