CLINICAL VALUE OF SEDIMENTATION SIGN IN DIAGNOSIS …

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Ali et al. World Journal of Pharmacy and Pharmaceutical Sciences

CLINICAL VALUE OF SEDIMENTATION SIGN IN DIAGNOSIS OF

LUMBAR SPINAL STENOSIS

1*Dr. Alaa Hussein Ali,

2Dr. Alaa Abdulhussein Salih Badi and

3Dr. Yahia Falih

Mohammad

1M.B.Ch.B.HDFOS.

2M.B.Ch.B.HDFOS.

3M.B.CH.B, DOS FACS.

ABSTRACT

Introduction: Lumbar spinal canal stenosis is described as a condition

in which there is diminished space available for the neural and vascular

elements in the lumbar spine. This may be due to age, injury, or

degeneration. Aim of the study: To evaluate the diagnostic accuracy,

discriminative ability, and reliability of the Sedimentation Sign in a

sample of patients with clinically diagnosed lumbar spinal stenosis.

Type of the study: Cross-sectional prospective study. Patients and

methods: Patients with low back pain referred to the orthopedic

consultant clinic, after history taking and examination, patients who were diagnosed

clinically to have lumbar spinal stenosis, referred for MRI of lumbosacral spine, looking for

sedimentation sign and measuring anteroposterior dimeter of spinal canal and dural sac.

Results: The results showed that 338 patients with low back pain,220 of them were

diagnosed to have lumbar spinal stenosis(65.1%),210(95.5%) of patients who were diagnosed

with lumbar spinal stenosis have sedimentation sign on MRI in our study, sedimentation sign

had a specificity of 100% and sensitivity of 95.5%, p value is<0.001,so it is highly

significant. Conclusion: The sedimentation sign was shown to have high reliability in the

present study. It was helpful to diagnose lumbar spinal stenosis in patients with low back

pain. The sign appears most sensitive in defining severe lumbar spinal stenosis cases, may

add specific diagnostic information beyond the traditional history, physical examination and

imaging studies that are standard in lumbar spinal stenosis diagnosis.

WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES

SJIF Impact Factor 7.632

Volume 9, Issue 12, 340-373 Research Article ISSN 2278 – 4357

*Corresponding Author

Dr. Alaa Hussein Ali

M.B.Ch.B.HDFOS.

Article Received on

11 October 2020,

Revised on 31 October 2020,

Accepted on 21 Nov. 2020

DOI: 10.20959/wjpps202012-17876


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INTRODUCTION

Lumbar spinal stenosis is described as a condition in which there is diminished space

available for the neural and vascular elements in the lumbar spine. This may be due to age,

injury, or degeneration.

Lumbar spinal stenosis occurs when the bony tunnels in the spine that transmit the spinal

cord and nerve roots become narrowed. The spinal nerves (or nerve roots) typically become

compressed, leading to pain in the lower back and legs.

When symptomatic, this causes a variable clinical syndrome of gluteal and/or lower

extremity pain and/or fatigue which may occur with or without back pain.

Symptomatic lumbar spinal stenosis has certain characteristic provocative and palliative

features. Provocative features include upright exercise such as walking or positionally-

induced neurogenic claudication. Palliative features commonly include symptomatic relief

with forward flexion, sitting and/or recumbency.[1]

The ancient historical description of LSS was by the Egyptian civilization, but the first

modern description of the condition is from 1803 by Antoine Portal.[2]

Verbiest was the first to describe the clinical symptoms of neurogenic claudication as a result

of spinal canal stenosis and established this pathology as a clinical entity in the 1950s.[3]

Arnoldi proposed one of the first definitions of spinal stenosis and classically defined the

pathology as ―any type of narrowing of the spinal canal, nerve root canals or intervertebral

foramina‖.[2]

More than 50 years later, there is still no widely accepted diagnostic or classification criteria

for the diagnosis of LSS and as a consequence studies use widely differing eligibility criteria

that limit the generalizability of reported findings. Among older individuals, LSS can be a

highly disabling condition, and is the most common reason for spinal surgery.

What is sedimentation sign?

Although there is a wide range of clinical, electrophysiological, and radiological findings to

reach the diagnosis, the indication for surgical treatment has still not been clearly defined, so

that additional diagnostic signs are important in guiding the choice of surgery.

https://en.wikipedia.org/wiki/Antoine_Portal


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Barz et al. demonstrated for the first time in 2010 that in patients without LSS a

sedimentation of the nerve roots to the dorsal region of the dural sac in magnetic resonance

images by gravitational force and defined its absence as a positive sedimentation sign.[4]

In a normal supine patient with no suspected LSS the nerve roots of the cauda equina will

‗settle‘ to the posterior aspect of the spinal canal under gravity. However, when a patient

suffers from symptomatic lumbar spinal stenosis the failure of the roots to form this

‗sediment‘ will be observed. In other words, they remain fairly evenly distributed throughout

the spinal canal, as they are effectively being held in place by the constriction of the anatomy

producing the stenosis (usually a combination of disc bulging, ligamentum flavum

hypertrophy and facet joint osteoarthrosis)(Fig.1).[5]

Fig.1 a.Normal nerve root sedimentation b.Absent nerve root sedimentation.[5]

1.1 Anatomy of Lumbar spine

1.2.1 Osteology

The lumbar vertebrae (Figs.2 and 3) are the largest segments of the movable part of the

vertebral column, and can be distinguished by the absence of a foramen in the transverse

process, and by the absence of facets on the sides of the body.[6]

The body is large, wider from side to side than from before backward, and a little thicker in

front than behind. It is flattened or slightly concave above and below, concave behind, and

deeply constricted in front and at the sides.


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The pedicles are very strong, directed backward from the upper part of the body;

consequently, the inferior vertebral notches are of considerable depth.

The laminae are broad, short, and strong; the vertebral foramen is triangular, larger than in

the thoracic, but smaller than in the cervical region.

The spinous process is thick, broad, and somewhat quadrilateral; it projects backward and

ends in a rough, uneven border, thickest below where it is occasionally notched.

The superior and inferior articular processes are well-defined, projecting respectively upward

and downward from the junctions of pedicles and laminae. The facets on the superior

processes are concave, and look backward and medialward; those on the inferior are convex,

and are directed forward and lateralward. The former are wider apart than the latter, since in

the articulated column the inferior articular processes are embraced by the superior processes

of the subjacent vertebra.

The transverse processes are long, slender, and horizontal in the upper three lumbar

vertebrae; they incline a little upward in the lower two. In the upper three vertebrae they arise

from the junctions of the pedicles and laminae, but in the lower two they are set farther

forward and spring from the pedicles and posterior parts of the bodies. They are situated in

front of the articular processes instead of behind them as in the thoracic vertebrae, and are

homologous with the ribs.

Of the three tubercles noticed in connection with the transverse processes of the lower

thoracic vertebrae, the superior one is connected in the lumbar region with the back part of

the superior articular process, and is named the mammillary process; the inferior is situated at

the back part of the base of the transverse process, and is called the accessory

process(Fig.2).[6]


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Fig. 2– A lumbar vertebra from behind.[7]

Fig. 3– Fifth lumbar vertebra, from above.[7]

The Fifth Lumbar Vertebra (Fig.3) is characterized by its body being much deeper in front

than behind, which accords with the prominence of the sacrovertebral articulation; by the

smaller size of its spinous process; by the wide interval between the inferior articular

processes; and by the thickness of its transverse processes, which spring from the body as

well as from the pedicles.[7]

1.2.2 Lumbar vertebral joints

The mobility of the vertebral column is provided by the symphyseal joints between the

vertebral bodies, formed by a layer of hyaline cartilage on each vertebral body and an

intervertebral disc between the layers.

The synovial joints between the superior and inferior articular processes on adjacent

vertebrae are termed the facet joints (also known as zygapophysial joints or Z-joints). They

permit simple gliding movements. The movement of the lumbar spine is largely confined to

flexion and extension with a minor degree of rotation (Fig.4).[6]


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Fig.4 The 3-joint complex is formed between 2 lumbar vertebrae. Joint 1: Disc between

2 vertebral bodies; Joint 2: Left facet (zygapophyseal) joint; Joint 3: Right facet

(zygapophyseal) joint.[6]

1.2.3 Lumbar Intervertebral Discs

Discs form the main connection between vertebrae. They bear loading during axial

compression and allow movement between the vertebrae. Their size varies depending on the

adjacent vertebrae size and comprises approximately one quarter the length of the vertebral

column.[6]

Fig.5 Intervertebral discs(Lateral and Superior views)[6]


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1.2.4 Lumbar Vertebral Ligaments

The ALL covers the ventral surfaces of lumbar vertebral bodies and discs. It is intimately

attached to the anterior annular disc fibers and widens as it descends the vertebral column.

The ALL maintains the stability of the joints and limits extension.

The PLL is located within the vertebral canal over the posterior surface of the vertebral

bodies and discs. It functions to limit flexion of the vertebral column, except at the lower L-

spine, where it is narrow and weak.

The ligamentum flavum (LF) bridges the interlaminar interval, attaching to the interspinous

ligament medially and the facet capsule laterally, forming the posterior wall of the vertebral

canal. It has a broad attachment to the undersurface of the superior lamina and inserts onto

the leading edge of the inferior lamina. Normally, the ligament is taut, stretching for flexion

and contracting its elastin fibers in neutral or extension. It maintains constant disc tension.

The intertransverse ligament joins the transverse processes of adjacent vertebrae and resists

lateral bending of the trunk. The iliolumbar ligament arises from the tip of the L5 transverse

process and connects to the posterior part of the inner lip of the iliac crest. It helps the lateral

lumbosacral ligament and the ligaments mentioned above stabilize the lumbosacral joint(Fig

6).[6]

A B

Fig.6(A) Anterolateral view of the lumbar spine demonstrating the multiple ligaments of

the lumbar spine. These ligaments include the following: ligamentum flavum (LF),

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anterior longitudinal ligament (ALL), posterior longitudinal ligament (PLL),

intertransverse ligament, interspinous ligament, supraspinous ligament, and facet

capsular ligament.[6]

(B)Lateral view

1.2.5 Spinal cord anatomy

The spinal cord normally terminates as the conus medullaris within the lumbar spinal canal at

the lower margin of the L2 vertebra, although variability of the most caudal extension exists

(fig.7).

Fig.7 Anatomy of cauda equine.

In a cadaveric study of 129 cadaveric specimens, the spinal cord terminated at L2 in 60%, L1

in 30%, and L3 in 10% of specimens. Differential growth rates in the spinal cord and the

vertebral canal are the cause of these disparities.[6]

Spinal nerves and roots

All lumbar spinal nerve roots originate at the T10 to L1 vertebral level, where the spinal cord

ends as the conus medullaris. A dorsal or posterior (somatic sensory) root from the

posterolateral aspect of the spinal cord and a ventral or anterior (somatic motor) root from the

anterolateral aspect of the cord join in the spinal canal to form the spinal nerve root. The roots

then course down through the spinal canal, forming the cauda equina, until they exit at their

respective neural (intervertebral) foramina as a single pair of spinal nerves. Thus, the lumbar

nerve roots exit the spinal canal at a lower level than where they arise.[6]


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Exit levels of spinal nerves

Lumbar spinal nerves exit the vertebral canal by passing inferior to the pedicles of the

corresponding vertebrae since early in development. In the lumbar region, the first division of

the spinal nerve takes place within the intervertebral foramen, resulting in the posterior and

anterior (dorsal and ventral) rami. The posterior rami pass posteriorly, skirting the articular

processes at that level, whereas the anterior rami proceed laterally to supply the body wall

and the lower limbs.[6]

Relations of the roots and spinal nerves

In the lumbar vertebral canal, the posterior and anterior roots of a given nerve (enclosed in

their dural sacs) cross the intervertebral disc that is located above the pedicle below which the

nerve exits. For example, the L2 nerve roots cross the disc between L1 and L2 vertebrae

before reaching the appropriate foramen, below the pedicle of the L2 vertebra.[6]

Lateral recess

Lateral to the dura is the lateral canal, which contains the nerve roots; compression in this

region results in radiculopathy.

The lateral recess, also known as ―Lee‘s entrance zone,‖ begins at the medial border of the

superior articular process and extends to the medial border of the pedicle. This is where the

nerve root exits the dura and courses distally and laterally under the superior articular facet.

The borders of the lateral recess are the pedicle laterally, the superior articular facet dorsally,

the disc and posterior ligamentous complex ventrally, and the central canal medially. Facet

arthritis most frequently causes stenosis in this zone, along with vertebral body spurring and

disc or anulus pathology. ―Lee‘s midzone‖ describes the foraminal region, which lies ventral

to the pars.[8]

Its borders are the lateral recess medially, the posterior vertebral body and disc ventrally, the

pars and intertransverse ligament dorsally, and the lateral border of the pedicle laterally. The

foramen is essentially the area between the cephalad and caudal pedicles. The dorsal root

ganglion and ventral motor root occupy 30% of this space. This also is the point where the

dura becomes confluent with the nerve root as epineurium. The exit zone is identified as the

area lateral to the facet joint. The nerve root is present in this location and can be compressed

by a ―far lateral‖ disc, spondylolisthesis and associated subluxation, or facet arthritis.[8]


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1.2.6 Anatomy of the spinal canal

The shape of the human upper lumbar vertebral canal is almost circular and this changes

gradually to a triangular shape in the lower lumbar vertebrae.[9]

The lumbar vertebrae thus

provide an appropriate transition between the obviously circular shape of the thoracic

vertebral canal and the markedly triangular shape of the sacral spinal canal.

The lower lumbar vertebrae frequently demonstrate a modification in the shape of the canal

in that the sides of the triangle are indented into the space of the triangle, tending to

compartmentalize the lateral corners into lateral recesses, the whole canal taking the shape of

a three-leaf clover or trefoil.[10]

The interlaminar angle is the ―third leaf‖ (Fig. 8).[11]

The

clinical relevance of the trefoil configuration lies in a possible predisposition to compression

of lumbar and sacral nerve roots. Epstein, Epstein and Lavine[12]

considered shallowness of

the lateral recesses to be the ― primary abnormality of clinical significance‖ in spinal stenosis.

Fig.8: Showing trefoil shape of spinal canal.[11]

The margins of the canal are formed by an anterior wall and a posterior wall, connected

through pedicles and intervertebral foramina.

The anterior wall consists of the alternating posterior aspects of the vertebral bodies and the

annulus of the intervertebral discs. In the midline these structures are covered by the posterior

longitudinal ligament, which widens over each intervertebral disc.

The posterior wall is formed by the uppermost portions of the laminae and the ligamentum

flavum. Because the superoinferior dimensions of the laminae tend to decrease at the L4 and

L5 levels, the ligamentum flavum consequently occupy a greater percentage of the posterior

wall at these levels. The posterolateral borders of the posterior wall are formed by the anterior


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capsule of the facet joint and the superior articular process, which is located well anterior of

the articulating inferior articular process.[13]

1.2 SPINAL STENOSIS

1.3.1 Pathophysiology of lumbar spinal stenosis

LSS can be monosegmental or multisegmental, and unilateral or bilateral. Anatomically, the

stenosis can be classified as central, lateral or foraminal. Depending on the extent of the

degeneration, central, lateral and foraminal stenosis can occur alone or in combination. The

L4–5 spinal discs are most frequently affected by LSS, followed by L3–4, L5–S1, and L1–

2.[14]

Multiple factors can contribute to the development of spinal stenosis, and these can act

synergistically to exacerbate the condition.

Degeneration of the vertebral disc often causes a protrusion, which leads to ventral narrowing

of the spinal canal (central stenosis; Figure 1a). As a consequence of disc degeneration, the

height of the intervertebral space is further reduced, which causes the recess and the

intervertebral foramina to narrow (foraminal stenosis), exerting strain on the facet joints

(Figure 9). Such an increase in load can lead to facet joint arthrosis, hypertrophy of the joint

capsules and the development of expanding joint cysts (lateral stenosis), which in

combination propagate spinal instability.

The reduced height of the segment leads the ligamentum flavum to form creases, which exert

pressure on the spinal dura from the dorsal side (central stenosis). Concomitant instability due

to loosened tendons (for example, the ligamentum flavum) further propagates preexisting

hypertrophic changes in the soft tissue and osteophytes, creating the characteristic trefoil -

shaped narrowing of the central canal.

LSS can also be subdivided into relative and absolute LSS—a classification that has not yet

been clinically validated—according to the anterior–posterior diameter of the spinal canal

(Figure 9 a,b and c). Relative LSS (spinal canal 10–12mm in diameter; physiological value is

22–25mm) is usually asymptomatic, whereas absolute LSS (spinal canal <10mm in diameter)

is often symptomatic and is associated with absence of free subarachnoid space (as observed

on lateral plain X-ray films). The lateral recess can be considered stenotic if it has a diameter

of <2mm (physiological diameter is 3–5mm).[14]


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Figure 9 a | distinct stenosis areas are depicted in red. ventral compression c caused by

medially bulging or protrusion of intervertebral discs. Lateral stenosis c caused by

lateral prolapse, stenosis of the neuroforamen or hypertrophy of the facet joints. b |

Dorsal view of lateral stenosis (red dots) caused by hypertrophic facet joints and

narrowing of the neuroforamen. c | Corresponding lateral perspective of narrowed

neuroforamen causing a lateral stenosis.[14]

1.3.2 Classification lumbar spinal stenosis

Etiological classification

• Acquired

Degenerative/spondylotic changes (most common)

Post surgical

Traumatic (vertebral fractures)

Inflammatory (ankylosing spondylitis)

• Congenital

Short pedicles with medially placed facets (e.g., achondroplasia).[15]


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Anatomical classification

• Central Canal stenosis

Cross sectional area of the spinal canal < 100mm2 or <10mm A-P diameter on axial CT

caused by ligamentum hypertrophy directly under the lamina posteriorly, and the bulging disc

anteriorly.

• Lateral recess stenosis (subarticular recess)

Associated with facet joint arthropathy and osteophyte formation overgrowth of superior

articular facet usually primary culprit.

• Foraminal stenosis

Occurs between the medial and lateral border of the pedicle exiting nerve root compressed by

ventral cephalad overhang of the superior facet and the bulging disc.

• Extraforaminal stenosis

Located lateral to the lateral edge of the pedicle lateral disc herniation causes impingement of

the existing nerve root.[15]

1.3.3 Symptoms

• Back pain, referred buttock pain

• Claudication.

• Pain worse with extension (walking, standing upright)

• Pain relieved with flexion (sitting, leaning over shopping cart, sleeping in fetal position)

• Leg pain (often unilateral)

• Weakness

• Bladder disturbances recurrent UTI present in up to 10% due to autonomic sphincter

dysfunction

• Cauda equina syndrome (rare).[16]

Clinical evaluation

In patients with spinal stenosis, symptoms include back pain (95%), sciatica (91%), sensory

disturbance in the legs (70%), motor weakness (33%), and urinary disturbance (12%). In

patients with central spinal stenosis, symptoms usually are bilateral and involve the buttocks

and posterior thighs in a nondermatomal distribution. With lateral recess stenosis, symptoms

usually are dermatomal because they are related to a specific nerve being compressed.


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Patients with lateral recess stenosis may have more pain during rest and at night but more

walking tolerance than patients with central stenosis.[8]

Can we predict diagnosis of LSS clinically?

The purpose of a clinical prediction rule is to improve the accuracy of diagnosis. The rule

which is developed by Konno et al[17]

was designed to help orthopedic specialists to identify

patients with LSS.

Q1 Numbness and/or pain in the thighs down to the calves and shins.

Q2 Numbness and/or pain increase in intensity after walking for a while, but are relieved by

taking a rest.

Q3 Standing for a while brings on numbness and/or pain in the thighs down to the calves and

shins.

Q4 Numbness and/or pain are reduced by bending forward.

Key questions for diagnosis of cauda equina symptoms:

Q5 Numbness is present in both legs.

Q6 Numbness is present in the soles of both feet

Q7 Numbness arises around the buttocks.

Q8 Numbness is present, but pain is absent.

Q9 A burning sensation arises around the buttocks.

Q10 Walking nearly causes urination.

Konno et al addressed that:

a score of 4 points on Q1–Q4 indicates the presence of LSS, a score of 4 on Q1–Q4 and < 1

on Q5–Q10 indicates the radicular type of LSS and a score of > 1 on Q1–Q4 and > 2 on Q5–

Q10 indicates the neurogenic claudication type of LSS.

In the validation cohort, the questionnaire had a sensitivity of 84% and a specificity of 78%

in diagnosing LSS.[17]

A clinical diagnosis support tool to identify patients with lumbar spinal stenosis.

Points

• Age: 60–70 1 >70 2

• Absence of diabetes 1


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• Intermittent claudication 3

• Exacerbation of symptoms when standing up 2

• Symptom improvement when bending forward 3

• Symptoms induced by having patients bend forward −1

• Symptoms induced by having patients bend backward 1

• Good peripheral artery circulation 3

• Abnormal Achilles tendon reflex 1

• Straight leg raise test positive -2

The total score range from −2 to 16., a score equal or greater than 7 has a sensitivity of 92.8%

and a specificity of 72.0% for the diagnosis of symptomatic lumbar spinal stenosis.[17]

The clinical syndrome of lumbar spinal stenosis should be considered in:

Older patients with back pain who also have pain in the buttocks or legs.

Neurogenic claudication is pain or discomfort with walking or prolonged standing that

radiates beyond the low back area and into 1 or both buttocks, thighs, legs, or feet.

In addition to this pain pattern, a provocative worsening with lumbar extension and

improvement with sitting or lumbar flexion is typical.

Radicular pain may occur with lumbar spinal stenosis, and this is characterized by a

distribution into 1 or more dermatomes that is present irrespective of activity.[18]

1.3.4 Can we predict spinal canal stenosis radiologically?

1. Plain radiography

Although plain radiography cannot confirm spinal stenosis, findings are:

. Short pedicles on the lateral view,

. Narrowing between the pedicles on the anteroposterior view,

. Ligament ossification,

. Narrowing of the foramen,

. Hypertrophy of the posterior articular facets can be helpful hints.[8]

2. Magnetic resonance imaging(MRI)

MRI should be confirmatory in patients with a consistent history of neurogenic claudication

or radiculopathy, but it should not be used as a screening examination because of the high


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rate of asymptomatic disease. Morphologic changes have been correlated with preoperative

findings, such as pain and function, however, only to a limited extent. Sagittal T2-weighted

MR images are a good starting point because they give a myelogram-like image. Sagittal T1-

weighted images are evaluated with particular attention focused on the foramen.

An absence of normal fat around the root indicates foraminal stenosis. Axial images provide

a good view of the central spinal canal and its contents on T1- and T2-weighted images. Far

lateral disc protrusions are identified on axial T1-weighted images by obliteration of the

normal interval of fat between the disc and nerve root .The foraminal zone is better evaluated

with sagittal T1-weighted sequences, which confirm the presence of fat around the nerve

root.[8]

3. Computed tomography(CT)

Despite the prevalence of MRI, myelography followed by CT is still accepted and widely

used for operative planning in patients with spinal stenosis; it has a diagnostic accuracy of

91%. The addition of CT after a myelogram allows detection of 30% more abnormalities than

with myelography alone.

Because of the dynamic nature of the study, stenosis not visible on MRI with the patient

recumbent may be identified on standing flexion and extension lateral views. CT after

myelography characterizes the bony anatomy better than MRI, which helps the surgeon plan

decompression surgery.[8]

Reversibility of sedimentation in lumbar spinal stenosis??

Christian Barz et al conducted a study of 30 patients [median age 73 years 16 males]. Three

months post-operation 27 patients had a negative Sed. sign. In this group, they found

improved clinical outcomes at follow-up. These changes were all statistically significant

(p < 0.001). Three patients had a positive Sed. sign at 3-month follow-up due to epidural fat

or a dural cyst following an intra-operative dural tear, but also showed improvements in

clinical outcomes.

They concluded that the reversibility of a pre-operative positive SedSign was demonstrated

after decompression of the affected segmental level and associated with an improved clinical

outcome. A persisting positive Sed. sign could be the result of incomplete decompression or


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surgical complications. A new positive Sed. sign after sufficient decompression surgery could

be used as an indicator of new stenosis in previously operated patients.[19]

1.3 Methods of measurement of spinal canal and dural canal diameters

1.4.1 Plain radiography

Hamdan and Al-Kaisy in their study measured the VBD and SCD in both anteroposterior and

lateral views of lumbosacral spine.[20]

VBD & SCD measured at each lumbar vertebral level,

the canal to body ratio was calculated on AP view based on Jones and Thompson

technique(Fig.10).[21]

Fig 10 Antero-posterior and lateral radiographs of a lumbar spine. A ı interpıdicuIar

distance. B antero posterior diameter of spinal canal. Cı transverse diameter of

vertebral body. Dı anterontero-posterior diameter of vertebral body. The products AB

and CD are compared.

100 patients were enrolled in the study, 50 patients were normal as a control group and 50

patients were diagnosed with LSS, they concluded that the C/B ratio 1:2.5-1:5.2 is considered

normal, whereas any ratio beyond this is stenotic canal.

C/B=A*B/C*D


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1.4.2 MRI measurements

1. Andrew Hughes et al proposed a method for measuring canal and dural diameters.[22]

37 patients, with L1 – L5 stenotic segments, have been involved, were diagnosed with lumbar

spinal stenosis by the MRI imaging.

The ratio of summary cross-sectional areas of lateral canals to cross-sectional area of dural

sac has been calculated for every stenotic segment. This parameter they called ―Coefficient of

Stenosis”. Value of this coefficient was compared with a control group values.

For evaluation multilevel lumbar spinal stenosis they used simple average value of

―Coefficient of Stenosis‖, they called ―Mean Coefficient of Stenosis‖(Fig 11 & 12).[22]

They improvised a new approach to determine optimal radiological criteria of a spinal canal

narrowing depending on (total cross sectional area of dural sac and lateral canals on middle

of intervertebral disc and facet joints level).But the sample was small, and they insisted on

checking the data on a large sample for recommendations about the clinical application of the

new method.

Fig.11 Scheme of the spinal canal areas measurement: 1. Cross-sectional area of lateral

recess; 2. Cross-sectional area of dural sac.


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Fitg 12 Measurements of linear sizes of the spinal canal. 1. Depth of the lateral recess; 2.

Ligamentous interfacet distance; 3. Anterio-posterior diameter of dural sac; 4.

Transverse diameter of dural sac; 5. Angle of the lateral recess.

2. Smita B. Shinde et al depended on MRI T2 weighted images performed in sagittal and

coronal plane. Anteroposterior diameter measured at sagittal section and transverse diameter

measured at coronal views. Both diameters measured at same intervertebral disc levels(Fig

13).[23]

In this study patients were 20 normal individuals,having normal spinal cord on MRI were

chosen for the study.When they compared mean anteroposterior diameter and transverse

diameter in 20 subjects the anteroposterior diameter is less.

Fig 13. Antero-posterior – Transverse diameter of lumbar L4 level.

3. Young Su Lim et al took the axial T2-weighted images at the level of facet joint for each

subject. DSCSA and SCCSA were measured at the L4-L5 intervertebral level (Fig 14

a&b).[24]


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Both DSCSA and SCCSA samples were collected from 135 patients with LSS, and from 130

control subjects who underwent MRI.

DSCSA and SCCSA were measured at the L4-L5 intervertebral level.

The average DSCSA value was 151.67±53.59mm2 in the control group and

80.04±35.36mm2 in the LSS group. The corresponding average SCCSA values were

199.95±60.96 and 119.17±49.41mm2.

A B

Fig 14. Measurement of dural sac cross-sectional area on MRI at the L4-5 level in the

(A) control group and (B) lumbar central canal spinal stenosis group.

4. Antonio Pierro et al proposed a method depended on the assessment of sagittal diameters

of the lumbar spine (spinal canal, dural sac, and vertebral body). The SCDs, DSD, and VBDs

were obtained at each level of the lumbar vertebral column from L1 to S1 vertebrae. At each

level, the DSR was calculated as the quotient of DSD to VBD(Fig 15 a,b and c).[25]

They concluded that the accurate and quantitative definition of the normality range for these

metrics may allow the physician to obtain more accurate diagnoses, avoiding duplication of

diagnostic tests, and speeding up the timing of the diagnosis.

SCD cutoff values from L1 to S1 ranged from 14.5–10.1 mm (males) to 15.0–9.9 mm

(females). DSD at S1 and L4 level show a significant difference in male and female groups.


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A B C

Fig 15. (T1‑weighted): Measurements were obtained on the sagittal images, in the

stretch between L1 and S1: (a) anterior‑posterior diameter of the vertebral body, (b)

anteroposterior diameter of the spinal canal, and (c) anteroposterior diameter of the

dural sac.[25]

5. D Premchandran et al described another method of measuring the VBD,DSD and SCD as

follows:

The Vertebral Body Diameter (VBD) measured between the anterior and posterior border at

the middle of each vertebral body of L1 to L5 lumbar vertebrae on T2 sagittal section MRI of

lumbar spine. The Dural Sac Diameter (DSD) measured between the posterior wall of the

vertebral body to the anterior border of the spinous process on T2 sagittal section MRI of

lumbar spine at L1 to L5.[26]

The Canal Body Ratio (CBR) calculated by dividing the DSD by the VBD.


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The cross-sectional area containing the dural sac is measured T2 axial section of MRI lumbar

spine at L1 to L5 lumbar vertebral levels.[27]

The ratio of the dural sac cross sectional area to the vertebral body cross sectional area of the

lumbar vertebrae L1 to L5 was calculated. Calculation of this ratio as a criteria to predict the

occurrence of canal stenosis was a new method that was performed in our study(Fig 16 a&

b).[28]

They concluded that the ratio between the area of the dural sac and the area of the vertebral

body being a constant at 0.2 can be used as a diagnostic marker to predict the lumbar canal

stenosis. This value is an additional to the canal body ratio which can also be used in

evaluating possible symptomatic or asymptomatic cases of lumbar canal stenosis.

a b

Fig 16

MRI T2 Sagittal section of the lumbar vertebrae illustrating the landmarks used for

measuring the area of the vertebral body and the area of the dural sac.

1.4.3 CT measurements

Abdoulatif Amadou et al used CT for measuring distances the anteroposterior diameter

(APD1) and inner pedicular diameter (IPD) of the lumbar canal(Figure 17)., the

anteroposterior diameter (APD2) and transverse diameter (TD) of the dural sac, followed by

the evaluation of APD2/APD1 (R1) and TD/IPD (R2) ratio(Figure 18).[29]


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In their study, the average APD of the lumbar canal (APD1) was 15.41±0.55mm, IPD was

23.27±1.67mm, the average APD of the dural sac (APD2) was 11.60±0.66mm, and the

average TD of the dural sac was 15.55±1.54mm.

They found that the lower APD of the lumbar canal would be in L3. The IPD of the lumbar

canal, the APD and TD of the dural sac would progressively decrease from L1 to L5.

Fig 17

Measurements of anteroposterior diameter (APD1) and interpedicular diameter (IPD) of

lumbar spinal canal.

Fig 18

Measurements of anteroposterior diameter (APD2) and transverse diameter (TD) of lumbar

dural sac.

2.1 MATERIAL AND METHODS

A cross-sectional prospective study was conducted in the consultant clinic of Basrah teaching

hospital and Ibn Al-Baitar private hospital from 13th

of July until 22th

of October 2018.

All data were collected from the patient himself by the same researcher with aid of clinical

history, physical examination and MR imaging studies.


363


Patients were of both sexes divided into 3 age groups; group 1(13-30 years), group 2(31-50

years), group 3(51-90 years).

Marital status was classified to married, unmarried, divorced and widow or widower.

Patients who are presented with back pain to the orthopedic consultation clinic in Basrah

teaching hospital (most of the patients presented to the outpatient clinic had plain radiograph

of lumbosacral spine) were referred to MRI study to the department of radiology or to Al-

Zahraa MRI clinic after history taking and clinical examination.

Three hundreds and thirty eight (338) patients with back pain divided into two groups

according to the clinical features that are predicting LSS clinically.

Group A who are diagnosed with LSS and group B who do not have LSS.

Then MRI study of each patient was interpreted carefully looking for MRI changes of LSS

and sedimentation sign which was examined by inter-observer.

After that groups A & B were divided into two sub-groups according to the sedimentation

sign in relation to its absence and presence.

The measurements of dural sac diameter and spinal canal diameter were achieved using

RADIANT and PHILIPS software for measuring the anteroposterior diameter of dura and the

canal on T1 and T2 weighted images.

Canal diameter will be measured on MRI T1 weighted images.

The anteroposterior SCD will be obtained perpendicularly to the long axis of the spinal canal

from the posterior wall of the vertebra at the midportion to the front edge of lamina.

The Dural Sac Diameter (DSD) measured between the posterior wall of the vertebral body to

the anterior border of the spinous process on the T2 sagittal section MRI of lumbar spine at

L1 to S1.

Back pain

Stenosis No stenosis

Sedsign + Sedsign - Sedsign + Sedsign -


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Exclusion criteria

(1) Lumbar vertebrae fracture

(2) Vertebral abnormalities

(3) Previous spinal surgery

(4) Spinal tumors

(5) Pott‘s spine

(6) Paget‘s disease

(7) Gross spinal pathology (e.g., spondylolisthesis, retrolisthesis and disc-space collapse).

2.2 RESULTS

A population of 338 patients presented with back pain were reviewed, their ages range from

13-81 years. The median is 49 while their mean was 48.18.Most age group of patients was

between 51-81 years of age (47.6%).[Table 1]

Tab 1: Age frequency.

Age Frequency Percent

13-30 43 12.7

31-50 134 39.6

51-90 161 47.6

Total 338 100.0

Most of the patients were from Basrah governorate (213), while 125 patients were from other

governorates. [Table 2]

Table 2: Residency.

Residency Numbers Percentages

Basrah 213 63.6

Other governorates 125 36.4

Total 338 100.0

Regarding the gender, females occupied the majority of the sample with 198 patients and 140

males [Table 3]

Table 3: Gender prevalence.

Gender Frequency Percent

Male 140 41.4

Female 198 58.6

Total 338 100.0


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Regarding the duration of back pain from its onset,28 patients were less than or equal to 12

weeks 8.3% and 310 patients were complaining for more than 12 weeks 91.7%.[Table 4]

Table 4: Duration of back pain.

Duration Frequency Percent

<= 12 weeks 28 8.3

>= 12 weeks 310 91.7

Total 338 100.0

The complaints of the patients that are related to LSS as following:

1-Numbness and/or pain in the thighs down to the calves and shins was very 94.5% of

patients.

2-Numbness and/or pain increase in intensity after walking for a while, but are relieved by

taking a rest 92.1% of patients.

3-Standing for a while brings on numbness and/or pain in the thighs down to the calves and

shins 92.7% of patients.

4-Numbness and/or pain are reduced by bending forward 91.5% of patients.[Table 5]

Table 5: the complaints of the patients that are related to LSS.

The complaints of the patients that are related to LSS

Numbness and/or pain in the thighs down to the calves and shins 94.5%

Numbness and/or pain increase in intensity after walking for a while,

but are relieved by taking a rest 92.1%

Standing for a while brings on numbness and/or pain in the thighs

down to the calves and shins 92.7%

Numbness and/or pain are reduced by bending forward 91.5%

The p value of this questionnaire (for the clinical diagnosis of LSS) in our study is p<0.001

Table 6 shows that the four signs used to diagnose spinal stenosis were all very sensitive and

very specific.


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Table 6: Showing specificity and sensitivity of the clinical symptoms for the diagnosis of

LSS.

Spinal stenosis Numbness and/or pain in the thighs down to the calves and shins

Yes No

Yes 201 19

No 2 116

Sensitivity = 91.4% Specificity =98.3%

Spinal stenosis

Numbness and/or pain increase in intensity after walking for a

while, but are relieved by taking a rest

Yes No

Yes 204 16

No 2 116

Sensitivity= 92.7% Specificity =98.3%

Spinal stenosis

Standing for a while brings on numbness and/or pain in the thighs

down to the calves and shins

Yes No

Yes 195 25

No 1 117

Sensitivity=88.6% Specificity=99.2%

Spinal stenosis Numbness and/or pain are reduced by bending forward

Yes No

Yes 198 22

No 1 117

Sensitivity=90% Specificity=99.2%

Of the three hundreds thirty eight (338) patients, 220 patients 65.1% diagnosed with LSS and

118 patients 34.9% do not present with LSS. [Tab 7]

Tab 7: Frequency of LSS.

The levels of LSS in our study were as follows, L1-L2 6%, L2-L3 3%, L3-L4 1.8%, L4-L5

8.9%, L5-S1 6.8%, Multiple levels 44.1%.[Table 8]

Table 8: Levels of LSS.

Levels Frequency Percent

L1-L2 2 6

L2-L3 10 3.0

L3-L4 6 1.8

L4-L5 30 8.9

L5-S1 23 6.8

Multiple 149 44.1

Total 220 100.0

LSS Frequency Percent

Yes 220 65.1

No 118 34.9

Total 338 110.0


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Regarding sedimentation sign in relation to LSS, 210 patients 95.5% have sed. sign on MRI,

10 patients 4.5% do not have sed. sign on MRI.

The specificity of Sed. sign was 100% and the sensitivity was 95.5%, the P value was

P<0.001. [Table 9]

Table 9. Sed.sign relation to LSS.

LSS with Sed. sign Frequency Percent

Positive 210 95.5

Negative 10 4.5

Total 220 100.0

Regarding the level of sed. sign in relation to the level of LSS sed. sign the results in our

study were as follows; L1-L2 9%, L2-L3 4.5%, L3-L4 2.7%, L4-L5 13.6%, L5-S1 10.5% and

Multiple level stenosis 67.7%[Table 10]

Table 10: Level of sed. sign in relation to level of LSS.

Sed. sign level with LSS level Frequency Percent

L1-L2 2 9

L2-L3 10 4.5

L3-L4 6 2.7

L4-L5 30 13.6

L5-S1 23 10.5

Multiple 149 67.7

Total 220 100.0

After measurements of both canal and dural sac diameters in both group A and B the results

were as follow: [From Table 11-14]

The diameter of the spinal canal for the patients who are diagnosed to have LSS [Table 11]:

Table 11: Measurement of spinal canal diameter from L1-S1 in patients with LSS.

Canal

diameter LCD1 LCD2 LCD3 LCD4 LCD5 SCD1

Mean 16.00 15.07 13.95 13.26 12.68 10.86

Median 15.90 14.80 13.95 13.20 12.65 10.90


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The diameter of spinal canal of the patients do not have LSS measured from L1-S1 was as

follows [Table 12]:

Table 12: Measurement of spinal canal diameter from L1-S1 in patients who do not

have LSS.

Canal

diameter LCD1 LCD2 LCD3 LCD4 LCD5 SCD1

Mean 17.85 16.91 16.28 15.77 14.75 12.37

Median 17.80 16.90 16.30 15.60 14.70 12.40

For the dural diameters the measurements were as follow:

In patients with LSS [Table 13]:

Table 13: Measurements of dural diameter from L1-S1 in patients with LSS.

Dural

diameter DSDL1 DSDL2 DSDL3 DSDL4 DSDL5 DSDS1

Mean 13.86 12.83 11.78 11.18 10.82 8.86

Median 13.80 12.80 11.60 11.00 10.30 8.60

For the patients who do not complain from LSS the measurements were as follow [Table 14]:

Table 14: measurements of dural diameter of patients with no LSS.

Dural

diameter DSDL1 DSDL2 DSDL3 DSDL4 DSDL5 DSDS1

Mean 15.54 14.57 13.79 13.00 12.23 9.92

Median 15.60 14.60 13.70 13.00 12.10 9.95

2.3 DISCUSSION

This study investigated the clinical value of sedimentation sign in patients who are diagnosed

clinically to have LSS according to Konno et al predicting questionnaire of LSS.

Regarding demographic distribution, most of our patients residency was in Basrah(63%) and

the rest came from neighboring governorates because Basrah is the main center of spine

surgery in south of Iraq.

Regarding the mean age of patients who are involved in the present study and diagnosed with

LSS, the mean age is 47.8 which is somewhat close to Leonoid kalichman et al[30]

as

described the mean age was 52.6(age range: 32–79).

Most of the studies showed the same results for the patients‘ gender, as in the present study

the female is affected more than males in 56.8%.


369


This agrees with VAC Resende et al where the female affected 70% more than male 30%.[4]

The standardized questionnaire used to reach the diagnosis of LSS was proposed by Konno et

al, According to the authors, it is a diagnostic support tool for lumbar spinal stenosis: a self-

administered, self-reported history questionnaire, a score of 4 points on Q1–Q4 indicates the

presence of LSS.

In our study the questionnaire has a sensitivity of 91.2 % and a specificity of 94.3% this

somewhat close to Konno et al the questionnaire had a sensitivity of 84% and a specificity of

78% in diagnosing LSS.

Regarding the sedimentation sign,95% of patients with LSS have Sed. Sign on MRI, showed

a sensitivity of 95.5% and a specificity of 100% and the P value is p<0.001 and it is strongly

significant result, this agrees with Barz et al 94% sensitive and 100% specific for LSS in their

study.[31]

The most level involved in LSS in this study is multilevel stenosis(44.1%),L4-5(8.9%).L5-

S1(6.8), L2-3(3%),L3-4(1.8%) and L1-2(0.6%),this result agrees with Hamdan et al that the

most common is multiple level stenosis than single level then followed by L4-5.[32]

The level of sedimentation sign and LSS level, above or below stenosis, as 3 patients above

the stenosis and 2 below the stenosis and the other patients sedimentation sign was at the

level of stenosis, this somewhat corresponding to VAC Resende et al.[4]

The anteroposterior diameter of spinal canal of the patients with LSS and patients who do not

have LSS is measured on MRI T1 weighted images from L1-S1,These results compared to

Antonio Pierro et al in a study similar to the present study with the same method of

measurements[25]

,the midsagittal diameters on MRI in patients diagnosed with LSS (the

mean) from L1-S1 were as follows:

(L1 16.0mm/L2 15.0mm/L3 13.9mm/L4 13.2mm/L5 12.6mm/S1 10.8mm)

The midsagittal diameter on MRI in patients who are not diagnosed with LSS (the mean)

from L1-S1were as follows:

(L1 17.8mm/L2 16.9mm/L3 16.2m/L4 15.5mm/L5 14.7mm/S1 12.3mm)


370


The mean midsagittal diameter showed a craniocaudal decrease in size and the measurements

of SCD in patients with LSS were narrower.

Regarding dural sac anteroposterior diameter in patients diagnosed with LSS and for the

patients who are not diagnosed to have LSS.

The results of dural sac diameter measurements on T2 weighted MRI compared to Divya

Premchandran et al.[28]

The midsagittal dural sac diameters on MRI in patients with LSS, (the mean) from L1-

S1were as follows:

(DSDL1 13.8mm/DSDL2 12.8mm/DSDL3 11.7mm/DSDL4 11.1mm/DSDL5

10.8mm/DSDS1 8.8mm)

The midsagittal dural sac diameter on MRI in patients who are not diagnosed with LSS, (the

mean) from L1-S1 were as follows:

(DSDL1 15.5mm/DSDL2 14.5mm/DSDL3 13.7mm/DSDL4 13.0mm/DSDL5

12.2mm/DSDS1 9.9mm)

The mean midsagittal diameter also showed a craniocaudal decrease in size and the

measurements of DSD in patients with LSS were narrower.

2.4 CONCLUSION

The Sed. sign was shown to have high reliability and acceptable inter-observer reliability in

the present study.

It was helpful to diagnose LSS in patients with LBP.

The Sign appears most sensitive in defining severe LSS cases, may add specific diagnostic

information beyond the traditional history, physical examination and imaging studies that are

standard in LSS diagnosis.

It may be that the Sed. sign is related to treatment outcome for individuals with LSS, yet

more research is warranted to determine whether or not this is the case.

Our study revealed that for each vertebral level from L1 to S1, a specific MRI cutoff value

can be associated to the narrowing of the spinal canal.


371


2.5 Recommendations

It may be that the Sed. sign is related to treatment outcome for individuals with LSS, yet

more research is warranted to determine whether or not this is the case.

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