Eur Radiol (2005) 15: 591–598

DOI 10.1007/s00330-004-2618-4 NEURO

Massimo Gallucci
Edoardo Puglielli
Degenerative disorders of the spine
Alessandra Splendiani
Francesca Pistoia
Giorgio Spacca

Received: 5 July 2004

Revised: 6 December 2004
Accepted: 6 December 2004
Published online: 31 December 2004
# Springer-Verlag 2004
M. Gallucci (*) . E. Puglielli .
A. Splendiani
Department of Radiology,
University of L’Aquila,
Via L. Natali,
67100 L’Aquila, Italy
e-mail: massimo.gallucci@cc.univaq.it
Tel.: +39-862-368512
Fax: +39-862-311277
F. Pistoia . G. Spacca
Department of Neuroscience,
S. Salvatore Hospital,
L’Aquila, Italy
Abstract Patients with back pain and Keywords Spine . Degenerative .
degenerative disorders of the spine Spondylosis . Disk pathology . Disk
have a significant impact on health herniation . Spine . Radiology
care costs. Some authors estimate that
up to 80% of all adults experience
back pain at some point in their lives.
Disk herniation represents one of the
most frequent causes. Nevertheless,
other degenerative diseases have to be
considered. In this paper, pathology
and imaging of degenerative spine
diseases will be discussed, starting
from pathophysiology of normal age-
related changes of the intervertebral
disk and vertebral body.

Introduction to pathophysiology
Even though several causes are responsible for physiolog-
ical (age-related) and pathological bony and articular
degeneration, the main mechanism implicated is trauma,
in the forms of sequels of acute traumatism, chronic multi-
traumatism and chronic overload. Among the mentioned
forms, the concept of “duration trauma” has certain rele-
vance: stresses not able to cause fractures when acutely
applied can be responsible for bony (and disk) damage
when applied for longer periods. The concept of functional
integrity of the spinal curves is also involved in the de-
generative processes of the spine. The presence of four
“sinusoidal” curves absorbs traumas several times more
than a straight structure (proportional to the square of the
curve numbers). Therefore, in the case of departure from the
correct alignment, an asymmetrical distribution of the load
may cause more or less severe, focal or diffuse, degener-
ative changes.
Study indications and techniques
Imaging in degenerative pathology of the spine comes from
the need for finding the reason for a clinical problem,
usually pain, which is rarely a nervous deficit. In the case of
typical back pain or monoradicular sciatica, it is invariably
accepted that imaging does not add significant information
during the acute phase [1] and patients have no theoretical
risk in waiting 4–6 weeks before performing any radiolog-
ical exam, having the possibility of a spontaneous regres-
sion of symptoms in the case of extraspinal diseases (neuritis,
muscular or insertional inflammation etc.) or even small
acute herniations. A typical pain associated with other
592
symptoms (fever, general compromission, altered hematic
formula) or in patients suffering from neoplastic pathology
or other systemic disease possibly responsible for spine
involvement (i.e. ostheoporosis, Cushing etc.) should be
investigated earlier.
As far as the techniques are concerned, it should be
considered that conventional plan X-ray examination still
plays an important and preliminary role: it is cheap, uni-
versally available, safe and offers a good panoramic view of
the affected spine, adding meaningful details on bone struc-
tures and the stability of the spine [2]. Mild signs of mis-
alignament will suggest upright X-ray and completion with
Fig. 1a–n Lateral bending (a, b). Mild instability on right bending at
the L4–L5 level. Same case, MR myelography and fast spin echo
(FSE) T2-w scans performed in rest condition (c, e) and during axial
loading (e, f). The load determines a mild increase of the degenerative
L4 anterolysthesis, with a narrowing of the lateral recesses (white
arrows) nicely demonstrated by MR myelography. Compression on
flexion–extension and left–right lateral bending exams
(Fig. 1a, b, g, h).
In the cases where conventional X-ray examination does
not fully justify the clinical symptoms, magnetic resonance
imaging (MRI) should be proposed. MRI is definitely the
modality of choice in studying cervical and thoracic spine.
In lumbar spine, computed tomography (CT) is considered
to be as equally sensitive, even though, due to safety con-
siderations, it should be reserved for elderly people or
secondary to MRI, with the aim of characterising a lesion
already demonstrated [3]. Contrast administration is equally
reserved for characterising lesion already documented and
nerve roots is clearly evident (white arrows) and assume the aspect of
“redundant” nerve roots (circle in f). (g–n) another case of L4–L5
lysthesis due to bilateral isthmic lysis is shown; (g, h) flexion–ex-
tension plan X-ray; (i, l) oblique projections with the typical “Scottish
terrier collar” sign (circles) indicating the lysis. The lysis is also
clearly demonstrated by lateral sagittal T2-w MRI cuts (arrows)
 593

is very rarely needed in the cases of degenerative spine

disease.
Finally, in the case of negative MRI exams, nuclear
medicine could play a role: bone scintigraphy is able to
recognise very circumscribed bony inflammations, tumours
or even methastases, and to better address a further MRI
investigation.
Other special techniques find rarer applications. Mag-
netic resonance (MR) myleography usually does not add
significant information to conventional MRI, with the sole
exception of instable spine studied by means of axial-
loader MR-compatible devices (Fig. 1c–f).
Conventional myelography is rarely performed, but is
still useful in the case of contra-indications to MRI, or in
spinal instability in which conventional MRI proved to be
unable to evaluate root compression, in case of metallic bars
proven to deteriorate significantly conventional MRI. This
last limit can be often overcome by means of T2-w turbo
spin echo (TSE) sequences with elevated turbo factor and
phase encoding directions in perpendicular planes in order
to obtain two sequences with the metal artifact projected in
the cranio-caudal direction (on the vertebral bodies, sparing
the canal) and in the anterior-posterior direction (on the
canal, sparing bodies and disks). Finally, nowadays, there is
no role for discography, except for the sole exception of
cases allocated to chemiodiscolysis.

Degenerative bony changes

Vertebral body marrow changes

Disk degeneration is almost always associated with bony

signal alterations. The changes, as described by Resnick in
1985 as “vertebral ostheochondrosis” [4], can be schemat-
ically reported as follows: (1) disk reduction in height and
hyaline degeneration (“chondrosis”); (2) end-plate cartilage
micro-fractures; (3) condroblastic proliferation; (4) sub-
condral neo-vascularisation; (5) trabecular bone deminer-
alisation; (6) ostheosclerosis. In 1988, Modic reviewed and
reduced these changes into three main radiological cate-
gories: Modic type (MT) I, II and III [5] (Fig. 2). In MT I
(discovertebritis or aseptic spondilytis), the bony marrow
has low T1 and high T2 signal, and schematically corre-
spond to points 2–4 described above [6]. The pattern can be
reversible or it can progress towards MT II, a condition
with fatty marrow prevalence in association with bone de-
mineralisation and an MR signal that is bright on T1 and
low on T2-w conventional spin echo (SE) sequences (on
TSE sequences, the signal is bright in both T2-w and T1-
w sequences). MT III is characterised by dark signals on
both T1 and T2-w SE and TSE sequences, consequent to
osteosclerosis.
Fig. 2a–f Modic type (MT) spongy bone changes. (a, b) MT I (also
called discovertebritis or aseptic spondilytis), the bony marrow has
low T1 and high T2 signal. (c, d) MT II, characterised by fatty
marrow prevalence and MR signal bright on T1 and T2-w FSE
sequences. (e, f) MT III, characterised by dark signals on both T1
and T2-w sequences consequent to osteosclerosis
Spondylosis
Spondylosis deformans concerns most of the age-related
vertebral alterations. The primary pathological findings are
antero-lateral osteophytes, which result from the weakening
of anular fibres with disk bulging and traction on Sharpey’s
fibres. Osteophytes typically develop where these fibres
attach to the vertebral body, usually some millimetres from
the diskovertebral junction. They are bony spurs or ledges
594
that extend first in the horizontal and then in the vertical
directions.
Different from the above are syndesmophytes. Syndes-
mophytes are slender, vertically oriented ligamentous calci-
fications and osseous excrescences that extend from the
margin of one vertebral body to another, often associated
with facet joint ankylosis and are one of the hallmarks of
ankylosing spondylitits. Osteophytes must also be distin-
guished from enthesophytes, the sweeping, asymmetric
lateral bony excrescences of psoriasic and Reiter syndrome,
and the flowing ossifications of diffuse idiopathic skeletal
hyperostosis (Fig. 3a–d) (DISH, see the Sect. 3.1) [7].
In the cervical spine, bony degenerative deformities often
involve unco-vertebral processes, causing the so-called
“unco-arthrosis” clearly visible on the anterior-posterior
plane X-ray films as smoothing and flattening, or even the
sharpening of uncal processes as a consequence of ostheo-
phytosis (Fig. 3e).
Finally, Schmorl’s nodes (herniation of disk material
through the end plate into the vertebral body) is another
common manifestation of spondylosis (Fig. 3f–h). Schmorl’s
nodes are found in up to 75% of the normal population and
are seen on CT scans as end-plate sclerotic areas surrounding
lucencies that represent herniation of the disk material.
Fig. 3a–h Different aspects of spondylosis deformans. Osteophytes
on longitudinal ligament (LL) X-ray (a) appears as bony excrescences
that originate from near the margin of vertebral bodies. Sindesmo-
phytes are vertically oriented ligamentous calcifications and osseous
excrescences that extend from the a vertebral body to another (in b:
conventional X-ray; in c: T2-w TSE). Enthesophytes (d) appears as
asymmetric lateral bony excrescences typical of the psoriasic and
Articular processes
Degenerative change of posterior articulations is seen path-
ologically as fibrillation and erosion of articular cartilage,
partial or complete denudation of the cartilagenous surface,
and new bone formation. Imaging findings of facet arthrosis
on plain film and CT scans includes joint space narrowing,
bone eburnation and osteophytosis. Facet osteophytes are
seen on CT axial images as a mushroom-like facet over-
growths with subchondral sclerosis. Sagittal scans through
the neural foramina show posterosuperior bony narrowing,
often combined with ligamentum flavum laxity that further
narrows the foramen [7, 8] (Fig. 4a, b, f–h).
Juxta-articular cysts, also known as “synovial cysts” or
“ganglionic cysts,” sometimes form next to degenerated
facet joints. The cysts’ contents range from serous or muci-
nous fluid to semi-solid gelatinous tissue. They may also
contain blood, hemosiderin or even air. Cyst density on CT
scan varies from hypo- to hyperdense compared to the ad-
jacent ligamentum flavum. The cyst can be percutaneously
treated under CT of fluoroscopic guidance by fixing a 22-
gauge needle inside the articular space, aspiring (when
possible) and breaking by filling it with steroids and local
anaesthetics (Fig. 4).
Reiter syndrome, and flowing ossifications of DISH. Cervical unco-
arthrosis is clearly visible on anterior-posterior plane X-Ray films
(e) as smoothing and flattening, or even sharpening of uncal pro-
cesses. (f, g, h) A LL radiograph, a T2-w MRI and a CT scan of a
typical Schmorl’s node (herniation of disk material through the end
plate into the vertebral body)

Fig. 4a–h Facet arthrosis (apophyseal joint osteoarthrosis). CT (a)
and T2-w MR on axial plane (b) show joint tickening, bone ebur-
nation and osteophytosis, which determines recess and intervertebral
canal stenoses. In c, d, e, a case of synovial cyst well shown at an MRI
examination. The interapophyseal leakage which is always associated
is a useful sign for differential diagnosis with other cystic pathology
(arrows in d). Percutaneous CT-guided therapeutic approach is shown
A peculiar condition consequent to conspicuous lumbar
lordosis and degenerative changes lead to a contact and
sclerosis of adjacent spinous processes with interspinous
garnulomatous reaction and a possible evolution towards
pseudoarticulation (Baastrup disease) (Fig. 4g).
Spondylolysis and lystesis
Spondylolisthesis is defined as the splitting of a vertebral
body in comparison with the lower levels. Six types of
lysthesis are distinguished: dysplastic (congenital, usually
associated with spina bifida), traumatic, pathologic (sec-
ondary to bone disease like Paget’s disease or a tumour),
iatrogenic (secondary to surgery), isthmic and degenerative.
In the isthmic form, lysthesis is a consequence of spondy-
lolisis, a condition due to the fracture of the pars inter-
articularis (isthmus), which is mostly a consequence of
chronic overload and relative chronic ischemic changes.
Two thirds of all spondylolyses occur at L5 and 30% are L4.
Plain X-ray examination is usually sufficient to detect lysis
and lystesis in L–L views as lucent defect in the pars in-
terarticularis with or without forward slippage of the upper
vertebral body. Oblique views are easier to be interpreted,
offering the classical sign of the “scottish terrier collar”
(Fig. 1i, l–n). If significant spondylolisthesis has occurred,
the anterio-posterior canal diameter is increased and the
interposed disk is nearly always degenerated and bulges,
but rarely herniates. The neural foramina are, thus, de-
formed and variably narrowed [7, 8].
595
in e. In f, g, h, a case of degenerative lateral stenosis with mild
antherolysthesis of L4 on L5 and a marked thickening of flava lig-
aments (black arrows in g and h), small synovial cysts associated with
intraarticular leakage (white arrows in f and thick arrows in h) and
Baastrup disease (arrows in g indicate pseudo-articulation between
adjacent spinous processes). “Redundant nerve root” sign is also
evident (circle in f)
Degenerative spondylolisthesis is a spreading of a ver-
tebral body anteriorly or posteriorly displaced due to severe
degeneration of interapophyseal joints. It is frequent at L4–
L5 level due to the more sagittal orientation of the joints
which, even in normal conditions, allow a mild posterior
spreading of L4 (10%) [7].
Degenerative stenosis
Spinal stenosis can be congenital, acquired or mixed, as the
result from a combination of congenital abnormalities with
superimposed degenerative changes. Apart from spinal ste-
noses occurring in the case of achondroplasia and inherited
metabolic disorders such as Morquio syndrome, most con-
genital stenoses happen in the case of a short peduncle
syndrome. As a consequence, lateral recesses and interver-
tebral canals are narrow (lateral stenosis) and, in most cases,
even the anterior-posterior diameter of the central canal is
reduced (central stenosis). Minimal disk bulge or spondi-
lotic change can, therefore, produce early neurological
deficits (mixed stenosis).
Acquired (degenerative) spinal stenosis is typically
caused by spondylosis, disk bulges or herniations, liga-
mentous degeneration, spondilolysthesis or a combination
of these disorders. Between 4% and 28% of CT or MR scans
in asymptomatic patients show signs of lumbar stenosis (i.e.
anterior-posterior diameter of the central canal inferior to
10 mm; lateral recesses less than 5 mm in the anterior-
posterior direction). More recently, attention has paid to
cases with bony canals that are normal in shape and di-
596

mension. In such cases, MR demonstrates that the dural sac
is small, with a prevalence of fatty extradural tissue in the
central canal. In extreme cases, the cauda equina nerve roots
may become edematous and redundant, mimicking vascular
malformation (“redundant nerve root sign”) (Figs. 1f, 4f, 5f)
[7–10].
Calcification and ossification in spinal ligaments may
also cause spinal stenosis and radiculomyelopathy. The two
most common posterior spinal ligaments that ossify are the
posterior longitudinal ligament and the ligamentum flavum.
Ossification of posterior longitudinal ligament (OPLL) is an
uncommon disorder that is also called “Japanese disease.”
It is most common in the midcervical (C3–C5) and mid-
thoracic (T4–T7) spine. Individuals with OPLL may be
entirely asymptomatic, but others have reported various
neurologic symptoms. The ossification of ligamentum flavum
(OLF) is one of most common causes of posterior thoracic
spinal cord compression [7–10].
Degenerative disk disease
Classification and pathophysiology
Three main pathogenetic mechanisms of intervertebral disk
degeneration are known: trauma and cyclical repetitive
loading on the disk (leading to damage of the annular fibres)
and decreasing of permeability of the vertebral end plates
(leading to compromising of the function of diskal fibro-
blasts and chondrocytes). Despite the presence of different
pathogenetic mechanisms, the first step in disk degenera-
tion is represented by dehydration of the nucleus pulposus
and consequent rigidity. MR can early detect disk degen-
eration by signal decrease on T2-weighted images. As a
consequence, fissures within the disk start producing. They
appear after 20 years of age and almost all people older
than 40 have virtually transverse intra-nuclear cleft. Con-
sidering the very high incidence in the healthy population,
dehydration and intra-nuclear cleft are to be considered as
para-physiological. On the other hand, the rupture of
collagen bridges among the peripheral fibres produce annular
weakness and disk bulge, while the rupture of the fibres and
radial tear of the annular fibres produces disk herniation.
The presence of radial tear is detectable by MR and
consists of a focal bright signal in T2-weighted sequences
(so-called “high intensity zone”) (Fig. 5) [11, 12]. Loss of
water content and annular fissures result in a dramatic
destruction of the intervertebral disk, which collapses and gas
and also calcifications within the disk are not uncommon in
degenerative diseases.
Many classifications and nomenclatures of the normal
and pathologic conditions affecting the lumbar disks have
been used by radiologists. The following (simplified) de-
finitions list is the one recently proposed by a task force of
radiologists, neuroradiologists, orthopaedists and neuro-
surgeons [13] (Fig. 5):
1. Bulge disk: when the contour of the outer annulus
extends in the axial plane beyond the disk space by
over than 50% (180°).
2. Disk herniation: localised displacement of disk mate-
rial beyond the normal margins of the intervertebral
disk space. Disk material may include nucleus, carti-
lage, fragmented apophyseal bone or fragmented anular
tissue. Disk herniation may take the form of protrusions
or extrusions:

Fig. 5a–f Different degenera-

tive changes of the disk as seen
in FSE T2-w MRI images. (a)
“High intensity zone,” likely
due to annular fissure. (b) An
asymmetrical left-sided bulging.
(c) A typical protrusion. (d) A
case of sequestered disk. (e, f)
Two cases of free fragments,
associated with an annular cleft
(black arrowhead in e) and
downward migrated (f). Note
the “redundant” aspect of the
nerve roots (white arrows in f)
 597

. Protrusion: when the greatest distance between the
edges of the disk material beyond the disk space is
less than the distance between the edge of the base
in the same plane. Protrusions with a base less than
25% of the circumference of the disk are focal, and
between 25% and 50% are broad based.
. Extrusion: when the distance between the edges of
the disk material beyond the disk space is greater
than the base. When no continuity exists between
the extruded material and the disk, it may be defined
as sequestrated or free fragment. Extruded disk ma-
terial displaced away may be called migrated.
Herniated disk material can be contained or uncontained,
depending on the integrity of the outer annulus; it can be
extra-ligamentous or trans-ligamentous, depending on the
crossing or not of the posterior longitudinal ligament.
Extra-ligamentous fragments usually do not cross the mid-
line nor migrate for more than one level due to the hard
adhesion of the posterior longitudinal ligament (PLL) in the
midline (Trolard’s ligament) and on each intersomatic level.
Intradural disk herniation is a rare condition in which the
displaced disk material penetrates the PLL and the dural sac.
In the axial plane, herniation is classified as central,
right–left central, right–left sub-articular, right–left foram-
inal, right–left extraforaminal.
The natural history of disk degeneration
Long-term follow-up studies of surgically and non-surgi-
cally treated patients indicate that, after a five-year period,
the success rate is similar, and even after a one-year pe-
riod, good clinical outcome is registered in 70–95% of
untreated patients [14–20].
The relief of pain is thought to be due to the subsidence of
sleeve root edema, inflammatory and fibrotic changes
around the disk material. The relief of pain usually occurs
within weeks or a month from the acute event. The main
mechanisms of regression are shrinkage due to dehydration,
fragmentation and phagocytosis of the disk herniation.
Shrinkage and dehydration of the disk material are related
to the loss of hydrophilic proteoglicans; on the other hand,
the inflammatory response of the acute phase should stim-
ulate the phagocytosis. Dehydration may have occurred in
those cases in which the disk fragment shows a hyper-
intense signal on T2-weighted images, as confirmed by the
loss of signal observed during the MR follow-up. In a
perspective study by our group, the herniated disk that
displayed a high signal intensity on T2-weighted sequences
regressed spontaneously in 83% of cases, while the free
fragment disappears spontaneously within six months in
100% of the cases studied. Protrusion or bulging tends to be
more stable from both anatomical and clinical points of
view [14, 20–24].
Finally, one should consider that radiology in the last 10
years has offered several possibilities to overcome the
diagnosis, and approach the disk pathology even from a
therapeutical view. The recently proposed mini-invasive
techniques (intra-discal or periganglionic steroid or O2–O3
mixture) are able to relieve symptoms in up to 80% of
patients with no risk and no meaningful complication, being
very easily tolerated by patients and easily administered by
radiologists [25].

References
1. Deyo RA, Weinstein JN (2001) Low
back pain. N Engl J Med 344:363–370
2. Almen A, Tingberg A, Besjakov J,
Mattsson S (2004) The use of reference
image criteria in X-ray diagnostics: an
application for the optimisation of
lumbar spine radiographs. Eur Radiol
14(9):1561–1567
3. Tsuchiya K, Katase S, Aoki C, Hachiya
J (2003) Application of multi-detector
row helical scanning to postmyelo-
graphic CT. Eur Radiol 13(6):1438–
1443. Epub 2002 Nov 19
4. Resnick D (1985) Degenerative disease
of the vertebral column. Radiology
156:3–14
5. Modic MT (1988) Degenerative disk
disease: assessment of changes in ver-
tebral body marrow with MR imaging.
Radiology 166:193–199
6. Mitra D, Cassar-Pullicino VN, McCall
IW (2004) Longitudinal study of ver-
tebral type-1 end-plate changes on MR
of the lumbar spine. Eur Radiol 14
(9):1574–1581
7. Ruscalleda J, Feliciani M, Rovira A
(1995) Degenerative changes of lum-
bosacral spine. Riv Neuroradiol 8
(s1):177–196
8. Gallucci M, Capoccia S, Colajacovo M
(2005) Spinal stenosis. In: van
Goethem JWM, van den Hauwe L,
Parizel P (eds) Medical radiology—
diagnostic imaging: imaging of the
spine. Springer, Berlin Heidelberg New
York (in press)
9. Postacchini L (1989) Lumbar spinal
stenosis. Springer, Berlin Heidelberg
New York
10. Yoshida M, Shima K, Taniguchi Y
(1992) Hypertrophied ligamentum fla-
vum in lumbar canal spinal stenosis:
pathogenesis, morphologic and immu-
nohystochemical observation. Spine
17:1353–1360
11. Saifuddin A, McSweeney E, Lehovsky
J (2003) Development of lumbar high
intensity zone on axial loaded magnetic
resonance imaging. Spine 28(21):
E449–E451
12. Haughton VM, Rogers B, Meyerand
ME, Resnick DK (2002) Measuring the
axial rotation of lumbar vertebrae in
vivo with MR imaging. Am J Neuro-
radiol 23(7):1110–1116
598
13. Fardon DF, Milette PC (2001) Recom-
mendations of the combined task forces
of the North American Spine Society,
American Society of Spine Radiology,
and American Society of Neuroradiol-
ogy. Spine 26(5):E93–E113
14. Bozzao A, Gallucci M, Masciocchi C,
Aprile I, Barile A, Passariello R (1992)
Lumbar disk herniation: MR imaging
assessment of natural history in patient
treated without surgery. Radiology 185
(1):135–141
15. Davis AR (1994) A long-term outcome
analysis of 984 surgically treated her-
niated lumbar disks. J Neurosurg
80:415–421
16. Kawaji Y, Uchiyama S, Yagi E (2001)
Three-dimensional evaluation of lum-
bar disc hernia and prediction of ab-
sorption by enhanced MRI. J Orthop
Sci 6(6):498–502
17. Saal JA, Saal JS (1990) The natural
history of lumbar intervertebral disk
extrusion treated nonoperatively. Spine
15:683–686
18. Bush K, Cowan N, Katz DE, Gishen P
(1992) The natural history of sciatica
associated with disk pathology. A
prospective study with clinical and
independent radiologic follow-up.
Spine 17(10):1205–1212
19. Gallucci M, Bozzao A, Orlandi B,
Manetta R (1995) Follow-up of surgi-
cally treated and untreated disk pathol-
ogy. Riv Neuroradiol 8(s1):85–96
20. Davis AR (1994) A long-term outcome
analysis of 984 surgically treated her-
niated lumbar disks. J Neurosurg
80:415–421
21. Saifuddin A, Mitchel R, Taylor BA
(1999) Extradural inflammation asso-
ciated with anular tear: demonstration
with gadolinium-enhancement lumbar
spine MRI. Eur Spine J 8:34–39
22. McCarron RF, Wimpee MW, Hudkins
P (1987) The inflammatory effect of
nucleus pulposus: a possible element in
the pathogenesis of low back pain.
Spine 12:760–764
23. Gallucci M, Bozzao A, Orlandi B,
Manetta R, Brughitta G, Lupattelli L
(1995) Does postcontrast MR en-
hancement in lumbar disk herniation
have a prognostic value? J Comput
Assist Tomogr 19(1):34–38
24. Splendiani A, Puglielli E, Delli Colli S,
de Amicis R, Masciocchi C, Gallucci
M (2004) Spontaneous involution of
disk herniation. Neuroradiology 46 (in
press)
25. Andreula CF, Simonetti L, De Santis F,
Leonardi M (2003) Minimally invasive
oxygen-ozone therapy for lumbar disk
herniation. Am J Neuroradiol 24:996–
1000