Optic Neuropathy.pdf

Optic Neuropathy ____________________________________________________________________________________________ Optic Nerve Anatomy Cranial nerve II, the second of twelve paired cranial nerves. Each human optic nerve contains 1.2 million nerve fibers. These fibers are axons of the retinal ganglion cel...

Optic Neuropathy ____________________________________________________________________________________________ Optic Nerve Anatomy Cranial nerve II, the second of twelve paired cranial nerves. Each human optic nerve contains 1.2 million nerve fibers. These fibers are axons of the retinal ganglion cells of one retina. Optic Nerve Anatomy The optic nerve is ensheathed in all three meningeal layers (dura, arachnoid, and pia mater). The optic nerve leaves the orbit (eye socket) via the optic canal, running postero-medially towards the optic chiasm. In optic chiasm there is a partial decussation (crossing) of fibers from the temporal visual fields (the nasal hemiretina) of both eyes. Temporal fibers or retina goes ipsilateral and detect nasal visual field. Nasal fibers or retina decussates (contralateral) in optic chiasm and detect temporal visual field. From there, the nerve fibers become the optic tract. Passing through the thalamus and turning into the optic radiation. Until they reach the visual cortex in the occipital lobe at the back of the brain. This is where the visual center of the brain is located. Optic Nerve Physiology The light stimulation of the retina, travel via the optic nerve as electrical signals to visual cortex and ultimately interpreted as visual images. The eye's blind spot is a result of the absence of photoreceptors in the area of the retina where the optic nerve leaves the eye. Fiber tracks of the mammalian central nervous system (as opposed to the peripheral nervous system) are incapable of regeneration, and, hence, optic nerve damage produces irreversible blindness. Classification of Optic Neuropathy I. GLAUCOMATOUS OPTIC NEUROPATHY. II. Non GLAUCOMATOUS OPTIC NEUROPATHY: - INFLAMMATORY OPTIC NEUROPATHY. - ISCHEMIC OPTIC NEUROPATHY. - INFILTRATIVE OPTIC NEUROPATHY. - COMPRESSIVE OPTIC NEUROPATHY. - Traumatic optic neuropathy III. Papilledema 1 Informations Inflammatory optic neuropathy (Optic Neuritis) Symptoms Is caused by a number of underlying conditions: - Autoimmune disease. - Systemic infection. The most commonly associated cause of inflammatory optic neuropathy is demyelinating optic neuritis secondary to multiple sclerosis (MS). Pathophysiology: - Patient is typically female, white, age 20 to 40 years. Typically present with ocular pain (exaggerated upon eye movement). Noticeable changes in color vision in the affected eye. Variable unilateral loss of vision, ranging from A complex cascade of inflammatory events begins 20/30 to no light perception. peripherally in the body. This is often accompanied by an afferent pupillary Activation of T lymphocytes. defect (APD). The activated cells cross the blood-brain barrier and gain Visual field defect in form of cecocentral scotomas access to the central nervous system. The initial inflammatory cascade leads to phagocytosis of In acute optic neuritis: the myelin sheath. Disc edema As a result, gliotic tissue is laid down in place of missing Disc hemorrhages myelin. This substitutive tissue lacks the conduction properties of Segmental or diffuse optic disc pallor Results from mechanical mass effect secondary to: ISCHEMIC OPTIC NEUROPATHY Non-Arteritic (NAION) 95% Arteritic (AAION). 5% No specific demographic predilection to age or gender Slowly progressive process with changes or fluctuations in visual acuity or missing visual field that occur over several months to years. Changes in color vision. Diplopia ( double vision), results from interruption of any of the cranial nerves innervating the extraocular muscles (CN III, IV, VI). The optic disc's appearance may vary greatly depending on the lesion's magnitude. Early in the compressive disease process, the optic disc may appear normal. Optic disc edema. Atrophic changes (most often due to chronic compression). Presence of optociliary shunt vessels. Is by accurately diagnosing and promptly treating the underlying cause of the compression is vital to preserve the patient's vision and medical health. Surgical and medical treatments directed at managing the underlying etiology may result in recovery of acuity, fields and symptoms. Non-Arteritic (NAION) 95%: Cause of NAION: Hypoperfusion or Non-perfusion of the optic nerve head. Risk factors of NAION: Diabetes mellitus Hypertension Hypercholesterolemia. Smoking. NAION: Mean age of onset: 60 years Patients present with Painless vision loss developing over hours to days. Visual loss less severe than AAION. No systemic symptoms. Segmental or diffuse disc swelling, hyperemic or pale. Peripapillary retinal heamorrhages. Disc in fellow eye “ disc at risk” : small, crowded, elevated with blurry margin NAION: observe , control risk factors Arteritic (AAION) 5%: The main cause of AAION is vasculitis of the short posterior ciliary vessels supplying the optic nerve head leading to ischemia. Associated with giant cell arteritis. Men age of onset: 70 years Headache is the most common symptom. Scalp tenderness Jaw claudication Malaise, anorexia, weight loss, fever Patients typically present with Severe visual loss, developing over hours to days. Pallid disc edema Disc of fellow eye: normal AION: High-dose ( steroid) oral prednisone or intravenous methylprednisolone followed by a course of oral prednisone. Most commonly found in association with Sarcoidosis Can result from: Systemic infection. Systemic lupus erythematoses SLE. Blood-borne cancers and metastatic disease. Pathophysiology "Infiltration Process": - Bloodstream carries pathologic cells to the meninges via the perivascular and subarachnoid space >> - Once present in meningeal tissue, these cells have the capability to invade the cranial nerves. - Infiltration of optic nerve tissue along with accompanying impairment to its blood supply lead to infarction and loss of axons. Reduction in visual acuity. Reduction in color vision. Reduction in contrast sensitivity that is typically painless, unilateral or asymmetric and variable. APD is often present. Associated ocular inflammation (iritis, vitritis, pars planitis, intermediate uveitis) can be present depending on the etiology. The optic disc is often diffusely edematous. To treat the underlying cause. Tumors ( Intracranial,Chiasmal, or Optic Nerve tumors). non-neoplastic lesions: - Retrobulbar hemorrhage. - Aneurysm. - Mucocele. - Orbital apex syndrome. These masses impinge on intra-orbital or intracranial structures of the visual pathway. Compression can be Unilateral or Bilateral. Traumatic Optic Classically divided into: - Direct injury: external object penetrates the tissues and Neuropathy impact the optic nerve. - Indirect injury: collision to the skull and the energy is absorbed by the optic nerve. Usually associated with mid-face trauma. Causes: Motor Vehicle Accident (MVA), most common cause. Bicycle Fall Assault Papilledema Intravenous steroid ( methylprednisone ) , administered over the course of three days followed by an 11-day course of oral prednisone. myelin, the nerve impulse is interrupted. Compressive Optic Neuropathy INFILTRATIVE OPTIC NEUROPATHY manegment Bilateral disc swelling due to increased intracranial pressure. Causes: Primary and metastatic intracranial tumors. Hydrocephalus. Pseudotumor cerebri: Often occurs in young, overweight females. Subarachnoid hemorrhage: Severe headache, may have preretinal hemorrhages (i.e., Terson syndrome). Arteriovenous malformation. Brain abscess: Often produces high fever. Meningitis: Fever, stiff neck, headache. Encephalitis: Often produces mental status abnormalities. Cerebral venous sinus thrombosis. AION: History of trauma Loss of vision after the trauma Commonly associated with loss of consciousness. Vision: is often significantly reduced. Pupillary reflex: afferent pupillary defect (APD) Associated ocular injury. Fundoscopy: - Acutely the optic nerve appears normal. - Weeks later, optic nerve pallor develops. - Vitreous hemorrhage - Retinal hemorrhage Episodes of transient, often bilateral visual loss (lasting seconds), often precipitated after rising from a lying or sitting position (altering intracranial pressure); Headache ; Double vision ; Nausea ; Vomiting ; Rarely , a decrease in visual acuity Bilaterally swollen, hyperemic discs Papillary or peripapillary retinal hemorrhages Dilated, tortuous retinal veins; Normal pupillary response and color vision; Enlarged physiologic blind spot by formal visual field testing. Done By Sara Alzahrani Best of luck Treatment should be directed at the underlying cause of the increased intracranial pressure.