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Occipital Nerve Stimulation


Occipital nerve stimulation (ONS) is a form of neuromodulation therapy aimed at treating headache and craniofacial pain. This therapy involves an implantable device composed of an electrode and pulse generator. The lead is placed into the subcutaneous tissues innervated by the greater and lesser occipital nerves, and the pulse generator is implanted into a subcutaneous pocket in the chest, abdomen, or back.

Prior to implantation, a trial is performed in which leads are placed under the skin and are connected to an external battery. The trial is performed under sedation, and the patient is discharged the same day. Afterward, the patient tries the therapy for 4–7 days and keeps a detailed pain diary.

A permanent device is implanted only if the patient reports significant improvements in pain and quality of life. The permanent implantation is placed under sedation or anesthesia, and the patient is discharged the same day.

The device is programmed by a clinical specialist appointed by the manufacturer.

This type of therapy has been evolving as a treatment for intractable occipital headache syndromes since the first implant in 1993, and the data to support its use are robust. Multiple authors have reported that successful neuromodulation for occipital headache syndromes can be accomplished with subcutaneous regional electrode placement. Available literature on the use of peripheral neurostimulation for headache includes occipital nerve stimulation, supraorbital nerve stimulation, and infraorbital nerve stimulation. Recently, other neurostimulatory techniques such as cervical epidural neurostimulation have been explored for cluster headaches, as well.

Neurostimulation is FDA-approved for the treatment of certain intractable pain syndromes, although it is not approved for headache, chronic migraine, and craniofacial pain and thus occipital nerve stimulation continues to represent an off-label use.

Mechanism of action

The theory of neuromodulation refers to therapeutic alteration of activity, electrically or chemically, in the central, peripheral, or autonomic nervous systems via the process of inhibition, stimulation, modification, or other forms of regulation. Occipital nerve stimulation is a form of neuromodulation that is reversible and adjustable and that can be tailored to an individual’s specific needs.

The mechanisms of action
for the paresthesia patterns and pain relief obtained from an occipital nerve stimulation are incompletely understood but appear to involve the following:

Subcutaneous electrical conduction

Dermatomal stimulation

Myotomal stimulation

Sympathetic stimulation

Local blood flow alteration

Peripheral nerve stimulation

Peripheral and central neurochemical mechanisms

Trigeminovascular system and Trigeminocervical tract

One prevalent theory is the involvement of the trigeminocervical system, which is the anatomic overlap of the trigeminal and occipital afferent systems at the level of C2 in the spinal cord. Trigeminal afferent pathways, and thus primary headache disorders, can be modulated at the C2 level by occipitally mediated afferents. In addition, electromodulation works to reduce blood flow to the pain-stimulating areas and to reduce abnormal excitation of the peripheral pain fibers, thus preventing central sensitization of trigeminal sensory nerve pathways, potentially reducing on-cell activity, and modulating the descending system at the level of the dorsal horn.

The gate control theory described by Melzack and Wall in 1965 (see image below) has been postulated to be one mechanism of action by which occipital nerve stimulation works for the treatment of local neuropathic pain.
According to this theory, stimulation activates large myelinated afferents, 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. Since pain states are maintained by continuous firing of unmyelinated and small myelinated afferents, a proportionately greater increase in the activation of large myelinated afferents closes the gate and stops pain transmission via presynaptic inhibition.

A schematic diagram of the gate control theory of

A schematic diagram of the gate control theory of pain.

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