Headache and neck pain are frequent manifestations of cervicocephalic artery dissection, with vertebral artery dissection most often producing unilateral occipito-nuchal pain. ^{Reference Matsumoto, Hanayama and Sakurai1} Headache may persist after cervicocephalic artery dissection, representing a long-term sequela that remains insufficiently described in the literature. ^{Reference Martins Bárbara, Iês, Sousa Jé, Abreu and Costa2} Accordingly, management strategies specific to dissection-associated headache have not been clearly delineated.

Here, we describe two patients with past medical history of episodic migraine who developed persistent post-dissection headaches with prominent cervical features responsive to peripheral nerve blockade; in one, benefit was durable, while in the other, waning response prompted escalation to onabotulinumtoxinA.

Case 1: A 42-year-old woman with episodic migraine presented with an abrupt unilateral occipito-cervical pain radiating to the ipsilateral eye, followed by a throbbing headache with photophobia, nausea and vertigo. Imaging demonstrated bilateral V3 vertebral artery dissections (Figure 1A-D) with a small right cerebellar infarct (Figure 1E). She was treated with dual antiplatelet therapy. She had a long-standing biomechanical cervical strain related to severe scoliosis and sacral agenesis with compensatory muscular overactivation from prolonged aerial performance activity. Although migrainous features gradually improved following the acute vascular event, she developed persistent daily suboccipital and cervical pain with mechanical neck sensitivity and radiation to the scalp, jaw and retro-orbital region. Headache frequency was 0–15 days per month. Pharmacologic options were limited by vascular disease and antiplatelet therapy; low-dose propranolol did not improve her headache. Given marked occipital tenderness and cervical trigger points on examination, multisite peripheral injections were initiated, including bilateral greater and lesser occipital, auriculotemporal and cervical trigger points using 0.5% bupivacaine, which improved her headache for 4–6 weeks each time. Repeated treatments maintained sustained benefit, with an estimated 80–85% reduction in headache frequency and intensity and prolonged headache-free intervals. She remains well controlled on periodic nerve blocks.

Figure 1.

Neuroimaging findings of Case 1. CT angiography demonstrates an abrupt cutoff of the right vertebral artery at the V3 segment (A) and luminal irregularity of the left vertebral artery at the V3–V4 junction (B). Axial T1-weighted fat-suppressed MRI shows marked subintimal hyperintense signal involving the V3–V4 segments of the right (C) and left (D) vertebral arteries, consistent with intramural hematoma from arterial dissection. Diffusion-weighted MRI reveals small foci of restricted diffusion in the right cerebellar hemisphere (E), consistent with subacute ischemic infarction.

Case 2: A 47-year-old woman with episodic migraine since adolescence (previously infrequent, characterized by throbbing pain with photophobia and nausea, and responsive to rizatriptan), hypertension and prior spontaneous coronary artery dissection developed a new unilateral occipital headache radiating to the neck, distinct from her usual migraine attacks and not responsive to simple analgesics. Neuroimaging showed an intracranial left V4 vertebral artery dissection (Figure 2A), treated with antiplatelet therapy. Within 2 months, she experienced a severe right occipital headache; repeat imaging demonstrated a new V4 dissection on the opposite side (Figure 2B). A comprehensive genetic panel for familial thoracic aortic aneurysm and dissection syndromes was negative, with unremarkable vasculitis screening and no evidence of fibromuscular dysplasia. She subsequently developed chronic daily headache with 16–20 moderate-to-severe headache days per month, characterized by bilateral suboccipital and neck pain, with superimposed medication overuse from combined acetaminophen-codeine use on 16 days per month. Rizatriptan was discontinued for vascular safety. Preventive therapy with amitriptyline and candesartan provided partial benefit, while ubrogepant and rimegepant offered inconsistent and incomplete acute relief. She underwent a series of peripheral nerve blocks similar to Case 1. Each block produced short-term improvement with several headache-free days, but the duration of benefit progressively shortened from 4–6 weeks down to 1–2 weeks. Given this pattern, she was transitioned to onabotulinumtoxinA for chronic migraine prevention due to progression from episodic to chronic migraine following the dissection events. After treatment initiation, headache frequency decreased with reduced attack severity and less reliance on acute medications, and she has remained clinically stable without further vascular events.

Figure 2.

Neuroimaging findings of Case 2. CT angiography shows luminal irregularity of the left vertebral artery at the V3–V4 junction (A). Follow-up T1-weighted fat-suppressed MRI demonstrates subintimal hyperintensity in the V3–V4 segments of both vertebral arteries (B), with new dissection involving the right vertebral artery.

The International Classification of Headache Disorders, 3rd edition (ICHD-3) ^{Reference Olesen, Bendtsen and Dodick3} classifies cervical artery dissection as a cause of secondary headache, defined by new unilateral head, neck or facial pain occurring in temporal association with the vascular injury, and acknowledges a persistent subtype when pain continues beyond vascular stabilization. Our two patients exemplify this clinical continuum, evolving from acute dissection-related vascular pain into persistent post-cervicocephalic artery dissection headache as described in post-dissection cohorts. ^{Reference Martins Bárbara, Iês, Sousa Jé, Abreu and Costa2,Reference Leys, Moulin, Stojkovic, Begey and Chavot4} Mechanistically, nociceptive input from the dissected arterial wall and upper cervical roots converges with trigeminovascular afferents within the trigeminocervical complex, facilitating referral of cervical pain and cross-sensitization of central migraine pathways. ^{Reference Martins Bárbara, Iês, Sousa Jé, Abreu and Costa2,Reference Doukhi, Debette and Mawet6} In susceptible individuals such as those with preexisting migraine or recurrent vascular injury, sustained cervical nociception may promote central sensitization and lower migraine activation thresholds beyond the period of arterial healing, providing a biologic explanation for the over-representation of migraine observed in cervicocephalic dissection cohorts. ^{Reference Matsumoto, Hanayama and Sakurai1–Reference Martins Bárbara, Iês, Sousa Jé, Abreu and Costa2}

Peripheral nerve blockade modulates this pain network by suppressing afferent input from occipital and adjacent cervical branches projecting to the trigeminocervical complex. ^{Reference Ashkenazi, Blumenfeld and Napchan5} In Case 1, cervical trigger point injections were included because examination revealed marked paraspinal and trapezius tenderness with reproducible pain referral to the occipital and retro-orbital regions, suggesting a significant myofascial component. Given her severe scoliosis and long-standing biomechanical cervical strain, the peripheral injection strategy was intentionally multimodal, targeting both occipital nerve afferents and muscular nociceptive sources converging on the trigeminocervical complex. Although this limits attribution of benefit to nerve blockade alone, the sustained and reproducible response supports the relevance of peripheral cervical pain generators in persistent post-dissection headache. Case 2, on the other hand, evolved into chronic migraine with medication overuse, consistent with transformation from episodic following the dissection events. In that context, escalation to onabotulinumtoxinA was undertaken to target the chronic migraine phenotype and given that onabotulinumtoxinA reduces trigeminal and cervical sensory input through inhibition of peripheral neurotransmitter release, thereby indirectly attenuating trigeminocervical sensitization. ^{Reference Burstein, Zhang, Levy, Aoki and Brin7}

Together, these cases illustrate the close interplay between cervical pain and migraine following vertebral artery dissection. Persistent cervical nociceptive input may interact with preexisting migraine biology, contributing to ongoing headache beyond vascular healing. Peripheral nerve blocks offer a vascular-safe approach to targeting cervical pain drivers, whereas escalation to onabotulinumtoxinA is appropriate when it is transformed to chronic migraine.