MRI Brain – Dedicated Protocol for Headache

1. Executive Summary

Headache is the third leading cause of disability worldwide and one of the most common reasons for neuroimaging requests. Yet it is also one of the most heterogeneous clinical questions in neuroradiology — the same symptom can represent a benign primary disorder requiring no imaging, or an immediately life-threatening pathology requiring emergent intervention. The clinical and imaging challenge is stratification: identifying the small minority of patients with secondary headache requiring specific diagnosis and treatment from the large majority with primary headache disorders where MRI is low-yield or frankly unnecessary.

The dedicated headache MRI protocol is not a single fixed protocol. It is a clinically-stratified framework in which the base sequence set of the generic brain MRI (described in the master page) is modified, augmented, or targeted based on the clinical phenotype of the headache and the specific secondary cause being excluded. A patient with suspected intracranial hypotension requires gadolinium and a specific sagittal T1 assessment; a patient with possible cluster headache requires pituitary protocol and MRA; a patient with thunderclap headache requires SWI/GRE and FLAIR with high sensitivity for subarachnoid blood. None of these requirements is met by the generic brain MRI template, and none should be imposed uniformly on all headache patients. For sequence-level protocol optimisation, vendor terminology and artefact management, see the dedicated MRIninja page FLAIR Sequence.

The cardinal principle of headache neuroimaging, explicitly endorsed by the ACR Appropriateness Criteria 2022 [1], is that imaging is not indicated for most patients with chronic headache, typical migraine or tension-type headache, and a normal neurological examination. The radiologist and technologist must understand which clinical features justify which protocol additions.

1.1 Added Value Over the Generic Protocol

The dedicated headache framework adds the following over the generic brain MRI:

• Contrast with pachymeningeal protocol: mandatory for intracranial hypotension, pachymeningitis, leptomeningeal enhancement, and cranial neuropathy — none of which can be adequately assessed without gadolinium
• SWI/GRE prioritised: haemorrhage screening in thunderclap headache; cortical superficial siderosis in headache + focal deficits; cavernoma bleeding
• Intracranial MRA: added for cluster headache, suspected aneurysm, reversible cerebral vasoconstriction syndrome (RCVS), and headache with focal deficits
• MR venography (MRV): added for suspected intracranial hypertension / idiopathic intracranial hypertension and for headache with papilloedema
• Thin-section pituitary protocol: added for cluster headache and suspected pituitary apoplexy
• Vessel wall imaging: for suspected vasculitis, RCVS, and giant cell arteritis
• Sagittal T1 pre- and post-contrast: specifically targeted for intracranial hypotension — brainstem sagging, pontomesencephalic angle, mamillo-pontine distance
• Positional FLAIR: DWI-FLAIR mismatch principle re-applied in the context of positional headache for CSF pressure changes
• Orbital sequences: added for suspected giant cell arteritis with ophthalmic artery involvement or orbital apex syndrome

1.2 Limits of the Dedicated Headache Protocol

Thunderclap headache: MRI is not the first-line investigation for thunderclap headache. Non-contrast CT remains the most appropriate first investigation because of its speed, availability, and established sensitivity for hyperacute subarachnoid haemorrhage. A negative CT in thunderclap headache within 6 hours of onset has very high negative predictive value, supported by the Ottawa Subarachnoid Haemorrhage Rule studies [6]. MRI is complementary — FLAIR and SWI can detect early SAH missed by CT, but this is a secondary role. The radiologist must communicate that a negative MRI in thunderclap headache does not exclude SAH within the first hours of onset.

Migraine: MRI is normal or shows non-specific white matter hyperintensities in migraine. There is no specific positive MRI finding that diagnoses migraine. The role of MRI in migraine is to exclude secondary causes — which is appropriate in new-onset migraine, particularly in patients > 50 years, but not in typical established migraine without red flags.

False reassurance from negative MRI: intracranial hypertension and hypotension can occasionally be associated with a normal MRI. Idiopathic intracranial hypertension (IIH) may show normal brain MRI without the classic finding of an empty sella or optic nerve sheath distension. CSF opening pressure measurement remains the gold standard for both conditions.

Incidental findings burden: headache MRI generates a high incidental finding rate — perivascular spaces, non-specific white matter lesions, unruptured intracranial aneurysms, arachnoid cysts, and pineal cysts are commonly found. The clinical and psychological burden of these incidental findings must be considered. Not all incidental findings in headache patients represent the cause of symptoms.

2. Clinical Context and Pre-Test Information

2.1 Clinical Presentation Relevant to MRI

The most critical clinical characterisation for MRI protocol design is the distinction between acute and chronic headache, and between specific and non-specific features.

Thunderclap headache — sudden onset, maximum severity within 60 seconds, often described as "worst headache of life" — is a neurological emergency until proven otherwise. The primary concern is subarachnoid haemorrhage (prevalence 1–3% in emergency thunderclap headache presentations), but the differential also includes cerebral venous thrombosis (CSVT), reversible cerebral vasoconstriction syndrome (RCVS), pituitary apoplexy, carotid or vertebral dissection, and the rare sentinel headache of unruptured aneurysm. CT without contrast remains the first investigation, but MRI adds SWI sensitivity for cortical superficial siderosis (RCVS) and FLAIR sensitivity for early SAH.

Progressive headache — gradually worsening over weeks to months — raises concern for mass lesion, hydrocephalus, or progressive intracranial hypertension. Post-contrast T1 is mandatory. FLAIR and T2 for white matter involvement.

Headache with focal neurological deficit — always suspicious for structural pathology. The protocol must include post-contrast T1 (mass, vascular malformation, demyelination, RCVS), DWI (ischaemic cause), and intracranial MRA. The specific deficit guides which vascular territory to prioritise.

Orthostatic headache — worsening on standing, relieved by lying — is the diagnostic hallmark of spontaneous intracranial hypotension (SIH). The protocol requires gadolinium with specific assessment of diffuse pachymeningeal enhancement, brain sagging, and venous sinus engorgement. The sagging brainstem on sagittal T1/T2 (reduced mamillo-pontine distance, reduced pontomesencephalic angle) is the most anatomically specific sign.

Positional headache with papilloedema — worsening when supine, improving on standing; visual obscurations — suggests idiopathic intracranial hypertension (IIH). The protocol requires MRI + MRV looking for empty sella, posterior globe flattening, optic nerve sheath distension, and transverse sinus stenosis.

Headache in temporal arteritis (giant cell arteritis — GCA) — patient > 50 years, scalp tenderness, jaw claudication, elevated inflammatory markers — may produce visual complications from ophthalmic artery involvement. Vessel wall MRI of temporal arteries and orbital apex sequences are relevant adjuncts. However, temporal artery biopsy remains the diagnostic gold standard.

Cluster headache and trigeminal autonomic cephalalgias (TAC) — strictly unilateral, periorbital/orbital, autonomic features — the ACR criteria [1] recommend MRI brain without and with contrast to exclude structural lesion (pituitary pathology, parasellar mass, cavernous sinus pathology) before the diagnosis of primary cluster headache is established.

Headache in pregnancy and postpartum — specific risk profile for CSVT (especially peripartum), posterior reversible encephalopathy syndrome (PRES), and cerebral artery dissection. Post-contrast T1 is relatively contraindicated in pregnancy (category C gadolinium agents). Non-contrast MRI + MRV and DWI are the appropriate protocol.

New headache in oncological or immunocompromised patient — broad differential including leptomeningeal carcinomatosis, brain metastases, abscess, fungal infection, and lymphoma. Post-contrast T1 is mandatory.

2.2 Pre-Test Information the Radiologist and Technologist Must Know

Onset pattern: sudden onset (thunderclap) vs progressive vs chronic — directly determines urgency and sequence priority. This must appear on the imaging request.

Neurological deficits: any deficit localising to cranial nerve, motor, sensory, visual, or cerebellar function requires post-contrast T1 and MRA.

Papilloedema: if clinically confirmed, IIH protocol is required — MRI + MRV, empty sella assessment, optic nerve sheath distension.

Positional component: upright-worsening → SIH protocol with gadolinium; supine-worsening → IIH protocol.

Prior malignancy: any known cancer — post-contrast T1 is mandatory; consider leptomeningeal carcinomatosis if multiple cranial nerve involvement.

Immunocompromise (HIV, transplant, immunosuppression): post-contrast T1 mandatory; DWI for abscess; SWI for toxoplasma-related haemorrhage.

Age > 50 with new headache: ACR Appropriateness Criteria [1] specifically flag this as a red flag scenario requiring imaging; temporal arteritis is an age-specific differential.

Pregnancy / postpartum status: modifies contrast strategy; increases probability of CSVT and PRES.

Prior SAH or known unruptured aneurysm: SWI/GRE and MRA essential; aneurysm growth assessment.

History of head trauma: even remote trauma in the context of positional headache may suggest chronic subdural; SWI sensitive for chronic blood products.

Fever or inflammatory syndrome: suggests infectious meningitis/encephalitis or granulomatous disease — post-contrast T1 with leptomeningeal assessment.

Anticoagulation: increases haemorrhagic transformation risk; SWI for microbleeds and intraparenchymal blood.

2.3 Differential Diagnosis Landscape

The headache MRI protocol must be designed to discriminate the following broad categories of secondary headache:

• Vascular: subarachnoid haemorrhage, intracerebral haemorrhage, CSVT, RCVS, dissection, unruptured aneurysm, giant cell arteritis, PRES
• Mass lesion: primary and secondary brain tumours, pituitary apoplexy, cavernoma
• Hydrocephalus: obstructive (colloid cyst, aqueductal stenosis, posterior fossa mass) and communicating
• Intracranial pressure disorders: idiopathic intracranial hypertension; spontaneous intracranial hypotension
• Inflammatory/infectious: meningitis, encephalitis, sarcoidosis, neurolupus, dural arteriovenous fistula with venous hypertension
• Sinus disease: sinusitis, mucocele, sinonasal neoplasm
• Primary headache disorders: migraine, tension-type, cluster — the latter requires structural exclusion by imaging

3. Indications, Appropriateness and Imaging Pathway

3.1 When the Dedicated Protocol Is Indicated

Based on ACR Appropriateness Criteria 2022 [1], dedicated headache MRI brain is appropriate for:

• Thunderclap headache: CT negative; FLAIR + SWI for SAH remnants, RCVS screening
• Headache with optic disc oedema (papilloedema): MRI + MRV mandatory to evaluate IIH, mass, hydrocephalus, CSVT
• Headache with neurological deficits: MRI with and without contrast; intracranial MRA
• New-onset headache in patient > 50 years: MRI without and with contrast to exclude mass, vasculitis
• New-onset headache in immunocompromised or cancer patient: MRI without and with contrast
• Headache of suspected trigeminal autonomic origin (cluster headache variant): MRI without and with contrast + thin pituitary section
• Chronic headache with new features or increasing frequency: MRI without and with contrast
• Orthostatic headache (positional — worse on standing): SIH protocol with gadolinium + spine MRI for CSF leak localisation
• Headache during or after pregnancy/postpartum: non-contrast MRI + MRV (CSVT exclusion)
• Headache following lumbar puncture or CSF leak procedure: SIH protocol
• Headache suspected to be cough/exertion/sexual activity-related: MRI with and without contrast per ACR (to exclude Arnold-Chiari, mass, Valsalva-related pathology)

Not appropriate per ACR 2022 [1]: Chronic migraine or tension-type headache without any red flags, normal neurological examination, no new features.

3.2 When the Generic Brain Protocol Is Sufficient

The generic brain MRI protocol (as described in the master page) is sufficient as an initial screen for:

• New-onset headache with moderate clinical suspicion but no specific red flags
• Headache requiring exclusion of mass lesion as a screening study when neurological examination is normal and no specific secondary diagnosis is being targeted

3.3 When Further Sub-Specialised Protocols Are Required

3.4 Red Flags Modifying Urgency or Protocol

4. Dedicated Protocol Design

The base protocol for headache MRI is the generic brain MRI as described in the master page. The modifications below are additions or targeted changes applied based on the specific clinical scenario.

4.1 Protocol Delta vs the Master Protocol

4.2 Mandatory Dedicated Sequences

4.3 Conditional and Advanced Sequences

4.4 Rationale per Disease-Specific Sequence

FLAIR — Sulcal Hyperintensity and Pachymeningeal Signal

In the headache context, FLAIR carries two specific diagnostic targets beyond its generic white matter lesion role.

Sulcal FLAIR hyperintensity: subarachnoid blood within the cortical sulci produces T1 and FLAIR hyperintensity by reducing CSF T1 (due to the paramagnetic effect of oxyhaemoglobin and haemorheological changes). Cortical sulcal FLAIR bright signal has sensitivity of approximately 80–90% for detecting SAH within 24–48 hours when CT is negative [7]. This is the primary use of FLAIR in thunderclap headache after a negative CT scan. However, sulcal FLAIR hyperintensity is non-specific — it is also seen in leptomeningeal carcinomatosis, meningitis, elevated protein, gadolinium (post-contrast FLAIR enhancement), and occasionally as a flow artefact. Correlation with SWI and clinical context is required.

Pachymeningeal signal on pre-contrast FLAIR: diffuse pachymeningeal T2/FLAIR hyperintensity without gadolinium is one of the SIH signs (Tosaka et al. sign) — visible on standard FLAIR before contrast as a linear dural hyperintensity, particularly at the tentorium and falx. This should be specifically assessed on the pre-contrast FLAIR in patients with orthostatic headache.

SWI — Subarachnoid Blood, Cortical Superficial Siderosis, and RCVS

As described in the master page, SWI detects haemoglobin degradation products (deoxyhaemoglobin, methaemoglobin, haemosiderin) through T2* dephasing. In the headache context, three specific targets beyond the generic SWI role are critical:

Cortical superficial siderosis: a thin line of haemosiderin deposition along the cortical surface (sulcal or gyral margin), appearing as SWI signal loss along the cortical surface. This is the hallmark of subacute or recurrent subarachnoid haemorrhage and is highly specific for cortical SAH in the setting of RCVS. In a patient with thunderclap headache and negative CT and FLAIR, cortical superficial siderosis on SWI establishes cortical SAH even when no gross blood is visible.

RCVS — beading pattern: SWI is less useful for the beading pattern of RCVS (which requires MRA or CTA), but detects the cortical superficial siderosis that accompanies the cortical SAH component of RCVS.

Cavernoma discovery in cluster headache differential: secondary cluster headache from cavernous malformation requires SWI for haemosiderin ring identification.

Post-Contrast T1 — Pachymeningeal vs Leptomeningeal Enhancement

The distinction between pachymeningeal enhancement (dura and outer arachnoid — T1 bright linear enhancement along the dural surface) and leptomeningeal enhancement (inner arachnoid and pia — enhancement within the cortical sulci) is diagnostically critical and requires careful post-contrast T1 assessment.

Diffuse pachymeningeal enhancement (dural enhancement only, not following sulci): characteristic of SIH; also seen in sarcoidosis and granulomatous dural disease; post-operative. Quantified as linear dural enhancement from vertex to posterior fossa tentorium, usually ≥ 2 mm thick.

Leptomeningeal enhancement (sulcal, cisternal, spinal): meningitis (bacterial, fungal, tuberculous), leptomeningeal carcinomatosis, neurosarcoidosis, RCVS (occasionally). Sulcal gadolinium enhancement on FLAIR (post-contrast FLAIR) is particularly sensitive for subtle leptomeningeal enhancement.

Post-contrast FLAIR: when subtle leptomeningeal enhancement is the clinical question, post-contrast FLAIR (acquired after standard T1 post-contrast) provides superior sensitivity by combining FLAIR signal suppression of CSF with T1 enhancement — very small amounts of enhancement in the sulci are more conspicuous against the dark CSF background on post-contrast FLAIR than on standard T1.

Sagittal T1 — Brain Sagging Assessment (SIH)

The sagittal T1 (or T2) provides the anatomical reference for brain sagging quantification in SIH. The specific measurements are:

• Mamillo-pontine distance: the perpendicular distance between the inferior surface of the mamillary bodies and the anterior pontine surface. Normal approximately 8–12 mm; reduced (< 7 mm) in significant SIH brain sagging.
• Pontomesencephalic angle: the angle between the anterior pons and the midbrain. Normal approximately 65–70°; reduced (< 50°) in significant brain sagging (Tsiouris et al. 2013 AJR criteria [5]).
• Brainstem descent: descent of the cerebellar tonsils below the foramen magnum (pseudoChiari pattern); flattening of the pons against the clivus; obliteration of the prepontine cistern.

The sagittal view should always be included in the initial headache MRI when orthostatic symptoms are present — even before contrast injection — because pre-contrast sagittal T1 already shows brainstem sagging, pituitary enlargement, and changes in CSF spaces.

Intracranial TOF MRA — Aneurysm, RCVS, and Cluster Headache

TOF MRA is added to the headache protocol for three specific clinical questions:

Post-negative CT thunderclap headache: identifies unruptured or incompletely ruptured aneurysm, sentinel leak, and the beading/constriction pattern of RCVS. In thunderclap headache with negative CT and negative LP, MRA is the next diagnostic step.

RCVS: the beading pattern of RCVS — multifocal segmental vasoconstriction of the large and medium intracranial arteries — is the imaging hallmark. TOF MRA at 3T provides adequate sensitivity for medium-calibre arterial beading (M1–M3 MCA, basilar, posterior cerebellar arteries), though subtle M3–M4 beading may require CTA.

Cluster headache and TAC: before labelling a headache as primary cluster headache, structural causes must be excluded — specifically an ipsilateral parasellar mass or cavernous sinus lesion that compresses the trigeminal-autonomic pathways. MRA identifies vascular compression and rules out arteriovenous malformation.

4.5 Dedicated Planes, FOV, Resolution and Coverage

Post-contrast T1 for pachymeningeal assessment: standard axial plus coronal planes are required for comprehensive pachymeningeal assessment. Coronal T1 post-contrast is particularly useful for the posterior fossa dura, tentorium, and cavernous sinus. Sagittal T1 post-contrast is required when SIH is the primary question (pituitary enlargement, dural enhancement at vertex).

Thin-section pituitary coronal T1: for cluster headache and TAC, a dedicated 2–3 mm coronal T1-weighted sequence covering the pituitary and parasellar region is standard practice. This sequence is not the same as the full dynamic pituitary protocol (which is described in the pituitary child page); it is a structural thin-section sequence specifically to exclude a parasellar mass.

MR venography coverage: phase-contrast MRV or 2D-TOF MRV should cover the entire brain from vertex to posterior fossa, with the superior sagittal sinus, transverse sinuses, sigmoid sinuses, and straight sinus fully displayed on the MIP reconstructions. CE-MRV (contrast-enhanced phase) provides superior delineation of the transverse sinus segments and is preferred when asymmetric CSVT is the primary concern.

Vessel wall imaging FOV: targeted at the circle of Willis for RCVS and intracranial vasculitis; at the posterior circulation for basilar vasculitis; at the carotid siphon for giant cell arteritis intracranial involvement.

4.6 Contrast Strategy Specific to Headache MRI

Contrast use in headache MRI must be explicitly stratified — indiscriminate gadolinium administration is not appropriate for all headache presentations and is specifically discouraged by the ACR Appropriateness Criteria [1] for chronic migraine and tension-type headache without red flags.

Contrast Usually Unnecessary

• Chronic migraine or tension-type headache, no new features, normal neurological examination
• New-onset headache in a young patient with typical migraine features and no red flags
• Pregnancy (relative contraindication; gadolinium is Category C; contrast should be deferred unless clinically essential)
• Paediatric headache without red flags

Contrast Recommended / Strongly Useful

• Orthostatic headache / suspected SIH: gadolinium is mandatory for pachymeningeal enhancement detection (present in virtually 100% of SIH [4]) — this is the most sensitive SIH brain finding
• Headache with papilloedema / suspected IIH: post-contrast T1 can identify dural venous sinus thrombosis and leptomeningeal enhancement
• Headache in oncological or immunocompromised patient: mandatory
• Headache with fever / suspected meningitis or encephalitis: mandatory
• Cluster headache / TAC: recommended for parasellar exclusion
• Headache with cranial nerve palsy: mandatory (leptomeningeal carcinomatosis, sarcoidosis, GCA, diabetes mellitus — cranial nerve enhancement is the primary finding)
• Headache after LP or dural puncture: gadolinium for SIH assessment
• Suspected RCVS or vasculitis: vessel wall imaging requires gadolinium

Contrast Mandatory

• Progressive headache in any patient: post-contrast T1 to exclude mass, metastasis, abscess
• New headache > 50 years (multiple differentials requiring enhancement assessment)
• Suspected leptomeningeal carcinomatosis: high-dose gadolinium (0.1 mmol/kg standard dose) and post-contrast FLAIR enhance sensitivity for subtle sulcal seeding

Specific Timing Notes

For SIH pachymeningeal enhancement assessment: standard 5-minute post-contrast T1 with axial and coronal acquisitions. The pachymeningeal enhancement in SIH is typically diffuse, linear, and persistent into the delayed phase. A 10-minute delayed coronal T1-FS acquisition may increase sensitivity for borderline cases.

For leptomeningeal enhancement: both standard T1 post-contrast and post-contrast FLAIR (acquired 4–6 minutes after injection) should be reviewed. Post-contrast FLAIR identifies sulcal enhancement that may be too subtle for standard T1 alone.

4.7 Sequence Matching, Reproducibility and Follow-Up

For known IIH on acetazolamide treatment: serial MRI should assess optic nerve sheath distension, posterior globe flattening, and empty sella — all reproducible on standard protocol. Transverse sinus stenosis on MRV should be compared at the same technical specifications.

For known SIH post-epidural blood patch: follow-up brain MRI should include gadolinium and specifically assess pachymeningeal enhancement resolution, brainstem position recovery, and subdural collection evolution.

For RCVS: follow-up MRA is recommended at 4–12 weeks after onset to document arterial normalisation (characteristic of RCVS) vs persistent beading (which suggests true vasculitis). This distinction has major treatment implications.

5. MRI Semiotics — Disease-Specific Imaging Findings

5.1 Direct Signs

Subarachnoid Haemorrhage — FLAIR and SWI

FLAIR sulcal hyperintensity: the most MRI-sensitive finding for subacute SAH. High signal within the cortical sulci (hyperdense on FLAIR relative to CSF) from blood products within the subarachnoid space. Sensitivity approximately 80–90% within 24–48 hours [7]; sensitivity decreases after 48 hours as oxyhaemoglobin degrades.

SWI sulcal signal loss: haemosiderin deposition along the cortical surface (cortical superficial siderosis) — the marker of remote or recurrent SAH. Seen in RCVS cortical SAH and in cortical SAH from other causes. Highly specific for blood products.

Spontaneous Intracranial Hypotension — The SEEPS Mnemonic

The classic SIH findings can be remembered as SEEPS [8]:

• Subdural fluid collections (hygroma or haematoma): bilateral thin subdural collections over the convexities; CSF or mixed signal
• Enhancement of the pachymeninges: diffuse linear T1 enhancement of the dura on post-contrast T1 — sensitivity 72%, specificity 93% per Kim et al. AJR 2019 [4]
• Engorgement of venous structures: distension of the transverse sinus, straight sinus, and superior sagittal sinus; the venous distension sign — transverse sinus diameter > 7 mm is sensitive [9]
• Pituitary enlargement: increased height of the pituitary gland > 8 mm, with convex superior margin; often bilateral uniform enlargement
• Sagging of the brain: downward displacement of the brainstem; reduced mamillo-pontine distance; pontomesencephalic angle < 50°; obliteration of prepontine cistern; flattening of the pons against the clivus; pseudoChiari pattern

Not all five features need to be present. Pachymeningeal enhancement is the most sensitive single finding. Brain sagging is the most specific single finding.

Idiopathic Intracranial Hypertension

• Empty sella: the pituitary gland is compressed against the sella floor by CSF; sella appears largely CSF-filled; best seen on sagittal T1
• Posterior globe flattening: flattening of the posterior scleral surface (the globe normally rounds convexly toward the posterior orbit); measured on axial T2 or T1
• Optic nerve sheath distension: optic nerve sheath > 5.5 mm diameter at 3 mm posterior to the globe on axial T2
• Transverse sinus stenosis or hypoplasia: bilateral or dominant transverse sinus narrowing on MRV; bilateral stenosis in up to 90% of IIH; this is now considered part of the pathophysiology, not just an epiphenomenon
• Slit-like ventricles: may be present, particularly in young patients with high ICP and small brain volume

RCVS — MRI Semiotics

• TOF MRA beading: multifocal segmental stenosis and dilation of large and medium arteries — the classic "string of beads" pattern; MCA, PCA, and basilar arteries predominantly
• Cortical superficial siderosis on SWI: indicating cortical SAH component
• PRES pattern: bilateral parieto-occipital FLAIR/T2 hyperintensity from posterior circulation vasospasm (present in approximately 30% of RCVS cases)
• Cortical/border zone infarcts on DWI: from vasospasm-related ischaemia — present in severe cases
• Normal MRA in first week: RCVS beading may not be visible on MRA in the first 1–2 weeks after onset — a negative initial MRA does not exclude RCVS; repeat MRA at 4–6 weeks recommended when suspicion is high

CSVT — MRI Semiotics

• Direct thrombus sign: T1-hyperintense thrombus within the venous sinus on non-enhanced T1 (subacute stage); T2* / SWI signal loss within the sinus (acute stage)
• Absence of flow void: loss of the normal flow void on T2 in the involved sinus (not reliable as sole criterion)
• Venous infarction: gyral oedema and haemorrhage in a non-arterial distribution; bilateral parasagittal involvement for SSS thrombosis; temporal lobe for transverse sinus thrombosis
• Empty delta sign on CT: not an MRI sign, but the classical CT finding for SSS thrombosis — relevant context for the radiologist reviewing prior CT
• MRV: absence of flow signal in the involved sinus; caution — hypoplastic transverse sinus can simulate thrombosis; bilateral assessment and T2 signal correlation essential

5.2 Indirect and Secondary Signs

Headache MRI incidental findings that are not the cause of headache but should be documented:

• Unruptured intracranial aneurysm: > 3 mm on MRA requires documentation and follow-up protocol
• Developmental venous anomaly (DVA): normal variant; does not cause headache; associated cavernoma must be excluded on SWI
• Pineal cyst: > 1 cm warrants dedicated thin-section sequences; most are benign
• Arachnoid cyst: location-dependent significance; posterior fossa arachnoid cysts with mass effect may cause headache

Migraine-related white matter lesions: small T2/FLAIR hyperintense foci in the periventricular and deep white matter are more common in migraineurs (especially women with aura) than in non-migraineurs — the OR is approximately 3.9 for any WML and 12.4 for infratentorial WML in migraineurs [10]. These are typically non-specific (< 3 mm), subcortical, not following typical MS distribution, and do not carry the same diagnostic weight as MS lesions. The radiologist must clearly distinguish migraine-pattern WML from demyelinating disease.

5.3 Severity, Extent and Activity Assessment

For CSVT: the extent of venous sinus involvement and the degree of collateral venous drainage determine clinical severity. Isolated sigmoid/transverse sinus thrombosis without cortical venous involvement carries better prognosis than SSS + cortical vein thrombosis.

For RCVS: the degree of arterial stenosis on MRA and the presence of cortical infarcts or haematomas indicate severity and guide the need for calcium channel blocker treatment.

For SIH: the degree of brain sagging (measured by mamillo-pontine distance and pontomesencephalic angle) and the presence of bilateral subdural haematomas indicate severity and urgency of blood patch or surgical treatment.

5.4 Validated Classification and Grading Systems

Fazekas Scale for White Matter Lesions

The Fazekas scale (Fazekas et al. 1987 [11]) provides a validated 0–3 grading system for periventricular and deep white matter hyperintensities on T2/FLAIR:

• Grade 0: absent
• Grade 1: punctate foci
• Grade 2: beginning confluence
• Grade 3: large confluent areas

Periventricular and deep WM are graded separately. This scale has good inter-rater reliability and is widely used for reporting non-specific WM lesions in headache patients. Fazekas Grade ≥ 2 should prompt further clinical assessment and vascular risk factor evaluation.

GLIMPSE criteria for IIH (modified Dandy criteria)

The diagnostic criteria for IIH require: papilloedema, normal neurological examination except cranial nerve VI palsy, normal brain MRI (or empty sella/optic nerve changes), elevated opening pressure (> 25 cm H₂O), and normal CSF composition. MRI contributes the structural exclusion component, not the diagnosis itself.

5.5 Differential Diagnosis on MRI

5.6 Mimickers, Pseudolesions and Normal Variants

Perivascular spaces (Virchow-Robin spaces): CSF-filled spaces following perforating arteries — round or linear, CSF signal on all sequences, FLAIR-attenuated (dark on FLAIR). Do not cause headache. Can be extensive in ageing patients and should not be reported as "lacunes" or "cystic lesions" without contextualisation.

Migraine-related WML: as described in 5.2 — do not report as MS unless distribution and characteristics meet McDonald criteria. State specifically that white matter foci are "non-specific, compatible with migraine-related changes."

FLAIR pseudo-sulcal hyperintensity (propofol/sedation/hyperoxia): FLAIR acquired under supplemental oxygen or sedation can show diffuse sulcal FLAIR hyperintensity from T1 shortening of CSF by dissolved oxygen. Symmetric, non-mass-forming; no corresponding SWI signal. Discriminate by clinical context.

Post-contrast FLAIR sulcal enhancement: gadolinium in the blood pool produces T1 shortening that can diffuse into CSF over time (approximately 20–30 minutes), producing FLAIR sulcal hyperintensity mimicking leptomeningeal enhancement. If post-contrast FLAIR is acquired > 20 minutes after injection, this artefact is prominent. Always acquire post-contrast FLAIR within 5–10 minutes of injection when possible.

Asymmetric transverse sinus on MRV: right transverse sinus is dominant in approximately 55% of individuals, left in 25%, co-dominant in 20%. Asymmetry alone does not indicate thrombosis. T2/FLAIR signal in the sinus, SWI signal, and T1 hyperintensity of thrombus are the discriminators.

Developmental venous anomaly (DVA): a normal variant that should not be reported as a "venous malformation" or "mass." DVAs appear as the classic "caput medusae" on post-contrast T1 — radially arranged medullary veins converging on a large collector vein. They do not spontaneously haemorrhage; associated cavernoma must be excluded on SWI.

6. Reporting Framework Specific to Headache MRI

6.1 Structured Reporting Template

Indication: state the headache phenotype (thunderclap / progressive / orthostatic / chronic with new features / cluster / postpartum) and the primary clinical question.

Technique: sequences performed; contrast administration (agent, dose, timing); specific additions (SWI, MRA, MRV, vessel wall MRI, pituitary protocol); field strength.

Comparison: prior brain MRI if available; prior CT.

Findings — in clinically relevant order:

Emergency findings first (haemorrhage screen — SWI/GRE):

• Intracranial haemorrhage: absent / present
• Cortical superficial siderosis: absent / present
• Sulcal FLAIR hyperintensity: absent / present / non-specific

Vascular findings (MRA, MRV if acquired):

• Intracranial arteries: patent / focal stenosis / beading / absent flow
• Dural venous sinuses: patent / flow gap / thrombus
• Aneurysm: absent / present (size, location, morphology)

Brain parenchyma:

• DWI: no restriction / focal restriction (location)
• FLAIR/T2 white matter: normal / non-specific WM foci (Fazekas grade) / specific pattern
• Post-contrast findings: no enhancement / pachymeningeal enhancement / leptomeningeal / parenchymal

SIH-specific assessment (sagittal T1, if orthostatic headache):

• Brain sagging: absent / present (state mamillo-pontine distance and pontomesencephalic angle)
• Subdural collections: absent / present
• Pituitary size: normal / enlarged

IIH-specific assessment:

• Empty sella: absent / partial / complete
• Optic nerve sheath: normal / distended (state diameter)
• Posterior globe flattening: absent / present
• Transverse sinus: patent / stenotic / hypoplastic

Impression:

• Address the specific headache clinical question explicitly
• State if findings support or argue against the suspected diagnosis
• State what is excluded (e.g., "No imaging evidence of subarachnoid haemorrhage, mass, or venous thrombosis")
• Classify incidental findings by clinical relevance
• State limitations

6.2 Mandatory Disease-Specific Reporting Checklist

• Haemorrhage screen explicitly stated (SWI/GRE reviewed)
• Sulcal FLAIR hyperintensity assessed in thunderclap headache
• Cortical superficial siderosis on SWI assessed in thunderclap headache
• Post-contrast pachymeningeal enhancement assessed (if orthostatic headache + contrast)
• Brain sagging measurements stated (if SIH suspected): mamillo-pontine distance + pontomesencephalic angle
• Pituitary size assessed (SIH and cluster headache)
• Dural venous sinuses assessed on MRV (if papilloedema, postpartum, CSVT suspected)
• Optic nerve sheath distension measured (if IIH suspected)
• Empty sella assessed (all headache MRI)
• White matter lesions graded (Fazekas scale) and characterised
• Incidental aneurysm documented (if MRA acquired)
• Contrast timing documented if pachymeningeal assessment was the indication
• Technical limitations stated (motion, absence of MRA/MRV if not acquired)

6.3 Critical Findings and Communication

Immediate verbal communication to the treating physician is required for:

• Sulcal FLAIR hyperintensity or SWI cortical siderosis in thunderclap headache (possible SAH)
• Hydrocephalus or obstructive lesion in progressive headache (neurosurgical emergency)
• CSVT with haemorrhagic infarction (anticoagulation decision)
• Significant brain sagging with subdural haematoma in SIH (blood patch urgency)
• Unexpected mass or metastasis in a patient with headache without known cancer
• Basilar artery occlusion in a headache patient (stroke emergency)
• Pituitary apoplexy (endocrine emergency + neurosurgical urgency)

6.4 Common Reporting Errors

7. Technical Pitfalls and Disease-Specific Optimisation

7.1 Technical Pitfalls Specific to Headache MRI

Sulcal FLAIR artefacts: the cortical surface and sulcal depths are prone to multiple FLAIR signal artefacts: CSF pulsation ghosting from third ventricle and basilar cisterns; partial-volume between cortex and CSF; flow artefacts from CSF motion in large sulci. These can simulate sulcal hyperintensity from SAH. The discriminator: true sulcal SAH produces consistent signal across multiple sulci in a haemorrhage-compatible distribution (basal cisterns, Sylvian fissures); pulsation artefacts are in the phase direction and produce a regular ghosting pattern.

Post-contrast FLAIR gadolinium diffusion: as described in Section 5.6, gadolinium diffuses into CSF over time, producing sulcal FLAIR hyperintensity that mimics leptomeningeal enhancement. Always document contrast injection time; if post-contrast FLAIR is the clinical question, acquire it within 5 minutes of injection to avoid this artefact. If it was acquired late, explicitly state "cannot exclude gadolinium-in-CSF artefact."

TOF MRA flow saturation in slow flow: RCVS beading involves stenotic segments where flow velocity is reduced. Slow flow through stenoses may produce saturation effects on TOF MRA that simulate complete vessel occlusion rather than stenosis. This is most relevant for M3/M4 MCA segments and small basilar perforators.

7.2 Sequence-Specific Disease Pitfalls

SWI in GCA: giant cell arteritis primarily affects the temporal arteries (superficial location) and the ophthalmic arteries — both outside the routine intracranial SWI coverage. Vessel wall MRI targeting the temporal arteries or orbital MRI for ophthalmic artery involvement adds diagnostic value but is not the same as standard brain SWI.

MRV false-negative CSVT: phase-contrast MRV may miss isolated cortical vein thrombosis (not the main sinuses). Isolated cortical vein thrombosis produces focal brain oedema and haemorrhage in a non-arterial distribution; SWI is more sensitive for the thrombosed cortical vein as a linear signal-loss structure.

FLAIR and meningitis sensitivity: bacterial meningitis can produce normal brain FLAIR — the FLAIR is positive for leptomeningeal enhancement only after gadolinium. A normal pre-contrast FLAIR does not exclude bacterial meningitis. Always include post-contrast imaging when meningitis is clinically suspected.

7.3 When the Exam Is Non-Diagnostic

• Thunderclap headache with negative MRI: MRI does not exclude SAH in the first 6 hours with the same reliability as CT. Negative FLAIR and SWI after a negative CT still warrants lumbar puncture for xanthochromia if the clinical suspicion is high.
• Orthostatic headache with normal brain MRI: up to 10% of SIH may have normal brain MRI — the absence of SEEPS signs does not exclude SIH. CSF opening pressure measurement and spinal MRI for epidural fluid collection are the next steps.
• Normal MRI in suspected IIH: opening pressure measurement on LP is required — normal MRI does not exclude IIH. Optic nerve sheath distension and empty sella are absent in a proportion of confirmed IIH.

8. MRI Technologist Pearls Specific to Headache MRI

8.1 Disease-Specific Positioning and Coil Tricks

For suspected SIH: the patient must remain supine for the entire examination (not semi-reclined, which is the default table angle in some departments). In SIH, even partial upright positioning during the scan changes the brain position and may reduce the conspicuity of sagging signs. Position the patient completely flat.

For suspected RCVS requiring MRA: MRA flow artefacts are reduced when the patient is breath-holding or motionless during the TOF acquisition. Clear verbal instruction before MRA is more effective for flow artefacts than for standard anatomical sequences.

8.2 Sequence Order Logic

For headache MRI, the sequence order must be adapted to the clinical urgency:

Thunderclap headache (emergency): DWI → SWI → FLAIR → post-contrast T1 → TOF MRA

Rationale: SWI is second (immediately after DWI) because haemorrhage detection is the primary emergency question; FLAIR sulcal assessment third; contrast and MRA after the emergency screen is completed.

Orthostatic headache (SIH workup): Sagittal T1 (non-enhanced) → FLAIR → Gadolinium → post-contrast T1 (coronal + axial + sagittal) → post-contrast FLAIR

Rationale: pre-contrast sagittal T1 assesses brainstem position and pituitary first; post-contrast T1 is the most diagnostically important sequence (pachymeningeal enhancement).

Progressive headache / oncological: DWI → FLAIR → T1 non-enhanced → Gadolinium → post-contrast T1 → SWI

Rationale: pre-contrast T1 before gadolinium for lesion T1 characterisation; post-contrast T1 is the primary finding sequence.

8.3 Fast Salvage Version of the Dedicated Protocol

In approximately 12–15 minutes, this five-sequence salvage protocol covers the major secondary headache diagnoses requiring immediate action.

8.4 Disease-Specific Avoidable Errors

9. Quality Control Checklist for the Dedicated Protocol

• SWI/GRE phase images saved (not just magnitude) in thunderclap headache
• FLAIR sulcal assessment documented in thunderclap headache
• Post-contrast T1 performed with stated timing relative to injection
• Sagittal T1 (non-enhanced) acquired in orthostatic headache
• Brain sagging measurements documented (mamillo-pontine distance, pontomesencephalic angle) when SIH is the question
• Optic nerve sheath measured at 3 mm posterior to globe when IIH is suspected
• MRV acquired and sinus patency confirmed for all postpartum headache and papilloedema cases
• Post-contrast FLAIR acquired within 5–10 minutes of injection when leptomeningeal enhancement is the question
• Pituitary size and morphology documented in cluster headache and SIH
• TOF MRA acquired and MIP reconstructions generated when aneurysm or RCVS is the question
• Vessel wall MRI performed and gadolinium timing for wall enhancement documented when vasculitis vs RCVS distinction is required
• Motion artefacts noted — if degrading SWI or FLAIR quality, state explicitly in report

11. Evidence Gaps and Ongoing Debate

Overuse of neuroimaging in headache: despite clear ACR guidance that chronic migraine and tension-type headache without red flags does not require imaging, the literature consistently documents over-utilisation of brain MRI for headache in primary care and emergency settings. The radiological and clinical community has not reached effective implementation of appropriate use criteria.

Incidental finding burden in headache MRI: the rate of clinically significant incidental findings on brain MRI performed for headache is approximately 0.4–0.9% in some series, but the rate of non-significant incidentals (unruptured small aneurysms < 3 mm, arachnoid cysts, WML, DVAs, pineal cysts) is substantially higher — approximately 10–20% depending on patient age and imaging indication. The downstream psychological, economic, and clinical burden of incidentalomas discovered during headache imaging is not well quantified.

Role of vessel wall MRI in RCVS vs vasculitis at 3T in routine practice: while the ASNR consensus [3] and multiple case series have established vessel wall enhancement as the key discriminator (vasculitis enhances; RCVS does not), the availability and technical quality of vessel wall MRI at 0.5–0.7 mm isotropic resolution is highly variable across clinical centres. Many published diagnostic claims for vessel wall MRI are based on academic tertiary centre protocols that cannot be replicated in general radiology departments.

MRI in migraine — beyond exclusion: the finding that migraineurs have higher rates of WML, iron deposition in deep grey nuclei, and morphometric cortical differences compared to non-migraineurs is well established but has no clinical management implications at present. Whether these findings have prognostic significance (relationship to cognitive outcomes or long-term disability) is an evolving research area without clinical guidance.

Abbreviated headache MRI protocols: whether a DWI + FLAIR + SWI three-sequence abbreviated protocol (approximately 8–10 minutes) provides adequate screening for the clinically important secondary causes of headache in red-flag presentations has not been prospectively validated. AI-assisted detection models for intracranial haemorrhage, mass lesions, and incidental aneurysms are in development but not validated for the specific clinical question of headache triage.

Thunderclap headache MRI vs CT vs LP pathway: the optimal diagnostic pathway for thunderclap headache (CT-first vs MRI-first; CT + LP vs CT + MRA; role of FLAIR + SWI) is not settled by high-quality prospective comparative studies. The Ottawa SAH rule supports a CT + LP standard, but MRI centres with rapid MRI access have proposed MRI-first pathways with equivalent or superior sensitivity.

12. Evidence-Based References

A. Guidelines / Consensus / Society Recommendations

B. Systematic Reviews / Meta-analyses

(Targeted systematic reviews for specific headache MRI questions are limited; the ACR Appropriateness Criteria documents above incorporate systematic review methodology.)

C. Important Prospective / Original Studies

D. Technical MRI Papers

E. Landmark Historical References

End of document — MRI Brain Headache Child Protocol — MRIninja v1.0 — May 2026 Page ID: 1106 | Slug: 1106-brain-headache-protocol Parent page: 1101-brain-generic-standard-protocol Future child pages building on this page: intracranial hypotension dedicated protocol; RCVS dedicated protocol; idiopathic intracranial hypertension; cerebral venous thrombosis; PRES imaging.