Headaches are one of the most common complaints seen in general practice and clinical neurology. Of the many types of headaches, the type that has historically been called a “vascular headache” is worthy of specific attention—not because it is still a formal diagnosis (it is not) but, as we will discuss, certain vascular/neurovascular factors behind many headache disorders inform our understanding, assessment and management of headaches today.
The following is a detailed discussion about vascular headaches: the history, modern counterparts, mechanisms, clinical features, assessment, and treatment and why this is important for patients and providers alike—particularly in the scope of outpatient neurology and neurointerventional practices.
- What is meant by the term “vascular headache”?
•The designation “vascular headache” is an outdated designation. It was originally used to apply to headaches where the primary pathway was thought to be due to changes in the blood vessels (e.g., vasodilation/vasoconstriction) in the head and neck.
•Now, major headache classification systems (i.e., International Headache Society classification changes) do not recognize “vascular headache” as a standalone category.
•However, many headaches that used to be contained under the label “vascular headache” relate to headaches that today are classified as a specific, primary headache disorder (i.e., migraines, cluster headaches) or are secondary headaches with vascular pathology (i.e., headaches in cerebrovascular disease).
•From a clinical neurology standpoint, it makes more sense to think of neurovascular mechanisms – rather than simply “vascular headaches”.
- Why the term changed and why it matters
• The move away from the term “vascular headache” is related to progress in our understanding of headache pathophysiology – particularly around neurovascular mechanisms (nerves + blood vessels) in conditions like headaches.
• That is, the overly simplified view that stretch/dilation of blood vessels causes headache is no longer the view taken by clinicians and researchers. The view is now more in line with where pain arises from the activation of the trigeminovascular system leading to the release of neuropeptides (e.g. CGRP), spreading cortical depression, vascular and endothelial effects, neuro-inflammation, etc.
• This matters, practically, because management – both preventive and acute – require neuro-modulatory strategies and not only vasoconstrictors or analgesic effects based on just vessel size. And mis-labelling headache can subsequently delay accurate diagnosis and impact treatment choices to achieve optimal treatment, or an injury can lead to a potentially overlooked secondary cause of headache.
• For patients and importantly clinicians, it is important to have a reminder that a headache can be a marker of risk of an underlying vascular event happen (depending on context). An example, migraine (especially with aura) is associated with an increased risk of ischemic stroke.
- Headaches that fall under the “Headache – Vascular umbrella.”
Although we no longer formally use the term “vascular headache,” it is probably appropriate to classify the relevant categories as:
a) Prevalent primary headache disorders with neurovascular mechanisms
• Migraine: Most relevantly migraine with aura. Symptoms are throbbing in quality, with photophobia or phonophobia, nausea, and sometimes aura phenomena may be visual, sensory, or speech based. Vascular or neurovascular changes are primarily central features.
• Cluster headache: Unilateral severe pain surrounding the eye/temple, with some autonomic symptoms (either tearing or nasal congestion). These headaches are less common but extremely disabling, and may also involve neurovascular or autonomic changes.
b) Secondary headaches with vascular disorders as causal or contributory factors
• Headache is a manifestation of a cerebrovascular event or vasculopathy – e.g. arterial dissection, intracranial bleed, cerebral venous sinus thrombosis.
• Headaches in the context of vascular risk states, or impaired reactivity of the cerebrovascular system. For example, there may be subtle vascular changes or endothelial dysfunction in the migraineur population.
- Mechanisms: What happens in the brain.
• The traditional “vascular” reason (near dilation of cerebral vessels producing pain) is too elementary. Vascular change occurs, but the right mechanism is the neurovascular system (combined system of blood vessels + nerves).
• In migraine:
- Cortical spreading depression (CSD) may initiate the chain of events: wave of neuronal and glial depolarization → change in blood flow → activation of trigeminal afferents.
- The trigeminovascular system activation: the trigeminal nerves innervate meningeal vessels (vasodilatation occurs via neuropeptide release, e.g. CGRP, substance P etc. subsequently leading to neurogenic inflammation and pain signaling).
- Endothelial dysfunction: biomarkers of vascular and endothelial injury, pro-thrombotic milieu, and impaired cerebrovascular reactivity appear in migraineurs, especially with aura.
- Clinical features: what to look for
There are key features that indicate the possibility of a “vascular-type” headache (or associated with vascular risk):
•Character of pain: throbbing or pounding oftentimes unilateral (in migraine); very severe, sharp/burning around eye/temple in cluster headache; ‘sudden onset worst headache’; ‘thunder clap’ (if has vascular event).
•Associated features
- Photophobia, phonophobia, nausea/vomiting (in migraine) and autonomic features (tearing/nasal congestion/eyelid swelling) in cluster headache.
- Neurological signs and/or systemic signs in secondary vascular headache (e.g. dissection/stroke).
•Aura in migraine: visual (flashing lights, zig-zag), sensory, speech.
•Frequency and pattern: Cluster headache typically occur in ‘clusters’ (eg. daily for weeks) and at similar times.
•Triggers/aggravating factors: stress, hormonal changes, sleep disturbance, weather changes, alcohol – particularly cluster headaches
•Risk factor context: if the patient has hypertension, with smoking, dyslipidemia, taking oral contraceptives (women), or with migraine with aura – must heighten suspicion of vascular risk.
- Diagnostics: what investigations and assessments are needed
•History & headache diary: importance of these for classification of the headache, noting triggers, duration, associated symptoms, and evolution.
•Medical investigation: a neurologic exam to assess for focal deficits; vascular exam as indicated (carotid bruit, pulse differences).
•Imaging/vascular work-up (important in the setting of a suspected secondary vascular process or atypical features):
- MRI/MRA or CT/CTA for intracranial vascular pathology
- MR/CT perfusion or diffusion imaging in the acute setting (stroke considerations) or during migraine aura investigations.
- Blood tests: vascular risk assessment (lipids, homocysteine), coagulopathy when clinically indicated.
•Risk-factor assessment: smoking status, blood pressure, lipid profile, family history of vascular disease.
•For migraineurs with aura, particularly young females using hormonal contraception, it is good practice to review vascular risk factors.
- Management: A Unified Strategy
- Acute management
•Migraine: NSAIDs, triptans (when indicated), antiemetics; rest in a dark, quiet room all are favoured options.
•Cluster headache: oxygen therapy, high flow and acute triptans/injectables based on protocol.
•Vascular event suspected (i.e., dissection, haemorrhage): neurology/neurovascular intervention needed immediately – with rapid imaging and specialist care.
- Preventative/long-term management
•Methodology that is more lifestyle modification-specific:
- Adequate and consistent sleep, regular meal patterns, hydration management.
- Avoidance of triggers (certain foods, alcohol, bright lights).
- Stress reduction and behaviour modification (biofeedback) when available.
•Risk-factor reduction: Especially the cases with migraine + aura or vascular risk: controlling hypertension, dyslipidaemia, weight and smoking cessation is required.
•Specific preventive therapies:
- For migraine patients: prophylactic medication (beta-blockers, antiepileptic medication, CGRP-targeted therapies) based on frequency/severity.
- Cluster headache: verapamil, lithium, neuromodulation for refractory cases.
•When to consider neurovascular/neurointervention input:
- Patients with headache related to vascular malformations (i.e., aneurysm, AVM, dissection) and may need to consider coiling, flow diverter stents or embolisation.
- At our centre we routinely see patients with headache and suspected vascular architecture (especially those refractory to usual therapy or with red-flag features) for possible intervention as well.
- When to raise an alert- red flag features
The following requires urgent assessment:
•Sudden onset (thunderclap) headache, at maximum intensity in seconds.
•Neurological deficits (weakness, speech disturbance, vision change) associated with headache.
•New headache onset in age over 50.
•Change in character, frequency, or severity of headache (particularly migraine > chronic transformation).
•Headache in the context of fever + neck stiffness (meningo-vascular cause).
•Headache with recent head trauma or on an anticoagulant.
•Migraine with aura who smokes, uses hormonal contraception or has multiple vascular risk factors – increased risk of stroke.
- Implications for practice and take home messages
•For Clinicians: “Vascular headache” may not be a term that is used formally, but the neurovascular basis remains highly relevant to headache evaluation.
•For Patients: if you experience recurrent headaches, particularly with features like aura, or you have vascular risk factors – seeing a neurologist/neurovascular specialist is a valuable discussion.
•Secondary prevention matters: supporting the broader aspects of vascular health (blood pressure, lipids, smoking), can improve headache outcomes and decrease long term cerebrovascular risk.
•Collaboration matters: Neurology and neurointervention teams are important to include in a case when headache has atypical features or where there is suspected vascular cause. A multidisciplinary neuro-vascular headache pathway is becoming the standard of care in many modern neurology practices (like here at Medanta).
- Conclusion
In summary, while “vascular headaches” may seem like an antiquated term, the concepts behind the term, still matter. Headaches in the context of neurovascular dysfunction – whether classic migraine, cluster headache or secondary vascular headaches – warrant thoughtful evaluation, localized management, and consideration of the full spectrum of headache care and cerebrovascular health.
At our centre, we refrain from calling them “headaches” and emphasize:
•Early identification of flags or vascular risk.
•Integrated care in the realm of neurology, intervention and imaging, lifestyle, and preventive medicine.
•Individualized therapy (because it’s never one size fits all in headache care).
If you or a loved one suffer recurrent, severe or extraordinary headaches – especially, with vascular risks – I recommend reaching out for a formal assessment by a specialist neurologist. Contemporary neurovascular medicine has a lot more to offer than exclusively opioids and other analgesics: it offers structure, intention and the future of improved outcomes.
