The acute headache – history, monitoring and investigations
Dr Kathleen White, Consultant Neurologist
8% of ED attendances and 3% of admissions.
- “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).
She then went on to discuss a standard full examination that might be expected, including fundoscopy.
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.
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.
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
- Other primary
- Facial pain disorders
You can simplify the diagnosis of migraine looking for high specificity features (Lipton 2002; Spectrum Study):
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
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!”