Urgent considerations
See Differentials for more details
Significant intracranial pathology is rare in children with headache.[6][7][8] However, the following conditions require immediate identification and intervention.
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.[12]
Possible aetiologies include:
Subarachnoid haemorrhage
Parenchymal haemorrhage
Sinovenous thrombosis
Arterial dissection
Pituitary apoplexy
Intracranial hypotension
Intermittent hydrocephalus
Initial management includes the following:[9]
Non-contrast head computed tomography (CT): may be used for speed and sensitivity in detecting a bleed when thunderclap headache or haemorrhage is suspected.
Magnetic resonance imaging (MRI): if intracranial hypertension or hypotension is suspected. Preferred over CT where available.
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 cerebrospinal fluid 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.
Magnetic resonance angiography or venography, and CT angiography or venography may be performed if a less common aetiology is clinically suspected in a child with thunderclap headache:[9][13]
Arterial dissection (i.e., recent neck injury, neck pain, focal neurological signs)
Intracranial hypertension (i.e., headache worse when lying down or headache on waking, tinnitus, optic nerve oedema, horizontal diplopia)
Intracranial hypotension (i.e., recent back or neck trauma, headache worse when upright)
Sinovenous thrombosis (i.e., evidence of intracranial hypertension, intracranial infection or mastoiditis, use of drug with hypercoagulable risk, focal neurological signs)
Tumour (i.e., worsening headache, optic nerve oedema, focal neurological signs)
Subarachnoid or subdural haemorrhage
Neurosurgical consult and intensive care admission are commonly required. Treatment is directed at the underlying aetiology.
Only after appropriate evaluation can more benign aetiologies be considered, including first or severe migraine, tension headache, or cluster headache.
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 hypertonic saline and hyperventilation to achieve a pCO₂ of 35 mmHg.[14][15] 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.[9] Head CT can be used if there are concerning symptoms and MRI is not possible.[9] 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:[16]
Suspicion of non-accidental injury
Post-traumatic seizure
Glasgow Coma Scale (GCS) <14 (children aged ≥1 year) on initial accident and emergency department assessment
Paediatric GCS <15 (children aged <1 year) on initial accident and 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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