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HEADACHE AND PROGRESSIVE VISUAL LOSS CASE CONFERENCE I DEPARTMENT OF NEUROLOGY LeeChuy, Katherine Lee, Sidney Albert Legaspi, Roberto Jose Lerma, Daniel Joseph Li, Henry Winston Li, Kingbherly Lichauco, Rafael Lim, Imee Loren Lim, Jason Morven Lim, John Harold Lim, Mary Lim, Phoebe Ruth Lim, Syndel Raina Lipana, Kirk Andrew 51 y/o, Male Chief complaint: Eight months of progressive visual loss and headache OPHTHALMOLOGIC FINDINGS Mild bilateral papilledema with some pallor of the right optic disc Visual fields with enlarged blind spot Concentric loss of the peripheral visual fields in both eyes (he could see only the center of the visual field with either eye) Other Exams The remainder of his neurologic exam was normal. LOCALIZATION AND DIFFERENTIAL DIAGNOSIS 1. Headache, papilledema and visual field loss of this kind is seen in what syndrome? 2. What is the appropriate test to perform next? APPROACH TO A NEUROLOGIC PROBLEM Three Questions Asked: 1. Is there a neurologic problem? 2. Where is the neurologic problem? 3. What is the neurologic problem? 1. Is there a Neurologic Problem? Focal Neurologic Deficits Cranial nerve deficit Increase ICP Headache Papilledema Visual Loss Meningeal Irritation Causes of optic disc swelling OPHTHALMIC ABNORMALITY UNDERLYING CAUSE VISUAL LOSS ASSOCIATED SYMPTOMS PUPILS Papilledema Increased intracranial pressure None or transient blurring; constriction of visual fields and enlargement of blind spot; findings almost always binocular Headache; signs of intracranial mass Normal unless succeed ed by optic atrophy Anterior ischemic optic neuropathy (AION) Infarction of disc and intraorbital optic nerve due to atherosclerosis or temporal arteritis Acute visual loss, monocular (usually); may be an altitudinal defect Headache with temporal arteritis Afferent pupillary defect Optic neuritis Inflammatory changes in disc and intraorbital part of optic nerve usually due to MS, sometimes to ADEM Rapidly progressive visual loss; usually monocular Tender globe, pain on ocular movement Afferent pupillary defect Hyaline bodies Congenital, familial Usually none; may be slowly progressive Enlargement of blind spot or arcuate inferior nasal defect Usually none; rarely transient visual obscurations Normal 2. Where is the Neurologic Problem Levelize Optic nerve Subarachnoid space directly communicates with sheaths of the optic nerve; increased CSF pressure leading to increased pressure in the optic nerve sheaths Lateralize Advanced papilledema due to increased ICP Almost always bilateral More pronounced on side with intracranial tumor Localize 3. What is the Neurologic Problem? Insidious Onset (weeks to months) Mass lesions Degenerative Disease TB/ fungal meningitis DIAGNOSTIC TESTS Imaging studies Computed Tomography (CT) scan Magnetic Resonance Imaging (MRI) Magnetic Resonance Angiography (MRA) MR spectroscopy Positron Emission Tomography (PET) scan Cerebral angiography Lumbar puncture CSF analysis measure levels of protein and glucose Detect RBC, WBC, cancer cell Done only after a CT or MRI Management for increased ICP Elevate head and body by 30 degrees to optimize venous drainage Reduce fever and control hyperglycemia Maintain osmolarity at 305-315 mOsm/L Prevent seizures Specific measures include: Hyperventilation Mannitol 1-2g/kg for severely increased pressure, followed by 50-300mg/kg q6 Corticosteroid Ventricular drainage Primary disorder should be treated General approach on brain tumors: Craniotomy Stereotactic techniques Radiosurgery Shunts Management of Meningitis Fungal meningititis: long course of high dose antifungals, such as amphotericin B and flucytosine TB meningitis: Isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months, followed by isoniazidanfrifampicin alone for a further ten months Steroids are always used in the first six weeks of treatment THANK YOU FOR LISTENING! HAVE A GOOD DAY