LeeChuy, Katherine Lee, Sidney Albert Legaspi, Roberto Jose Lerma, Daniel Joseph Li, Henry Winston Li, Kingbherly Lichauco, Rafael Lim, Imee Loren Lim,

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Presentation transcript:

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 ABNORMALITYUNDERLYING CAUSEVISUAL LOSS ASSOCIATED SYMPTOMSPUPILS PapilledemaIncreased 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 neuritisInflammatory 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 bodiesCongenital, familialUsually 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

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

Further Diagnostic Tests  Perform MRI or CT scan  (+) mass  tumor  (-) mass  IIH

Modified Dandy Criteria for Idiopathic Intracranial Hypertension According to the Dandy criteria, an IIH diagnosis is appropriate if a person: has signs and symptoms of increased intracranial pressure, such as papilledema and headache; has no localizing findings on neurological examination has a normal MRI/CT scan with no evidence of venous obstructive disease; has high intracranial pressure of 250mm/H 2 O or above on a spinal tap, with no abnormalities of cerebrospinal fluid; is awake and alert; has no other cause of increased intracranial pressure found.

Management for increased ICP  Elevate head and body by 30 degrees to optimize venous drainage  Reduce fever and control hyperglycemia  Maintain osmolarity at mOsm/L  Prevent seizures

 Specific measures include:  Hyperventilation  Mannitol  1-2g/kg for severely increased pressure, followed by mg/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

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