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Extra case 1
HEADACHE AND VOMITING
PRESENTATION
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22 year old female
PC: 2/52 headache
HPC: daily throbbing headache involving entire head
Worse upon waking, get better as day goes on
Has nausea, vomiting and intermittent diplopia (2/7)
Some alleviation by paracetamol and ibuprofen
PMHx: asthma
Meds: COCP
Allergies: sulphurs
FHx: An aunt died of a brain tumour in her 50s
SHx: Receptionist, shares a flat with friend
EXAMINATION
O/E: Afebrile, BP 110/70, PR 80 reg
 Neck supple, no meningismus
 CVS/ RESP/ABDO: normal
 Neuro: alert, uncomfortable from pain
 Cranial nerves: pupils reactive, bilateral
papilloedema, right sixth nerve palsy.
 Motor Examination: normal strength
 Reflexes: Normal, plantar response down going
bilaterally. Normal co-ordination and gait.
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WHAT IS PAPILLOEDEMA? WHAT ARE THE
COMMON CAUSES OF PAPILLOEDEMA?
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= swelling of the optic disc due to raised intracranial
pressure
Intracranial mass lesions (eg. tumour, hematoma)
Cerebral oedema (eg. Due to acute hypoxic ischemic
encephalopathy, large cerebral infarction, severe
traumatic brain injury)
Increased CSF production (eg. choroid plexus papilloma)
Decreased CSF absorption (eg. arachnoid granulation
adhesions after bacterial meningitis)
Obstructive hydrocephalus
Obstruction of venous outflow (eg. venous sinus
thrombosis, jugular vein compression, neck surgery)
Idiopathic intracranial hypertension (pseudotumor
cerebri)
WHAT IS THE DIFFERENTIAL DIAGNOSIS?
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Idiopathic (benign) intracranial hypertension
Migraine; tension-type headache; medication overuse
headache  but these would not have papilloedema
Malignant hypertension  optic neuropathy can be mistaken
for papilloedema
Secondary intracranial hypertension
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Metastatic tumour, hematoma  intracranial mass lesion
Acute hypoxic ischemic encephalopathy, large cerebral infarction,
severe traumatic brain injury  cerebral oedema
Choroid plexus papilloma  inc CSF production
Arachnoid granulation adhesions after bacterial meningitis  dec
CSF absorption
Obstructive hydrocephalus
Venous sinus thrombosis, jugular vein compression, neck surgery
 obstruction of venous outflow
WHAT TEST(S) WOULD YOU PERFORM?
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Neuroimaging then lumbar puncture (to rule out other Dx and
determine opening pressure)
MRI > CT  if IIH, MRI may show
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Flattening of the posterior sclera (80%)
Distension of perioptic subarachnoid space (50%)
Enhancement (with gadolinium) of the prelaminar optic nerve (45%)
Empty sella (70%)
Intraocular protrusion of the prelaminar optic nerve (30%)
Vertical tortuosity of the orbital optic nerve (40%)
MRV is more sensitive than MRI for finding cerebral venous
thromboses
LP: measure opening pressure; analyse CSF for cell count, glucose
and protein  may indicate need for culture for microbial agents;
CSF cytology or; antigen testing (eg, CSF VDRL)
Also need to check visual fields (assess severity and monitor
response)  either Goldmann kinetic perimetry or computer-assisted
static perimetry
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May find: enlarged blind spot; generalized constriction; inferonasal
vision loss
WHAT IS THE PROBLEM WITH THE
PATIENT’S VISION?
Intermittent diplopia  believed to be due to
fluctuations in perfusion of the nerve head
 Papilloedema: inc ICP  transmitted to the optic
nerve sheath  mechanical disruption of
axoplasmic flow  swelling of the axons and
leakage of water/protein/other cellular contents
into the extracellular space of the optic disc 
optic disc oedema
 CNVI palsy  due to inc ICP; CNVI has long
intracranial course before exiting the skull
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INVESTIGATIONS
Contrast-enhanced MRI of the brain  normal
 LP  30mL CSF drained
 Lumbar puncture:
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Headache improves considerably
 Nausea and vomiting resolve over 1-2/7
 Diplopia resolves over 1/52
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HOW IS A LUMBAR PUNCTURE PERFORMED?
WHAT ARE THE CONTRAINDICATIONS, SIDE
EFFECTS AND COMPLICATIONS?
TECHNIQUE
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Lateral recumbent position (or sitting upright)  for accurate measurement
of opening pressure
Level of entry for spinal needle: use highest points of iliac crests as guide
for L4 vertebral body  palpate spinous processes and interspaces of L3,
L4 and L5  insert needle into subarachnoid space at L3/4 or L4/5
interspace  below the termination of the spinal cord
Pt must be in foetal position  neck, back and limbs in flexion; lower
lumbar spine flexed  determines success of obtaining CSF
Clean and disinfect skin  local anaesthetic for lumbar intervertebral space
 insert 20 or 22 gauge spinal needle with a stylet  advance needle
slowly, angling slightly towards head (aim for umbilicus)  transiently
remove stylet at subarachnoid space to confirm CSF flow
pt should slowly straighten legs (allow CSF flow)  measure opening
pressure with manometer  collect fluid (usually 8-15mL, but can be up to
40mL for culture)  replace stylet  remove spinal needle
Queckenstedt manoeuvre: measure CSF pressure then manually compress
both jugular veins and note change in pressure  old method to show flow
from ventricles to lumbar space
http://www.youtube.com/watch?v=R2_0gOI8uV0
INDICATIONS AND CONTRAINDICATIONS
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Indications: diagnosis of CNS infections and sometime to help
diagnose subarachnoid haemorrhage, CNS malignancies,
demyelinating diseaes and Guillain-Barre syndrome
Urgent LP for suspected CNS infection (except for brain abscess or a
parameningeal process) and suspected subarachnoid haemorrhage
with a negative CT scan
Nonurgent LP is indicated for diagnosis of: IIH, carcinomatous
meningitis, tuberculous meningitis, normal pressure hydrocephalus,
CNS syphilis, CNS vasculitis
LP in therapy: spinal anaesthesia; intrathecal
chemotherapy/antibiotic administration; injection of contrast media
for myelography/cisternography
Contraindications: no absolute contraindications, but take care with
Possible raised intracranial pressure
Thrombocytopenia or other bleeding diathesis (including
anticoagulant therapy)
Suspected spinal epidural abscess
SIDE EFFECTS AND COMPLICATIONS
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Complications: post-LP headache; infection; bleeding; cerebral
herniation; minor neurologic symptoms (radicular pain, numbness);
late onset of epidermoid tumours of the thecal sac; back pain
Post-LP headache: due to leakage of CSF from dura and traction on
pain-sensitive structures
Infection: either meningitis or other (discitis or vertebral
osteomyelitis)  but uncommon
Back pain and/or neurologic symptoms: can suggest haematoma 
take care if bleeding disorder
Cerebral herniation:  take care if suspected inc ICP
Epidermoid tumour: rare, may only be evident years after procedure
is performed  can be due to epidermoid tissue being transplanted
into the spinal canal when not using a stylet or if the stylet is poorly
fitting
CNVI palsy: results from intracranial hypotension, generally
accompanied by other features of post-LP headache
WHAT IS THE NORMAL CONSTITUENTS AND
OPENING PRESSURE OF CSF?
Opening pressure: 50–200 mm H2O CSF
 Colour: colourless
 Turbidity: crystal clear
 Mononuclear cells: <5 per mm3
 Polymorphonuclear leukocytes: 0
 Mean total protein: 22–38 mg/dl
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 Range:
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9–58 mg/dl (mean ± 2.0 SD)
Glucose: 60–80% of blood glucose
HOW DO THESE TESTS AND FINDINGS
HELP IN THE DIAGNOSIS?
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Opening pressure – pressures over 180 are considered abnormal
Can compare opening and closing pressure to estimate the volume of CSF
reservoir.
Clarity - pleocytosis (inc cell count) is the usual reason for cloudy fluid.
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>200 white cells per cubic millimeter can be present without altering the clarity
>500 white cells per cubic millimeter usually produces cloudiness.
Red cell concentrations between 500 and 6000 per mm3 can cause the fluid to
appear cloudy; concentrations of over 6000 give a grossly bloody appearance.
A markedly elevated protein can also alter the clarity of the CSF.
But little clinical use as a large number of cells can be present without affecting
the clarity.
Colour - Xanthochromia commonly indicates spontaneous subarachnoid
hemorrhage. A variety of conditions, however, can also produce
xanthochromia: a traumatic tap; bilirubin due to jaundice; protein; etc.
Cells – CNS infections produce 3 basic CSF types which suggest diagnoses
WHICH CONDITIONS ARE ASSOCIATED
WITH BIH?
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Affects the brain, appears to be (but is not) a tumour; often reversible.
Clinical criteria: include headache, papilloedema, vision loss, elevated ICP
with normal cerebrospinal fluid composition, and no other cause of
intracranial hypertension evident on neuroimaging or other evaluations.
Despite its prior name (BIH), it is not a benign disorder. Many patients suffer
from intractable, disabling headaches, and there is a risk of severe,
permanent vision loss.
Pathogenesis is unknown.
Associated conditions:
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Medication – may just be anecdotal
Systemic illnesses — In addition to obesity, systemic illnesses reportedly
associated with IIH include:
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Addison disease
Hypoparathyroidism
Anaemia, usually severe
Sleep apnoea
Systemic lupus erythematosus (SLE)
Behcet's syndrome
Polycystic ovary syndrome
Coagulation disorders
Uremia
DISCUSS TREATMENT OF THIS CONDITION
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The treatment of IIH has two major goals: the alleviation of
symptoms (usually headache) and the preservation of vision.
Weight loss – low sodium wt reduction program
Medications - carbonic anhydrase inhibitors, loop diuretics,
and corticosteroids
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Carbonic anhydrase inhibitors – believed to reduce rate of CSF
production
Cautious with corticosteroids because of weight gain, steroid
withdrawal may cause severe rebound intracranial hypertension
Headache prophylaxis
Serial lumbar punctures – not recommended as CSF reforms
within 6 hours, therefore short term treatment,
uncomfortable, complications
Surgery – CSF shunting, optic nerve sheath fenestration
ARE THERE ANY LONG-TERM
COMPLICATIONS OF THIS CONDITION?
Permanent vision loss is the major morbidity
associated with IIH.
 A recurrence of symptoms may occur in 8 to 38
percent of patients after recovery from an
episode of IIH or after a prolonged period of
stability. Weight gain is a common but not
universal antecedent to recurrent IIH
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