Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Neuro-Ophthalmic Disease Cases Kelly A. Malloy, OD, FAAO, Diplomate Clinical cases will be used to demonstrate the varied presentations related to neuro-ophthalmic disease. These will include both afferent and efferent manifestations of neuro-ophthalmic disease, as well as associated ocular health and neurologic manifestations. Conditions that may be demonstrated through clinical cases are included in the outline below. Course Learning Objectives: 1. To emphasize the importance of the optometrist’s role in identifying signs and symptoms which suggest a neuro-ophthalmic disease process. 2. To understand how to conduct an examination oriented to the detection of neuro-ophthalmic disease. 3. To discern the differential diagnoses for a variety of clinical neuro-ophthalmic presentations. 4. To become familiar with the necessary diagnostic testing for a variety of neuro-ophthalmic presentaions. 5. To emphasize the need to promptly identify and refer patients presenting with emergent neuro-ophthalmic disease conditions. 6. To have a better understanding of the work-up, management, and treatment of neuro-ophthalmic disease conditions. Neuro – Ophthalmic Disease Cases - OUTLINE Conditions that may be demonstrated through actual clinical cases are included in the outline below. PAPILLEDEMA Papilledema - Bilateral/Asymmetric (anatomic difference in lamina) ICP (Intracranial pressure) greater than 200 - 250 mm H2O RARELY Unilateral Features of edema Axoplasmic stasis in pre-laminar optic nerve Obscuration of retinal vessels coursing over the disc margin Paton’s lines temporally Symptoms of Increased Intra-Cranial Pressure Headache Nausea Vomiting Diplopia (Abduction deficit – CN VI) Pulsatile tinnitus Transient Visual Obscurations (TVOs) Last few seconds (uni or bi-lateral) Transient optic nerve ischemia Pattern of Edema Corresponds with NFL thickness Superior, Inferior > Nasal > Temp Superior and Inferior NFL swell first Last to swell is Temporal NFL NFL swelling blurs disc margins and obscures underlying vessels Spontaneous Venous Pulsation Presence of SVP means ICP normal (at that moment - can fluctuate) 10-20 % of normals may not have SVP PSEUDOTUMOR CEREBRI IMPOSTERS Tumor Cerebri Anomalous Discs, Obesity, Migraine Venous Sinus Thrombosis Arteriovenous Malformation Spinal Cord Tumors PSEUDOTUMOR CEREBRI IS A SYNDROME BASED UPON: MODIFIED DANDY’S DIAGNOSTIC CRITERIA PATIENT MUST BE AWAKE & ALERT SIGNS & SYMPTOMS OF INCREASED ICP NO NEUROLOGIC SIGNS EXCEPT CN VI PARESIS CSF OPENING PRESSURE > 200MM. H20 & NORMAL COMPOSITION NORMAL MRI, CT PSEUDOTUMOR CEREBRI - EPIDEMIOLOGY 92% Women Ages 11-58 No Racial Bias 13/100,000 In Women - 10% Above Ideal Body Weight 19/100,000 - 20% Above Ideal Body Weight PSEUDOTUMOR CEREBRI INVESTIGATIONS MRI and MRV (MRA) LUMBAR PUNCTURE with opening pressure and analysis of CSF TREATMENT WEIGHT LOSS (6%) CARBONIC ANHYDRASE INHIBITORS acetazolamide (diamox); up to 1000 mg. reduces CSF by 50% but may be unsustained! Contraindicated in renal disease SURGICAL TREATMENT Lumboperitoneal Shunt Optic Nerve Sheath Fenestration Gastric Bypass Surgery PROGNOSIS 49% Have Some Visual Loss (Corbett 1982; Orcutt 1984) 25% Severe & Permanent Visual Loss (Folley 1955; Boddle 1974) 80% Improve In 8 Months (Corbett 1982) 10% Recurrence Rate CRANIAL NERVE III PALSY Hyper Deviation Which Increases In Upgaze And Reverses In Downgaze Exo Which Increases Across From The Vertically Limited Eye DEATH FROM SUBARACHNOID HEMORRHAGE (SAH) (LOCKSLEY 1969) 20% Of Patients With SAH Die Within 48 Hours need to consider aneurysm in all CN III palsy ANSWER BY PUPIL INVOLVED=ANEURYSM SPARED=VASCULOPATHIC DOES NOT APPLY IF: Complicated CNIII Incomplete CNIII Relative Sparing 20-50 Years Of Age ABERRANT REGENERATION OF CN III Pseudo Graefe Sign Eyelid Synkinesia •Light-Gaze Disassociation Pupils ABERRANT REGENERATION OF CN III - CAUSES COMMON CAUSES: Aneurysm, Tumor, Trauma UNUSUAL: Inflammation NEVER: Diabetes Mellitus ISOLATED CN III PALSY IN ADULTS Undetermined 24% Aneurysm 21% Ischemia 18% Trauma 13% Neoplasm 12% CN III PALSY Work-up ADULTS 20-50 YEARS CT, MRI, MRA, Arteriogram 50+ YEARS (pupil, palsy, pain) Neuroimaging Vasculopathic Evaluation CNIV PALSY Vertical Diplopia , Worse at Near, Object Tilting, Relief With Head Position A Hypertropia That Increases Across From The Vertically Limited Eye And On Ipsilateral Head Tilt MEASURING EXCYCLOTORSION Subjective, Maddox Rod, Bagolini Striated Lenses, Fundus, Plot Blindspot OBJECTIVE vs. SUBJECTIVE EXCYCLOTORSION Objective = Subjective - Acute Objective > Subjective - Longstanding Objective Without Subjective - Congenital “CHECKLIST” EXAMINATION what to look for: CONTRA HORNER’S CONTRA INO IPSI RAPD DMS BILATERAL CNIV TRUNCAL ATAXIA & IPSI DYSMETRIA IPSI CN III, V1, VI, OSP anatomic localization: LOCUS CERULEUS (Copetto 1983) MLF (Vanooteghem 1992) BRACHIUM SUP COLL (Elliot 1991) ANT MEDULLARY VELUM ANT MEDULLARY VELUM SUP CEREBELLAR PEDUNCLE CAVERNOUS SINUS BILATERAL CNIV R HYPER> IN L GAZE & RHT, L HYPER> IN R GAZE & LHT V PATTERN ESO > 25 PD, EXCYCLOTORSION > 10 deg (LOOK FOR THE DORSAL MIDBRAIN SYNDROME) ISOLATED CN IV IN KIDS (CAUSE) Trauma, Congenital ISOLATED CN IV IN ADULTS 10% Aneurysm, 20% Ischemic, 30% Undetermined, 40% Trauma TRAUMATIC CNIV PROGNOSIS (SYDNOR 1982) SPONTANEOUS RECOVERY: UNILATERAL: BILATERAL: 65% 25% WHAT DO I DO? History Of Trauma?, Old Photos, Vertical Vergences, Neuro-Imaging, Vasculopathic Eval, MG?, Graves?, Skew? CNIV: MANAGEMENT? Segmental Prisms & Patches X 9-12 Months Monitor For Secondary Contracture - Surgical Intervention _______________________________________________________________________ ABDUCTION DEFICIT/ CN VI PALSY F ABDUCTION DEFICIT CN VI PALSY KEY POINTS - Measure At Distance Imposters – Abduction Deficits Graves Disease / Thyroid Orbitopathy, Myasthenia Gravis, Loss Of Fusional Reserves, Spasm Of The Near Reflex, Duane’s Retraction Syndrome “THE SIGNATURE OF CN VI PARESIS” At Distance: Eso Which Increases In The Action Of The Palsied Eye CN VI PALSY - ANSWER BY MOTILITY Duction > Version, “Glissades” (Slowed Saccades), Asymmetric OKN (Optokinetic Nystagmus), Negative Forced Duction ANATOMIC LOCALIZATION FASICULAR CN VI + Contralateral Hemiplegia = (Raymond’s) VII + Contralateral Hemiplegia = (Millard-Gubler) Etiology: Infarction, Demyelination, Tumor SUBARACHNOID Increased Intracranial Pressure (Papilledema), AICA Aneurysm, Subarachnoid Hemorrhage, Trauma, Meningitis, Clivus Tumor, Post Infectious, Neurosurgical PETROUS Petrous Apex/ Mastoid Infection, Inferior Petrosal Sinus Infection, Petrous Bone Fracture, Trigeminal Schwannoma, Lumbar Puncture, Myelography, Spinal/ Epidural Anesthesia CAVERNOUS SINUS/ SOF Aneurysm, Thrombosis, CCF (Carotid Cavernous Fistula), Dural AVM (Arterio-venous Malformation), Tumor, Tolossa-Hunt, Herpes Zoster WORK-UP? CBC (Complete Blood Count), BS (Blood Sugar) / HEMOGLOBIN A1c, LYME TITER, RPR/ FTA-ABS (tests for syphilis), ANA (Anti-Nuclear Antibody), ESR (Erythrocyte Sedimentation Rate), C-REACTIVE PROTEIN, PLATELETS, & HEMOGLOBIN (tests for Giant Cell Arteritis), Exclude Trauma, MRI With Gadolinium, Lumbar Puncture CHRONIC CNVI PALSY (= OR > 6 months) – Harbingers of Serious Intracranial Disease _______________________________________________________ HORNER SYNDROME MIOSIS, PTOSIS, ANHYDROSIS Anisocoria > Dim “Lazy Dilator” (Dilation Lag) Anisocoria > 5 Sec Than 12 Sec Measure in bright AND dim - Greater anisocoria in dim illumination Pancoast’s Tumor (Apical lung tumor) TRIAD: Ptosis, Miosis, Arm Pain CAROTID ARTERY DISSECTION CLASSIC TRIAD: Pain On Side Of Face, Head Or Neck, Oculosympathetic Paresis Without Anhydrosis, Delayed Retinal Or Cerebral Ischemia (50-95% Of Patients) SYMPTOMS Exploding, Ipsilat Headache Transient Monocular Blindness Diplopia Orbital, Facial, Neck, Jaw Pain Dysguesia Facial Numbness Neck Swelling SIGNS Horner’s Syndrome Neck Bruit Or Swelling CN VI, IX-XII CRAO Cerebral Ischemia Need to consider CAROTID DISSECTION in EVERY PAINFUL HORNER SYNDROME Can occur with or without trauma Medical Emergency Horner’ s with eye, head, neck pain - Pt to hospital (MRI, MRA, CTA, angiogram) ____________________________________________________________________________ OPTIC NEURITIS Most common acute monocular vision loss in young and middle-aged 3rd and 4th decades, Females Association with Multiple Sclerosis Typical ON Unilateral Painful (with eye movements) Visual loss progressing over one week Young / middle age adult Normal fundus or minimal ON edema Atypical ON NLP vision Optic disc or retinal hemes Severe disc swelling Macular exudates No pain Uveitis Bilateral vision loss (adults) DDX of Optic Neuritis Inflammatory / Autoimmunine Diseasesn ( SLE, Antiphospholipid Syndrome, Primary Sjogren’s Syndrome, Neurosarcoidosis, Neuro-Bechet’s Disease, Wegener’s Granulomatosis) Infectious Etiologies ( Lyme , Neurosyphilis, HIV-related disorders of the CNS) Genetic / Hereditary Disorders Demyelinating Disorders 50% of MS pts develop ON at some point ON is 1st clinical symptom of MS in 20% Work-Up lab testing to R/O other etiologies ACE, ANA, Lyme titer, FTA-ABS, RPR MRI of brain and orbits with contrast Spinal tap ? Recommended ON Tx IV Methylprednisolone 250 mg q 6 hr x 3 days Oral prednisone taper 1 mg/kg/day x 11 days, 4 day taper MS treatments High-risk ON and 2 or more lesions on MRI Immunomodulators [20 mg day 1; 10 mg days 2 and 4] Copaxone Interferons Interferon beta-1a (Avonex or Rebif) Interferon beta-1b (Betaseron) Lower risk of further demyelinating events Reduce MRI activity OPTIC NEURITIS (CLINICAL PROFILE) F (77.2%) M (22.8%) CAUCASION (85%) > BLACK (15%) AGES 15-40 YEARS (MEDIAN 31.8) 92.2% PAIN! VISUAL NADIR: 4.7 DAYS RECOVERY: 2-3 MONTHS FELLOW EYE: 20% (68.8%, 33.2%, 31.4%) IDIOPATHIC OPTIC NEURITIS SYMPTOMS 92.2% PAINFUL, BLURRED VISION DISCOMFORT ON EYE MOVEMENT IDIOPATHIC OPTIC NEURITIS FUNDUS EXAM RETROBULBAR OPTIC NEURITIS 65% PAPILLITIS 35% IDIOPATHIC OPTIC NEURITIS VISUAL RECOVERY RECOVERY BEGINS WITHIN 3 WEEKS OF ONSET OF SYMPTOMS PLATEAU’S @ 6 WEEKS; IMPROVES UP TO 1 YEAR @ 5 YEARS: 87%: > 20/25 94%:> 20/40 VISUAL RECOVERY IS WORSE IN PATIENTS WITH FC/LP RECURRING OF 20% IN 5 YEARS ONTT(Beck 1992) Optic Neuritis= MS (Relapsing/ remitting) DxMS: Clinical Diagnosis + MRI findings Oral steroids double risk of recurrence (30%) Treatment affects course of disease (IV sol medrol halves risk of CDMS at 2 years in patients with + MRI). IV steroids speed visual recovery MRI can predict CDMS ONTT TREATMENT RECOMMENTATIONS FOR IDIOPATHIC OPTIC NEURITIS 8 DAYS OF ONSET MRI SHOULD BE PERFORMED ASSESS CRITICAL NUMBER OF WHITE MATTER LESIONS IV METHYLPREDNISOLONE X 3 DAYS (short course of prednisone) ONTT – 10 year results Overall risk of MS in 10 yrs = 38% CDMS One or more brain lesions = 56% CDMS > 40% with one or more lesions did NOT develop CDMS in 10 yrs No brain lesions = 22% CDMS 78% with no lesions did NOT develop CDMS in 10 yrs Risk significantly higher with 1 lesion No increased risk with greater number of lesions Mean time to DX = 3 years Almost 75% of Dx occurred in 5 years _______________________________________________________________________ GIANT CELL ARTERITIS ELDERLY - Mean age :72 years Consider in patients over age 50 Preference for Caucasians (2/3) Preference for women (2/3) 27% men 73% women Attacks medium and large sized arteries Specifically targets arteries with ILM Elastin likely is inciting antigen (auto-immune) Thrombosis and Occlusion SYSTEMIC SYMPTOMS OF GCA Fever , Headache, Anorexia/Weight Loss, Malaise, Myalgia GCA SYMPTOMS (Keltner 1982) HEADACHE TENDER TEMPORAL ARTERY MYALGIA/ ARTHRALGIA FEVER WEIGHT LOSS JAW CLAUDICATION ANOREXIA MALAISE LEG 4-100% 28-91% 28-86% 30-100% 16-76% 4-67% 14-69% 12-97% 2-43% OCCULT GCA Ocular involvement No systemic symptoms / signs 21% of GCA cases Have LOWER values of ESR and CRP May be a more localized disease process OCULAR INVOLVEMENT 50% of GCA pts. present with ocular involvement Characteristics of pts with ocular involvement OLDER, LOWER ESR (&CRP) LESS SYSTEMIC SYMPTOMS VISUAL LOSS The fellow eye can be affected (28-31%): Simultaneously Within days to weeks BILATERAL ischemic visual loss – CONSIDER GCA! AMAUROSIS FUGAX Transient monocular blindness Most often caused by ON ischemia, can be light-induced Present in 31-46% of GCA pts. Precedes permanent visual loss 50-63% of time Prodrome to AAION OCULAR SIGNS OF GCA Arteritic Anterior Ischemic Optic Neuropathy (AAION) (81%) Central Retinal Artery Occlusion (9 - 14%) Cilioretinal Artery Occlusion Posterior Ischemic Optic Neuropathy Ocular Ischemia (CWS, Choroidal Hypoperfusion, Chorioretinal Degen.) Ocular Motility Restrictions / Cranial Neuropathies Nystagmus / Internuclear Ophthalmoplegia AAION 81% of GCA pts Most common cause of severe vision loss in GCA Poor visual prognosis Fellow eye commonly involved (65% if untreated) Simultaneously or within weeks (usually) More severe visual dysfunction than N-AION (usually!) Extremely poor visual prognosis “Chalky white” disk swelling Cupping & parapapillary atrophy (Hayreh et al.2001) LAB TESTING / WORK-UP Westergren Sedimentation Rate (ESR) C-Reactive Protein (CRP) Platelet count CBC c differential Erythrocyte Sedimentation Rate Westergren / STAT A normal ESR does NOT R/O GCA Normal in 12-13% of GCA patients NON-SPECIFIC FOR GCA Indicator of inflammatory and neoplastic disease Non-specific marker of an acute phase reaction ESR High Normal Cut-Off MEN: Age / 2 WOMEN:{Age + 10} / 2 C-Reactive Protein Immunoassay Normal Value: <2.54 mg/dL Elevated in GCA One of major Acute Phase Reactants Independent risk factor for coronary artery disease Returns to normal more rapidly than ESR with resolution of disease process Elevated CRP and ESR : 97% specific for GCA CBC with Differential Anemia associated with GCA (normochromic, normocytic) Platelet Count Thrombocytosis: platelet count (>400x10 9/L) Marker of systemic inflammatory response Linked with increased cerebral ischemic events Severe thrombocytosis (> 600x109) associated with risk of permanent visual loss If suspicion remains, get GSTA Biopsy! BIOPSY OF Greater Superficial Temporal Artery PERFORMED WITHIN 14 days SKIP LESIONS in 28 % (17/60), BIOPSY 3-7 mm. SEGMENT DO NOT WAIT UNTIL AFTER BIOPSY TO TREAT Try to perform biopsy within 2 weeks of treatment TEMPORAL ARTERY BIOPSY 2cm sample (preferably more) Ipsilateral side of any ocular invovement Skip Lesions (4 - 5% false negatives) TREATMENT Visual Involvement: PROTECT OTHER EYE STAT IV Methylprednisolone (Solumedrol 250mg IV q 6 hrs x 3 days) Followed by Oral Prednisone No Visual Involvement: PROTECT VISION Oral Prednisone (60-80 mg daily) PROGNOSIS UNTREATED: 30-40% BILATERAL BLIND (highest risk of vision loss within 10 days) 5-10% GO BLIND DESPITE TREATMENT 15-34% HAVE SLIGHT IMPROVEMENT WITH TREATMENT 26% RELAPSE RATE ANY NEW-ONSET NEUROLOGIC DEFICIT IN A PATIENT OVER 50 YRS. SHOULD BE INVESTIGATED FOR GCA! ______________________________________________________________________________________ MYASTHENIA GRAVIS NEUROMUSCULAR DISORDER WEAKNESS & FATIGABILITY OF VOLUNTARY MUSCLE DECREASE OF Ach RECEPTORS AUTOIMMUNE ATTACK PEAK INCIDENCE YOUNGER WOMEN (15-20) OLDER MEN (50-60) OVERALL F:M 2:1 UNDER 3O: F:M 4.5:1 23% HAVE AN ASSOCIATED IMMUNOLOGIC DISORDER 60% INITIAL PRESENTING SIGN IS AN OCULAR MANIFESTATION 90% WILL DEVELOP EYE SIGNS 15% WILL DEVELOP ONLY EYE SIGNS MG WORK-UP AChR ANTIBODY ASSAY (binding, blocking & modulating) MuSK Antibody TSH, T4, T3, thyroid antibodies (to r/o associated thyroid dysfunction) EMG (SINGLE FIBER) CHEST CT (to r/o thymoma in MG) PROGNOSIS IN 5 YEARS 40% STAY OCULAR 40% CONVERT TO GENERALIZED 11% SPONTANEOUS REMISSION 85% CONVERT TO GENERALIZED SYMPTOMATIC THERAPIES ACh ESTERASE INHIBITORS (MESTINON (pyridostigmine) / PROSTIGMIN (neostigmine)) IMMUNOTHERAPIES ANTICYTOKINE AGENTS CORTICOSTEROIDS, CYCLOSPORIN CYTOTOXIC: IMMURAN (azathioprine) HUMORAL THERAPY PLASMAPHERESIS, INTRAVENOUS GAMMA GLOBULIN SURGICAL THERAPY THYMECTOMY DRUGS TO AVOID IN MG IODINATED CONTRAST AGENTS CALCIUM CHANNEL BLOCKERS BETA-BLOCKERS: PROPRANOLOL, TIMOPTIC NEUROMUSCULAR BLOCKING AGENTS SUCCINLYCHOLINE, VECURONIUM QUININE, QUINIDINE, PROCAINAMIDE SELECTED ANTIBIOTICS AMINOGLYCOSIDES, CIPROFLOXACIN __________________________________________________________________________ METASTATIC DISEASE PRIMARY CANCERS CAN METASTASIZE TO BRAIN OR BONE LEADING TO NEURO-OPHTHALMIC DISEASE MANIFESTATIONS CRANIAL NERVE VI PALSY HORNER SYNDROME DORSAL MIDBRAIN SYNDROME OPTIC NEUROPATHY METS TO BONE (clivus, anterior skullbase) prostate and breast cancers METS TO CNS kidney, lung, stomach and thyroid cancers DORSAL MIDBRAIN SYNDROME symptoms upgaze paresis (sometimes downgaze) eyelid retraction convergence retraction nystagmus skew deviation _____________________________________________________________________________ NEURO-SARCOID 10-20 x MORE PREVALENT IN African Americans & Scandinavians OCULAR INVOLVEMENT: 22% NEUROSARCOIDOSIS: 5% FEATURES OF ANY OPTIC NEUROPATHY OPTIC DISC PALLOR DECREASED COLOR VISION (DYSCHROMATOPSIA) VISUAL FIELD LOSS RELATIVE AFFERENT PUPILLARY DEFECT SARCOID OPTIC NEUROPATHY SYSTEMIC SIGNS LYMPHADENOPATHY ERYTHEMA NODOSUM, SKIN NODULES, MACULOPAPULAR RASH, LUPUS PERNIO NASOPHARNGITIS HEPATOMEGALY, SPENOMEGALY, PORTAL HYPERTENSION, BONE CYSTS, POLYARTHRALGIAS SARCOID OPTIC NEUROPATHY LABORATORY NORMOCHROMIC, NORMOCYTIC ANEMIA ELEVATED ESR SERUM ACE (+66%) HYPERCALCEMIA (+18%); HYPERCALCURIA ELEVATED SERUM LYSOZYME LIVER FUNCTION TESTS (+SERUM ALKALINE PHOSPHATASE) CSF: NORMAL OR PLEOCYTOSIS SARCOID OPTIC NEUROPATHY INVESTIGATIONS CHEST X-ray, CT GALIUM SCAN LUMBAR PUNCTURE PULMONARY FUNCTION STUDIES BRONCOALVEOLAR LAVAGE FIBEROPTIC BRONCHOSCOPY WITH TRANSBRONCHIAL BIOPSY BIOPSY (conjuntiva, lung, skin, lymph node, optic nerve sheath) SARCOID OPTIC NEUROPATHY TREATMENT & PROGNOSIS CORTICOSTEROIDS PREDNISONE IMMUNOSUPPRESSANTS CYCLOSPORIN METHOTREXATE 50% SPONTANEOUSLY REMIT _____________________________________________________________________________ OTHER AUTO-IMMUNE DISEASES LUPUS – SLE 90% WOMEN MORE COMMON IN BLACKS SYSTEMIC SYMPTOMS – FATIGUE, MALAISE, FEVER, WEIGHT LOSS ARHTRALGIAS, MYALGIAS, ARTHRITIS RASH HAIR LOSS EDEMA KIDNEY PROBLEMS + ANA IN 98% + ANTI ds-DNA IN 70% MANY OTHER AUTO ANTIBODIES CAN BE ASSOCIATED AS WELL SJOGREN’S SYNDROME MAINLY WOMEN MAINLY MIDDLE-AGED, BUT CAN ALSO OCCUR IN CHILDHOOD MAY BE ASSOCIATED WITH OTHER AUTOIMMUNE DISEASES DIMINSIHED LACRIMATION AND SALIVATION ARTHRALGIAS / ARTHRITIS CAN BE ASSOCIATED WITH LYMPHOMA, MENINGITIS, AND MULTIPLE SCLEROSIS Has been associated with optic neuropathy Lab Tests: ANA, SSA & SSB Antibodies _____________________________________________________________________________ LYME DISEASE LYME TITER WESTERN BLOT IgG AND IgM STUDIES NEURO-LYME – Optic neuropathy, Diplopia, Disc edema _____________________________________________________________________________ CAT-SCRATCH DISEASE BARTONELLA TITERS (Henselae and Quintana) Transmitted by a cat (typically a kitten) Usually occurs in patient’s under age 20 Disc Edema Neuro-retinitis – macular star Treatment: Antibiotics – Rifampin, Azithromycin, Bactrim ____________________________________________________________________________ GRAVES’ DISEASE DISORDER OF IMMUNE REGULATIONS CYTOTOXICITY DIRECTED AT THYROID GLAND & EOM HYPERTHYROIDISM INFILTRATIVE ORBITOPATHY INFILTRATIVE DERMOPATHY GRAVES’ DISEASE - WOMEN 5:1 GRAVES’ ORBITOPATHY - WOMEN 3:2 GRAVES’ = INFLAMMED ORBIT TUMOR (exophthalmos; eyelid edema) LOSS OF FUNCTION (eyelid retraction; motility defect; optic neuropathy) REDNESS PROPTOSIS RARELY AN ISOLATED FINDING ABSENCE MAY MEAN POSTERIOR DECOMPRESSION EYELID EDEMA “JELLY ROLL” “FINGER-LIKE” DIURNAL IMPROVEMENT LOSS OF FUNCTION (upper eyelid retraction) MOST RELIABLE SIGN 50% GRAVES’ DISEASE 90% GRAVES’ ORBITOPATHY EYELID LAG = UNRELIABLE LOSS OF FUNCTION (restricted motility defect) INFERIOR RECTUS 60-70% MEDIAL RECTUS 25% SUPERIOR RECTUS 10% DIURNAL VARIATION GAZE INDUCED IOP RISE Thyroid Work-Up TSH T3 T4 Thyroid Stimulating Immunoglobulin Thyroperoxidase Antibody Thyroglobulin Antibody GRAVE’S MANAGEMENT PRISMS & PATCHES DROPS & OINTMENTS ELEVATED HEAD POSITION STOP SMOKING !!! STEROIDS IMMUNOSUPPRESSIVES RADIATION THERAPY ?? ORBITAL DECOMPRESSION EXTRAOCULAR MUSCLE SURGERY EYELID MARGIN REPOSITIONING BLEPHAROPLASTY __________________________________________________ ARNOLD-CHIARI MALFORMATION Herniation of cerebellar tonsils through the foramen magnum SYMPTOMS: Headache Neck pain Oscillopsia Diplopia Ataxia Weakness SIGNS: Down-beat nystagmus, especially in lateral gazes Ocular misalignment Ataxia WORK-UP: Neuro-imaging, preferably mid-sagital MRI Treatment: Neuro-surgical decompression if warranted due to symptoms