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Clinical Case Challenges In NeuroOptometry I Thomas J. Landgraf, O.D., F.A.A.O. “Clinical Case Challenges in Neuro-Optometry” Thomas Landgraf, O.D., F.A.A.O. Clinical Associate Professor, UMSL College of Optometry My Background Graduate of ICO…Chicago Residency at PCO…Philadelphia SCO x 15 years…Memphis Now at UMSL College of Optometry In terms of Neuro-Eye… Dr. Lawrence Gray at ICO & PCO My Background At SCO…Chief of Ocular Disease Goals for this lecture Not an expert Share patient care experiences Share “optometric legal consultant” experiences Resources Journals and Internet Review of Optometry Review of Ophthalmology Handbook of Ocular Disease Management Clinical Guide To Ophthalmic Drugs Neuro-Optometry Why spend 3 hours on it? Conditions are both: Vision threatening Life threatening “True” ocular emergencies Case #1: ONH Edema? Always A Tough DDx (Differential Diagnosis) S: 52 yo Caucasian male referred to me Tentative diagnosis of CRVO OS Case #1: ONH Edema? Always a Tough DDx S: Painless vision loss OS x 2 weeks Prosthetic OD due to trauma No significant medical or ocular conditons Low daily dosage of methadone Nicotine patch Case #1: ONH Edema? Always a Tough DDx O: BVA OS: 20/400 OS pupil round and reactive to light Normal SLX Tonometry 17 mm Hg BP: 280/170 RAS: not done at previous visit Case #1: ONH Edema? Always a Tough DDx O: DFE OS: Optic nerve head edema Accompanied by flame hemes, exudates, cotton wool spots, and macular edema Normal peripheral retina Case #1: ONH Edema? Always a Tough DDx A: Malignant Hypertension and Resultant Retinopathy OS P: Immediate referral to medical center For lowering of BP Referral to retinal specialist Level Of Comfort Confirmation Case #1: ONH Edema? Always a Tough DDx Follow-up 4 months later Current meds: minoxidil, norvasc, coumadin HTN and its complications Noted improved vision But some glare, distortion, “wavy lines” in central vision Case #1: ONH Edema? Always a Tough DDx Follow-up 4 months later BVA OS: 20/20 BP: 160/85 DFE OS: exudative macular star, healthy ONH (.2/.2), normal peripheral retina Case #1: ONH Edema? Always a Tough DDx Follow-up 4 months later Resolving Malignant Hypertensive Retinopathy Improved Blood Pressure Educated on compliance Case #1: ONH Edema? Always a Tough DDx Bottom Lines Primary Care OD’s need to take BP’s Especially on those with retinal vascular disease Consider typically bilateral retinal conditions In monocular patients Case #1: ONH Edema? Always a Tough DDx Timely diagnosis for malignant HTN Can significantly reduce morbidity and mortality Like Neuro-Eye Disease: sight and life threatening Pseudotumor Cerebrii (PTC) Background “false brain tumor” Increased intracranial pressure without an intracranial mass Major diagnosis of exclusion: a true intracranial tumor All patients with papilledema must have neuro-imaging studies PTC: Why? Poor CSF absorption By meninges surrounding brain and spinal cord Increased intra-abdominal pressure From obesity elevated intrathoracic pressure decreased venous drainage from the brain PTC: Diagnosis Who? Obese women of childbearing age Secondary Obstruction to venous drainage: cerebral venous thrombosis Exongenous agents: tetracycline, vitamin A, corticosteroids, BCP’s Medical conditons: lupus, sarcoidosis, anemias, blood dyscrasias PTC: Diagnosis Symptoms Bad HA’s: frontal, around the eyes, pressure-like, throbbing Transient visual loss Intracranial noises: heartbeat or whooshing sound in ears, tinnitus Vision loss: blur, temporal VF defect PTC: Diagnosis Signs Optic disc edema Unilateral, bilateral, asymmetric VA, pupils, EOM’S usually normal VF: blind spot enlargement, inferonasal loss, generalized constriction PTC: Differential Diagnosis Intracranial mass Meningitis: abrupt onset, fever and chills, stiff neck Bilateral inflammatory optic neuropathy: early and central vision loss, pain on eye movement, retrobulbar PTC: Differential Diagnosis Pseudopapilledema: optic disc drusen or tilted discs, ultrasound may aid Neuroretinitis: macular exudate, early central vision loss Bilateral ION: older, vascular risk factors, painless, early vision loss PTC: Ancillary Tests Optometric In-Office: VF B scan ultrasound Photos or optic nerve imaging PTC: Ancillary Tests Neurologist or neuro-eye doc referral Neuroimaging before lumbar puncture Standard MRI of the brain CT scan with contrast if patient markedly obese Neuroimaging Major Scans Used To Evaluate NeuroEye Disease CT (Computerized tomography) MRI (Magnetic Resonance Imaging) Neuroimaging CT Good to view bony abnormalities, calcifications, acute hemorrhages Valuable to diagnosis of orbital processes Test of choice for thyroid eye disease Neuroimaging MRI Far better at characterizing soft tissues Preferable for most intracranial processes Not subject to bone artifact Contrast media and special studies can sharpen Gadolinium is a contrast material that can increase signal intensity PTC: Ancillary Tests Lumbar Puncture Required for the diagnosis of PTC Neurologist, radiologist or ER physician Usually > 200 mm Lumbar Puncture Procedure Patient positioned on side in fetal position with back fully flexed 18 g needle inserted at L4-L5 interspace Opening pressure measured when needle penetrates subarachnoid space HA is most common complication Lumbar Puncture Opening pressure Normal: 60-80 mm of H20 Borderline elevated: 180-210 mm of H20 Lumbar Puncture CSF evaluation Color Clear and colorless is normal Cloudy: infection Xanthochromic (yellow): subarachnoid hemorrhage Cell count and differential, cytology, chemical analysis, serologic analysis, microscopy, culture PTC: Management “Comanage” with neurologist Initial LP improved signs and sxs VF, DFE, photos or optic nerve imaging every month x 3 months Every 2-3 months thereafter for about a year Individual case variability PTC: Management “Comanage” with neurologist Other options for some persistent signs and sxs CAI’s : acetazolamide Other diuretics Weight loss HA management PTC: Management Diamox Not just for angle closure Decreased CSF production up to 50% 1-3 grams qd 500 mg bid, tid, qid Side effects: taste alteration, nausea, fatigue, diarrhea, tingling Not with sulfa allergies, kidney disease PTC: Management Headache management Topamax (topiramate) Migraine prophylaxis and epilepsy PTC: HA relief and mild inhibition of carbonic anhydrase, also causes weight loss Recently: development of angle closure glaucoma from choroidal expansion PTC: Management For signs and symptoms unresponsive to LP, severe vision loss Corticosteroids Surgery Optic nerve sheath fenestration CSF diversion (shunt) PTC: My Clinical Experience Relatively rare condition? Not at SCO “Comanagement” turns into MANAGEMENT Optometrists take the time Need to be familiar with ancillary diagnostic tests and treatment options Case #2: Monocular Acute Vision Loss In A Golden Girl S: 85 yo Caucasian female Cx: acute vision loss OD 2 weeks earlier Earache Sore temporal veins Jaw claudication Past medical hx: non-contributory Case #2: Golden Girl O: BVA LP OD, 20/30 OS +APD OD BP: 150/100 No carotid bruits SLX: NS consistent with 20/30 VA Case #2: Golden Girl O: DFE: pallid swelling of the optic nerve OD Othewise normal retina and posterior pole OU Case #2: Golden Girl A: Provisional Diagnosis: Giant Cell Arteritis OD P: FLAN: increased arterial filling time OD Choroidal nonfilling defect OD 80 mg Prednisone po daily Case #2: Golden Girl P: R/O all causes of Anterior Ischemic Optic Neuropathy CBC: Elevated monocyte and platelet counts ESR: 44 FTA-ABS and VDRL non-reactive Case #2: Golden Girl One week later….. Right temporal artery biopsy Ear pain and temporal HA resolved Case #2: Golden Girl Two weeks later….. ESR: 4 Plan: Monitor with ESR And for prednisone side effects Case #2: Golden Girl Eventually….. VA did not improve OD But remained stable OS Anterior Ischemic Optic Neuropathy (AION) Arteritic Or….. Giant Cell Arteritis Nomenclature following vision loss Temporal Arteritis AION-artertic Background Granualomatous vasculitis of mediumsized arteries “True” ocular emergency The Goal: Prevention of contralateral vision loss AION-arteritic Background Contralateral vision loss 2/3 if untreated Within weeks if untreated AION-arteritic Why Granulomatous vasculitis of temporal artery Occlusion of short posterior ciliary arteries (supply anterior optic nerve) AION-artertic AION-arteritic Diagnosis: Who? Rose Nylen on the Golden Girls Average age of onset = 70 years Female and Scandanavian Lower incidence rates Tennessee & Israel AION-arteritic Diagnosis: symptoms Unilateral decreased VA, temporal HA, scalp tenderness VA usually < 20/200 Amaurosis fugax Anorexia, fever, malaise, depression Onset is variable AION-arteritic Clinical Features Vasculitis of coronary arteries: MI, CHF, angina pectoris Neurologic: peripheral neuropathies, ischemic brain damage Polymyalgia Rheumatica: pain and stiffness of the neck, shoulders, hips AION-arteritic Diagnosis: signs AION-arteritic Optic nerve edema, hemes, cotton wool spots APD VF defects: central, altitudinal, arcuate AION-arteritic Diagnosis: signs AION-arteritic Pallor described as chalky white CRAO in up to 10% of patients Disc eventually glaucoma-like with cupping BUT with pallor AION-arteritic Differential Diagnosis Vs. non-arteritic AION Worse VA Worse VF HA and scalp tenderness Constitutional symptoms Older Worse ESR, CRP, CBC variables AION-arteritic Ancillary Tests Optometric In-Office VF Optic nerve imaging Photos FLAN considered to check for choroidal perfusion defects AION-arteritic Ancillary Tests Referral ESR (erythrocyte sedimentation rate) CRP (C-reactive protein) Westergren 15% of GCA patients: normal ESR Elevated in > 91% Also elevated WBC, platelet counts; IgG anticardiolipin antibodies AION-arteritic Ancillary Tests Referral Temporal artery biopsy Should be performed on all suspects > 95% sensitive, 100% specific Can be done shortly after steroid treatment Inflammatory cells in the muscular walls of the artery AION-arteritic Diagnosis: Summary History and clinical impression ESR and CRP Confirm with temporal artery biopsy AION-arteritic Management Referral: neurologist, internist (PCP), rheumatologist For suspects or diagnosed: Systemic steroids AION-arteritic Management Systemic steroids Hospital admission 1-2 gm IV methylprednisone x 2-3 days 60-100 mg of oral prednisone: tapered very slowly AION-arteritic Management Systemic steroids Anecdotal vision recovery? Poor prognosis? No solid support for anti-steroid medications (Rheumatrex aka methotrexate) AION-arteritic My Clinical Experience This is rare? Most important from an educational perspective Presume the worst if suspect Vs. glaucomatous optic neuropathy Combination of AION + OAG in my patients