1. An interesting case ofAn interesting case of
headacheheadache
G.Balaji med.pgG.Balaji med.pg
Prof.Dr.G.sundharamurthy’s unitProf.Dr.G.sundharamurthy’s unit
2. historyhistory
• 35 year old female presented with c/o headache35 year old female presented with c/o headache
of 2 weeks duration.of 2 weeks duration.
• Headache -generalised throbbing pain presentHeadache -generalised throbbing pain present
through out the day.through out the day.
• Aggravated by bending forward , coughing andAggravated by bending forward , coughing and
sneezing. Pain reduced by NSAIDs but notsneezing. Pain reduced by NSAIDs but not
completely absent.completely absent.
• Headache associated with nausea and vomitingHeadache associated with nausea and vomiting
occasionally.occasionally.
3. • No h/o loc, seizures, fever, altered sensorium,No h/o loc, seizures, fever, altered sensorium,
weakness of limbs, hard of hearing ,tinnitus.weakness of limbs, hard of hearing ,tinnitus.
• H/o blurring of vision for both distant and nearH/o blurring of vision for both distant and near
objects. No h/o double vision, deviation of eyesobjects. No h/o double vision, deviation of eyes
to one side.to one side.
• No h/o trauma, head injury, falls.No h/o trauma, head injury, falls.
• No h/o any drug in take.No h/o any drug in take.
4. • Past history:Past history:
not a known case of type 2 dm, sht, ihd,not a known case of type 2 dm, sht, ihd,
pulmonary tb.pulmonary tb.
no chronic drug intake.no chronic drug intake.
No similar episodes in the past.No similar episodes in the past.
No h/o any hospitalisation.No h/o any hospitalisation.
5. • Personal historyPersonal history::
Nil addictions.Nil addictions.
bowel and bladder habits normal.bowel and bladder habits normal.
• Menstrual& marital historyMenstrual& marital history::
Married with 2 children. Last child birth 7 yearsMarried with 2 children. Last child birth 7 years
ago. Underwent sterilisation after birth of 2 childago. Underwent sterilisation after birth of 2 child
Menstrual cycles regular.Menstrual cycles regular.
6. On examinationOn examination
Patient conscious, oriented, afebrile.Patient conscious, oriented, afebrile.
pulse- 80/ minpulse- 80/ min
Bp- 110/70 mm hg.Bp- 110/70 mm hg.
No pallor, icterus, lymphadenopathy, cyanosis,No pallor, icterus, lymphadenopathy, cyanosis,
clubbing.clubbing.
Cvs –S1,S2 heard, no murmurs.Cvs –S1,S2 heard, no murmurs.
Rs – nvbs heard, no added sounds.Rs – nvbs heard, no added sounds.
Per abdomen- soft, no organomegaly. No mass.Per abdomen- soft, no organomegaly. No mass.
7. • Cns:Cns:
Pt is conscious, oriented ,Pt is conscious, oriented ,
No cranial nerve palsiesNo cranial nerve palsies
Motor- no weakness of limbs. Reflexes normal.Motor- no weakness of limbs. Reflexes normal.
No sensory deficitNo sensory deficit
No cerebellar signs.No cerebellar signs.
No signs of meningeal irritation.No signs of meningeal irritation.
Fundus- bilateral papilledema.Fundus- bilateral papilledema.
13. DefinitionDefinition
1.1. Clinical features of raised intracranialClinical features of raised intracranial
pressure (ICP)pressure (ICP)
2.2. Absence of space-occupying lesionAbsence of space-occupying lesion
(SOL) on brain imaging(SOL) on brain imaging
3.3. Exclusion of other causesExclusion of other causes
15. EpidemiologyEpidemiology
• General population = 1 / 100,000 / yrGeneral population = 1 / 100,000 / yr
• Women aged 15 – 44 = 3.5 / 100,000 / yrWomen aged 15 – 44 = 3.5 / 100,000 / yr
• Women BMI >29 = 20 / 100,000 / yrWomen BMI >29 = 20 / 100,000 / yr
16. Clinical features ofClinical features of
Idiopathic Intracranial HypertensionIdiopathic Intracranial Hypertension
• HeadacheHeadache
• VomitingVomiting
• Visual symptoms / signsVisual symptoms / signs
– Transient visual obscurationsTransient visual obscurations
– Diplopia (VIth Nerve palsy)Diplopia (VIth Nerve palsy)
• ““false localising sign”false localising sign”
– Enlarged blind-spotEnlarged blind-spot
• Papilledema on fundus examinationPapilledema on fundus examination
• Rest of neurological examination should beRest of neurological examination should be
normalnormal
17. LUMBAR PUNCTURELUMBAR PUNCTURE
• Measure CSF opening pressure with ptMeasure CSF opening pressure with pt
lyig in left lateral position.lyig in left lateral position.
• If opening pressure elevated, removeIf opening pressure elevated, remove
enough CSF to decrease closing pressureenough CSF to decrease closing pressure
to about 150 mm H2O.to about 150 mm H2O.
• Send for cell count, protein, glucose,Send for cell count, protein, glucose,
cultures (bacterial, viral, and fungal), andcultures (bacterial, viral, and fungal), and
cytology.cytology.
18. NEUROIMAGINGNEUROIMAGING
• MRI preferred over CTMRI preferred over CT
• Possible MRI FindingsPossible MRI Findings
– Empty sella – 70%Empty sella – 70%
– Flattening of posterior sclera – 80%Flattening of posterior sclera – 80%
– Enhancement of prelaminar optic nerve – 50%Enhancement of prelaminar optic nerve – 50%
– Distention of perioptic subarachnoid space – 45%Distention of perioptic subarachnoid space – 45%
– Vertical tortuosity of orbital optic nerve – 40%Vertical tortuosity of orbital optic nerve – 40%
– Intraocular protrusion of prelaminar optic nerve – 30%Intraocular protrusion of prelaminar optic nerve – 30%
• Consider Magnetic Resonance Venography toConsider Magnetic Resonance Venography to
r/o cerebral venous thrombosisr/o cerebral venous thrombosis
25. DIAGNOSIS OFDIAGNOSIS OF
PSEUDOTUMOR CEREBRIPSEUDOTUMOR CEREBRI
• Based onBased on modified Dandy criteriamodified Dandy criteria
– Awake, alert pt.Awake, alert pt.
– Signs and symptoms of increased ICPSigns and symptoms of increased ICP
– Absence of localized neurological findings,Absence of localized neurological findings,
except for CN VI paresisexcept for CN VI paresis
– Normal CSF fluid findings except forNormal CSF fluid findings except for
increased pressureincreased pressure
– Absence of deformity, displacement, andAbsence of deformity, displacement, and
obstruction of ventricular systemobstruction of ventricular system
– No other identifiable cause of ICP,SOLNo other identifiable cause of ICP,SOL
26. How do we make theHow do we make the
diagnosis?diagnosis?
• Clinical features of raised ICP without apparentClinical features of raised ICP without apparent
causecause
• Normal brain imagingNormal brain imaging
• Normal imaging of venous systemNormal imaging of venous system
• LP (serves 3 purposes):LP (serves 3 purposes):
1.1. Checks pressure – establishes diagnosisChecks pressure – establishes diagnosis
2.2. CSF analysis – excludes infectious, inflammatory andCSF analysis – excludes infectious, inflammatory and
neoplastic etiologiesneoplastic etiologies
3.3. Symptomatic improvementSymptomatic improvement
27. Associated FactorsAssociated Factors
• Female > MaleFemale > Male
• ObesityObesity
• DrugsDrugs
– TetracyclinesTetracyclines
– Vitamin AVitamin A
• Iron Deficiency AnemiaIron Deficiency Anemia
• Endocrine abnormalitiesEndocrine abnormalities
– HypothyroidismHypothyroidism
– HypoparathyroidismHypoparathyroidism
– PCOS (probably independent of obesity, acnePCOS (probably independent of obesity, acne
treatment)treatment)
29. ““Benign Intracranial Hypertension?”Benign Intracranial Hypertension?”
- No longer!- No longer!
May lead to irreversible visual lossMay lead to irreversible visual loss
Normal Optic atrophy
30. Follow upFollow up
• Symptoms of raised ICPSymptoms of raised ICP
• Neuro-opthalmological assessmentNeuro-opthalmological assessment
- Visual Field TestingVisual Field Testing
- Fundus ExaminationFundus Examination
31. treatmenttreatment
• T. acetaolamide 250 mg tdsT. acetaolamide 250 mg tds
• T.furesamide- 40 mg od.T.furesamide- 40 mg od.
• Lumbar puncture- about 30 ml of csfLumbar puncture- about 30 ml of csf
drained till 200 mm water pressuredrained till 200 mm water pressure
reached.reached.
• Patietnt improved with above therapy andPatietnt improved with above therapy and
was discharged with t.acetazolamide 250was discharged with t.acetazolamide 250
mg tds. To review after 15 days.mg tds. To review after 15 days.
32. British medical bulletin-june 2006.British medical bulletin-june 2006.
pg 233-244pg 233-244
• Idiopathic intracranial hypertension and
visual function
• James F. Acheson*
• Department of Neuro-Ophthalmology, National
Hospital for Neurology and Neurosurgery,
London,
and Neuro-Ophthalmology and Strabismus
Service, Moorfields Eye Hospital, London, UK
