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GRAND ROUND

GRAND ROUND . Cc. Headache of 04 months - globbal,dullaching,inc. in severity - Sts. awaken her from sleep - temporal improv’t with analgesics ass’d nausea and vomiting diplopia and blurring of vision of 2 months tinnitus but no dizziness or vertigo. Ctd.

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GRAND ROUND

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  1. GRAND ROUND • Cc. Headache of 04 months - globbal,dullaching,inc. in severity - Sts. awaken her from sleep - temporal improv’t with analgesics • ass’d nausea and vomiting • diplopia and blurring of vision of 2 months • tinnitus but no dizziness or vertigo

  2. Ctd. • no similar history in the past • no abnormal body mov’t or weakness of extremitis • no history of fever • no chronic cough;no intake of drugs • increase 8kg of wt. Over 1yr • no chronic illnesses in the past

  3. ctd • has regular menses • single and lives with her family P\E GA:healthy looking BP=100\80 PR=80 RR=16 BMI=24.7 • no pallor , NIS • no LAP

  4. ctd • Chest,Cvs,Abdomen/NAD • CNS:conscious,oriented to TPP - language,memory,attention/Intact -cranial nerves: Normal findings -Fundoscopy:swollen disc with blurred disc marigin -visual acuity:6/6

  5. CNS exam’n ctd • Visual field-normal by confront’n method • motor and sensory :normal findingsr • reflexes:2/4 allover • plantar-downgoing bilaterally • cerebellar signs-absent

  6. summary • 24 yrs old female patient with 04 months history of headache and 02 months history of visual complaints • Fundoscopy showing evidence of papilledema

  7. Differential Diagnosis • Intracranial mass • Hydrocephalus • Meningeal process(infectious,inflammatory, neoplastic) • Inc’d venous press./Cerbral venous thromb. • Idiopathic intracranial HPNm

  8. Lab. Results • WBC=4500 Hgb=14.8gm/dl Plt=76000 • ESR=45mm/hr serum VDRL-NR • CT scan of brain-Normal CT findings • LP-opening press. >300mm of water clear CSF No cell,glucose 70mg/dl,protein0.2gm/l CSF VDRL-NR,gram s.and AFB-No organism.

  9. Idiopathic intracranial HPN • also called pseudotumor cerebri,benign ICH • a disorder of unknown etiology • primary problem is chronically inc. ICP • most important neurologic manifestation is papilledema

  10. Pathophysiology • Unclear • multiple studies with conflicting results • some of proposed mechanisms increased CSF production;decd. absorp’n cerebral edema elevated cerebral venous pressure • role of obesity

  11. Frequency • variable from country to country • Annual incidence at Mayo clinic(1976-90) 0.9/100000 pop’n 1.6/100000 women 3.3/100000 females aged 15-44 yrs 7.9/100000 obese women aged 15-44 yrs • F:M=8:1 obese women of child bearing age

  12. Clinical Findings • Symptoms of increased ICP -headache,pulsatile tinnitus,diplopia • symptoms of papilledema -transient visual obscursions,progressive -loss of vision,blurring of vision -sudden visual loss • There are pts. with IIH without papilledema -In one study of 65 adults with refractory migrane,12(18% had IIH without papilledema

  13. Cont’d • Visual function testing -fundoscopy,visual field,visual acuity -color vision,ocular motility • characteristics,Sxs,Sns in pts. with IIH - pt. Characterstics - symptoms female(65-95%)Headache(75-99%) Age peak:21-34yrs Visual dist.(30-68%) obesity (44-94%) diplopia (20-38%) Intracranial noises(0-80%)

  14. Cont’d • Signs - papilledema(98-100%) -VF defects (3-51%) - abducent palsy(14-35%) -Dec’d VA (2-25%) • Risk Factors Conditions Endocrine diseases • female sex Addisons disease • Reproductive age gp. Cushing’s disease • Obesity Hypoparathyroidism • Recent weight gain Hypothyroidism

  15. Risk Factors cont’d • Miscellaneous diseases CRF,SLE,Anemia,Hypervitaminosis A,Dural AV malf. • Medications - Multivitamines(vit. A),steroids and steroid withdrwal TTC,sulfa Abics.,cimetidine,naldixic acid,nitrofurantoin amiodarone,tamoxifen,cyclosporine,lithium carbonate

  16. Diagnosis • a dignosis of exclusion • Based on modified Dandy criteria 1.signs and symptoms of raised ICP 2.No localizing neurologic signs,in an alert patient, other than abducens n. palsy 3.Normal neuroimaging studies,except for small ventricles and empty sella 4.Documented inc’d opening pressure(>250mm of water) but normal CSF composition 5.Primary structural or systemic causes of elevated intracranial venous sinus pressure excludedM

  17. Diagnosis cont’d • Neuroimaging - for structural abns. or mass lesions - Brain MRI with gadolinium enhancement - MRI venography,CT scan • LP • Orbital ultrasonography • Other lab tests - CBC,ESR,ACLA,ANA,Full procoagulant profile

  18. Treatment • Joint Mx with ophthalmologist and neurologist • Treatment goals • to detect and prevent visual loss • to reduce ICP • to relieve headache • Medical and surgical options

  19. Medical therapy • Treatment of associated condition - withdrawal of offending agent - treatment of obesity as low as 6%loss of wt. results in dec’d ICP and papilledema • Diuretics - Acetazolamide-first line medical therapy -250mg po qid or 500mg po bid - Loop diuretics,Eg. Furesemide: as an adjunct to acetazolamide

  20. Medical therapy cont’d • Corticosteroids -rapidly lower ICP -long term use not recommended -for patients who continue to have visual loss • Repeated LP -in patients with infrequent exacerbationsof symptoms

  21. Surgical therapy • When visual function is severly impaired • To those with incapacitating headache • Options -optic nerve sheath decompression (fenestration) -lumboperitoneal or ventriculoperitoneal shunting

  22. Prognosis • Encouraging in early intervetion • Prognosis for visual loss,varied in d/f series -studies of 1960’s and 1970’s ,<25% of pts. Had significant blindness -recent study ,visual dysfunction in close to ½ of patients

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