Emergency red flags: go to hospital immediately if headache is:
- Sudden onset: worst headache of your life (thunderclap headache)
- Associated with neck stiffness, fever, or rash (possible meningitis)
- Following a head injury
- With new neurological symptoms: vision loss, weakness, speech difficulty
- Waking you from sleep progressively worsening over days-weeks
Blood tests ordered for headache
| Test | What it checks for |
|---|---|
| ESR | Very high ESR >50 in elderly: suggests giant cell arteritis (temporal arteritis) |
| CRP | Active inflammation: infection, vasculitis, autoimmune |
| CBC | Infection (high WBC), anaemia (low Hb can cause headache) |
| Glucose | Hypoglycaemia and very high blood sugar both cause headache |
| TSH | Hypothyroidism and hyperthyroidism cause headaches |
| Sodium | Low sodium (hyponatraemia) causes severe headache and confusion |
| Blood pressure check | Hypertensive headache: BP >180/120 |
| Lumbar puncture (CSF) | If subarachnoid haemorrhage or meningitis suspected |
Common headache types and their features
Tension headache (most common: 70% of headaches)
Bilateral pressing or tightening sensation, mild to moderate severity, not worsened by activity. Not pulsating. No nausea. Often related to stress, poor posture, eye strain or dehydration. Blood tests normal. Treatment: paracetamol, ibuprofen, rest, hydration.
Migraine
Moderate-to-severe pulsating pain, usually one-sided, lasting 4-72 hours. Often accompanied by nausea, vomiting, sensitivity to light (photophobia) and sound (phonophobia). May have aura (visual zig-zag lines, blind spot, tingling) before headache. Triggered by stress, hormones, certain foods (red wine, cheese, chocolate), sleep changes. Blood tests normal. Requires specific migraine treatment (triptans).
Cluster headache
Excruciating, strictly one-sided pain around one eye, with watering eye and blocked nostril on same side. Occurs in clusters over weeks, then remits for months. Predominantly affects men. Blood tests normal. Treated with high-flow oxygen and sumatriptan injection.
Giant cell arteritis (temporal arteritis)
Occurs almost exclusively in people over 50. Severe temporal (side of head) pain, jaw claudication (pain when chewing), scalp tenderness, and risk of sudden vision loss. ESR is typically extremely high (>50, often >100 mm/hr). CRP also elevated. Treated urgently with high-dose prednisolone to prevent blindness. Temporal artery biopsy confirms diagnosis.
Medication overuse headache (rebound headache)
Paradoxically, taking too many painkillers (>10-15 days per month) for headache causes chronic daily headache. All painkillers worsen it. Treatment: gradual painkiller withdrawal, preventive medication.
Blood pressure and headache
Hypertension alone rarely causes headache except at very high levels (>180/120 mmHg: hypertensive crisis). Most patients with chronic hypertension do not have headache. However, a hypertensive crisis with headache, confusion or visual changes is a medical emergency.
Questions to ask your doctor
- Is my headache pattern concerning for a serious cause?
- Should I have an ESR to rule out giant cell arteritis?
- Do I need a brain CT or MRI?
- Is medication overuse contributing to my headaches?
- Should I see a neurologist?
References
Sources cited on this page. PubMed links open the original abstract.
- GBD 2016 Headache Collaborators. Global, regional, and national burden of migraine and tension-type headache, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018;17(11):954–976. PMID 30353868 · doi:10.1016/S1474-4422(18)30322-3
Red flag headaches – the features that mandate urgent imaging
The vast majority of headaches are primary – tension-type, migraine, or cluster – and require no imaging. However, certain headache patterns signal potentially life-threatening secondary causes that require urgent investigation:
- Thunderclap headache: A headache that reaches maximal severity within 60 seconds – "the worst headache of my life." Subarachnoid haemorrhage (SAH) from a ruptured cerebral aneurysm must be excluded urgently. CT head without contrast detects SAH in 95–98% of cases within 6 hours; if negative, lumbar puncture at 12 hours looks for xanthochromia (yellow discolouration of CSF from haemoglobin breakdown).
- Progressive headache over weeks: New daily headache steadily worsening suggests raised intracranial pressure – from a space-occupying lesion (tumour, cerebral abscess, subdural haematoma), idiopathic intracranial hypertension, or hydrocephalus. Associated with morning headaches (worse on waking, improved by sitting up), vomiting, or visual obscurations.
- Fever + headache + neck stiffness: Bacterial meningitis – blood cultures and lumbar puncture (if safe – CT first to exclude raised ICP preventing LP) + immediate IV antibiotics without delay for diagnostic results. Every hour of delay in bacterial meningitis treatment significantly worsens outcomes.
- Headache + new neurological deficit: Focal weakness, speech disturbance, visual field loss, or unilateral sensory change with headache suggests stroke, TIA, or cerebral venous sinus thrombosis.
- Temporal headache in adults over 50: New-onset headache in an older adult, especially with scalp tenderness over the temporal artery, jaw claudication, visual disturbance, or a raised ESR – giant cell arteritis (GCA) until proven otherwise. Immediate high-dose prednisolone (60–100 mg) to prevent irreversible blindness; temporal artery biopsy for confirmation.
Migraine – the mechanism and evidence-based treatment
Migraine is a complex neurovascular disorder, not simply "a bad headache." The pathophysiology involves cortical spreading depression (a wave of neuronal and glial depolarisation moving across the cortex at 3–5 mm/minute – the electrophysiological basis of aura), followed by activation of the trigeminal-vascular system and release of CGRP (calcitonin gene-related peptide) – the key pro-migraine neuropeptide. CGRP causes dilation of meningeal vessels, inflammation, and the transmission of pain signals to the brain cortex.
Treatment implications of the CGRP mechanism: triptans (5-HT1B/1D agonists – sumatriptan, rizatriptan, zolmitriptan) are the gold-standard acute treatment, working by constricting dilated meningeal vessels and blocking CGRP release. For prevention, the newest class of targeted therapies – anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) – directly block CGRP or its receptor and are NICE-approved for chronic migraine (15+ headache days per month, 8+ of which are migraine).
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