Headache – Evening Medical Update Series at Royal College of Physicians Edinburgh 27th March

The acute headache – history, monitoring and investigations
Dr Kathleen White, Consultant Neurologist

8% of ED attendances and 3% of admissions.

5 patterns:

  • “thunderclap” (sudden onset, severe)
  • with fever
  • with focal neurology
  • new onset persistent headache
  • chronic headache presenting for analgesia

Dr White talked about taking a good history of the pain, and then the red flags (which indicate a secondary cause).

Image result for red flags for headache

She then went on to discuss a standard full examination that might be expected, including fundoscopy.

SAH

Acute sudden onset headache – 1/3 have serious intracranial pathology – 1/4 will have intracranial haemorrhage, though this reduces to 1/8 if there are no other symptoms.

Subhyloid pressure is a bleed in the preretinal space seen on fundoscopy – caused by raised ICP in subarachnoid haemorrhage (SAH).

For SAH, 15% of CT brain scans are normal.

Follow up is cerebral angiography (most often MRA) to identify source of bleeding. This is to stop rebleeding – risk of 20% in first 14 days and 50% in first 6 months – and it is often fatal.

Sudden onset headache with reduced consciousness

Central Venous Sinus Thrombosis

85% are associated with risk factors. 12% are idiopathic. Mortality is high 20-50%. Only 25-30% of patients make a recovery.

Carotid/vertebral dissection

The leading cause of stroke in young (<40) people.

Management of primary headache
Dr Anish Bahra, Consultant Neurologist

Classification of headaches – primary (98% = benign = morbidity) and secondary (2% = not benign = mortality).

The following are not reliable predictors of secondary headache – severity, recurrence & chronicity, clinical syndrome, response to treatment. The only isolated secondary headache phenotype is thunderclap headache. (Locker et al 2006).

What does help is the following (for identifying secondary headache):

  • abnormal neurological examination*
  • age >50 years*
  • additional features
  • sudden onset*

* any one = 98.6 % sensitivity

So what is thunderclap?

Thunderclap signifies 1-5 minutes of onset time. Any time over than that and you can relax.

Primary headache

RE migraine – a polygenic network problem with ion channel dysfunction – and at least 3 genes have been classified. It often starts in the neck due to V1/C1 nucleus area. During the last decade, blocking calcitonin gene-related peptide (CGRP) has emerged as a possible mechanism for prevention of migraine attacks. CGRP has been shown to be released during migraine attacks and it may play a causative role in induction of migraine attacks

  • Tension type headache ~87%
  • Migraine 12%
  • Cluster headache and related
    • paroxysmal hemicrania
    • hemicrania continua
    • SUNA
  • Other primary
  • Facial pain disorders

You can simplify the diagnosis of migraine looking for high specificity features (Lipton 2002; Spectrum Study):

  • disability
  • nausea
  • photophobia

RE Medication overuse headache (8 days / month), can take 6-8 weeks to improve – happens more quickly with triptans. Triptans are the worse in terms of speed to onset. 45% get better, 45% don’t change, 10% get worse – but now they can respond to prophylaxis which they didn’t before. For people that don’t respond, they need a clinical psychologist.

When treating migraine, go in with the domestos in A&E! Eg large ibuprofen, paracetamol, sumatriptan + antiemetic like metoclopramide or prochlorperazine (Ferrari Lancet 2001). If no response to a combination, don’t try it again. You expect the drug to work within 2 hours – that’s the aim.

Regarding preventative treatment, it’s about:

  • amitriptyline – start 10mg, up to 50-75mg
  • candesartan – start 2mg, up to 16mg
  • propranolol – start 20mg, up to 320mg
  • topiramate
  • flunarizine

Cluster headache

Where people with migraine will go to sit down, cluster will be fidgeting and rocking – it’s not motion sensitive.

Acute management is sumatriptan SC and oxygen. Prevention is verapamil, lithium, steroids.

Vasculitic causes of headache – investigation through to management
Dr Lisa Hutton, Consultant in Rheumatology

How to recognise the pattern of when vasculitis may be the diagnosis? Recognise it as a multi-system disease.

ANCA associated vasulitis

Granulomatosis with polyangiitis (new name for Wegeners)

Eosinophilic granulomatosis with polyangiitis (new name for Churg-Strauss)

C-ANCA = GPA

P-ANCA = MPO/MPA/EGPA

Dr Hutton went through some really interesting cases of vasculitis before talking about the EULAR guideline for AAV (ANCA-associated vasculitis). Specifically she discussed giant cell arteritis (GCA) or temporal arteritis.

Talked about the side effects of steroids and the tapering regimen over 8 months. New drugs include tocilizumab (Actemra).

A key point that Dr Hutton made is that you can get GCA without a rise in inflammatory markers – it is rare but not unique. Therefore, if you have a convincing clinical picture but normal inflammatory markers, you should treat anyway. This is corroborated in a paper I’ve just found, “Giant cell arteritis with normal ESR and/or CRP is rare, but not unique!”

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