Headaches Flashcards
Covers migraine, tension, cluster, temporal arteritis, venous sinus thrombosis
What is an occipital nerve block?
May be used to treat WHAT
What is the epidemiology of migraine?
More common in women
Most commonly start between 15-24yrs
Occur most frequently in those 35-45yrs
In women, majority resolve after the menopause
What are some precipitants of migraine?
CHOCOLATE
Chocolate – due to high phenylethylamine content
Hangovers
Oral contraceptive
Caffeine (or withdrawal from) or Cheese(→due to high tryptamine content)
Orgasms
Lie ins/relaxation
Alcohol
Travel or Tumult
Exercise
Other factors: Noise/lights Obesity Patent foramen ovale Common around puberty, menstruation, pregnancy, menopause
Though in 50% of cases triggers are not identified and even if triggers are avoided, doesn’t necessarily mean won’t have a migraine
What is the pathophysiology of migraine?
Not entirely known
Genetic predisposition
Related to dilation/constriction of cerebral blood vessels: Neuropeptide CGRP (calcitonin gene related peptide) is thought to be important
Initial local (occipital cortex) hypovolaemia cause aura → hyperaemia/blood vessel dilatation/oedema → stimulation of nerve endings and causes pain
How does migraine present?
Visual arua – perceived visual disturbances i.e. zig-zag lines, bright flashing lights, distorted objects etc – precede the attack and last 15-60 mins
Sensory aura – pins/needles spreading up limbs
Speech aura – temporary dysarthria
Gradual onset, unilateral, pulsatile, moderate-severe headache aggravated by movement; lasting 4-72hrs; may also be bilateral +/- neck pain
Photophobia
N+V
Heightened sensitivity to all stimuli – become painful i.e. brushing hair
What is necessary for a diagnosis of migraine?
Headaches lasting 4/72hrs with aura = classical migraine
Headaches lasting 4/72hrs with no aura but with N+V or photophobia + 2x following (common migraine):
Unilateral
Pulsating
Interferes with normal life
Worsened by normal activities i.e. walking, climbing stairs
What is necessary for a diagnosis of migraine?
Headaches lasting 4/72hrs with aura = classical migraine
Headaches lasting 4/72hrs with no aura but with N+V or photophobia + 2x following (common migraine):
Unilateral
Pulsating
Interferes with normal life
Worsened by normal activities i.e. walking, climbing stairs
Get patients to keep a headache diary
What do you give for acute management of migraines?
Triptan e.g. sumatriptan + NSAIDs/paracetamol
What do you give for prophylaxis against migraines?
If episodes >2 month:
Propanolol PO daily 60-180mg
Amitriptyline PO at night 25–75 mg
Topiramate (anticonvulsant) PO daily 50-100mg
Acupuncture, CBT
What is an analgesic rebound headache?
Headaches following stopping long term/excessive use of analgesia
Worse with mixing analgesics i.e. Parecetamol + codeine/opiates
Management:
Withdraw analgesics and limit future use
Aspirin or naproxen may be used to improve symptoms whilst withdrawing from analgesics
What are the features of a tension headache?
Bilateral, non-pulsatile headache ± scalp muscle tenderness
No N+V or sensitivity to head movements
Management:
Stress relief
Scalp massage (mmm)
What is the epidemiology of trigeminal neuralgia?
More common in men but more common in Asian women than Asian men
Presents >50yrs
What is the aetiology and pathophysiology of trigeminal neuralgia?
Exact mechanisms unknown but believed to be due to loss of myelin sheath around trigeminal nerve
Secondary causes:
Compression of the trigeminal root by arteriovenous malformation or aneurismal intracranial vessels or a tumour (superior cerebellar artery implicated)
Chronic meningeal inflammation
MS
Herpes zoster
Skull base malformation
How does trigeminal neuralgia present?
Paroxysms of intense, stabbing pain lasing a few seconds (→hours) in the trigeminal nerve distribution
Unilateral, affecting mandibular or maxillary divisions
Triggered by:
Washing affected area, shaving, eating, talking
How do you manage trigeminal neuralgia?
Carbamazepine
Also: Lamotrigine, Phenytoin, Gabapentin
Surgery
i) If medications are ineffective
ii) Microvascular decompression – moving of any overlying blood vessels over the nerve and placing pads between vessel and nerve
What is the epidemiology of giant cell arteritis/temporal arteritis?
Common in the elderly
Rare under 50
Strongly associated with polymyalgia rheumetica (PMR)
What is the aetiology and pathophysiology of giant cell arteritis?
Inflammation of walls of arteries
Inflamed superficial temporal or occipital arteries cause pain → touching skin over vessels will cause pain
Vessel may become hardened (due to the chronic inflammation) → loss of pulse
How does giant cell arteritis present?
Generalised headache
Scalp tenderness
Claudication of the jaw
Painless temporary or permanent visual loss (if more than one of the temporal or occipital arteries are affected)
Generalised malaise, fever, fatigue
How does polymyalgia rheumetica present?
Pain, stiffness and inflammation of the muscles of the shoulders, neck and hips - mostly in the morning, lasting longer than 45 mins
Fatigue
Loss of appetite and weight
Depression
Similarly rare in the under 50’s (most are in 70’s)
How do you investigate giant cell arteritis?
Bloods:
Raised ESR/CRP
LFT - Low albumin, Raised ALP, Raised gamma-glutamyltransferase
Temporal arterial biopsy = diagnostic
Do not hesitate to start steroids though as risk of slight loss is high and biopsy should still remain +ve for a few weeks after starting treatment
Hypertrophy and inflammation of the intima
Degredation and presence of giant cells, lymphocytes and plasma cells in the elastic lamina
How do you manage giant cell arteritis?
Corticosteroids: Predinsolone – ASAP - probably a long course (1-2+yrs)
To reduce the risk of sight loss
75mg aspirin PO OD - to reduce clot risks
PPI - gastroprotection as long course steds + NSAID
What is the epidemiology of venous sinus thrombosis?
Rare but most common in the 3rd decade and in women
What are some risk factors/aetiology for developing a VST?
Thrombophilia
Nephrotic syndrome, dehydration
IBD, lupus
Pregnancy and recent birth
Polycythaemia rubra vera, sickle cell
Oestrogen contraceptives
Meningitis, sepsis
Trauma/head/neck surgery
What is the pathophysiology of VST?
Blood clot in the dural venous sinuses – congestion – venous infarction due to insufficient blood supply – cerebral oedema – further hypoxic injury
