Mechanisms of Neurovascular Compression
Within the Spinal and Intervertebral Canals

This section is compiled by Frank M. Painter, D.C.
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FROM:   J Manipulative Physiol Ther. 2000 (Feb); 23 (2): 107–111 ~ FULL TEXT

Lynton G.F. Giles, DC, PhD

National Unit for Multidisciplinary Studies of Spinal Pain,
The University of Queensland,
Townsville General Hospital,
Townsville, Australia.

OBJECTIVE:   To describe some possible causes of encroachment on human spinal and intervertebral canal (foramen) neurovascular II structures.

DATA SELECTION AND SYNTHESIS:   A review of some imaging films of patients aged 38 to 52 years and some human autopsy histopathologic sections from 40– to 60–year-old cadavers to determine what structures may be responsible for neurovascular compression in individuals in this relatively young-to-middle-age group and to illustrate some examples.

RESULTS:   Stenosis of the spinal and intervertebral canal neurovascular structures can be caused by various bony and soft-tissue structures. Stenosis can be related to osteophytosis of the vertebral body, uncoverte-intervertebral disc protrusion, ossification of the posterior longitudinal ligament, and ligamentum flavum hypertrophy or buckling.

DISCUSSION:   Various forms of spinal and intervertebral canal stenosis can cause compression of neurovascular structures that may, in turn, be responsible for symptomatology. Of course, autopsy findings cannot be equated with painful syndromes in patients.

Keywords:   Spine, Stenosis, Neurovascular Compression, Pathology

From the Full-Text Article:


Spinal stenosis (ie, narrowing of the spinal canal, lateral root canals, or both) may result in mechanical compression of the spinal cord, nerve roots, or both, [1] as well as compression of vascular structures. Symptoms and signs of spinal cord compression, nerve root compression, or both occur when degenerative tissues impinge on the spinal cord1 or nerve roots (eg, when intervertebral disc protrusion causes spinal stenosis). [2, 3]

Encroachment on neurovascular structures in the spinal and intervertebral canals can be due to many causes (eg, overt pathology, bony and/or soft-tissue degenerative changes, and axial loading leading to spinal canal and intervertebral canal stenosis). [4–6] The purpose of this article is to record possible mechanisms of neurovascular encroachment in the spinal and intervertebral canals caused by bony, intervertebral disc, ligamentous degenerative changes, or a combination of these.

Degenerative changes, such as spondylosis, osteophytosis, intervertebral disc protrusion, or other soft-tissue abnormalities, are usually the result of trauma on the spine and may be viewed with both computed tomography (CT) and magnetic resonance imaging (MRI) techniques to accurately assess the degree of canal narrowing. [7] Plain film radiographs can provide very useful information when taken in the weight-bearing position, [8] and the addition of flexion and extension stress views, such as those of the cervical [2, 9] and lumbar spines, [10, 11] may provide additional information, although instability remains a controversial issue. [12] However, the role of plain x-ray films of the spine is limited because normal soft tissues of the spine cannot be seen. CT scans can provide more bony information and some degree of soft-tissue visualization, whereas MRI scans show greater soft-tissue detail, and bone scans may provide information in cases of overt pathology and trauma.

During MRI, lumbar spine axial compression in slight extension with compression of approximately half the body weight can demonstrate stenotic changes, as was clearly demonstrated by Willen et al. [6] This phenomenon should be remembered as an important functional component able to cause stenosis, which would be overlooked in routine MRI investigations looking for pathology in the supine position.

It is not the purpose of this article to discuss the pathophysiologic effects of mechanical compression on neurovascular structures because this has been done elsewhere in the literature. [13–17]


A review of some images from patients aged 38 to 52 years and histopathologic sections from autopsy material aged 40 to 60 years indicates how neurovascular compression may occur within the spinal canals, intervertebral canals, or both.


In the lumbar, thoracic, and cervical spines, spinal and intervertebral canal stenosis leading to compression of neurovascular structures occurred because of degenerative bony or soft-tissue structures. In particular, the underlying pathologic reactions to degenerative changes in the spine that lead to stenosis were degenerative changes in the intervertebral disc, facet, and/or uncovertebral joints and ligamentum flavum hypertrophy with or without calcification or buckling of this ligament. The causes of stenosis were classified as shown in Table 1, and some of these examples are presented.

Table 1   Some bony and soft-tissue structures that cause spinal canal
                 or intervertebral canal stenosis as a result of degenerative changes

A: Bony tissue structures

Vertebral body posterior or posterolateral osteophytes
Zygapophysial (facet) joint osteophytes
Osteophytes of the posterolateral margins of the joints of von Luschka (uncovertebral joints) in the cervical spine
B: Soft tissue structures Intervertebral disc protrusion ± calcification
Ossified posterior longitudinal ligament
Ligamentum flavum hypertrophy ± calcification or ossification
Ligamentum flavum degenerative buckling

     Lumbar spine     

Erect posture radiography showed some useful findings, one example of which is shown in Figure 1, A, where the lateral lumbosacral view of a 38–year-old man with chronic low back pain showed a thin disc at L5–S1 with some retrolisthesis of L5 on S1 caused by facet subluxation and a decrease in both the superior-inferior and the anteroposterior (A-P) diameters of the intervertebral canals at this level compared with the L4–5 level.

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Figure 1:

A,   Lateral lumbosacral view showing thinning of the L5 disc height with some retrolisthesis of L5 on S1 causing A-P narrowing of the spinal canal at this level. Note the resulting smaller diameters of the L5–S1 intervertebral foramen compared with those of the L4–5 level.

B,   Axial scan of the L5 disc of the patient in panel A showing the mainly central disc protrusion (with partial calcification) causing some A-P stenosis of the spinal canal and compromise of the anterior epidural space in which blood vessels such as Batson's venous plexus and the recurrent meningeal nerve are located.

Intervertebral disc protrusion was confirmed by a lumbosacral CT examination (Figure 1, B) that showed some narrowing of the A-P diameter of the L5–S1 spinal canal caused by the protrusion.

Intervertebral disc protrusion with resultant subluxation of the L5–S1 facet surfaces and stenotic changes in intervertebral canal dimensions can affect the spinal ganglion and its related blood supply because of ligamentum flavum buckling, as shown in an L5–S1 autopsy histopathologic section cut in the parasagittal plane (Figure 2).

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Figure 2:

Autopsy histopathologic parasagittal plane section of the L5–S1 level of a 59–year-old woman showing subluxation of the hyaline articular cartilage-lined (H) facet surfaces caused by disc protrusion (white arrow) and resulting thinning of the L5–S1 intervertebral disc. Stenosis of the intervertebral canal has occurred with deformation of the spinal ganglion (G) caused by buckling of the ligamentum flavum (black arrow).

IAP, Inferior articular process of L5 vertebra;
S, superior articular process of first sacral segment (S1)
(Bar scale = 1 cm).

Midline intervertebral disc protrusion can efface or compress the anterior aspect of the dural tube and compromise the intervening blood vessels and recurrent meningeal nerve (Figure 3).

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Figure 3:

Autopsy histopathologic axial plane section through an L5 intervertebral disc protrusion containing some early calcifying nuclear material (arrow) in a 51–year-old woman. Note how little space can be available between the disc protrusion and the sensitive dural tube (DT) for Batson's venous plexus and the recurrent meningeal nerve.

H, Hyaline articular cartilage on the L5–S1 zygapophysial joint facet surfaces.

     Thoracic spine     

An MRI example of a T6–7 intervertebral disc protrusion compromising the thoracic dural tube of a neurologically intact 39–year-old man with symptoms of midthoracic spine pain that had occurred intermittently over a 15–year period and was aggravated by coughing, sneezing, and bearing down is shown in Figure 4, A and B.

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Figure 4:

MRI sagittal view (A) showing a T6–7 disc protrusion and early deformation of the anterior aspect of the thoracic cord (black arrow) and axial view (B) showing the focal centrolateral protrusion impressing on the dural tube and the spinal cord (white arrow).

An autopsy thoracic spine histopathologic section cut in the axial plane showing some hypertrophy and ossification of the ligamenta flava that could cause stenosis of the spinal canal in a 40–year-old man is shown in Figure 5.

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Figure 5:

Autopsy histopathologic horizontal (axial) view from a 40–year-old man showing how ossification (arrows) and hypertrophy (tailed arrow) of the ligamentum flavum can cause spinal canal stenosis.

B, Blood vessels;
D, dural tube;
S, spinal cord.

     Cervical spine     

An example of cervical spine intervertebral canal stenosis caused by osteophytosis of the left uncovertebral joint and spinal canal encroachment by intervertebral disc protrusion is shown in Figure 6, A and B, respectively.

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Figure 6:

A,   Oblique-view radiograph showing the lower left intervertebral foramina with osteophytes projecting from the joint of von Luschka into the C6–7 intervertebral foramen.

B,   CT axial scan view at C6–7. Note the broad-based central and left posterolateral disc protrusion (large arrow) causing A-P spinal canal narrowing, with osteophytic lipping of the uncovertebral joint (small arrow) resulting in marked left-sided foraminal stenosis suspicious for neural infringement (arrow head).

The oblique radiograph of the lower cervical spine (Figure 6, A) shows osteophytes projecting into and stenosing the left C6–7 intervertebral foramen of a 46–year-old man with symptoms of C6–7 central spinal pain radiating to the left arm with thumb numbness. A CT scan axial view of this patient at C6–7 (Figure 6, B) shows intervertebral disc protrusion deforming the dural tube and causing A-P spinal canal narrowing, as well as joint of von Luschka (uncovertebral) osteophytosis, resulting in left-sided marked foraminal stenosis.

A photograph comprised of 2 autopsy histopathologic sections cut in the axial plane and prepared from 2 slightly different levels of the cervical spine is shown in Figure 7, A and B, with an axial CT scan for orientation.

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Figure 7:

A,   An axial CT scan at the C5–6 level of a 52–year-old man showing the approximate area of the histopathologic sections in panel B. The CT scan also shows some posterior spondylosis of the vertebral body with some disc herniation on the right side, both of which cause some narrowing of the spinal canal and the right intervertebral canal.

B,   A montage representing 2 histopathologic sections from a midcervical spine region of a 60–year-old woman. Note how osteophytosis of the posterolateral region of the uncovertebral joint (arrow) can deform the nerve roots.

AT, Anterior tubercle;
C, capsule of synovial joint;
D, dural tube;
G, spinal ganglion (highly vascular) and intermediate neural branch blood vessel (arrow head);
H, hyaline articular cartilage on the facet of the inferior articular process;
L, lamina;
MR, motor root;
P, pedicle;
PT, posterior tubercle;
S, superior articular process;
SR, sensory root;
V, thin-walled vein adjacent to the vertebral artery.

These histopathologic sections clearly indicate important neurovascular structures that could be compressed in the intervertebral and spinal canals when stenosis of the canals occurs. For example, an osteophyte projecting from the right joint of von Luschka can distort and compress the nerve roots.


The imaging and autopsy material results show some possible causes of spinal stenosis. Of course, they do not show painful structures nor can imaging in patients be compared directly with histopathologic sections of spines. Nonetheless, autopsy material enables some of the various possible pathologic changes responsible for spinal or intervertebral canal stenosis to be illustrated for different levels of the spine in order to complement imaging. Most of these changes can be found at each level of the lumbar, thoracic, and cervical spines, bearing in mind that only the cervical spine has uncovertebral joints.

To obtain maximum information from an imaging investigation, weight-bearing images can be far more useful than nonweight-bearing images. This is important when using even sophisticated imaging, such as MRI, which, unfortunately, is not normally designed to show weight-bearing or stress views of the spine, even though some attempts have been made to incorporate such techniques. [6, 18] Axial compression of the lumbar spine during MRI will show structural changes within the spinal and intervertebral canals (Figure 8), and therefore mechanisms of neurovascular compression within the spinal and intervertebral canals must be considered from the point of view of existing pathology and possible functional pathology if clinicians are to be able to successfully explain to patients why they have spinal pain syndromes.

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Figure 8:

Axial representation of spinal canal and intervertebral canal structural changes at the L4–5 spinal canal (A) and spinal recess levels (B), respectively, in both the psoas relaxed position and in axial compression with slight extension.

DT, Dural tube;
F, fat pad;
IAP, inferior articular process of L4;
LF, ligamentum flavum;
L4, fourth lumbar nerve;
L5, fifth lumbar root sleeve;
SAP, superior articular process of L5.

Note the disc bulge, buckled ligamentum flavum, and the changed configuration of the posterior epidural fat pad and neural structure during axial compression with slight extension.

Modified with permission from Willén et al. [6]


I thank Mike Shapter, Photographer, Townsville General Hospital, for the printing of the photographs.


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