Dorsal Root Ganglion Stimulation for Pain Control

The DRG’s Role in Pain

The DRG is located inside the dural capsule in the lateral vertebral foramen in the spinal canal. It is a bilateral bulbous structure on the dorsal roots and houses the cell bodies and proximal processes of primary sensory neurons (PSNs) as well as satellite glial cells (SGCs) and immune cells ( ). PSNs are pseudounipolar cells; their dendrites, located throughout the body, transmit action potentials (APs) toward the central nervous system (CNS) and pass the T-junction of the DRG (the point at which the peripheral and central dendrites bifurcate from the process that extends from the soma) along the way. Depending on levels of activity and cellular conditions, the T-junction may function as a filter that restricts some APs from reaching the spinal cord or may enhance/propagate peripheral activity due to the intrinsic activity arising from the DRG itself ( ). Each DRG is somatotopically organized ( ), with up to 15,000 cell bodies per DRG at segmental levels where a major plexus innervates limbs ( ). Each DRG subserves sensory information specific to that spinal level in an approximately dermatomal fashion, although considerable cross-linkages and functional overlap exist between DRGs at adjacent spinal levels ( ).

The pathological events leading to neuropathic pain often begin with peripheral injury at the sensory nerve. The PSNs respond with pathological changes, including increased receptor expression, increased membrane excitability, and repetitive ectopic firing originating in the DRG ( ). The hyperexcitable state of DRG sensory neurons may be caused by the loss of inward calcium currents, alterations in sodium channels, and release of intracellular second messengers ( ). At projection sites within the spinal cord and elsewhere in the CNS there is increased release of excitatory amino acids and other neurotransmitters and signaling molecules, the functional consequence of which may be long-term potentiation and central sensitization. Other cellular populations may also be activated, as there is proliferation among SGCs in the DRG and microglia in the spinal cord, and sympathetic fiber baskets sprout around PSN somata ( ). Thus the DRG area is an important neuromodulation target because it plays a pivotal role in the development and maintenance of chronic pain. For a more complete discussion of the role of the DRG in the development of chronic neuropathic pain see ).

DRG Stimulation

Electrical stimulation reduces the ectopic firing rate of in vitro DRG neurons ( ). It is thought that the clinical pain-relieving effect of DRG stimulation is achieved by a similar mechanism, in which the overactivity/hypersensitivity of the DRG is reversed by exogenous electrical pacing ( ).

Stimulation of the DRG can be achieved via a minimally invasive epidural approach. Because the DRG is located within the vertebral canal and can be identified on the basis of landmarks such as the vertebral pedicles ( ), small flexible leads can be navigated through the intraforaminal ligaments and placed consistently near the DRG. The relative lack of cerebrospinal fluid around the DRG allows for increased energy efficiency, so DRG stimulation uses approximately 15% of the power consumption of tonic SCS systems ( ). The bony enclosures around the DRG ensure that the relationship between the lead and DRG remains constant, i.e., the strength of electrical field on neural tissue remains constant despite changes in bodily position and gravitational effects ( ).

The outcomes of DRG stimulation are different from those of SCS in regards to the distributions of paresthesia that can be generated. SCS generally covers broad swathes of the body and can be more easily directed to the limbs than the trunk. DRG stimulation, on the other hand, is generally characterized by smaller subdermatomal coverage patterns that can be readily applied to both axial and radicular pain distributions. It is theorized that DRG stimulation preferentially recruits the PSNs that have altered membrane properties due to neuropathological pain-initiated changes, given that the threshold for firing is halved in a genetic mutation animal model of chronic pain ( ). This selectivity may be responsible for the localized treatment that is possible with DRG stimulation. Contrast this with SCS, in which broad regions of the dorsal columns, including fibers which may or may not play a role in pain perception, are stimulated to create broad paresthesias ( ). Thus DRG stimulation may allow direct and specific modulation of algogenic sites.