A Case Series in a Tertiary Care Headache Center: Ultrasound-Guided Proximal Greater Occipital Nerve Pulsed Radiofrequency is Effective in Migraine with Aura for Six Months

About 30% of migraineurs have migraine with aura (MwA). Aura symptoms can be very distressing and temporarily disabling for those affected.[1] As imaging studies show, migraine with aura (MwA) differs from migraine without aura (MwoA) in terms of heredity, a stronger association with various diseases, including stroke, and different changes in brain structure and function. The same treatment is recommended in the current guidelines. This is not unexpected as the subtypes of MwA and MwoA attacks have been poorly documented in studies examining acute and preventive therapy for migraine.[2,3] Ultrasound (US)-guided proximal greater occipital nerve (PGON) block at the level of C2 is more effective than distal GON blockade at the level of the external occipital spine in chronic migraine patients. Radiofrequency (RF) treatment of GON has recently been used in the treatment of headaches with promising results.[4] US-guided pulsed RF (PRF) of the GON is effective in chronic migraine patients.[5] Case studies have found that the GON block can heal the extended auras.[6,7] However, we could find no evidence that GON PRF is effective for the aura. The authors defined the six-month efficacy of US-guided PGON PRF in six patients with MwA. The efficacy was assessed by the intensity and number of migraine attacks with and without aura from the patient’s medical records and headache diaries. The numeric rating scale (NRS) was used to measure intensity. Case History Records of six female patients with MwA who were followed up for at least six months after the procedure and gave informed consent were retrospectively obtained [Figure 1]. Table 1 summarizes the characteristics of the cases. Migraine attacks had a mean NRS of 9.333 ± 0.516 with a frequency of 10.333 ± 3.502 times per month and a duration of 60.666 ± 12.436 hours. Patients’ auras included visual and/or sensory deficits that lasted 28.333 ± 7.527 minutes and occurred 7.666 ± 2.875 times per month.Figure 1: Flowchart Diagram of Case Series: PGON: Proximal greater occipital nerve, PRF: Pulsed radiofrequency, MwA: Migraine with aura, MwoA: Migraine without auraTable 1: Characteristics of patientsIn the event of a subsequent migraine attack, patients were invited for a US-guided PGON diagnostic block. The immediate efficacy of the PGON block was assessed by aural relief (5 complete relief, 1 partial relief) and NRS decrease from baseline to 20 minutes after blockade from 9.333 ± 0.500[8,9] to 0.500 ± 0.002 (0–2) (P: 0.001). One week after the diagnostic blockade, patients were contacted for PRF. We performed diagnostic blockade and PRF of PGON in a sterile operating room without anesthesia. We used an ultrasound machine with a 13–5 MHz linear probe (GE Healthcare, VolusonTM E6, Turkey). During the diagnostic blockade, a 3-mL injection of lidocaine %2 (Aritmal %2, Osel) was administered. PRF was performed with RF technology (Top Lesion Generator TLG-10, Japan). A 60-mm-long 21 G 5-mm radiofrequency needle with an active tip (SC-K; Top Neuropole, Tokyo, Japan) was used. Using the in-plane technique, the nerve was treated from medial to lateral at the level of C2 between the inferior oblique muscle and the semispinalis capitis [see Figure 2]. PRF treatment was given with 5 Hz and 5 ms pulse width for 360 s at 45 V, assuming that the electrode points were not over 42°C after the patient felt occipital dysesthesias and sensation with a voltage of less than 0.2 V.Figure 2: (a) Sonoanatomy of The Proximal GON: GON: Greater occipital nerve, SSCM: Semispinalis capitis muscle, OCIM: Obliquus capitis inferior muscle, SP: Spinous process, (b) Radiofrequency needle placementThe efficacy of the treatment is shown in Table 2. A significant drop in the aura days and aura duration was noted [baseline: 7.67 ± 2.875 (5–12); after six months: 1.333 ± 1.032 (0–3), P: 0.002 for aura days/baseline: 28.333 ± 7.527 (20–40); after six months 7.500 ± 5.244 (0–15), P: 0.001 for aura duration]. The headache days [baseline: 10.333 ± 3.502 (5–15), after six months: 3.833 ± 1.602 (2–6), P: 0.002], headache intensity [NRS baseline: 9.333 ± 0.516 (9–10), after six months: 3.666 ± 1.032 (2–5), P: 0.001], and headache duration [baseline: 60.666 ± 12.436 min (48–72), after six months: 4.833 ± 2.316 min (1–8), P: 0.001] all showed a statistically significant decrease. Six patients experienced no mild or severe adverse effects during the six-month treatment.Table 2: Efficacy of PRF of PGON in timeDiscussion This manuscript demonstrates the efficacy of PGON’s PRF in the treatment of MwA over six months. Aura and headache development should be considered to understand the underlying basis of efficacy. Cortical spreading depression (CSD) is most likely the source of the aura. In rodents, CSD is associated with delayed activation of the trigeminovascular pathway by activating nociceptors innervating the meninges and central neurons in the spinal trigeminal nucleus at the C2 level.[3] In addition, the release of potassium, arachidonic acid, hydrogen ions, and nitric oxide can be facilitated by CSD waves moving slowly through the cortex, resulting in central sensitization (CS) and activation of the trigeminocervical complex (TCC). Furthermore, CSD is linked to alterations in the release and dispersion of many chemicals in the interstitial space, including excitatory neurotransmitters, serotonin, noradrenaline, and calcitonin gene-related peptide (CGRP).[2,3] CGRP sends sensations of pain to the thalamus and upper cortical pain locations via the trigeminal nucleus caudalis (TNC) and C2 level. Furthermore, studies have shown that CGRP might increase the sensitivity of neurons, potentially leading to CSD by increasing the propagation of neuronal activity across the cortex and causing prolonged depolarization.[10] GON blockade has been utilized in an acute treatment for migraine as well as a short- and long-term preventive therapy for refractory migraine.[4] Previously, in a small study of 18 patients with MwA, a complete response was reported in 11 attacks and a partial response in six of 22 attacks treated with the GON block. The aura symptoms disappeared within 5 to 90 minutes.[7] Using functional magnetic resonance imaging and quantitative sensory assessment, the impact of the GON block on pain thresholds has been studied before. The occipital nerve enters the TCC, converges on the same central nuclei, crosses the midline, and passes to higher processing units at the C2 level, which is most likely where trigeminal nociceptive activity is blocked.[8] Also, reduction in CGRP levels was demonstrated after GON block previously.[9] By generating a dense electric current surrounding an active electrode tip, PRF can heat the area around the nerves to temperatures of 42 to 44°C. By altering the synaptic impulses of the pain pathways, this technique specifically targets the pain fibers, particularly the nonmyelinated C-fibers. PRF’s analgesic properties may also exert benefits through noradrenergic, serotonergic, and endogenous opioid-inhibitory pain pathways, resulting in central and peripheral modulation.[11] The intervention in the current study was designed to target GON at the C2 level. The method by which GON blockade effectively inhibits aura, and headache attacks could include lowering CGRP levels in addition to inhibiting pain transmission from occipital neurons to the TNC. The efficacy may have been enhanced by the PRF of PGON through the modulatory effects. This multimodal mode of action may have contributed to the reduction in average monthly migraine aura days reported in the current study. It is important to highlight that our observational study, which had a small sample of subjects, demonstrates promising outcomes regarding the effectiveness of PGON in treating MwA over six months. However, further research is necessary to fully understand how it works and establish the scope of these findings. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.