Urgent considerations

See Differentials for more details

Thunderclap headache

Thunderclap headache (or sudden severe headache onset) is uncommon. However, it is often associated with a serious underlying brain disorder that requires specific and urgent therapy.[8]

Possible aetiologies include:

  • Subarachnoid haemorrhage

  • Parenchymal haemorrhage

  • Sinovenous thrombosis

  • Arterial dissection

  • Pituitary apoplexy

  • Intracranial hypotension

  • Intermittent hydrocephalus.

Initial management includes the following.

Non-contrast head computed tomography (CT)

  • After a history and physical examination, diagnostic testing often begins with a non-contrast head CT on which acute bleeding will be hyperdense.[7]

Lumbar puncture

  • Neuroimaging may be indicated prior to lumbar puncture to rule out a large mass lesion and assess risk for herniation.

  • If subarachnoid haemorrhage is strongly suspected (i.e., thunderclap headache with severe rapid onset), and the head CT is non-diagnostic, lumbar puncture should be performed. Examination of centrifuged supernatant CSF for xanthochromia (yellow colouration) is the most sensitive method for detecting subarachnoid haemorrhage and is best identified and quantified in the laboratory, rather than visually. Xanthochromia can persist up to several weeks following a subarachnoid haemorrhage. If this method is not available, sending tubes 1 and 4 for a cell count can also enable differentiation between true subarachnoid blood and blood from a traumatic tap.

  • If intracranial hypertension is suspected (i.e., headache worse when lying down or headache on waking, tinnitus, optic nerve oedema, horizontal diplopia) or hypotension is suspected (i.e., recent back or neck trauma, headache worse when upright) then a lumbar puncture with opening pressure in the relaxed lateral recumbent position is indicated.

Other imaging modalities include magnetic resonance imaging (MRI) without contrast, magnetic resonance angiography and CT angiography.[7][9]

These may be performed if the following are clinically suspected:

  • Arterial dissection (i.e., recent neck injury, neck pain, focal neurological signs)

  • Sinovenous thrombosis (i.e., evidence of intracranial hypertension, obesity or recent weight gain, use of medications with hypercoagulable risk such as oral contraceptive pills, focal neurological signs)

  • Tumour (i.e., slowly worsening headache, optic nerve oedema, focal neurological signs)

  • Subarachnoid or subdural haemorrhage (identify arteriovenous malformation or aneurysm; identify amount and severity of injured brain parenchyma).

Only after appropriate evaluation can more benign aetiologies be considered, including first or severe migraine, tension headache, or cluster headache.

Treatment is directed at the underlying aetiology. Non-specific pain medications may be used symptomatically for headache relief as needed. Often neurosurgical consultation and intensive care admission are required.

Acute herniation

Patients with intracranial lesions causing intracranial hypertension may present initially with:

  • Headache, usually positional (worse when lying down)

  • Vomiting, may be projectile

  • Diplopia

  • Depressed level of consciousness

  • Ophthalmoplegia or pupil asymmetry (optic nerve oedema may be absent depending on acuity of presentation)

  • Cushing triad: hypertension, bradycardia with or without apneustic breathing (breathing characterised by a prolonged inspiratory phase followed by expiration apnoea, most often associated with head injury).

If a space-occupying lesion is present, urgent neurosurgical consultation is required. Maintaining a neutral neck position and elevated head of bed (at 20 to 30 degrees) may improve venous drainage. Initial management of critically raised intracranial pressure includes intravenous hyperosmolar therapy (mannitol or sodium) and hyperventilation to achieve a pCO₂ of 35 mmHg. Further reduction in pCO₂ may be necessary to achieve rapid but temporary reductions in cerebral blood flow and thus intracranial pressure, but excessive or prolonged hyperventilation may compromise cerebral perfusion, resulting in further hypoxic ischaemic injury.

Traumatic brain injury

A detailed history of the mechanism of injury and any associated symptoms is essential. Examination should include a full neurological assessment and examination for injuries including signs of basal skull fracture. Non-contrast MRI is indicated.[7] Head CT can be used if there are concerning symptoms and MRI is not possible.[7] Immobilisation and imaging of the cervical spine might also be needed.

In the UK, the National Institute for Health and Care Excellence recommends that children aged 16 years and under who have sustained a head injury should have a CT head scan within 1 hour if any of the following apply:[10]​​

  • Suspicion of non-accidental injury

  • Post-traumatic seizure

  • Glasgow Coma Scale (GCS) <14 (children aged ≥1 year) on initial emergency department assessment

  • Paediatric GCS <15 (children aged <1 year) on initial emergency department assessment

  • GCS <15 2 hours after the injury

  • Suspected open or depressed skull fracture or tense fontanelle

  • Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ears or nose, Battle’s sign)

  • Focal neurological deficit

  • Bruise, swelling, or laceration of more than 5 cm on the head in children aged under 1 year

  • Two or more of: witnessed loss of consciousness lasting more than 5 minutes; abnormal drowsiness; three or more discrete episodes of vomiting; antegrade or retrograde amnesia lasting more than 5 minutes; dangerous mechanism of injury (high-speed road traffic accidents as a pedestrian, cyclist, or vehicle occupant, fall from a height >3 metres, high-speed injury from projectile or other object); any current bleeding or clotting disorder.

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