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Interspinous Oedema

From WikiMSK

Written by: Dr Jeremy Steinberg, Dr Mike Cleary; peer reviewer: Dr Mike Cleary ā€“ created: 5 October 2020; last modified: 11 April 2025

This page or section deals with a topic that is not widely recognised or accepted.
Please use your clinical judgement and note that this is not necessarily standard practice in NZ.
Median sagittal section of two lumbar vertebrae and their ligaments. High signal intensity (oedema) can occur in the interspinous space (between spinous processes).
Interspinous Oedema
Definition Pain potentially arising from pathology, including inflammation and/or oedema (seen as high signal intensity on MRI), within the interspinous space.
Epidemiology Common incidental finding, especially with age. Symptomatic prevalence estimated around 12% in one MSK clinic audit based on injection response. Further research required.
Causes Trauma (e.g., lifting, falls), Degenerative changes (potentially leading to Baastrup's disease), Rheumatological conditions (e.g., PMR, RA).
Clinical Features Highly variable. May include midline pain, worse with extension, relieved by flexion, tenderness over the interspinous space. In traumatic cases: often definite link to inciting event, severe pain impacting function/sleep.
Tests MRI (fluid-sensitive, fat-suppressed sequences like STIR, T2-FS), Clinical correlation, Diagnostic image-guided local anaesthetic injection into the interspinous space.
Treatment Conservative management (physiotherapy, NSAIDs), Image-guided interspinous space corticosteroid +/- local anaesthetic injection. Surgery reserved for refractory cases (e.g., Baastrup's).

Interspinous high signal intensity is a finding seen on fluid-sensitive magnetic resonance imaging (MRI) sequences, such as Short Tau Inversion Recovery (STIR) or T2-weighted fat-suppressed (T2-FS) images.[1] This signal alteration, often interpreted as interspinous oedema or inflammation, can reflect changes within the interspinous ligament (ISL), associated bursae (interspinous bursitis), or surrounding soft tissues. The terminology often overlaps significantly with the imaging features seen in Baastrup's disease ("kissing spines").[2] As advanced MRI sequences utilizing fat suppression have become more commonplace, there has been improved visualisation and detection of these subtle changes in the posterior spinal elements.[1]

This finding is typically seen in the lumbar spine but also occurs in the cervical spine. While implicated as a potential source of mechanical low back pain (LBP),[2] its clinical significance is debated. A clear correlation with LBP is not consistently established, as high signal intensity is frequently found in asymptomatic individuals, particularly with increasing age.[1][3] This highlights the challenge of differentiating clinically relevant findings from incidental changes. Recent evidence suggests a link between ISL high signal and segmental instability, especially in degenerative lumbar spondylolisthesis.[4]

Anatomy

There are several soft tissue structures located in the posterior aspect of the lumbar spines. Namely, the multifidi muscles, interspinalis muscles, interspinous ligaments, and fat.

There are a variable number of bursal cavities located between the spinous processes of the cervical and lumbar segments in the interspinal ligaments. Bursal cavities are more common with increasing age, with L3/4 and L4/5 being most common. The interspinous ligament is thin centrally and undergoes fatty degeneration and cavitation in the sixth decade.[5]

Interspinous ligament

The ISL is a complex structure between adjacent spinous processes, extending from the ligamentum flavum anteriorly towards the supraspinous ligament/fascia posteriorly. It is composed of ventral, middle, and dorsal parts.[6] Descriptions of fiber orientation vary: classical descriptions suggest posterocranial fibers,[7] while recent studies report orientations ranging from horizontal[8] to variable depending on the level (postero-cranial superiorly, horizontal centrally, vertical inferiorly).[9] Biomechanically, the ISL offers relatively little resistance to spinous process separation in flexion compared to other spinal structures, with tensile strength decreasing at lower lumbar levels.[8]

Viewed anteriorly but not posteriorly, there are two interspinous ligaments that are separated by fat. The interspinous ligaments provide little resistance to spinous process separation with forward flexion.

Supraspinous ligament

The supraspinous ligament is not a true ligament, but rather largely consists of tendinous fibres from the back muscles, and is only well developed at the upper lumbar levels. It's caudal extent is variable. It terminates at L3 in 22%, L4 in 73%, bridges L4-5 in 5%, and is routinely absent at L5-S1.

The anatomical discontinuity or modification of the posterior ligamentous complex at the most commonly affected levels provides a structural basis for increased vulnerability. The absence of a robust SSL, combined with the inherently greater mobility of the L4-S1 segments, may mean that forces generated during movement, muscle contraction, or unexpected loading are less effectively distributed and become more concentrated on the remaining ISL and the fascial/tendinous attachments.

The superficial layer is collagenous and thought to represent superficial fascial condensation, and anchors the skin to the thoracolumbar fascia. It provides little resistance to spinous process separation. The middle layer consists of intertwining fibres of the thoracolumbar fascia and the aponeurosis of longissimus thoracis. The deep layer consists of strong tendinous fibres from the aponeurosis of longissimus thoracis. The tendons aggregate in a parallel manner towards the spinous processes, creating the impression of a ligament.

At the caudal levels of L4 and L5 there are only oblique fibres of the thoracolumbar fascia that intersect over the spinous processes and fuse with the aponeurosis of the longissimus thoracic that attach to the spinous processes.[10]

Relationship with Muscles

The ISL/SSL complex is intimately related to the surrounding musculature. Fibers from the multifidus muscle and erector spinae muscles attach directly into or blend with these ligaments and the associated thoracolumbar fascia.[10] Contraction of these muscles, especially forceful or unexpected co-contraction, could exert significant tensile stress on the intervening ligamentous and fascial tissues, potentially concentrating forces at their attachments on the spinous processes due to anatomical disparities (e.g., broad multifidus origin vs. focused insertion).

Innervation

The ISL, SSL, periosteum of the spinous processes, and associated thoracolumbar fascia are innervated primarily by the medial branches of the lumbar dorsal rami ā€“ the same nerves that supply the facet joints.[10] These structures contain nerve endings, including nociceptors, making them potential sources of pain.[8] Crucially, the thoracolumbar fascia is now recognized as a densely innervated structure with significant sensory functions.[11] Histological studies reveal a rich network, predominantly of free nerve endings.[12] These include nociceptors (signaling potential damage, often containing Substance P/CGRP) and low-threshold mechanoreceptors (signaling light touch/pressure).[11] Autonomic fibers are also present.[13] This dual innervation implies a role in both pain perception and proprioception. Importantly, fascial nociceptors can become sensitized following injury or inflammation, contributing to persistent pain states.[13][11]

Aetiology

Interspinous oedema simply refers to a radiological finding, and does not presuppose any underlying cause. Bogduk theorises that the pain arises as a result of a periostitis of the spinous processes, or inflammation of the interspinous ligament, with nociception arising from the medial branches of the dorsal rami [10] Some authors use the term interspinous bursitis. The term bursitis, implying bursal pathology, is not able to be proven on imaging as the oedema could be from any number of causes. The term oedema is therefore preferred, although a bursal process is probably more likely in rheumatological cases.

While some research indicates a higher prevalence of interspinous ligament oedema in patients with LBP compared to asymptomatic controls , other studies highlight its presence in a substantial proportion of individuals without symptoms, particularly with increasing age in the mid and lower lumbar segments.[14] This underscores the challenge of differentiating clinically relevant findings from incidental, age-related, or asymptomatic degenerative changes. [15]

Nonetheless, pathology in the interspinous region is implicated as a potential source of mechanical LBP, characteristically presenting as midline pain exacerbated by lumbar extension and relieved by flexion. Recent evidence also links high signal intensity in the ISL to segmental instability, particularly in the context of degenerative lumbar spondylolisthesis.[16]

Asymptomatic/Incidental

Despite its frequent detection, interspinous high signal can be an incidental finding unrelated to the patient's symptoms. Its prevalence increases with age and is common in asymptomatic individuals.[1][17][3] A negative response to a diagnostic local anaesthetic injection into the interspinous space confirms the finding is not the source of the patient's pain.[18]

Trauma

Acute trauma may be a common cause of symptomatic interspinous high signal intensity.[18] Mechanisms include:

  • Lifting (often in flexion): May involve eccentric muscle loading (e.g., multifidus strain), sudden forceful muscle co-contraction leading to tensile stress on the ISL/fascial complex ("surprise loading" effect generating high spinal forces[19]), or microtrauma at the entheses.
  • Falls: Sudden unguarded muscle contraction might cause avulsion-type injuries.
  • Hyperextension: Less common, but can cause compression of interspinous tissues.[18]

The exact tissue injured is speculative (ligament sprain, muscle strain, fascial injury, enthesopathy, periostitis). Bogduk theorised pain could arise from periostitis of the spinous processes or inflammation of the ISL itself, involving nociception via the medial branches.[10]

Baastrup's Disease

Baastrup's disease, first described in 1933, is thought to be rare. Also known as "kissing spines," Baastrup's disease involves close approximation or contact between adjacent spinous processes, leading to mechanical irritation, inflammation, development of adventitial bursae, and secondary degenerative bony changes (sclerosis, flattening, hypertrophy).[2]

It is more common in older individuals (especially over 70) with degenerative spine changes (e.g., disc height loss, spondylolisthesis).[20][2] While classically associated with excessive lordosis, this link has been questioned.[2] However in this study, the authors used Baastrup's and interspinous oedema interchangeably, and did not differentiate between traumatic and atraumatic causes, nor did they differentiate whether there was lumbar spine impaction.

The term Baastrup's should ideally be reserved for cases with clear spinous process impaction and associated bony changes, though imaging overlap with isolated interspinous high signal is significant. True Baastrup's may represent a more chronic, mechanically driven end of the spectrum. Surgical outcomes (spinous process excision) have been historically poor in some cohorts.[21]. True Baastrup's disease probably reflects only a minority of cases of interspinous oedema.

The hallmark finding suggestive of Baastrup's is close approximation and contact of adjacent spinous processes along with interspinous with or without bone oedema oedema, cystic lesions, sclerosis, flattening and enlargement of the articulating surfaces of the two affected spinous processes, bursitis and occasionally epidural cysts or midline epidural fibrotic masses. Usually generalised degenerative spinal changes are seen, most prominent at the affected level, including facet joint hypertrophy, disc herniation, and spondylolisthesis. On MRI gadolinium administration may show enhancement of the affected area.[2]

  • MRI, STIR sequence, sagittal reconstruction illustrating bone oedema at both the spinous processes of L3-L4 level.[2]
    MRI, STIR sequence, sagittal reconstruction illustrating bone oedema at both the spinous processes of L3-L4 level.[2]
  • Lumbar spine X-ray, AP (left image) and lateral (right image) views illustrating close approximation and contact of spinous processes at L4-L5 level with sclerosis and flattening of the articulating surfaces (white arrow).[2]
    Lumbar spine X-ray, AP (left image) and lateral (right image) views illustrating close approximation and contact of spinous processes at L4-L5 level with sclerosis and flattening of the articulating surfaces (white arrow).[2]
  • MRI, sagittal reconstruction: STIR sequence (a) illustrating high signal intensity and fat-suppression T1-weighted sequence, post intravenous gadolinium injec
    MRI, sagittal reconstruction: STIR sequence (a) illustrating high signal intensity and fat-suppression T1-weighted sequence, post intravenous gadolinium injec
  • L3/4 Baastrups on Xray
    L3/4 Baastrups on Xray
  • L3/4 Baastrups on coronal fat sat MRI
    L3/4 Baastrups on coronal fat sat MRI
  • L3/4 Baastrups on T2 sagittal MRI
    L3/4 Baastrups on T2 sagittal MRI

Rheumatological Conditions

Interspinous bursitis has been associated with several rheumatological conditions, especially polymyalgia rheumatica (47% of RA patients), but also rheumatoid arthritis (10%), and crystalopathies. In rheumatological cases, interspinous oedema is likely to be incidental, rather than related to any pain, and the patient is likely to have already been diagnosed or there will be other features to make the diagnosis of an inflammatory condition. Lumbar spine involvement is more common than cervical spine, even though neck pain is more common than low back pain. Overall the relationship with pain in these patients is not clear, but in a control group the findings were only seen in 1 out of 65 patients.[22][23] There may be additional factors in the patients pain such as facet joint irritation or disc pain which may need to be addressed.

Pathophysiology

The mechanisms driving pain associated with interspinous high signal intensity are debated. Two main models are considered. It is possible these models are not mutually exclusive, potentially representing a spectrum where initial trauma/sensitization might precede or coexist with chronic mechanical changes.

Feature Trauma/Neuropathic Model (Cleary) Inflammatory/Mechanical Model
Initiating Event Tensile (micro)trauma to ISL/fascia/tendon complex from excessive muscle forces (e.g., surprise loading). Chronic mechanical stress/impingement between adjacent spinous processes (e.g., due to excessive lordosis, degeneration).
Primary Pathology Initial inflammation followed by persistent sensitization of peripheral nociceptors in fascia/ligament/tendon. Mechanical irritation, inflammation of interspinous tissues, development of adventitial bursitis, bony remodeling.
Pain Mechanism Primarily driven by ongoing firing of sensitized peripheral nerves (neuropathic component); potential central sensitization. Primarily driven by inflammation and mechanical irritation of innervated tissues (nociceptive/inflammatory pain).
Interpretation of MRI Oedema Represents fluid accumulation secondary to initial trauma/inflammation, but pain persists due to neural changes. Represents active inflammation within the ISL and/or fluid within an interspinous bursa, directly related to ongoing mechanical irritation.

Traditional Inflammatory/Mechanical Model

This model, closely linked to Baastrup's disease, attributes pain primarily to chronic mechanical stress. Impingement between adjacent spinous processes causes irritation and inflammation of the intervening soft tissues (ISL, bursa). Pain is considered nociceptive/inflammatory, driven by chemical mediators and mechanical stimulation of local nerve endings.[2] MRI high signal directly reflects this active inflammation or bursal fluid.

Traumatic/Neuropathic Model

Dr Cleary proposes a significant shift in the conceptualisation of this condition, away from a simple tendinopathy or inflammatory model towards a neuropathic pain mechanism, or more specifically neurogenic inflammation.

The trauma to the interspinous structures is conceptualised not necessarily as a single major event but potentially even microtrauma resulting from excessive tensile forces to the complex network of the interspinous ligaments, associated fascia, and the entheses of the erector spinae and multifidus muscles.

Specific biomechanical scenarios are proposed as triggers for this trauma. "Surprise loading," as investigated by Mannion et al.[24] , is highlighted as a situation generating high reflex muscle forces and spinal compression. In this model, these forces, potentially involving forceful co-contraction of the agonist (ESA) and antagonist (multifidus) muscles acting on the spinous processes, concentrate stress at the interspinous attachments. The anatomical arrangement, including the disparity in muscle attachment areas (broad origin vs. focused insertion) and the relative weakness of the ISL, makes this region vulnerable. The analogy of a "Christmas cracker" is used to depict the ISL/fascial complex being pulled apart by opposing muscle forces acting on the spinous processes.  

The initial tissue injury could trigger a local inflammatory response, involving the release of mediators like histamine and bradykinin. This leads to vasodilation and increased vascular permeability, resulting in oedema, which manifests as high signal intensity on fluid-sensitive MRI sequences. Critically, alongside this inflammatory response, it is proposed that there is subsequent sensitisation of local nociceptors ā€“ specifically, free nerve endings located within the fascia, ligaments, and tendons of the interspinous complex, drawing on the work of researchers like Mense on fascial innervation.[25][26][27]

The persistence of pain, particularly chronic LBP in some individuals following such events, is attributed primarily to the ongoing activity of these sensitised peripheral nociceptors. This shifts the focus from ongoing inflammation or structural damage alone to a neuropathic component involving hyperexcitable nerve endings. There could be recruitment of silent nociceptors and neurogenic inflammation, where the nerve endings themselves releases substances that perpetuate inflammation and sensitisation. This increased afferent input ("afferent barrage") could like to secondary sensitisation changes in the dorsal horn.

The often rapid and significant pain relief observed following the injection of a mixture of local anesthetic (LA) and corticosteroid into the interspinous space is evidence supporting the neuropathic component. Dr. Cleary argues this rapid response (within minutes to days) is best explained by the LA "switching off" the sensitised free nerve endings, rather than solely by the slower anti-inflammatory action of the steroid. The maintenance of improvement at 2 years in his series is noted.

Epidemiology

Useful data has been obtained from an audit of a Musculoskeletal Medicine Specialist's practice. The term symptomatic was denoted when there was evidence of lumbar interspinous oedema on MRI and significant improvement with a fluoroscopically guided injection. Of 178 new cases of low back pain +/- leg pain, there were 21 cases of symptomatic interspinous oedema (12% prevalence), 6 cases of asymptomatic interspinous oedema (3.3% prevalence), and 10 inconclusive cases (5.6% prevalence).[18]

An MRI study using of 539 patients with back or leg pain found lumbar interspinous oedema to be present in 8.2% of cases. When present, it was seen at multiple levels in 47.7%; 71.4% of these cases had two levels involved, and 28.6% had 3 levels involved. The machine was 1.5 Tesla, fat suppression was not routinely used, and coronal sequences were not obtained. There was no control group, and no correlation with diagnostic blocks. The authors found an association with anterolisthesis and central spinal canal stenosis, and theorised that "bursitis" may develop due to translational movements of the spinous processes abutting each other. There was no association with lordosis.[28]

Clinical Features

See also: Case:02_Low_Back_Pain

Certain patterns have been found in the presentation of symptomatic interspinous oedema. The onset of pain is closely linked to the time of the accident/forces, and the patient is definite about the accident. The pain distribution is highly variable. The pain is significant, and affects sleep, work, and recreation. On examination there is tenderness of the interspinous soft tissues.[18]

Case Examples of Symptomatic Interspinous Oedema
Age Duration of Pain Injury Interspace Pain Drawing
31 2 months lifting and throwing concrete into skip bin L4/5
39 8 months Lifting rail 'ping' L4/5 L5/S1
55 3 months Fall L4/5
41 3 months Lifting at gym L4/5 L5/S1
30 1 month Lifting child L5/S1
65 11 months Pulling out pallet which snagged

In kissing spines, patients may have midline back pain that worsens with extension and relieved by flexion. On examination the patient may be tender over the suspected level. Rarely an epidural cystic mass may cause neurogenic claudication with extension.[2]

Imaging

The diagnosis is supported by finding interspinous oedema on MRI. The two key sequences are the coronal fat sat Dixon and the T2 sagittal sequence. The coronal fat sat sequence needs to be specifically requested at certain radiology providers in New Zealand.

  • MRI T2 coronal Dixon and sagittal images showing interspinous oedema at the L4/5 interspace.
    MRI T2 coronal Dixon and sagittal images showing interspinous oedema at the L4/5 interspace.
  • Another case MRI T2 coronal SPAIR showing interspinous oedema at the L4/5 interspace. It is not well seen on the sagittal.
    Another case MRI T2 coronal SPAIR showing interspinous oedema at the L4/5 interspace. It is not well seen on the sagittal.

Diagnosis

The interspinous space is supplied by the medial branches of the dorsal rami, and so are anaesthetised with medial branch blocks

In the appropriate clinical setting and imaging findings, the diagnosis can be confirmed by finding resolution of pain with a diagnostic injection of local anaesthetic under fluoroscopic guidance.[18] Injections at non-involve segments may theoretically confirm the clinical response.

The interspinous soft tissues are supplied by the medial branches of the dorsal rami. Therefore medial branch diagnostic blocks would be positive, and radiofrequency neurotomy of the medial branches would relieve the pain. There is discussion amongst the Musculoskeletal Medicine community as to whether, if the history fits, should symptomatic interspinous oedema be excluded by the appropriate MRI sequences before embarking on MBBs?[18]

Treatment

In most cases symptoms can be treated with conservative management and corticosteroid injection. Surgery is not indicated. Injections are performed at the level of the interspinous ligament and have been used with good therapeutic benefit. There is usually durable fast relief by an interspinous injection of steroid and local anaesthetic. This should ideally be done with imaging guidance to ensure accurate needle positioning. In New Zealand, fluoroscopic guidance is normally used.[18] Ultrasound could theoretically be used as an alternative, however this has not been studied.

The fluoroscopic technique is as follows:[18]

  • Advance a 9 cm 22-gauge spinal needle into the interspinous space using AP and lateral projections.
  • Infiltrated 1 mL Omnipaque 300 into the interspinous space to ensure position.
  • Infiltrate a mixture of 40 mg Kenacort A and 0.5 mL 0.75% Ropivacaine into the affected interspinous space.
Fluoroscopic corticosteroid injection of the interspinous space of L4/5

Resources

Supraspinous and interspinous ligaments - Heylings 1976.pdf
Supraspinous and Interspinous ligaments - Rissanen 1960.pdf
Baastrups - Filippiadis 2015.pdf
An open access review of Baastrup's
interspinous bursitis - depalma 2004.pdf
case report with a useful discussion and literature review.

Summary

  • Interspinous oedema can be asymptomatic, but is more common in symptomatic patients.[Level 5]
  • The symptomatic patient is definite about an accident with the pain being closely linked to the inciting event. The pain distribution is quite variable, but the pain intensity is often severe with marked effects on function. There is tenderness in the affected interspinous space.[Level 5]
  • For diagnosis the MRI needs to include a coronal T2 fat sat Dixon sequence, and the diagnosis is supported by abolition of pain with image guided injection.[Level 5]
  • If looking at doing medial branch blocks, consider first excluding the presence of interspinous oedema on MRI.[Level 5]
  • There is usually durable fast relief by an interspinous injection of steroid and LA. [Level 5]

References

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