disc extrusion versus enclosed disc herniation

[promethius]

So what are the implications of a disc extrusion versus an enclosed disc herniation with associated radicular pain in terms of prognosis for recovery and treatment options? I heard that radicular pain from a disc extrusion compared to that from an enclosed disc herniation is less likely to improve with physical therapy because it is difficult if not impossible to get the material to go back into the disc rather than to just get the enclosed herniated disc to go back into the disc space. Will epidural injections be equally effective for treatment of both conditions? Just curious to hear what everyone's thoughts are. Thanks!

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[willabeast]

disc extrusions heal faster than enclosed disc herniations however they usually are more painful. PT will not get a HD to go back into the disc.
the function of PT is to teach the patient how not to make the injury worse, and how to prevent another HD in the future. sending a patient to PT thinking PT will cure a HD would require quite a leap of faith. if a therapist can get the patient walking again i would applaud his or her efforts.

 

[SSdoc33]

disc extrusions heal faster than enclosed disc herniations however they usually are more painful. PT will not get a HD to go back into the disc.
the function of PT is to teach the patient how not to make the injury worse, and how to prevent another HD in the future. sending a patient to PT thinking PT will cure a HD would require quite a leap of faith. if a therapist can get the patient walking again i would applaud his or her efforts.

im not sure i agree with anything you just typed.

i dont think you can make a clear statement about protrusion vs. extrusion other than extrusions are "typically" a bit more severe.

 

[jadedphysiotherapist]

disc extrusions heal faster than enclosed disc herniations however they usually are more painful. PT will not get a HD to go back into the disc.
the function of PT is to teach the patient how not to make the injury worse, and how to prevent another HD in the future. sending a patient to PT thinking PT will cure a HD would require quite a leap of faith. if a therapist can get the patient walking again i would applaud his or her efforts.

Not quite. Management is key but there are before and after MRI pics showing disc herniation actually receding. That may be some good interdisciplinary coordination with you if some clinicians have had success with it in your surroundings area.

The difficult part is patient compliance avoiding movements that continue to exacerbate the area. There aren't general practice guidelines yet for how to maximize the receding effects that I know of currently which is why research in this area can be promising.

Best thing? Keep them away from chiropractic "spinal adjustment" as the acute pain relief can actually lead to worse neurological symptoms and disability (I have seen this)...rvus come from manip only from them as well....so it will be utilized in excess for your patients due to their reimbursement.

From what I've read, strengthening multifidi and erector spinae, neurodynamic exercise, as well as general sagittal plane exercise with progressive loading and motor control postural exercise helps well if the patient has a heavy flexion bias that has radicular pain centralize to testing.

Many of these patients have lateral trunk shifts when observing their posture due to postural compensation to avoid certain positions as well. Usually have positive straight leg and crossed straight leg raise for pain reproduction (due to central disc herniation) It's really interesting actually

Hope this was informative

 

[Aether2000]

The natural history of disc displacement is largely resolution, regardless of whether extruded or not, but by different mechanisms. Extruded discs migrate inferiorly (usually) and thin out as they go while the supply of nutrients from the annulus and nucleus pulposis have been disrupted. Extruded discs are usually larger than contained disc prolapse and the Japanese longitudinal studies reflect the relatively more rapid volumetric resolution of the larger disc herniations compared to smaller disc herniations, with a 50% resolution in size in 4 months and 11 months respectively. Non-extruded discs continue to have nutrient and oxygen supply from the nucleus pulposis, and create an inspissated fragment of physiologically active disc material lodged through the 11 lamellar layers of the posterior annulus fibrosis. Therefore, these require longer to resolve via the metalloproteinase mechanisms. Radicular pain is caused by inflammation primarily from the inflammatory disc content contacting the nerve which partially degrades the myelin. Acute compression of the nerve does not lead to radicular pain, but instead leads to numbness and weakness. This was demonstrated in awake neurosurgery during which time the nerve was cross-clamped. There was no pain, but there was instant numbness and weakness. On the other hand, chronic compression may lead to vaso nervorum venous compression and venous engorgement with subsequent intraneural edema, and more of an achy, rather than sharp or lancinating pain. Of course a synovitis adjacent to an exiting nerve may lead to neural inflammation and simultaneously with compression. For extruded discs, it is not clear to me that physiotherapy or chiropractic or traction or central disc decompression would make any difference given the anatomy. There may be some benefit from these treatments to contained disc herniations. The real kicker is how to avoid reinjury of the same area since the collagen cross bridges require so much greater time in the disc than anywhere else. Re-herniation in the absence of repair is estimated between 30 and 70%. Frequently the annulus has not sufficiently healed even though the pain has resolved, thereby giving patients a false sense of security they may go back to the same types of activities that may have caused the problem in the first place.

 

[lobelsteve]

The natural history of disc displacement is largely resolution, regardless of whether extruded or not, but by different mechanisms. Extruded discs migrate inferiorly (usually) and thin out as they go while the supply of nutrients from the annulus and nucleus pulposis have been disrupted. Extruded discs are usually larger than contained disc prolapse and the Japanese longitudinal studies reflect the relatively more rapid volumetric resolution of the larger disc herniations compared to smaller disc herniations, with a 50% resolution in size in 4 months and 11 months respectively. Non-extruded discs continue to have nutrient and oxygen supply from the nucleus pulposis, and create an inspissated fragment of physiologically active disc material lodged through the 11 lamellar layers of the posterior annulus fibrosis. Therefore, these require longer to resolve via the metalloproteinase mechanisms. Radicular pain is caused by inflammation primarily from the inflammatory disc content contacting the nerve which partially degrades the myelin. Acute compression of the nerve does not lead to radicular pain, but instead leads to numbness and weakness. This was demonstrated in awake neurosurgery during which time the nerve was cross-clamped. There was no pain, but there was instant numbness and weakness. On the other hand, chronic compression may lead to vaso nervorum venous compression and venous engorgement with subsequent intraneural edema, and more of an achy, rather than sharp or lancinating pain. Of course a synovitis adjacent to an exiting nerve may lead to neural inflammation and simultaneously with compression. For extruded discs, it is not clear to me that physiotherapy or chiropractic or traction or central disc decompression would make any difference given the anatomy. There may be some benefit from these treatments to contained disc herniations. The real kicker is how to avoid reinjury of the same area since the collagen cross bridges require so much greater time in the disc than anywhere else. Re-herniation in the absence of repair is estimated between 30 and 70%. Frequently the annulus has not sufficiently healed even though the pain has resolved, thereby giving patients a false sense of security they may go back to the same types of activities that may have caused the problem in the first place.

A, But not A+. You forgot to include "lamellae" in your answer. 😍

 

[jadedphysiotherapist]

The natural history of disc displacement is largely resolution, regardless of whether extruded or not, but by different mechanisms. Extruded discs migrate inferiorly (usually) and thin out as they go while the supply of nutrients from the annulus and nucleus pulposis have been disrupted. Extruded discs are usually larger than contained disc prolapse and the Japanese longitudinal studies reflect the relatively more rapid volumetric resolution of the larger disc herniations compared to smaller disc herniations, with a 50% resolution in size in 4 months and 11 months respectively. Non-extruded discs continue to have nutrient and oxygen supply from the nucleus pulposis, and create an inspissated fragment of physiologically active disc material lodged through the 11 lamellar layers of the posterior annulus fibrosis. Therefore, these require longer to resolve via the metalloproteinase mechanisms. Radicular pain is caused by inflammation primarily from the inflammatory disc content contacting the nerve which partially degrades the myelin. Acute compression of the nerve does not lead to radicular pain, but instead leads to numbness and weakness. This was demonstrated in awake neurosurgery during which time the nerve was cross-clamped. There was no pain, but there was instant numbness and weakness. On the other hand, chronic compression may lead to vaso nervorum venous compression and venous engorgement with subsequent intraneural edema, and more of an achy, rather than sharp or lancinating pain. Of course a synovitis adjacent to an exiting nerve may lead to neural inflammation and simultaneously with compression. For extruded discs, it is not clear to me that physiotherapy or chiropractic or traction or central disc decompression would make any difference given the anatomy. There may be some benefit from these treatments to contained disc herniations. The real kicker is how to avoid reinjury of the same area since the collagen cross bridges require so much greater time in the disc than anywhere else. Re-herniation in the absence of repair is estimated between 30 and 70%. Frequently the annulus has not sufficiently healed even though the pain has resolved, thereby giving patients a false sense of security they may go back to the same types of activities that may have caused the problem in the first place.

This was awesome.
Do you have sources for further reading on the resolution timeframes?

It also looks like subtle myotomal weakness will be what to look for on compression rather than just a reproducible pain symptom due to inflammation

 

[sloh]

Thanks for that response algosdoc. Just to add to the discussion as well

Incidence of Spontaneous Resorption of Lumbar Disc Herniation: A Meta-Analysis. - PubMed - NCBI

"The phenomenon of LDH (Lumbar Disc Herniation) reabsorption is well recognized. Because its overall incidence is now 66.66% according to our results, conservative treatment may become the first choice of treatment for LDH. More large-scale, double-blinded, randomized, controlled trials are necessary to study the phenomenon of spontaneous resorption of LDH."

 

[Aether2000]

http://www.josonline.org/pdf/v9i1p1.pdf

 

[jadedphysiotherapist]

http://www.josonline.org/pdf/v9i1p1.pdf

So I had seen before and after pics showing healing but what's unnerving is that the sensorimotor changes may be there to stay.....and if the pain stimulus dissipates from the initial inflammation, then habits may continue to lead to sensorimotor change and new complaints of "oh my leg has just never been as strong but gee my back pain is gone" from the patient.

Thanks for the share and the general healing timeframes you stated.

I wonder how this will affect spine, pm&r, ipm, and physical therapy more in the future

 

[ampaphb]

The natural history of disc displacement is largely resolution, regardless of whether extruded or not, but by different mechanisms. Extruded discs migrate inferiorly (usually) and thin out as they go while the supply of nutrients from the annulus and nucleus pulposis have been disrupted. Extruded discs are usually larger than contained disc prolapse and the Japanese longitudinal studies reflect the relatively more rapid volumetric resolution of the larger disc herniations compared to smaller disc herniations, with a 50% resolution in size in 4 months and 11 months respectively. Non-extruded discs continue to have nutrient and oxygen supply from the nucleus pulposis, and create an inspissated fragment of physiologically active disc material lodged through the 11 lamellar layers of the posterior annulus fibrosis. Therefore, these require longer to resolve via the metalloproteinase mechanisms. Radicular pain is caused by inflammation primarily from the inflammatory disc content contacting the nerve which partially degrades the myelin. Acute compression of the nerve does not lead to radicular pain, but instead leads to numbness and weakness. This was demonstrated in awake neurosurgery during which time the nerve was cross-clamped. There was no pain, but there was instant numbness and weakness. On the other hand, chronic compression may lead to vaso nervorum venous compression and venous engorgement with subsequent intraneural edema, and more of an achy, rather than sharp or lancinating pain. Of course a synovitis adjacent to an exiting nerve may lead to neural inflammation and simultaneously with compression. For extruded discs, it is not clear to me that physiotherapy or chiropractic or traction or central disc decompression would make any difference given the anatomy. There may be some benefit from these treatments to contained disc herniations. The real kicker is how to avoid reinjury of the same area since the collagen cross bridges require so much greater time in the disc than anywhere else. Re-herniation in the absence of repair is estimated between 30 and 70%. Frequently the annulus has not sufficiently healed even though the pain has resolved, thereby giving patients a false sense of security they may go back to the same types of activities that may have caused the problem in the first place.

Algos has stated a couple of dogmatic points that run contrary to accepted axioms.

Healthy discs have only minimal blood supply. Feeder vessels arising from the spinal artery recede out of the disc in infancy, and the normal adult disc is relatively avascular, relying on diffusion for a supply of nutrients. Nerve fibers in the disc are largely confined to the outer layers of the annulus fibrosus. Discs are enervated by branches of the recurrent sinuvertebral nerves, which arise in the drg. An injured disc develops radial fissures. The proinflammatory nuclear material leaks out, leading to an inflammatory response. As the injury heals, the healing process is accompanied by new vessel formation, or neovascularization within the annulus or endplate..Sensory nerve endings spread into the inner layers ofthe annulus and the endplate.

 

[Aether2000]

I did not discuss blood supply. I discussed nutrient supply to the disc herniations. The nutrient supply to the nucleus pulposis of the disc is via the endplate (primarily superior), and does not arise from blood vessels. I agree with everything ampaphb contends about the healing of the residual disc within the confines of the annulus fibrosis.

 

[ampaphb]

A herniation receives nutrients via the ingrowth of blood vessels through the process of neovascularization. There is an argument that the disc itself can hurt after being injured, secondary to the ingrowth of nascent nerve fibers

 

[ampaphb]

Additionally, Howe, Loeser, and Calvin Demonstrated mechanosensitivity in animals (which included pain) when the DRG was squeezed. (Pain1977; 3:25-41). Norton showed the same in humans in Acta Chir Scandinav 1944; Supp 95:1-96. Smyth and Wright showed stretching the DRG and nerve root also produced pain (JBJS 1959; 40A:1401-1418.

This all comes from Dr. Bogduk's powerpont presentation entitled Lumbar Radicular Pain

 

[Aether2000]

The DRG is not mechanically involved in the vast majority of disc herniations since they are paracentral, far removed anatomically from the DRG. The DRG does have some increase in sensitivity. But most disc herniations produce radicular pain from inflammatory substances.

Spine (Phila Pa 1976). 1993 Sep 1;18(11):1425-32.
Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots.
Olmarker K1, Rydevik B, Nordborg C.
Author information

Abstract
Epidural application of autologous nucleus pulposus in pigs, without mechanical nerve root compression, induced a pronounced reduction in nerve conduction velocity in the cauda equina nerve roots after 1-7 days, compared to epidural application of retroperitoneal fat in control experiments. Histologically, the nerve fiber injury was more pronounced after application of nucleus pulposus than after control tissue application. The results demonstrate that nucleus pulposus may induce nerve tissue injury by mechanisms other than mechanical compression. Such mechanisms may be based on direct biochemical effects of nucleus pulposus components on nerve fiber structure and function and microvascular changes including inflammatory reactions in the nerve roots.

There is neurovascular growth within both injured central discs and within disc herniations but the vessels are microscopic, and the primary nutrient supply has not been demonstrated to arise from these microvascular ingrowths in disc herniations.

 

[ampaphb]

What you said was "Acute compression of the nerve does not lead to radicular pain, but instead leads to numbness and weakness." I was addressing that. I completely agree that most radicular pain is chemically mediated.

 

[Aether2000]

Ok. Thanks. As we understand the growth factors within the disc, it gets even more complex. There are differences in the expression of the growth factors in prolapsed vs extruded discs.... The plot thickens!

Mol Med Rep. 2017 Apr;15(4):2195-2203. doi: 10.3892/mmr.2017.6221. Epub 2017 Feb 20.
Molecular profile of major growth factors in lumbar intervertebral disc herniation: Correlation with patient clinical and epidemiological characteristics.
Tsarouhas A1, Soufla G1, Tsarouhas K2, Katonis P3, Pasku D1, Vakis A4, Tsatsakis AM5, Spandidos DA1.
Author information

Abstract
The involvement of growth factors (GFs) in the pathogenesis of lumbar intervertebral disc (ID) herniation and the spontaneous resorption of herniated ID fragments remains only partially elucidated. A simultaneous assessment of the transcript levels of numerous GFs and their association with clinical and epidemiological profiles of human ID herniation would provide valuable insight into the biology and clinical course of the disease. In the present study, we examined simultaneously the transcript levels of vascular endothelial growth factor (VEGF), transforming growth factor β1 (TGF‑β1), basic fibroblast growth factor 2 (bFGF2), platelet derived growth factor (PDGF) isoforms and receptors, epidermal growth factor (EGF) and insulin growth factor‑1 (IGF‑1) in herniated and control ID specimens and investigated their correlation with the clinicopathological profiles of patients suffering from symptomatic lumbar ID herniation. GF mRNA expression levels were determined by RT-qPCR in 63 surgical specimens from lumbar herniated discs and 10 control ID specimens. Multiple positive correlations were observed between the transcript levels of the GFs examined in the ID herniation group. VEGF mRNA expression was significantly increased in the protruding compared with the extruded discs. Intense and acute pain significantly upregulated the PDGF transcript levels. Significant negative correlations were observed between the patient body mass index and the transcript levels of VEGF and PDGF receptors. Our findings support the hypothesis of the involvement of GFs in the natural history of ID herniation. GFs synergistically act in herniated IDs. Increased VEGF expression possibly induces the neovascularization process in the earliest stages of ID herniation. PDGF‑C and ‑D play a role in the acute phase of radiculopathy in a metabolic response for tissue healing. A molecular effect, in addition to the biomechanical effect of obesity in the pathogenesis of ID herniation is also implied.

 

[ampaphb]

Let's not forget

Genet Mol Res. 2016 Sep 9;15(3). doi: 10.4238/gmr.15038669.
Effects of MMP-1 and MMP-3 gene polymorphisms on gene expression and protein level inlumbar disc herniation.
Eser B1, Eser O2, Yuksel Y3, Aksit H4, Karavelioglu E5, Tosun M3, Sekerci Z6.
Author information

Abstract
The aim of this study was to identify the possible correlation between polymorphisms in matrix metalloproteinase (MMP)-1 and MMP-3 and their corresponding protein levels in disc tissues obtained from patients with lumbar disc herniation (LDH) using biochemical and immunohistochemical analyses. Blood and disc samples were obtained from 100 patients with LDH who underwent a lumbarmicrodiscectomy. Based on the radiological degeneration, the patients were diagnosed with grade 2, 3, or 4 LDH. MMP-1 -1607 1G/2G and MMP-3 -1171 5A/6A were analyzed by real-time polymerase chain reaction. The expressions of MMP-1 and MMP- 3 were detected by biochemical and immunohistochemical analyses. We found no association between the MMP-1 polymorphism and discdegeneration and MMP-1 expression. However, patients expressing the 6A/6A and 5A/6A alleles of MMP-3 -11715A/6A showed higher MMP-3 expression, compared to those expressing the 5A/5A genotype. Additionally, the radiological degeneration grades were correlated with the histological degeneration scoring. Protein levels and immunopositive cell rates of MMP-1 and MMP-3 were associated with disc degeneration grades. Moreover, the MMP-1 and MMP-3 expression and the histological and radiological scores were positively correlated and the MMP-3 -11715A/6A polymorphism was associated with MMP-3 expression in herniated disc tissues. This study is the first to investigate polymorphisms in MMP-1 and MMP-3, as well as their corresponding protein expressions. We also quantified an association between the radiological degeneration grades and MMP-1 and MMP- 3 expression. Further genomic studies on MMPs could focus on the utilization of MMP-1 and MMP-3 as markers for the prevention and treatment of this disease.
PMID: 27706715


J Orthop Surg Res. 2016 Jan 16;11:12. doi: 10.1186/s13018-016-0343-8.
Interleukin-23 may contribute to the pathogenesis of lumbar disc herniation through the IL-23/IL-17 pathway.
Jiang H1, Deng Y2, Wang T3, Ma J4, Li P5, Tian P6, Han C7, Ma X8,9.
Author information

Abstract
BACKGROUND:
Studies have indicated that interleukin 23 (IL-23) plays an important role in many inflammatory- and autoimmune-related diseases. However, there is little knowledge about IL-23 in lumbar disc herniation (LDH). Thus, in this study, we aimed to find out whether IL-23 is expressed in intervertebral discs (IVDs) and what roles it may play.

METHODS:
Human IVD tissues were collected from 29 LDH patients and 8 vertebral fracture patients (normal control, NC group). According to the integrity of annulus fibrosus, LDH patients were divided into two groups: R group (ruptured group, n = 16) and NR group (non-ruptured group, n = 13). Morphological changes of IVDs were assessed by hematoxylin and eosin (HE staining), and expression of IL-23 in IVD tissues was detected by immunohistochemical staining. Besides gene expression of IL-23, IL-17, IL-6, IL-1β, and TNF-α was also evaluated by reverse transcription polymerase chain reaction (RT-PCR).

RESULTS:
The results showed that the R group was more degenerated than the other two groups and NC group showed the least degenerated performance; stronger positive IL-23 expression was observed in herniated IVDs, especially in the R group. Meanwhile, higher gene expression of IL-23, IL-17, IL-6, IL-1β, and TNF-α was found in the tissues from LDH patients and a positive correlation between IL-17 and IL-23 gene expression was also observed.

CONCLUSIONS:
Taken all above results together, it may be deduced that higher expression of IL-23 may contribute to the deterioration of IVDs through the IL-23/IL-17 pathway.
PMID: 26774625


Arthritis Res Ther. 2016 Jan 7;18:3. doi: 10.1186/s13075-015-0887-8.
Serum levels of the proinflammatory cytokine interleukin-6 vary based on diagnoses in individuals with lumbar intervertebral disc diseases.
Weber KT1, Alipui DO2, Sison CP3,4,5, Bloom O6,7,8, Quraishi S9,10, Overby MC11, Levine M12, Chahine NO13,14,15,16.
Author information

Abstract
BACKGROUND:
Many intervertebral disc diseases cause low back pain (LBP). Proinflammatory cytokines and matrix metalloproteinases (MMPs) participate in disc pathology. In this study, we examined levels of serum cytokines and MMPs in human subjects with diagnoses of disc herniation (DH), spinal stenosis (SS), or degenerative disc disease (DDD) relative to levels in control subjects. Comparison between subjects with DH and those with other diagnoses (Other Dx, grouped from SS and DDD) was performed to elaborate a pathological mechanism based on circulating cytokine levels.

METHODS:
Study participants were recruited from a spine neurosurgery practice (n = 80), a back pain management practice (n = 27), or a control cohort (n = 26). Serum samples were collected before treatment and were assayed by multiplex assays for levels of interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, interferon-γ, tumor necrosis factor-α, MMP-1, MMP-3, and MMP-9. Inflammatory and degradative mediator levels were compared for subjects with LBP and control subjects, by diagnosis and by treatment groups, controlling for effects of sex, age, and reported history of osteoarthritis. Spearman's correlation coefficient was used to examine relationships with age, body mass index (BMI), symptom duration, and smoking history.

RESULTS:
Serum levels of IL-6 were significantly higher in subjects with LBP compared with control subjects. Participants with LBP due to Other Dx had significantly higher levels of IL-6 than DH and controls. Serum levels of MMP-1 were significantly lower in LBP subjects, specifically those with DH, than in control subjects. Positive correlations were found between IL-6 levels and BMI, symptom duration, and age. MMP-1 levels were positively correlated with age.

CONCLUSIONS:
The findings of the present clinical study are the results of the first examination of circulating cytokine levels in DDD and SS and provide evidence for a more extensive role of IL-6 in disc diseases, where patients with DDD or SS have higher serum cytokine levels than those with DH or control subjects. These findings suggest that LBP subjects have low-grade systemic inflammation, and biochemical profiling of circulating cytokines may assist in refining personalized diagnoses of disc diseases.
PMID: 26743937