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  • The Incidence of Vascular Conflict with the Trigeminal Nerve in Cluster Headache

    Final Number:

    Tsinsue Chen MD; Arthur Andre MD; Indran Davagnanam MD; Daisuke Danno; Ludvic Zrinzo MD, MSc, FRCS; Manjit Matharu MD

    Study Design:

    Subject Category:

    Meeting: 2018 ASSFN Biennial Meeting

    Introduction: Cluster headache (CH) is one of the most disabling primary headache syndromes. Although neurovascular conflict is implicated in facial pain syndromes such as trigeminal neuralgia, its role in CH has not been systematically reviewed. In this study, we assess the incidence of radiographic arterial and venous conflict with the trigeminal nerve in symptomatic versus asymptomatic trigeminal nerves in a cohort of patients with CH.

    Methods: Patients with confirmed CH at a single institution underwent high-resolution MRI of the prepontine cistern between 2007 and 2017. Prospectively acquired images were retrospectively reviewed by a neuroradiologist and two neurosurgeons blinded to symptom severity and lateralisation. Each trigeminal nerve was classified into one of the following groups based on its relationship to adjacent vasculature: (1) no vessel within 1 mm, (2) vessel within 1 mm, (3) vascular contact, (4) vascular distortion of the nerve and (5) vascular contact nerve atrophy or signal change.

    Results: 136 patients (mean age at imaging: 44.5 years, mean age of symptom onset: 31.0 years) had 153 symptomatic and 119 asymptomatic nerves (55 left-sided; 64 right-sided; 17 side-alternating attacks). The incidence of arterial conflict (groups 3, 4 and 5) was significantly higher in symptomatic compared to asymptomatic nerves (40.5% vs. 26.9%, p=0.02). The incidence of venous conflict was not significantly different between symptomatic versus asymptomatic nerves (42.5% vs. 42.0%, p=0.94).

    Conclusions: We hypothesize that arterial contact is neither required nor sufficient to drive CH attacks but that it may interact with a central (hypothalamic) generator to drive symptoms in a subgroup of patients. These findings suggest a rationale for microvascular decompression of the trigeminal nerve in patients with refractory CH and radiological arterial contact with the nerve on the symptomatic side.

    Patient Care: Initial evidence that arterial contact with the trigeminal nerve on the symptomatic cluster headache side proposes a rationale for microvascular decompression as a potential tool for the surgical treatment of cluster headache. Microvascular decompression would be a definitive treatment option, given that the current surgical treatment modalities remain neuromodulatory in nature.

    Learning Objectives: To evaluate the association between vascular contact with the trigeminal nerve and symptomatic cluster headache.

    References: 1. Guerreiro R, Casimiro M, Lopes D, Marques JP, Fontoura P. Video NeuroImage: symptomatic SUNCT syndrome cured after trigeminal neurovascular contact surgical decompression. Neurology 2009; 72(7): e37. 2. Mjaset C, Russell MB. Secondary chronic cluster headache due to trigeminal nerve root compression. Acta Neurol Scand 2010; 122(6): 373-6. 3.Irimia P, Gonzalez-Redondo R, Dominguez PD, Diez-Valle R, Martinez-Vila E. Microvascular decompression may be effective for refractory SUNCT regardless of symptom duration. Cephalalgia 2010; 30(5): 626-30.

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