Neuro - Life/Sight Threatening Secondary Headaches Flashcards
NOTIS Mnemonic for Red Flags for Headaches
N
O
T
I
S
1.) Neurological Symptoms - new sx
- cognitive dysfunction, ↓conscious level
- intracranial haemorrhage, SOL
- stroke: dizziness, weakness, speech etc
- visual sx: acute glaucoma, temporal arteritis, CNIII palsy (posterior communicating artery aneurysm)
2.) Onset new/changed OR Over 50yrs
- malignancy, acute glaucoma
3.) Thunderclap Headache - extremely painful sudden onset headache, often in an occipital location
- subarachnoid haemorrhage
4.) Intracranial Pressure - raised ICP
- papilloedema, pulsatile tinnitus,
- vomiting (also present in CO poisoning)
- postural: worse standing, lying or bending over
- pressure: worse on coughing or straining
5.) Systemic Symptoms
- cranial infections: fever, photophobia, neck stiffness
- SOL: weight loss, fatigue, night sweats etc.
- pre-eclampsia: pregnancy sx
Subarachnoid Haemorrhage (SAH)
Pathophysiology
Risk Factors
Clinical Features
Imaging/Investigations
1.) Pathophysiology - arterial bleed between the arachnoid and pia mater
- spontaneous SAH: often due to a ruptured ‘berry’ aneurysm (85%), other causes include: infective (mycotic) aneurysm, arteriovenous malformation, arterial dissection, pituitary apoplexy, perimesencephalic SAH (venous)
- traumatic SAH: occurs due to head injury
2.) Risk Factors
- conditions associated with berry aneurysms: ADPKD, CT disorders (Marfan’s or Ehlers-Danlos), coarctation of the aorta
- smoking, alcohol, hypertension, family history
- cocaine use, sickle cell anaemia, neuro-fibromatosis
- peak incidence is 40-50, more common in women and Afro-Caribbean
3.) Clinical Features
- thunderclap headache: sudden onset occipital headache that occurs during strenuous activity, the pain is maximal at onset of the headache
- neuro sx: speech, weakness, seizures, LOC
- visual sx: diplopia, orbital pain
- meningism sx (blood leaks into CSF): photophobia and neck stiffness (not meningitis as it is sudden onset and there is no fever present)
- dizziness, N+V, high blood pressure, coma, seizures, sudden death
- ECG changes (including ST elevation)
4.) Imaging/Investigations
- 1°non-contrast CT Head: ‘star sign’ acute (hyperdense/bright) blood accumulates in basal cistern –> hyper attenuation in subarachnoid
- 2°LP (if CT is negative): done >12hrs from sx onset to allow xanthochromia (bilirubin in RBCs) to be seen, RBCs also increased
- 3°CT/MR Angiography (once SAH is confirmed): to locate the source of the bleeding and identify a causative pathology that needs urgent treatment
Management of a Subarachnoid Haemorrhage
Acute Management
Surgical Intervention
Complications
1.) Acute Management - referral to neurosurgery when confirmed
- intubation and ventilation if reduced consciousness
- vasospasm: nimodipine (CCB) used for prevention
- hydrocephalus: LP or insertion of a shunt
- seizures: antiepileptic medications
2.) Surgical Intervention - repair the vessel and prevent re-bleeding
- most intracranial aneurysms are treated with a endovascular coil (IR): insert a catheter into aneurysm sac to seal it off from the artery
- a minority require a craniotomy and clipping by a neurosurgeon: cranial surgery to clamp neck of aneurysm
3.) Complications - re-bleeding (occurs in 30% of cases)
- vasospasm: vasoconstriction due to CSF irritant, vasospasm can lead to global cerebral ischaemia
- cerebral oedema: hypoxia and extravasated blood
- acute hydrocephalus: blood blocks CSF drainage
- embolus: thrombi occlude smaller distal arteries
- hyponatraemia (SIADH), seizures
Meningitis
What is it?
Causes
Clinical Features
Complications
1.) What is it? - inflammation of the leptomeninges and the CSF of the subarachnoid space
2.) Causes
- bacteria: N. meningitidis (young), S. pneumoniae (old), Listeria monocytogenes (immunosuppressed)
- viral: HSV, CMV, HIV, measles, mumps, enteroviruses
- others: TB, fungal
3.) Clinical Features
- fever, neck stiffness, photophobia, vomiting
- headache, confusion,
- septicaemia: non-blanching purpuric rash, ↓BP (late)
- meningoencephalitis: seizures, focal neuro deficits
- Kernigs’s: knee extension is met with resistance
- Brudzinki: neck flexion –> involuntary knee/hip flexion
4.) Complications
- sensorineural hearing loss, epilepsy, paralysis
- sepsis, intracerebral abscess
- brain herniation, hydrocephalus
- posterior communicating artery aneurysm: headache + third nerve palsy
Management of Meningitis
Investigations
CSF Analysis
Management
Management of Close Contacts
1.) Investigations
- lumbar puncture: must exclude ↑ICP, L3/L4, between arachnoid mater and pia mater
- FBC: ↑WCC, ↓plts, ↑CRP, coagulation screen, VBG, blood glucose, blood cultures
2.) CSF Analysis
- bacterial: cloudy, low glucose (<50% of CBG), high protein (>50mg/dL), majority neutrophils
- viral: clear/cloudy, normal glucose (>50% of CBG), normal/raised protein, majority lymphocytes
- TB/fungal: slightly cloudy, low glucose, high protein, majority lymphocytes
3.) Management
- GP: call an ambulance, give high flow oxygen, give IV (IM if no IV access) benzylpenicillin,
- IV ceftriaxone (or cefotaxime)
- IV dexamethasone to ↓risk of neuro complications unless septic or immunocompromised or post-op
- IV fluids, analgesia, ?sepsis 6
4.) Management of Close Contacts
- notify public health England
- prophylactic Abx (PO cipro or rifampicin) for close contacts (<7days) for meningococcal meningitis
- meningococcal vaccine for close contacts
Raised Intracranial Pressure
Pathophysiology
Clinical Features
Papilloedema
Management
1.) Pathophysiology - due to a space-occupying lesion
- ↓space for other skull contents e.g. CSF to squeeze in to –> rise in pressure within the intracranial space
- differentials: tumour, intracranial haemorrhage, abscess/infection, idiopathic intracranial hypertension
2.) Clinical Features - constant headache worse on:
- waking, lying down, bending over, coughing/straining
- other symptoms inc: nausea and vomiting
- ↓consciousness, focal seizures, CN palsies (3 and 6)
- visual field defects, ↓pupil reaction, ptosis
- papilloedema on fundoscopy
- cushing’s reflex: ↑BP, ↓HR, abnormal breathing (inc Cheyne-Stokes respiration)
3.) Papilloedema - swelling of the optic disc due to high pressure causing CSF to flow into optic nerve sheath
- the sheath is connected to the subarachnoid space
- seen in fundoscopy, alongside other changes:
- elevated optic disc, blurring of the optic disc margin
- loss of venous pulsation, engorged retinal veins
- haemorrhages around optic disc, Paton’s lines which are creases in the retina around the optic disc
4.) Management
- investigate and treat the underlying cause
- head elevation to 30º
- controlled hyperventilation: to reduce pCO2 –> vasoconstriction of the cerebral arteries –> ↓ICP
- IV mannitol may be used as an osmotic diuretic
- removal of CSF: repeated LP (IIH), VP shunt (hydrocephalus), drain from intraventricular monitor
Idiopathic Intracranial Hypertension (IIH)
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - syndrome of unknown aetiology that results in ↑ICP (>25cmH2O)
- demographic: obese, young-middle aged woman
- drug: OCP, steroids, tetracyclines, lithium, vitamin A
2.) Clinical Features
- headache: non-pulsatile, bilateral, and worse in the morning (after lying down or bending forwards)
- morning vomiting, key differential is sleep apnoea
- transient blurred vision due to optic nerve ischaemia
- if untreated permanent visual damage may result
3.) Investigations
- fundoscopy: bilateral papilloedema with the blurring of the optic disc margin
- non-contrast CT: to exclude a SOL before a LP
- LP: elevated opening pressure w/ normal CSF
- MRI: normal
4.) Management
- weight loss is first-line management
- medical: acetazolamide (many side effects), topiramate and furosemide are also commonly tried
- ↓CSF pressure: therapeutic LP, surgical CSF shunting
- optic nerve sheath fenestration may protect vision
Giant Cell (Temporal) Arteritis
Pathophysiology
Diagnostic Features
Management
1.) Pathophysiology - chronic vasculitis of large and medium-sized vessels causing inflammation of arteries
- superficial temporal artery is most common
- can cause acute visual loss as occlusive arteritis –> anterior ischaemic optic neuropathy (AION)
- associated with HLA-DR4 gene
- risk factors: >50s, FH, caucasian, female, PMR
2.) Diagnostic Features - >50 w/ 2+ of the following:
- unilateral headache localised in the temporal region
- tenderness/↓pulsation of temporal artery
- visual sx: blurring, diplopia, blindness, amau.. fugax
- other sx: jaw claudication, tongue discomfort
- constitutional sx: fever, night sweats, weight loss
- bloods: ↑ESR, ↑CRP
- temporal artery biopsy: reveals necrotizing arteritis
3.) Management - steroids (don’t wait for biopsy)
- PO prednisolone (40mg, 60mg if visual sx) OD for 2wks then taper
- visual sx: IV methylpred (1g) pulse therapy (1-3d)
- low dose aspirin to reduce thrombotic risk
Acute-Angle (Acute) Glaucoma
Pathophysiology
Risk Factors
Clinical Features
Initial Management
1.) Pathophysiology - ↑IOP –> damage to optic nerve
- iris bulges forward and seals off the trabecular meshwork from the anterior chamber
- this prevents drainage of aq humour –> fast ↑IOP
2.) Risk Factors
- ↑age, females, FH, hyperopia, shallow ant chamber
- Chinese and East Asian, rare in black ethnic origin
- medication: noradrenaline, anticholinergics e.g. oxybutynin, solifenacin, TCA e.g. amytriptyline
3.) Clinical Features
- painful red eye, blurred vision, halos around lights
- teary, hazy cornea, ciliary injection, ↓visual acuity
- associated headache, nausea and vomiting
- fixed and dilated pupil, firm eyeball on palpation
4.) Initial Management - ophthalmic emergency
- lie patient on their back without a pillow
- pilocarpine eye drops (2% for blue, 4% for brown): pupil constriction and ciliary muscle contraction opens up flow of aq humour into the trabecular meshwork
- PO/IV acetazolamide 500mg: carbonic anhydrase inhibitor (CAi) which ↓production of aqueous humour
- analgesia and antiemetic if required
