Fig. 1
Intraoperative anterior-posterior (AP) radiograph demonstrating bilateral placement of octrode neurostimulator arrays (A). This patient is a 58-year-old male who developed left V1 and V3 distribution pain, after a brain stem infarct. Trigeminal branch stimulation, a form of peripheral field stimulation, trial leads were placed in V1 (a) and V3 (b) regions, corresponding to the painful areas (B). Intraoperative lateral radiograph of the same patient demonstrating final position of the implanted V1 (a) and V3 (b) region leads (C)
Pathophysiology
Neuromodulation refers to alteration of electrical or chemical activity of the peripheral or central nervous system for relief of pain through the process of inhibition, stimulation, modification, or other forms of regulation. ONS is a form of neuromodulation, which is reversible, adjustable, and may be individualized to the patient’s specific therapeutic needs. While the mechanisms of action for the pain relief obtained from an ONS are incompletely understood, the following are thought to play some role: subcutaneous electrical conduction, dermatomal stimulation, myotomal stimulation, sympathetic stimulation, local blood flow alteration, peripheral nerve stimulation, peripheral or central neurochemical mechanisms, and the trigeminovascular system or trigeminocervical tract. Ultimately, peripheral neurostimulation may exert its effect by multiple mechanisms, which may differ in the various headache and pain syndromes [7].
One theory postulates the involvement of the trigeminocervical system – the anatomic overlap of the trigeminal and occipital afferent systems at the spinal cord vertebral level of C2. These afferents have been cited to converge on second-order nociceptors in the spinal trigeminal nucleus. As such, trigeminal afferent pathways, and thereby primary headache disorders, may be controlled at the C2 level by occipitally mediated afferents. Others suggest that electromodulation reduces blood flow to areas of pain as well as abnormal excitation of the peripheral pain fibers. Therefore, the central sensitization of the trigeminal sensory nerve pathways is prevented, while the descending system at the level of the dorsal horn may be modulated.
Another possible mechanism of action of ONS is described by the gate control theory. Described initially by Melzack and Wall in 1965, the gate control theory describes the enhancement of inhibitory actions of the local circuit neurons in the dorsal horn on the central transmission cells. Stimulation of somatosensory pathways, such as the peripheral nerves or dorsal columns, results in activation of large myelinated afferents (Aß fibers), which “close the pain gate” in the substantia gelatinosa, by enhancing the inhibitory actions of local circuit neurons in the dorsal horn on central transmission cells. The preferential activation of larger, myelinated Aß fibers thus reduces nociceptive transmission in the smaller, thinly myelinated and unmyelinated A∂ and C fibers, effecting a reduction in pain.
Patient Selection
Occipital nerve stimulation has been used for the management of a variety of headache disorders, including Chiari I malformation headache, migraine headache, cluster headache, cervicogenic headache, occipital neuralgia, and posttraumatic headache. In a recent publication by the authors, a single center’s experience with ONS was analyzed, with patients being retrospectively diagnosed (Table 1). The authors have observed that with those patients with the following conditions, a substantial success rate was expected: migraine, Chiari malformation, and occipital neuralgia. However, patients with recent MRSA infections, unrealistic expectations, and psychiatric comorbidities are those who are generally avoided. These issues underscore the importance of using a trial and requiring a psychiatric evaluation for all patients [10].
Table 1
Patient outcomes from a study by Mammis et al. on Peripheral Neuromodulation for Headache and Craniofacial Pain [10]. For each diagnosis, codes from the 2nd edition of the International Headache Classification (ICHD-2) system are listed
ICHD-2: Diagnosis | Number of patients | Number of successful trials | Trial success rate (%) | Number of permanent systems still used at last follow-up | Long-term implanted success rate (%) | Intent-to-treat success rate (%) |
---|---|---|---|---|---|---|
7.7: Headache attributed to Chiari malformation type I | 28 | 18 | 64 | 15 | 83 | 54 |
1.1 or 1.2: Migraine headache with or without aura | 24 | 21 | 88 | 19 | 90 | 79 |
5.2.2: Chronic posttraumatic headache attributed to mild head injury | 11 | 10 | 91 | 8 | 80 | 73 |
13.8: Occipital neuralgia | 8 | 7 | 88 | 7 | 100 | 88 |
5.7.2: Postcraniotomy headache | 7 | 7 | 100 | 6 | 86 | 86 |
3.1.2: Chronic cluster headache | 5 | 4 | 80 | 4 | 100 | 80 |
6.1.1: Headache attributed to ischemic stroke | 5 | 3 | 60 | 1 | 33 | 20 |
13.7: Other trigeminal or terminal branch neuralgias | 5 | 4 | 80 | 1 | 25 | 20 |
11.2.1: Cervicogenic headache | 4 | 3 | 75 | 3 | 100 | 75 |
4.7: Hemicrania continua | 1 | 1 | 100 | 1 | 100 | 100 |
7.4.4: Headache attributed to hypothalamic or pituitary hyper- or hyposecretion | 1 | 1 | 100 | 0 | 0 | 0 |
7.7: Headache attributed to Chiari malformation type I | 28 | 18 | 64 | 15 | 83 | 54 |
1.1 or 1.2: Migraine headache with or without aura | 24 | 21 | 88 | 19 | 90 | 79 |
5.2.2: Chronic posttraumatic headache attributed to mild head injury | 11 | 10 | 91 | 8 | 80 | 73 |
13.8: Occipital neuralgia | 8 | 7 | 88 | 7 | 100 | 88 |
5.7.2: Postcraniotomy headache | 7 | 7 | 100 | 6 | 86 | 86 |
3.1.2: Chronic cluster headache | 5 | 4 | 80 | 4 | 100 | 80 |
6.1.1: Headache attributed to ischemic stroke | 5 | 3 | 60 | 1 | 33 | 20 |
13.7: Other trigeminal or terminal branch neuralgias | 5 | 4 | 80
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