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Radicular Pain and Radiculopathy

From WikiMSK

Written by: Dr Jeremy Steinberg ā€“ created: 5 September 2021; last modified: 13 April 2025

This article is still missing information.

Radicular pain is commonly confused with radiculopathy, and also with somatic referred pain. This article should be read in conjunction with that on referred pain.

Descriptions

Radicular Pain

Definition
Radicular Pain
Pain perceived as arising in a limb or the trunk wall caused by ectopic activation of nociceptive afferent fibers in a spinal nerve or its roots or other neuropathic mechanisms

Radicular pain is a subset of neuropathic pain, and refers to pain that is evoked with stimulation of the dorsal root or dorsal root ganglion of a spinal nerve - i.e. the peripheral axons or cell bodies rather than the peripheral nerve endings as occurs with nociceptive pain. In radicular pain, the pain is felt in the peripheral innervation of the affected nerve. Therefore it is a form of referred pain, but doesn't involve the convergence mechanism. The pain is felt in the periphery because of stimulation to the nerve proximal to the peripheral distribution. The older now obsolete term for neuropathic pain was "neurogenic pain."

Various authors commonly confuse radicular pain distributions with dermatomes, and also confuse somatic referred pain with dermatomes. There is in fact no good correlation between dermatomes and radicular pain patterns (sometimes called dynatomes), or somatic referred pain and dermatomes. If anything, radicular pain patterns tend to follow myotomal distributions of innervation more than a dermatomal distribution.

Notably, it is not possible to differentiate between L4, L5, and S1 lumbar radicular pain patterns alone.[1] A segmental diagnosis can only be made with some accuracy in combination with radiculopathy. In the cervical spine there are some differences between nerve dynatomes found in a derivation study.[2] This is especially true of non-adjacent dynatomes, however there is a lot of overlap and the maps hasn't been externally validated as a way of localising the segment.

It is this authors opinion that radicular pain should viewed as the pain perceived in the distribution of a specific spinal nerve root that follows any combination of its dermatome (skin), myotome (muscle), and sclerotome (other deep structures).

Radiculopathy

Definition
Radiculopathy
Objective loss of sensory and/or motor function as a result of conduction block in axons of a spinal nerve or its roots.

Radiculopathy is commonly confused with radicular pain. Radiculopathy is distinct, it is not defined by pain, but rather refers to conduction block along a spinal nerve or its roots with some combination of weakness, numbness, and hyporeflexia. With sensory fibre block numbness develops in a dermatomal distribution. With motor fibre block weakness develops in a myotomal distribution. Reduced reflexes can occur through either sensory or motor blockade.

Some level of localisation can be made with patterns of radiculopathy, especially with motor and reflex changes. In the presence of pure sensory changes differentiation between adjacent segments can't be achieved in the cervical spine[3]; but may be variably possible in the lumbar spine.[4]

While it is true that muscles receive innervation from more than one spinal nerve root, sufficient injury to one root usually still causes significant loss of power. There are two characteristics of the motor findings in radiculopathy[5]

  1. Weakness affects two or more muscles from the same spinal segment but different peripheral nerves. For example C6 radiculopathy can affect muscles supplied by the musculocutaneous nerve and the radial nerve. (all the muscles down the C6 column in the myotome chart)
  2. There may be weakness of muscles supplied by the proximal nerves (i.e. dorsal scapular, suprascapular, axillary, long thoracic). Proximal nerves originate from the nerve roots but quickly innervate the shoulder muscles, and move away from the course that the peripheral nerves of the arm travel. If there is weakness of both proximal muscles and distal muscles then the lesion is near the nerve roots. For example, a C7 radiculopathy can cause both scapular winging (weak serratus anterior, long thoracic nerve) and triceps weakness. The serratus anterior weakness helps localise the lesion proximal to the radial nerve or brachial plexus.

Pain Patterns

Distinguishing Somatic Referred From Radicular Pain

The following table can serve as a guide in differentiating somatic referred from radicular pain.

Note, burning is not a helpful differentiating descriptor in lumbar radicular pain.[6]

It is important to note that patients may have a combined state, experiencing both somatic referred and radicular pain.

In low back pain some patients may get pain that seems to spread to the buttocks. The buttocks and lumbosacral spine are both innervated by spinal nerves L4, L5, and S1. However the lumbar spine is innervated by the dorsal rami, while the buttock is innervated by the ventral rami (superior and inferior gluteal nerves, sensory branches). A prolapsed disc may irritate the dura of the nerve root (somatic) as well as the nerve root itself (radicular).

Somatic Referred vs Radicular Pain[7]
Somatic Referred Radicular
Primary Source Bone, periosteum, ligament, joint capsule, fascia, disc annulus Dorsal nerve root / Dorsal Root Ganglion (DRG)
Pain quality Dull, deep ache, or pressure-like, perhaps like an expanding pressure Shooting, lancinating, or electric-shocks
Relation to back pain Referred pain is always concurrent with back pain. If the back pain ceases then so does the referred pain. If the back pain flares then so does the leg pain intensity and spatial spread. Not always concurrent with back pain.
Distribution Anywhere in the lower limb, fixed in location, commonly in the buttock or proximal thigh. Spread of pain distal to the knee can occur when severe even to the foot, and it can skip regions such as the thigh. It can feel like an expanding pressure into the lower limb, but remains in location once established without traveling. It can wax and wane, but does so in the same location. Entire length of lower limb, but below knee > above knee. In mild cases the pain may be restricted proximally.
Pattern Felt in a wide area, with difficult to perceive boundaries, often demonstrated with an open hand rather than pointing finger. The centres in contrast can be confidently indicated. Travels along a narrow band no more than 5-8 cm wide in a quasi-segmental fashion but not related to dermatomes (dynatomal).
Depth Deep only, lacks any cutaneous quality Deep as well as superficial
Neurological signs Not characteristic Favours radicular pain, but not required.
Neuroanatomical basis Discharge of the peripheral nerve endings of AĪ“ and C fibres from the lower back converge onto second order neurons in the dorsal horn that also receive input from from the lower limb, and so the frontal lobe has no way of knowing where the pain came from. Heterotopic discharge of AĪ“, AĪ², and C fibres through stimulation of a dorsal root or dorsal root ganglion of a spinal nerve, typically in the presence of inflammation, with pain being felt in the peripheral innervation of the affected nerve

Ventral vs Dorsal Root Pain

Main article: Pain from Ventral Root Afferents

There may be a distinct pain pattern arising from the "wrong way" unmyelinated afferents in the ventral root (see section below). This is a type of somatic referred pain.

Classically, radicular pain has been described as having two components. Dorsal root irritation (involving the dorsal root ganglion sensory fibers) produces the well-known ā€œelectric,ā€ shooting pain radiating along the limb in a band. Ventral root involvement can produce an additional deep, aching pain that is felt proximally (e.g. in the low back, buttock, or scapular region) rather than distally. [8]

This proximal pain is diffuse and ā€œmyalgic,ā€ and in cervical radiculopathy it may localize to the interscapular or scapular area (sometimes termed a sclerotomal pain pattern). Historic experiments showed that stimulating ventral nerve roots in awake patients evoked aching pain, confirming that ventral roots do contain afferent (sensory) fibers.[9]

Modern anatomical studies have verified that up to 20ā€“30% of fibers in human ventral roots are unmyelinated pain-conducting axons.[10] These ā€œventral root afferentsā€ usually originate from the dorsal root ganglion and loop into the ventral root, innervating meninges, blood vessels, and other deep structures.[11]

Consequently, a compressed spinal nerve root can generate both a band-like dermatomal pain (via dorsal root fibers) and a non-dermatomal deep pain (via ventral root or recurrent meningeal fibers). Clinically, this explains why radicular pain often does not strictly follow dermatomes ā€“ studies show that in the majority of cases, patientsā€™ pain maps extend outside the textbook dermatomal zones.

Instead, radicular pain should be viewed as a combination of neuropathic pain traveling along the nerveā€™s distal distribution and a dull ache in the segmental region of the spine. Both components result from nerve root irritation. Importantly, the presence of proximal deep pain (for example, shoulder blade and chest pain in C7 radiculopathy or buttock pain in S1 radiculopathy) does not exclude a radicular diagnosis; rather it is a common feature.[12]

This has practical implications: treatments like selective nerve root blocks may temporarily alleviate both the shooting limb pain and the proximal ache, further supporting their common origin in the affected nerve root.

Mechanisms

In animal studies, squeezing a lumbar dorsal root only elicits a momentary burst of activity in AĪ“ and C fibres. However, squeezing a lumbar dorsal root ganglion elicits a sustained but temporary response in all fibres i.e. AĪ², AĪ“, and C fibres. For sustained activity to occur in squeezing a dorsal root, the root must be previously injured and inflamed. In the presence of an inflamed nerve root there is heterotopic activity in all fibres: AĪ², AĪ“, and C fibres, like with squeezing a non-inflamed DRG.[13]

Human studies have found similar results. Squeezing or pulling normal nerve roots doesn't cause radicular pain, pain only occurs if they are inflamed. The DRG compression findings in animals haven't been attempted in humans. The human studies have found further qualitative features of the pain that has contributed to our understanding such as it being lancinating and traveling in a band no more than 2-3 inches wide.[14][15][16]

The AĪ² involvement in inflamed nerve roots means that radicular pain is not exactly pure "nociception," and this is probably where the qualitative in the experienced pain differences lie compared to simple nociceptive pain.

The inflammatory soup contains a variety of cells, neuropeptides, and cytokines. Macrophages, lymphocytes, and fibroblasts attend the scene. There is the production of nitric oxide, prostaglandin A2 and E2, TNFĪ±, interleukins 8 and 12, leukotriene B4, thromboxane, interferon Ī³, metalloproteinases, and immunoglobulins. This leads to the generation of action potentials and pain propagation.

There are no equivalent data for cervical radicular pain. Apply a sufficiently strong stimulus to a normal dorsal nerve root leads to peripheral radiation of pain. While gentle stimulation of dorsal roots that have already been compressed causes pain and paraesthesia. Herniated cervical discs produce nitric oxide, metalloproteinases, interleukin-6, and prostaglandin E2.

One study showed that applying a sufficiently strong stimulus to a normal dorsal nerve root is always followed by a peripheral radiation of pain; but gentle stimulation of dorsal roots previously affected by compressive lesions, evoked a sensation of pain or paraesthesia.[17] Herniated cervical intervertebral discs have been shown to produce nitric oxide, metalloproteinases, interleukin-6 and prostaglandin E2[18]

Aetiology

Studies often confuse the definitions of radicular pain and radiculopathy and so this clouds the picture as to any potentially differing causes.

Disc herniation is the cause in 98% of cases. The remaining 2% is made up of a large number of other causes which include the various causes of foraminal stenosis, epidural disorders, meningeal disorders, and neurological disorders. See Lumbar Radicular Pain

Treatment

Treatment for lumbar radicular pain has included intramuscular steroids, caudal epidural steroids, interlaminar epidural steroids, transforaminal steroids, conservative therapy, and microdiscectomy. (See Lumbar Radicular Pain)

Treatment for cervical radicular pain has included conservative therapy, transforaminal steroids, and surgery. (See Cervical Radicular Pain)

Reading

On_the_definitions_and_physiology_of_back_pain,_referred_pain,_and_radicular_pain_-_Bogduk_2009.pdf
Sciatica and the Intervertebral Disc_An Experimental Study.pdf

See Also

References

  1. ā†‘ Furman MB, Johnson SC. Induced lumbosacral radicular symptom referral patterns: a descriptive study. Spine J. 2019 Jan;19(1):163-170. doi: 10.1016/j.spinee.2018.05.029. Epub 2018 May 22. PMID: 29800710.
  2. ā†‘ Slipman CW, Plastaras CT, Palmitier RA, Huston CW, Sterenfeld EB. Symptom provocation of fluoroscopically guided cervical nerve root stimulation. Are dynatomal maps identical to dermatomal maps? Spine (Phila Pa 1976). 1998 Oct 15;23(20):2235-42. doi: 10.1097/00007632-199810150-00019. PMID: 9802168.
  3. ā†‘ Rainville J, Laxer E, Keel J, Pena E, Kim D, Milam RA, Carkner E. Exploration of sensory impairments associated with C6 and C7 radiculopathies. Spine J. 2016 Jan 1;16(1):49-54. doi: 10.1016/j.spinee.2015.07.462. Epub 2015 Aug 4. PMID: 26253986.
  4. ā†‘ Nitta H, Tajima T, Sugiyama H, Moriyama A. Study on dermatomes by means of selective lumbar spinal nerve block. Spine (Phila Pa 1976). 1993 Oct 1;18(13):1782-6. doi: 10.1097/00007632-199310000-00011. PMID: 8235861.
  5. ā†‘ McGee, Steven R. Evidence-based physical diagnosis. Philadelphia, PA: Elsevier, 2018.
  6. ā†‘ Scholz J, Mannion RJ, Hord DE, Griffin RS, Rawal B, Zheng H, Scoffings D, Phillips A, Guo J, Laing RJ, Abdi S, Decosterd I, Woolf CJ. A novel tool for the assessment of pain: validation in low back pain. PLoS Med. 2009 Apr 7;6(4):e1000047. doi: 10.1371/journal.pmed.1000047. Epub 2009 Apr 7. PMID: 19360087; PMCID: PMC2661253.
  7. ā†‘ Bogduk et al. Medical Management of Acute and Chronic Low Back Pain: An Evidence Based Approach. Elsevier Science. 2002
  8. ā†‘ SMYTH, M. J.; WRIGHT, V. (1958-12). "Sciatica and the Intervertebral Disc". The Journal of Bone & Joint Surgery. 40 (6): 1401ā€“1418. doi:10.2106/00004623-195840060-00016. ISSN 0021-9355. Check date values in: |date= (help)
  9. ā†‘ Frykholm, R.,Hyde, J., Norlen, G. and Skoglund, C. R. (1953) On pain sensations produced by stimulation of ventral roots in man. Acta Physiol. Scand., 29 (suppl. 106): 455469.
  10. ā†‘ Coggeshall, R. E.; Applebaum, M. L.; Fazen, M.; Stubbs, T. B.; Sykes, M. T. (1975). "UNMYELINATED AXONS IN HUMAN VENTRAL ROOTS, A POSSIBLE EXPLANATION FOR THE FAILURE OF DORSAL RHIZOTOMY TO RELIEVE PAIN". Brain (in English). 98 (1): 157ā€“166. doi:10.1093/brain/98.1.157. ISSN 0006-8950.
  11. ā†‘ Risling, M.; Dalsgaard, C.ā€J.; FrisĆ©n, J.; Sjƶgren, A.ā€M.; Fried, K. (1994-01-15). "Substance Pā€, calcitonin geneā€related peptide, growthā€associated proteinā€43, and neurotrophin receptorā€like immunoreactivity associated with unmyelinated axons in feline ventral roots and pia mater". Journal of Comparative Neurology (in English). 339 (3): 365ā€“386. doi:10.1002/cne.903390306. ISSN 0021-9967.
  12. ā†‘ Slipman, Curtis W.; Plastaras, Christopher T.; Palmitier, Randal A.; Huston, Christopher W.; Sterenfeld, Elliot B. (1998-10). "Symptom Provocation of Fluoroscopically Guided Cervical Nerve Root Stimulation". Spine. 23 (20): 2235ā€“2242. doi:10.1097/00007632-199810150-00019. ISSN 0362-2436. Check date values in: |date= (help)
  13. ā†‘ Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain. 1977 Feb;3(1):25-41. doi: 10.1016/0304-3959(77)90033-1. PMID: 195255.
  14. ā†‘ Norlen G. On the value of the neurological symptoms in sciatica for the localization of a lumbar disc herniation; a contribution to the problem of the surgical treatment of sciatica. Stockholm 1944.
  15. ā†‘ McCulloch JA, Waddell G. Variation of the lumbosacral myotomes with bony segmental anomalies. J Bone Joint Surg 1980; 62B:475-480. DOI. Full Text.
  16. ā†‘ SMYTH MJ, WRIGHT V. Sciatica and the intervertebral disc; an experimental study. J Bone Joint Surg Am. 1958 Dec;40-A(6):1401-18. PMID: 13610969.
  17. ā†‘ FRYKHOLM R. Lower cervical vertebrae and intervertebral discs; surgical anatomy and pathology. Acta Chir Scand. 1951;101(5):345-59. PMID: 14868335.
  18. ā†‘ Kang JD, Georgescu HI, McIntyre-Larkin L, Stefanovic-Racic M, Evans CH. Herniated cervical intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine (Phila Pa 1976). 1995 Nov 15;20(22):2373-8. doi: 10.1097/00007632-199511001-00001. PMID: 8578386.

Literature Review

Literature Review

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