Spine Study Archives 
MMoohhaammeedd MMoohhii EEllddiinn , MB-BCH , 
M.Sc., MD 
Professor of Neurosurgery 
Faculty of Medicine 
Cairo University 
EGYPT 
Weekly Neurosurgical Conference – Kasr El Aini, 25 November 2010
Spine Study Archives 
Schmorl’s nodes (SN) 
(Intervertebral Disc Herniation)
Schmorl’s nodes (SN) 
• Commonly observed 
– on routine radiographs 
– at autopsy 
• Represent herniation of the nucleus 
pulposus into the adjacent end plate. 
• Forms a defect in the upper or lower 
surface of the involved vertebra. 
• Tend to occur near the central or 
posterior axis. 
• SN are also a common radiographic 
feature of 
– Scheuermann’s disease 
– Chondrodysplasias such as multiple 
epiphyseal dysplasia.
Intervertebral Herniation 
• The EP has less 
resistance to expansile 
pressure of nucleous 
pulposus than the 
normal annulus fibrosus 
• Disc herniation in the 
craniocaudal direction, 
through a defect or 
break in the VEP
EP Defects can be 
• Developmental (intrinsic abnormality of EP) 
– Previous vascular channels 
– Ossification gaps 
– Small indentation defects left during the 
regression of chorda dorsalis (notochord) 
• Weakening of EP (numerous local and 
systemic) 
– Infection 
– Metabolic: osteomalacia, hyperparathyroidism 
– Paget disease 
– Degenerative 
– Neoplastic 
• Traumatic: axial loading 
• Scheuermann disease 
• Osteoporosis ?!!
SN Location 
• Intervertebral Location: 
– almost 2/3 in the posterior part of the VEP, 
– 1/3 in the middle part; 
– anterior nodes rare 
• However, traumatic Schmorl nodes occur 
– Predominantly in the posterior VEP 
– Mostly in sites that are particularly susceptible to 
injury 
• lower thoracic, 
• thoracolumbar junction and 
• upper lumbar spine
Pathologically Schmorl’s nodes 
• Represent the nucleous 
pulposus with degenerative 
or inflammatory changes & 
a sclerotic response in the 
adjacent vertebral 
spongiosa (trabeculat bone) 
• The herniated NP may 
become vasularised, and 
lately ossified or calcified
Schmorl’s nodes Detection 
• Conventional radiography depicts fewer SNs than cross-sectional 
imaging methods 
• Recently developed SNs may not be seen on 
conventional radiographs due to the absence of 
surrounding sclerosis 
• Slab contact radiographs obtained with the use of 
finegrain film allow detailed assessment of the presence 
of SNs 
• The size of SNs and the height of the intervertebral disk 
space can be measured without any magnification. 
Subtle bone changes accompanying those nodes also 
can be depicted.
Forms of the VEP 
VEP variations 
A: A Schmorl node defined as 
a focal indentation of the 
VEP 
B: The normal concave form of 
the VEP 
C: The cupid’s bow contour 
has a smooth concavity in 
the posterior portion of the 
VEP 
D: A straight VEP is present 
when a line drawn from the 
anterior edge to the 
posterior edge of the 
vertebral body is in contact 
with the central portion of 
the VEP 
E: A fractured VEP 
anterior posterior 
The lower part of the vertebral body, 
in a sagittal plane, is demonstrated
SN appear to be 
VEP Reaction to Vertical Loading 
• Normal concave VEP (negative association), 
• A straight VEP seems to be more susceptible to 
the formation of SN 
• Explanations 
– expansive pressure of the nucleus pulposus per 
surface ratio, lower in a concave VEP (surface is 
larger than straight VEP) 
– there is more space for the nucleus pulposus, 
therefore, there is less pressure because the volume 
of an intervertebral space with concave VEPs is larger 
than that associated with a straight VEP.
Frequency of Schmorl’s Nodes 
Literature Discrepancy 
• 58% in our elderly population 
• 57% in the 2nd decade of life and 5% in the 6th decade of life 
NO Discrepancy… WHY? 
Schmorl Nodes of Elderly Persons 
tend to be smaller and 
have more surrounding sclerosis (healing) 
less likely to have reactive concomitant bone marrow changes 
that facilitate their detection with MR imaging (18).
• A common finding in the spines of the 
elderly, with a frequency similar to that 
reported for a younger population
Size and Volume of SN 
• Mean anteroposterior 
diameter 
– 6 mm (range, 2–15 mm) 
– 8.2 mm (range, 4–20 
mm) by using MR 
imaging 
• Mean height of 3.3 mm 
(range, 1–9 mm). 
• No correlation between the 
size and volume of the 
Schmorl nodes and the 
degree of disc degeneration 
• Patients with LBP tended to 
have larger Schmorl nodes 
than those of asymptomatic 
patients.
Clinical Controversy of SNs 
• Most consider them to be asymptomatic ( frequent 
finding in persons without back pain) 
• However, in patients with back pain MR-based studies 
showed 
– a significantly higher frequency in the symptomatic group (19%) 
in comparison with the control group (9%) 
– more frequent frequency of enhanced signal intensity after IV 
gadolinium 
– more frequent frequency of those accompanied by bone marrow 
changes 
• An autopsy study showed 
– 10% acute Schmorl nodes 
– Acute or chronic trauma due to excessive axial loading may 
cause Schmorl nodes that initially are symptomatic
SN and LBP 
• On MRI: detected in 19% without back pain 
• SN generally considered asymptomatic 
• However, acute SN may be painful 
• SN may give rise to disc degeneration 
• The relationship of SN with disc disease and 
their clinical significance as a source of low back 
pain remain unknown 
• Factors have been shown to have only modest 
effects, have yet to be formally evaluated and 
variability remains unexplained 
– Environmental factors 
• occupational physical loading, 
• trauma, and 
• smoking 
– Genetic factors.
MRI SN-Characteristics 
MRI SN-Characteristics 
• Localized defect in a vertebral end plate 
• With a well-defined herniation pit in the 
vertebral body 
• With or without a surrounding sclerotic 
rim (low signal on all sequences) 
• Small erosive defects of the end plate in 
degenerate segments are not considered 
SN 
MR score 
• Absent (score 0) or 
• present (score 1) at cranial and caudal 
vertebral levels T9 to L5. 
• Multiple nodes at a particular vertebral 
level were recorded as present (score 1)
Although MRI is considered the most 
sensitive method for assessing the spine, 
there is no accepted or standard definition 
of SN, nor their size.
• a) Sagittal slab contact radiograph at the L3-4 level in a 74-year-old man 
shows a 
• Schmorl node (black arrow) in the distal VEP of L3 and shows a vacuum 
phenomenon in the 
• intervertebral disk (white arrow). (b) Gross specimen of the same slab 
shows the Schmorl node, 
• with displacement of the intervertebral disk (white arrow) in the VEP of L3. 
Cleft formation (black 
• arrow) in the intervertebral disk corresponds to the site of the vacuum 
phenomenon.
Sagittal slab contact radiograph of 
the L2-3 interspace in a 72-year-old 
man shows 
a Schmorl node (black arrow) in the 
lower endplate 
of L2 with traction osteophyte formation 
(white arrow). 
Sagittal slab contact radiograph of 
the L2-3 interspace in a 59-year-old 
man shows 
a Schmorl node (black arrow) in the 
lower endplate 
of L2 and claw osteophyte formation 
(white arrows).
Sagittal slab contact radiograph of 
the T11 to L1 levels of the spine 
in a 61-yearold 
man shows Schmorl nodes 
(straight arrows) 
at the T11-12 level, with a straight 
configuration 
of the VEP and moderate disk 
space 
loss. A cupid’s bow contour 
(curved arrows) is 
at the T12-L1 level.
Anteroposterior and (b) 
lateral specimen 
radiographs 
of the T11-L5 segment in a 
60-year-old man show 
the transition of 
Schmorl nodes (white 
arrows) in the VEPs of 
T11 to L2 to a cupid’s 
bow contour (black arrows) 
of the VEP of L3 and L4.
Heritability of SN 
• A number of genes have been implicated in disc degeneration 
including 
– an aggrecan gene polymorphism 
– a vitamin D receptor and 
– matrix metalloproteinase 3 gene alleles 
• Several mechanisms may be proposed to account for genetic 
factors influencing SN. 
• Synthesis and breakdown of disc anatomic and biochemical 
structures could be genetically determined and lead to accelerated 
degenerative changes in some persons; for example, 
• SN are more common in premature disc degeneration 
– Scheuermann’s disease and 
– the chondrodysplasias 
• Disc disease may therefore be a constellation of several related 
phenotypes, and SN may be at the more severe end of the 
spectrum.
AGE and SN 
• SN present during skeletal maturation are 
unlikely to be the result of disc degeneration 
• In subjects under 50 years of age 
• disc degeneration in the T10–L1 region is more 
frequent in discs with SN than in those without 
SN; 
• In subjects over 50 years of age this difference 
becomes even more marked 
• So, in the T10–L1 region, SN originating in 
childhood or adolescence predispose to earlier-onset 
disc degeneration.

Schmorl’s nodes (spine 2010)

  • 1.
    Spine Study Archives MMoohhaammeedd MMoohhii EEllddiinn , MB-BCH , M.Sc., MD Professor of Neurosurgery Faculty of Medicine Cairo University EGYPT Weekly Neurosurgical Conference – Kasr El Aini, 25 November 2010
  • 2.
    Spine Study Archives Schmorl’s nodes (SN) (Intervertebral Disc Herniation)
  • 3.
    Schmorl’s nodes (SN) • Commonly observed – on routine radiographs – at autopsy • Represent herniation of the nucleus pulposus into the adjacent end plate. • Forms a defect in the upper or lower surface of the involved vertebra. • Tend to occur near the central or posterior axis. • SN are also a common radiographic feature of – Scheuermann’s disease – Chondrodysplasias such as multiple epiphyseal dysplasia.
  • 4.
    Intervertebral Herniation •The EP has less resistance to expansile pressure of nucleous pulposus than the normal annulus fibrosus • Disc herniation in the craniocaudal direction, through a defect or break in the VEP
  • 5.
    EP Defects canbe • Developmental (intrinsic abnormality of EP) – Previous vascular channels – Ossification gaps – Small indentation defects left during the regression of chorda dorsalis (notochord) • Weakening of EP (numerous local and systemic) – Infection – Metabolic: osteomalacia, hyperparathyroidism – Paget disease – Degenerative – Neoplastic • Traumatic: axial loading • Scheuermann disease • Osteoporosis ?!!
  • 6.
    SN Location •Intervertebral Location: – almost 2/3 in the posterior part of the VEP, – 1/3 in the middle part; – anterior nodes rare • However, traumatic Schmorl nodes occur – Predominantly in the posterior VEP – Mostly in sites that are particularly susceptible to injury • lower thoracic, • thoracolumbar junction and • upper lumbar spine
  • 7.
    Pathologically Schmorl’s nodes • Represent the nucleous pulposus with degenerative or inflammatory changes & a sclerotic response in the adjacent vertebral spongiosa (trabeculat bone) • The herniated NP may become vasularised, and lately ossified or calcified
  • 8.
    Schmorl’s nodes Detection • Conventional radiography depicts fewer SNs than cross-sectional imaging methods • Recently developed SNs may not be seen on conventional radiographs due to the absence of surrounding sclerosis • Slab contact radiographs obtained with the use of finegrain film allow detailed assessment of the presence of SNs • The size of SNs and the height of the intervertebral disk space can be measured without any magnification. Subtle bone changes accompanying those nodes also can be depicted.
  • 9.
    Forms of theVEP VEP variations A: A Schmorl node defined as a focal indentation of the VEP B: The normal concave form of the VEP C: The cupid’s bow contour has a smooth concavity in the posterior portion of the VEP D: A straight VEP is present when a line drawn from the anterior edge to the posterior edge of the vertebral body is in contact with the central portion of the VEP E: A fractured VEP anterior posterior The lower part of the vertebral body, in a sagittal plane, is demonstrated
  • 10.
    SN appear tobe VEP Reaction to Vertical Loading • Normal concave VEP (negative association), • A straight VEP seems to be more susceptible to the formation of SN • Explanations – expansive pressure of the nucleus pulposus per surface ratio, lower in a concave VEP (surface is larger than straight VEP) – there is more space for the nucleus pulposus, therefore, there is less pressure because the volume of an intervertebral space with concave VEPs is larger than that associated with a straight VEP.
  • 11.
    Frequency of Schmorl’sNodes Literature Discrepancy • 58% in our elderly population • 57% in the 2nd decade of life and 5% in the 6th decade of life NO Discrepancy… WHY? Schmorl Nodes of Elderly Persons tend to be smaller and have more surrounding sclerosis (healing) less likely to have reactive concomitant bone marrow changes that facilitate their detection with MR imaging (18).
  • 12.
    • A commonfinding in the spines of the elderly, with a frequency similar to that reported for a younger population
  • 13.
    Size and Volumeof SN • Mean anteroposterior diameter – 6 mm (range, 2–15 mm) – 8.2 mm (range, 4–20 mm) by using MR imaging • Mean height of 3.3 mm (range, 1–9 mm). • No correlation between the size and volume of the Schmorl nodes and the degree of disc degeneration • Patients with LBP tended to have larger Schmorl nodes than those of asymptomatic patients.
  • 14.
    Clinical Controversy ofSNs • Most consider them to be asymptomatic ( frequent finding in persons without back pain) • However, in patients with back pain MR-based studies showed – a significantly higher frequency in the symptomatic group (19%) in comparison with the control group (9%) – more frequent frequency of enhanced signal intensity after IV gadolinium – more frequent frequency of those accompanied by bone marrow changes • An autopsy study showed – 10% acute Schmorl nodes – Acute or chronic trauma due to excessive axial loading may cause Schmorl nodes that initially are symptomatic
  • 15.
    SN and LBP • On MRI: detected in 19% without back pain • SN generally considered asymptomatic • However, acute SN may be painful • SN may give rise to disc degeneration • The relationship of SN with disc disease and their clinical significance as a source of low back pain remain unknown • Factors have been shown to have only modest effects, have yet to be formally evaluated and variability remains unexplained – Environmental factors • occupational physical loading, • trauma, and • smoking – Genetic factors.
  • 16.
    MRI SN-Characteristics MRISN-Characteristics • Localized defect in a vertebral end plate • With a well-defined herniation pit in the vertebral body • With or without a surrounding sclerotic rim (low signal on all sequences) • Small erosive defects of the end plate in degenerate segments are not considered SN MR score • Absent (score 0) or • present (score 1) at cranial and caudal vertebral levels T9 to L5. • Multiple nodes at a particular vertebral level were recorded as present (score 1)
  • 17.
    Although MRI isconsidered the most sensitive method for assessing the spine, there is no accepted or standard definition of SN, nor their size.
  • 18.
    • a) Sagittalslab contact radiograph at the L3-4 level in a 74-year-old man shows a • Schmorl node (black arrow) in the distal VEP of L3 and shows a vacuum phenomenon in the • intervertebral disk (white arrow). (b) Gross specimen of the same slab shows the Schmorl node, • with displacement of the intervertebral disk (white arrow) in the VEP of L3. Cleft formation (black • arrow) in the intervertebral disk corresponds to the site of the vacuum phenomenon.
  • 19.
    Sagittal slab contactradiograph of the L2-3 interspace in a 72-year-old man shows a Schmorl node (black arrow) in the lower endplate of L2 with traction osteophyte formation (white arrow). Sagittal slab contact radiograph of the L2-3 interspace in a 59-year-old man shows a Schmorl node (black arrow) in the lower endplate of L2 and claw osteophyte formation (white arrows).
  • 20.
    Sagittal slab contactradiograph of the T11 to L1 levels of the spine in a 61-yearold man shows Schmorl nodes (straight arrows) at the T11-12 level, with a straight configuration of the VEP and moderate disk space loss. A cupid’s bow contour (curved arrows) is at the T12-L1 level.
  • 21.
    Anteroposterior and (b) lateral specimen radiographs of the T11-L5 segment in a 60-year-old man show the transition of Schmorl nodes (white arrows) in the VEPs of T11 to L2 to a cupid’s bow contour (black arrows) of the VEP of L3 and L4.
  • 22.
    Heritability of SN • A number of genes have been implicated in disc degeneration including – an aggrecan gene polymorphism – a vitamin D receptor and – matrix metalloproteinase 3 gene alleles • Several mechanisms may be proposed to account for genetic factors influencing SN. • Synthesis and breakdown of disc anatomic and biochemical structures could be genetically determined and lead to accelerated degenerative changes in some persons; for example, • SN are more common in premature disc degeneration – Scheuermann’s disease and – the chondrodysplasias • Disc disease may therefore be a constellation of several related phenotypes, and SN may be at the more severe end of the spectrum.
  • 23.
    AGE and SN • SN present during skeletal maturation are unlikely to be the result of disc degeneration • In subjects under 50 years of age • disc degeneration in the T10–L1 region is more frequent in discs with SN than in those without SN; • In subjects over 50 years of age this difference becomes even more marked • So, in the T10–L1 region, SN originating in childhood or adolescence predispose to earlier-onset disc degeneration.