Headache and vomiting

1. Extra case 1 Headache and vomiting

2. 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  Presentation

3. 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.  examination

4. = 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 (pseudotumorcerebri) What is papilloedema? What are the common causes of papilloedema?

5. 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 • 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 is the differential diagnosis?

6. Neuroimaging then lumbar puncture (to rule out other Dx and determine opening pressure) • MRI > CT  if IIH, MRI may show • 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 • May find: enlarged blind spot; generalized constriction; inferonasal vision loss What test(s) would you perform?

7. 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 What is the problem with the patient’s vision?

8. Contrast-enhanced MRI of the brain  normal LP  30mL CSF drained Lumbar puncture: Headache improves considerably Nausea and vomiting resolve over 1-2/7 Diplopia resolves over 1/52 investigations

9. How is a lumbar puncture performed? What are the contraindications, side effects and complications?

10. 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 technique

11. Indications: diagnosis of CNS infections and sometime to help diagnose subarachnoid haemorrhage, CNS malignancies, demyelinatingdiseaes 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 Indications and contraindications

12. 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 Side effects and complications

13. Opening pressure: 50–200 mm H2O CSF • Colour: colourless • Turbidity: crystal clear • Mononuclear cells: <5 per mm3 • Polymorphonuclearleukocytes: 0 • Mean total protein: 22–38 mg/dl • Range: 9–58 mg/dl (mean ± 2.0 SD) • Glucose: 60–80% of blood glucose What is the normal constituents and opening pressure of CSF?

14. 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. • >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- Xanthochromiacommonly 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 How do these tests and findings help in the diagnosis?

15. 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: • Medication – may just be anecdotal • Systemic illnesses — In addition to obesity, systemic illnesses reportedly associated with IIH include: • Addison disease • Hypoparathyroidism • Anaemia, usually severe • Sleep apnoea • Systemic lupus erythematosus (SLE) • Behcet's syndrome • Polycystic ovary syndrome • Coagulation disorders • Uremia Which conditions are associated with BIH?

16. 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 • 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 Discuss treatment of this condition

17. 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 Are there any long-term complications of this condition?