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Pain from Ventral Root Afferents

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A and B show two different routes that may be followed by ventral root afferent fibres into the dorsal horn. From Coggeshall (1979)[1]

The Bell-Magendie law states that anterior spinal nerve roots contain only efferent motor fibres, and posterior roots contain only afferent sensory fibres. A clinical consequence of this is that dorsal rhizotomy should provide relief of segmental pain. The truth is a little more complex, there are actually also sensory fibres in the ventral roots.[1]

Ventral roots in reality also carry nociceptive fibers (i.e. "wrong way" fibres) that produce a dull, aching pain quality. These ventral root afferents are not a separate ā€œpain pathwayā€ per se ā€“ they usually reunite with the dorsal root in the intervertebral foramen ā€“ but they explain why pure dorsal root lesions donā€™t encompass all root-related pain. The concept of ventral root afferents is well established anatomically, but current clinical practice simply addresses the patientā€™s symptoms as ā€œradicular painā€ without parsing which root division is causing which aspect. This article discusses afferent fibres within the ventral roots and their potential clinical relevance.

Ventral Root Pain in Radicular Pain

Radicular pain usually does not usually follow a dermatomal pattern, and this fact has lead to fascinating research which is directly clinically relevant.

Mid-20th-century texts on radiculopathy described two qualitatively different pain types depending on whether ventral or dorsal spinal nerve roots were affected. A 1957-era notion was that ventral root compression produces a dull, deep, aching ā€œmyalgicā€ pain, whereas dorsal root compression produces sharp, shooting, electric ā€œneuralgicā€ pain. This concept can be traced to earlier physiological discoveries. As early as 1822, FranƧois Magendie observed that pinching or injuring a ventral spinal root in animals could still evoke pain behaviors ā€“ a paradox, since ventral roots were thought purely motor. Magendie showed that severing the corresponding dorsal root eliminated these pain responses, implying some sensory fibers travel via ventral roots and then loop back to the dorsal root (ā€œrecurrent sensibilityā€)ā€‹.

Claude Bernard later coined the term ā€œrecurrent sensibilityā€ in 1858 and confirmed that unmyelinated fibers in ventral roots can carry nociceptive signals into the dorsal hornā€‹.

Early neurologists like Moritz Schiff and Sir Charles Sherrington further differentiated ā€œdeepā€ vs. ā€œsuperficialā€ pain qualities, aligning deep diffuse pain with muscle/tissue afferents and sharp pain with cutaneous afferents. By the mid-20th century, clinicians such as Otfried Foerster noted that stimulating or compressing nerve roots could produce two components of pain. Foerster and Gagel (1932) had reported that some pain fibers cross in the ventral spinal commissureā€‹, hinting that not all pain travels exclusively in dorsal pathways.[2]

These ideas culminated in the following classic teachings: dorsal root (sensory) lesions cause lancinating pain radiating along the limb, while ventral root (motor) lesions cause a more diffuse, aching pain in proximal regions. For example, Smyth and Wright in 1958 experimentally compressed lumbosacral nerve roots in post-operative sciatica patients and noted two pain components: ā€œa sharp pain which ranā€¦down the extremity, and a deep, boring, aching, unpleasant sensation felt diffusely in the soft tissueā€ā€‹.[3] They explicitly described the latter as ā€œdull aching pain, myalgic more than neuralgic in characterā€ā€‹. Thus, early clinical research recognized a potential dichotomy in radicular pain quality corresponding to dorsal vs. ventral root involvement.

Early Experimental Findings (Magendie to 1950s)

Magendie (1820s) ā€“ Demonstrated the functional separation of dorsal and ventral roots (sensory vs. motor) but also observed that ventral root injury could still elicit pain reflexes unless the dorsal root was cutā€‹. This was the first evidence of sensory afferents in ventral roots, violating the simple Bell-Magendie law and introducing the concept of recurrent sensory fibers.

Claude Bernard (1858) ā€“ Investigated ā€œrecurrent sensitivityā€ in depth. He confirmed that unmyelinated sensory fibers exit the spinal cord via ventral roots and then re-enter the dorsal horn (often via the mixed spinal nerve and dorsal root) to transmit painā€‹. Bernardā€™s experiments in dogs showed that stimulation of ventral roots could cause pain behaviors and that these were abolished by dorsal root section. This firmly established that some afferent nociceptive information can travel in ventral roots before reaching the CNS.

Moritz Schiff (19th c.) ā€“ As an early neurophysiologist, Schiff participated in debates about recurrent sensibility. He and others confirmed the existence of ventral root afferents but also noted controversies in interpretation. These 19th-century studies set the stage for distinguishing ā€œdeepā€ pain arising from muscle/viscera vs. ā€œsurfaceā€ pain from skin, a distinction later elaborated by Sherrington.

Sir Charles Sherrington (early 20th c.) ā€“ Sherringtonā€™s work on reflexes and nociception did not directly focus on ventral root afferents, but he introduced the idea of nociceptive specificity: that certain ā€œslow-conductingā€ afferents (now known as C-fibers) evoke dull, diffuse pain, as opposed to the fast, sharp pain from A-delta fibers. This framework aligns with the ventral vs. dorsal root pain dichotomy: ventral root afferents tend to be unmyelinated C-fibers mediating slow, aching pain, whereas dorsal root carries the full range including fast pain. Sherringtonā€™s concept of ā€œthe pain reflexā€ (1906) and subsequent work by others helped explain why deep muscle or joint pain (likely carried by smaller fibers, some traveling via ventral routes) feels qualitatively different from cutaneous pain.

Frykholm and colleagues (1950s) ā€“ By the mid-20th century, neurosurgeons and physiologists revisited ventral root pain in humans. In 1953, R. Frykholm et al. electrically stimulated ventral lumbar nerve roots during surgery on awake patients. Remarkably, this produced conscious pain sensations, proving ventral root stimulation can be painfulā€‹. Patients described a deep, aching pain rather than the classic dermatomal sharp shooting pain. This work directly supported the notion of ventral root pain in humans. Frykholm also noted that compressive cervical radiculopathy often caused shoulder girdle ache in addition to arm pain, an observation consistent with ventral root (or ventral ramus) afferent involvement.[4]

White and Sweet (1955) ā€“ Neurosurgeons J. White and W. Sweet reported clinical cases and neurosurgical findings supporting ventral root pain. They noted that both the ventral nerve root and even the pia mater over the ventral cord are pain-sensitiveā€‹. In their pain mechanism writings, White & Sweet concluded that dorsal root section (rhizotomy) sometimes failed to relieve pain because some sensory fibers travel with the ventral root. By 1955, they hypothesized that ventral root afferents could explain certain otherwise puzzling pain distributions. White and Sweet advocated targeting the dorsal root ganglion or performing dorsal root ganglionectomies in intractable cases ā€“ essentially removing the cell bodies of both dorsal and any ventral root afferents ā€“ after observing that dorsal rhizotomy alone often did not cure painā€‹ā€‹.[5]

Other early researchers ā€“ Windle and Oā€™Donnell (1930s) performed anatomical studies in cats, showing that some dorsal root ganglion cells send a branch into the ventral root (the ā€œthird branchā€ of bifurcating sensory neurons)ā€‹. Foerster (1911) had noted that compressing anterior (ventral) spinal nerve elements could cause aching pain in patients with spinal root injuries, and Gagel (with Foerster in 1932) documented unmyelinated fibers in ventral root samples. Gagelā€™s histological studies suggested up to 18ā€“20% of fibers in ventral lumbosacral roots were sensory, even in that early era. By the 1940s, surgeons like Zacharides (sometimes spelled Zacharidis) also reported that ventral root manipulation during surgery caused ā€œsclerotomalā€ deep pain, lending clinical credence to the concept. In summary, a wealth of early experiments established the presence of afferent pain-conducting fibers in ventral roots and linked them to a dull, diffuse pain quality.

Post-1950s Research

Modern research has clarified ventral root afferents' existence and role.

Anatomical studies: Advanced histology and electron microscopy in the 1970s demonstrated that a significant portion of ventral root fibers are unmyelinated sensory axons. For example, a 1975 study by Coggeshall et al. found about 27% of human lumbar ventral root axons are unmyelinated, likely sensory in functionā€‹.[6]. These small fibers often contained substance P and CGRP (neuropeptides typical of nociceptors) as later shown by immunohistochemistryā€‹ā€‹.

Risling and colleagues (1980sā€“1990s) in Sweden traced many of these ventral root afferents back to dorsal root ganglion cellsā€‹.[7] Consistent with Magendieā€™s law, most ventral-root sensory fibers eventually turn and enter the spinal cord via the dorsal root entry zone (maintaining the general rule that afferents enter dorsally)ā€‹.

Willis (1980s) further confirmed ventral root afferents exist anatomically, entering the spinal cord directly via ventral roots, particularly at sacral levels, though many loop back dorsally. He noted visceral nociceptive fibres commonly traverse ventral roots, explaining persistent pelvic or visceral pain post dorsal rhizotomy. This ventral afferent input contributes substantially to visceral referred pain.[8]

In other words, ventral root afferents are essentially sensory fibers whose pathways loop back to the dorsal side near the cord. Notably, a minority of sensory neurons may even have cell bodies located aberrantly in ventral roots, but the bulk share the dorsal root ganglion originā€‹. The presence of these fibers is not an artifact of injury; they exist in normal development and even increase postnatally in some speciesā€‹. Overall, modern anatomy has robustly validated that ventral roots carry pain-conducting afferents in both animals and humans.

Electrophysiological evidence: Building on Frykholm, more refined experiments continued in animals. Electrophysiologic recordings in cats showed that stimulating dorsal roots can evoke action potentials traveling out the ventral roots ā€“ evidence of dorsal root ganglion cells with processes in both rootsā€‹.[9].

In 1977, Coggeshall et al. used horseradish peroxidase tracing to map sensory neurons with ventral root projectionsā€‹.[10] By the late 1970s, the clinical neuroscience community recognized this; a 1979 review by Coggeshall declared that ā€œthe law of separation of functionā€¦may not be entirely accurateā€ given the discovery of numerous ventral root afferentsā€‹ā€‹. He noted the clinical implication: dorsal rhizotomy often failed to relieve pain because ventral root afferents remained intactā€‹ā€‹. True to White & Sweetā€™s prediction, surgeons began to consider dorsal root ganglionectomy in refractory cases to remove both dorsal and ventral root sensory fibersā€‹. Another study in 1975 suggested that sensation ā€œalso reaches the cord through the ventral root,ā€ explaining why pain could return after cordotomy or rhizotomyā€‹ā€‹.[11]

Ventral Root Avulsion models: More recently, ventral root avulsion (VRA) models in rodents have been used to study neuropathic pain. Avulsing lumbosacral ventral roots (which injures motor neurons and any afferents in them) produces at-level neuropathic pain behaviors (allodynia in adjacent dermatomes), although some studies debate the extent of ventral afferentsā€™ contributionā€‹.[12]

Notably, Hoang and Havton (2006) showed reimplanting an avulsed ventral root (allowing afferents to reconnect to the cord) could alleviate some pain behaviors, again implicating ventral root sensory fibers in the pain generation after root injuriesā€‹.[13][14] Electrophysiologically, ventral root afferents are mostly C-fibers or thin A-delta fibersā€‹. They typically have higher thresholds and slower conduction, consistent with mediating slow, aching pain. Meanwhile, classic sharp radicular pain is linked to ectopic firing of injured dorsal root ganglion neurons or their peripheral axons (often A-delta fibers).

Imaging and neurochemical data: While standard clinical MRI cannot resolve dorsal vs ventral root fiber composition, advanced neuroimaging supports the anatomical findings. Diffusion tensor imaging (DTI) has demonstrated intact microstructural continuity of many unmyelinated fibers in ventral roots. Functional MRI (fMRI) studies specifically on radicular pain are limited, but one can infer differences: cutaneous nerve root pain (dorsal root) tends to activate primary somatosensory cortical areas with somatotopic representation, whereas deep muscle/joint pain (which could involve ventral root afferents or dorsal ramus afferents) also engages insular and limbic regions related to aching pain. Additionally, modern tract-tracing confirms that ventral root afferents often innervate the meninges and blood vessels around the cord (the nervi nervorum of the root)ā€‹.[15]

For example, small fibers leave the ventral root to innervate the pia mater and ligaments; these contain substance P/CGRP and can be sources of pain when stretched or inflamedā€‹ā€‹. Thus a compressive disc lesion might activate pain by irritating the ventral rootā€™s nervi nervorum (causing diffuse, local pain) in addition to compressing dorsal root ganglion axons (causing shooting distal pain).

Ventral Root Pain: Accepted Clinical Entity or Artifact?

Modern clinical literature tends not to explicitly mention ā€œventral root painā€ as a distinct entity, leading some to wonder if it was an artifact of older experiments. The concept is generally valid and accepted among neuroanatomists and pain researchers, but it has been deemphasized in clinical teaching for several reasons:

Integration into broader concepts: Today, radicular pain is usually described as resulting from dorsal root or dorsal root ganglion irritation. This is a simplification ā€“ effectively lumping all nerve-root-derived pain together. Because ventral root afferents ultimately join the dorsal root pathway near the cord, most sources simply attribute radicular pain to dorsal root ganglion compression (the most sensitive structure). In practice, a disc herniation compressing a spinal nerve will affect both ventral and dorsal root fibers (since they are in close proximity). Thus, rather than teaching two separate pain syndromes, textbooks say ā€œnerve root compression causes radiating neuropathic painā€ and mention it can be accompanied by motor deficits. The dual-component nature may be acknowledged (e.g. ā€œradicular pain often has a sharp component and a deep acheā€), but not explicitly linked to ventral vs. dorsal root anatomy in many sources.

Historical over-interpretation concerns: Some early clinicians may have over-attributed certain pain patterns to ventral roots when other explanations exist. For instance, deep ā€œmyalgicā€ proximal pain in radiculopathy could also result from muscle spasm or from irritation of the dorsal primary ramus. Modern studies like Mizutamari et al. (2014) found that C6ā€“C7 cervical root lesions produce deep scapular pain without cutaneous distribution, and they speculated this pain might travel via the medial branches of dorsal rami (which innervate muscles/joints) rather than via ventral root afferentsā€‹.[16]

In the lumbar spine, buttock pain in sciatica could stem from the sinuvertebral (recurrent meningeal) nerve or the dorsal ramus supplying the multifidus muscle. Thus, some authors have attributed the ā€œdeep achingā€ component to somatic referred pain from musculoskeletal structures sharing the same root level, rather than directly to the ventral root itself. This ambiguity may make clinicians less confident in labeling something ā€œventral root pain.ā€ Itā€™s worth noting, however, that those dorsal ramus and meningeal nerves themselves originate from the mixed spinal nerve, meaning they carry sensory signals from the same dorsal root ganglion ā€“ in essence another route for ā€œrecurrentā€ afferents. Whether one calls it ventral root afferent or a branch of the mixed nerve, the result is similar: a deep sclerotomal ache from nerve root irritation.

Teaching focus on dermatomes and myotomes: Medical education focuses on dermatomal maps and the Bell-Magendie law for clarity. Emphasizing that ventral roots also carry sensory fibers could confuse the basic message. Hence, most contemporary neurology texts stick to the classic rule (dorsal = sensory, ventral = motor) with an asterisk or footnote, if any, about ventral root afferents. The phenomenon is sometimes mentioned in neurosurgical contexts (e.g. for dorsal rhizotomy failures or DRG stimulation therapies) but is not highlighted in general pain management guidelines.

Despite this de-emphasis, ventral root pain is indeed a real clinical phenomenon and not an artifact. Cases of ventral root schwannoma, for example, have shown that patients can present with predominantly deep, aching pain until the tumor compresses the dorsal root properā€‹.[17]

During selective rhizotomy procedures for spasticity or pain, surgeons have noted that stimulating ventral root filaments can cause patients to report discomfort, supporting the existence of some sensory function. The lack of widespread discussion seems to be more about convenience and prevailing models of radiculopathy, rather than any repudiation by evidence. In fact, when patients with chronic radiculopathy are carefully interviewed, they often describe both sharp, radiating pain (classic neuropathic pain shooting along the limb) and dull, proximal pain in the back or shoulder. The latter is sometimes called ā€œsclerotomal painā€ or ā€œdeep referred pain.ā€ Clinically it may be indistinguishable whether this comes from ventral root afferents in the nerve root or from structures like facet joints and paraspinal muscles that share innervation. Thus, ventral root pain as a separate entity has blurred into the broader concept of radicular versus referred pain.

Implications for Current Teaching of Radicular Pain

Current evidence supports a refined understanding of radicular pain pathways: Both dorsal and ventral root contributions should be acknowledged to fully explain patientsā€™ pain patterns. Teaching can be updated as follows:

Radicular pain often has two components: a sharp, shooting pain radiating along the limb (from stimulation of dermatomal afferents in the dorsal root/dorsal root ganglion) and a deep, aching, poorly localized pain (from stimulation of non-dermatomal afferents, e.g. ventral root afferents or recurrent branches). Importantly, clinical studies confirm that radicular pain frequently is not strictly dermatomal. In a large series by Murphy et al. (2009), over 2/3 of patients with cervical or lumbar nerve root pain had pain distributions that were non-dermatomal, especially for C5ā€“C8 and L2ā€“L5 rootsā€‹.[18] Only the S1 root reliably produced true dermatomal pain in most casesā€‹.

This finding aligns with the concept that deeper structures innervated by the affected root (muscles, ligaments, periosteum via ventral rami or ventral root afferents) generate pain outside the classic skin dermatome map. Thus, educators should caution against using dermatomal patterns as the sole diagnostic criterion ā€“ it has low sensitivity/specificity for many rootsā€‹. Instead, the composite ā€œdynatomalā€ pattern (a term coined by Slipman et al. for the combined pain map) should be taughtā€‹ā€‹.

Dermatomes vs. myotomes vs. sclerotomes: The traditional dermatome maps reflect cutaneous innervation via dorsal root fibers. Myotomal innervation (motor axons to muscles) and sclerotomal innervation (to bone, fascia, dura) follow different segmental patterns. Because ventral root afferents often innervate the meninges and possibly contribute to muscle pain, radicular pain can appear to follow a ā€œsclerotomal or myotomalā€ distribution. For example, C7 nerve root compression may cause deep pain between the shoulder blades (interscapular area) corresponding to the territories of muscles/joints innervated by C7 dorsal rami, rather than the C7 dermatome on the skinā€‹. Teaching should emphasize that radicular pain referral is complex, and students should recognize proximal deep ache (e.g. scapular or buttock pain) as part of the radicular symptom complex, not dismiss it as unrelated. This also helps differentiate radicular pain from pure cutaneous neuropathy.

Dorsal Root Ganglion (DRG) emphasis: Modern teaching rightly emphasizes the DRG as a key player in radicular pain. The DRG contains the sensory neuron cell bodies and is extremely sensitive to mechanical compression and chemical inflammation. Dorsal root (or spinal nerve) compression that impacts the DRG can generate ectopic discharges (felt as shooting pain). However, instructors can integrate ventral root afferents into this narrative by explaining that some DRG neurons have dichotomous axons: one branch going out the dorsal root into the limb, another small branch looping into the ventral root or meningeal branch. Irritation of such a neuron can cause pain that radiates both along the limb and locally near the spine. This explains why, for instance, compressive radiculopathy often presents with back pain or neck pain in addition to limb pain. Rather than attributing all local spine pain to ā€œmuscle strain,ā€ it should be taught that the nerve root itself (via recurrent meningeal nerves and ventral root afferents) can produce proximal aching pain.

Clinical examination and treatment: Understanding the dual nature of radicular pain can improve clinical evaluation. For example, a patient with L5 radiculopathy might have a sharp pain down the lateral leg (dorsal root component) and a deep ache in the buttock or low back (ventral root/referred component). Both are radicular in origin. During a straight-leg raise test, the sharp leg pain might be the limiting factor, but the baseline buttock ache might indicate ongoing root irritation. In treatment, a selective nerve root block (anesthetic around the nerve root) often relieves both components ā€“ supporting that both originate from the nerve root. If only dorsal fibers carried pain, one might expect only the distal pain to improve; in practice patients often report relief of deep ache as well after an epidural or nerve block. Thus, current practitioners implicitly address ventral root pain even if they donā€™t label it as such.

Article Authors thoughts: Looking at pain referral patterns with respect to both myotomes (ventral root) and dermatomes (dorsal root) can be helpful diagnostically. For example in C7 radicular pain, the chest pain could be myotomal (e.g. pectoralis major supply includes C7, and the arm pain dermatomal). However some individuals may have more prominent ventral root than dorsal root pain, potentially delaying the correct diagnosis by confusing the uneducated clinician.

Conclusion

In conclusion, there is strong current evidence for a ventral root pain mechanism, backed by anatomical, electrophysiological, and clinical data. While modern summaries often simplify radicular pain to dorsal root irritation, a comprehensive teaching would note that some sensory fibers travel via ventral roots, contributing to the non-dermatomal, deep components of radicular pain. Recognizing this helps reconcile historical findings with present-day clinical observations and ensures that the full spectrum of radicular pain is appreciated.

Reading

Afferent fibres in the ventral root coggeshall 1979.pdf
Visceral inputs to sensory pathways in the spinal cord - willis 1986.pdf
Bernard-Claude.pdf
Sciatica and the Intervertebral Disc_An Experimental Study.pdf

References

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