The dorsal root ganglia (or spinal ganglia) (▶ Fig. 19.1) are described as nodulelike structures found on the posterior root of each spinal nerve, which contains the soma (or cell bodies) of the afferent sensory nerves carrying signals back to the central nervous system. ¹ These structures develop from neural crest cells migrating into the rostral mesoderm, and each is described as oval and reddish in nature with size depending on its root for the corresponding level. ² Histologically, the ganglia are described as containing the cell bodies of the pseudounipolar sensory neurons, which are spherical and lack dendrites. Since the cell bodies have no dendrites and are not directly involved in conducting sensory signals, the ganglion also has glial cells (satellite cells) within it to insulate the cell bodies electrically. Nerve fibers and connective tissue are also noted on histology, but the predominant image is the circular cell bodies of the sensory nerves with the glial cells interspersed between them. ³

There is a dorsal root ganglion (DRG) associated with each spinal nerve, the only possible exception being the C1 spinal nerve, which is primarily a motor neuron. The DRG of the C1 spinal nerve may be rudimentary or absent. ⁴ The pseudounipolar nature of the sensory nerves in the peripheral nervous system means that the cell body is located between the two branches, which act as axons. These branches can be labeled the distal and proximal processes. Signals in these nerves begin in the distal process via communication between sensory cells, travel proximally, can bypass the soma, and continue into the spinal cord via the posterior root into the posterior (or dorsal) horn to synapse in one of the sensory pathway tracts. ²

19.2 Location

The locations of DRG depend on the level at which the corresponding nerve is found. From the cervical down to the lumbar spine, the DRG for these nerves are generally located in or marginally outside the midpoints of the intervertebral foramina, immediately lateral to the perforation of the dura mater by the dorsal root. However, in the lower lumbar, sacral, and coccygeal regions they can be intraspinal or within the dura mater itself. ⁵ One consequence of the positioning of these ganglia is clinical manifestations with compression. Proximally located DRG is more likely to be associated with radicular syndromes. ⁶ This is especially true in L4 and L5 radiculopathy as DRG become more proximal the further caudal they are. These ganglia are vulnerable to compression owing to the narrow epiradicular space, larger size, and risk of compression from spinal disc herniation. They can also have indentations. ⁶ Kikuchi et al noted variations in the appearance of these indentations, which were more common in older patients and patients with radiculopathy and were absent in the S1 nerve roots. ⁷ These findings suggest that the main causes of ganglionic indentation are compression by the superior facets at the intervertebral foramina and bulging discs causing compression. The highest incidence for indentation was in the intraspinal DRG; more distal DRG had a lower incidence. ⁸

19.3 Blood Supply

The DRG receive their blood supply from nutrient arteries that branch directly from the dorsal division of each spinal segmental artery. ⁹ Compression of the spinal nerve distal to a DRG decreased blood flow by up to 45%, while compression proximal to it caused only a 10 to 15% decrease. ¹⁰ The ganglion has more abundant intrinsic vessels than the nerve root, consisting of continuous and fenestrated capillaries. The association of such capillaries with the DRG suggests the blood–nerve barrier around the ganglion is not as impervious as originally thought, similar to peripheral nerves, so the DRG could be subject to more hemodynamic stress and/or injury. This is especially true for patients with diabetes mellitus, who in postmortem studies had statistically significantly thicker DRG perineural capillary basement membranes than nondiabetics. ¹¹ This finding is not surprising in view of findings with diabetic peripheral neuropathy, but could implicate DRG pathology in neuropathic manifestations of dysesthesia and anesthesia in diabetics.

19.4 Lumbar Dorsal Root Ganglion

The lumbar DRG are clinically important owing to their proximal position in the foraminal spaces from which the nerves exit. This set of ganglia has been proved to be important in lower back pain and sciatica because of their susceptibility to mechanical irritation from injury. ¹²

Studies to visualize the lumbar DRG have elucidated their role in pain when they are subject to compression through lumbar disc herniation. ⁷ In one study, the location of the DRG from the L1–L3 nerves were found to be extraforaminal or foraminal, while the L4 DRG were in the foraminal region, and the L5 DRG were predominantly in the foraminal region with the possibility of being intraspinal. ¹³ Only at the L5 level were intraspinal ganglia noted, more in females than males, though there was no statistically significant difference. ¹⁴ The same studies showed the more caudally located ganglia to be wider and longer. The architecture of the lumbar DRG proved unique. The L5 and L2 DRG have a trigangliar architecture, which is considered an anatomical variant as they are predominantly singular at those levels. The L3 and L4 DRG tend to show a near 1:1 ratio of singular and bigangliar architecture, and the L1 DRG is almost always single. ⁷

19.5 Pathologies of the Dorsal Root Ganglia

19.5.1 Sensory Ganglionopathies

Sensory ganglionopathies (or sensory neuronopathies) are a distinct group of peripheral neuropathies that affect the cell bodies of sensory neurons. They can occur in a DRG or in the trigeminal ganglia and lead to the degeneration and destruction of both their central and peripheral sensory projections. This pathological process causes degeneration of both short and long axons. The clinical presentation of a sensory ganglionopathy entails severe sensory loss in the effect region of the ganglion. An assortment of disease conditions can cause ganglionopathies especially since, as discussed earlier, the blood–nerve barrier around the DRG is permeable, rendering the ganglion vulnerable to infection, tumor metastasis, autoimmune disorders, and toxins. Hereditary disorders such as Tay–Sachs can also be implicated in sensory ganglionopathies. Ganglionectomy of the DRG can be used to diagnose the condition causing the sensory ganglionopathy. ^{15,​ 16}

A sensory ganglionopathy can begin with patchy, asymmetrical sensory loss involving proximal regions. As it progresses, it can involve more distal regions and become more symmetrical. This is different from peripheral neuropathy, where distal sensory loss precedes proximal sensory loss. ¹⁷ Necrosis of the sensory cell bodies within the ganglia results in the degeneration of the axons, which is important as the patients show clinical symptoms of gait ataxia (due to denervation of the muscle spindles), loss of vibratory sense, loss of tendon reflexes, and dysesthesias. Ganglionopathies have been dubbed “ataxic neuropathies” in view of the gait ataxia, but this title is misleading as ataxic neuropathies also include other conditions such as demyelinating neuropathies, where ataxia is the main symptom.

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