What are the mechanisms of action of occipital nerve stimulation?

Updated: Oct 11, 2018
  • Author: Antonios Mammis, MD; Chief Editor: Jonathan P Miller, MD  more...
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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 [2] 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. [3] 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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