HEADACHE AND PROGRESSIVE VISUAL LOSS Case Conference I Department of Neurology
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Transcript of HEADACHE AND PROGRESSIVE VISUAL LOSS Case Conference I Department of Neurology
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LeeChuy, KatherineLee, Sidney Albert
Legaspi, Roberto JoseLerma, Daniel Joseph
Li, Henry WinstonLi, Kingbherly
Lichauco, RafaelLim, Imee Loren
Lim, Jason MorvenLim, John Harold
Lim, MaryLim, Phoebe RuthLim, Syndel Raina
Lipana, Kirk Andrew
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51 y/o, Male
Chief complaint: Eight months of progressive visual loss and headache
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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)
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Other Exams The remainder of his neurologic exam was normal.
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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?
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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?
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1. Is there a Neurologic Problem?
Focal Neurologic DeficitsCranial nerve deficit
Increase ICPHeadachePapilledemaVisual Loss
Meningeal Irritation
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Causes of optic disc swellingOPHTHALMIC
ABNORMALITY UNDERLYING CAUSE VISUAL LOSSASSOCIATED 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 succeeded 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
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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
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3. What is the Neurologic Problem?
Insidious Onset (weeks to months) Mass lesions Degenerative Disease TB/ fungal meningitis
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Imaging studies
Computed Tomography (CT) scan Magnetic Resonance Imaging (MRI) Magnetic Resonance Angiography
(MRA) MR spectroscopy Positron Emission Tomography (PET)
scan Cerebral angiography
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Lumbar puncture
CSF analysis measure levels of protein and glucose Detect RBC, WBC, cancer cell Done only after a CT or MRI
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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
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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
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General approach on brain tumors: Craniotomy Stereotactic techniques Radiosurgery Shunts
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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
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