Transcript HEADACHE AND PROGRESSIVE VISUAL LOSS Case Conference

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