Background

Migraine is a common neurological disorder that has a wide variety of subtypes, many comorbidities, and a variable prognosis [1]. Migraine that undergoes progression clinically evolves to high-frequency episodic migraine or chronic migraine. Functional changes may accompany migraine progression, including the development of allodynia, and changes in the periacqueductal gray matter. These findings support the hypothesis that migraine is not just an episodic disorder but a chronic disorder with episodic manifestations [2]. Moreover, headache syndromes often involve occipital and neck symptoms, suggesting a functional connectivity between nociceptive trigeminal and cervical afferents. The most likely mechanism for this observation is “referred pain” originating from structures in the neck and projecting to facial areas and vice versa at the level of second-order neurons in the brainstem, which receive convergent input from both trigeminal and cervical territories [3]. Several studies have suggested that pain relief in migraine, cervicogenic headache and cluster headache can be achieved by local injections of steroids, local anaesthetics, or a mixture of both in the area of greater occipital nerve (GON), offering a toll for the management of these form [4, 5]. The GON is composed of sensory fibres that originate predominantly at the C2 level. Its cutaneous distribution covers the posterior part of the head up to the vertex. Usually greater occipital nerve block (GONB) is performed by using local anaesthetics alone or with steroid and bilateral GON, trigger-points in the cervical paraspinal and trapezius muscles are treated. The rationale of performing a GONB for the treatment of chronic headache states on the anatomical connections between trigeminal and upper cervical sensory fibres at the level of the trigeminal nucleus caudalis [6, 7]. However, the reason for the improvement of clinical symptoms after occipital nerve blockade in primary headache patients is unknown. Several hypotheses have been suggested, including inhibition of central-pain processing mechanisms at the brainstem level, a systemic steroid effect and placebo effects.

Migraine patients, especially when affected by chronic and aura subtype forms, often have increased skin sensitivity to non-noxious stimuli and GONB may play a role in cutaneous allodynia in migraine. In fact, allodynia is thought to be caused by the headache and the activation of nociceptors with the development of central sensitization in subjects with an altered regulation of the central nociceptive pathway [8]. The persistence of pain sensation seems to be able to induce central sensitization in the caudal nucleus of the trigeminal nerve by lowering the neuronal pain threshold [9].

GONB alleviate head pain by altering the nociceptive input to the trigeminal-cervical complex. Based on findings from experimental studies, electrical stimulation and local anaesthetic blocks of the GON has been shown to have a facilitatory effect on dural nociceptive stimulation suggesting the subsequent induction of central sensitization on the second-order neurone receiving cervical and trigeminal input [10].

A disturbance in the region of the head can provoke pain in the distribution of the trigeminal and upper cervical nerves due to a convergence of the afferent fibres of the three superior cervical roots on the neurones of the trigeminal nerve nucleus [11], so the analgesic action of GONB is a process most likely initiated by a diffuse inhibitory process.

Conclusion

In conclusion, neurophysiological and clinical data suggests a functional connectivity between the sensory occipital segments and the trigeminal nociceptive system in humans. GON block for migraine, and in particular in unresponsive chronic migraine patients, should be in this way considered an effective management tool.