Review Article
Lumbar Spinal Stenosis: A Review
Abstract
Lumbar Spinal Stenosis (LSS) is one of the most common
radiologic-anatomical syndromes in all population. Magnetic Resonance Imaging
(MRI) of lumbar spine is the standard test to identify the narrowing of the
spinal canal and adjacent vascular structures. Population of least developed
countries those work for bread and butter are at highest risk of this disorder.
This review attempts to describe the types, patho-anatomy, patho-physiology,
clinical presentation, diagnosis, treatment and complication of lumbar
stenosis. The effectiveness of conversative treatment and the need for surgery
according to the severity of the stenosis play a crucial role for patient
management. Spinal stenosis is categorized as primary and secondary. MRI
provides detail anatomic structures which is adequate for surgical planning.
Introduction
Lumbar spinal stenosis (LSS)) is a one of the commonest disorder
in aging as well as adolescent population.[1] It
is characterized by the narrowing of the spinal canal and the nerve root canals.[2] Aching,
cramping, or heaviness in the buttocks, hips, thighs, knees or lower legs with
standing or walking, is the classic clinical symptom of neurogenic claudication.
LSS thus have become most common cause for spinal surgery in patients
over age 65 years.1 LSS is not life threatening, but it negatively
impacts the quality of life (QOL) due to substantial disability, with
limitations in performing routine daily life activities.[3]
MRI is suggested as the standard non-invasive test to
confirm the presence of anatomic narrowing of the spinal canal or the presence
of nerve root impingement. It seems to be useful to consider the dynamic aspect
of LSS and assess neural and vascular tissue impingement based on morphology of
the dural sac and its content.[4] Machado
et al, (2015) investigated the effectiveness of spinal surgery. They concluded
that the relative efficacy of various surgical options remained uncertain.4
Supe et al. (2015) stated the spinal synovial cyst are
associated with pain in back with radicular pain and are most common at L4-L5
as this region is the most mobile. They recommended MRI scan of the spine is
best diagnostic modality for these cysts.[5] In
appropriately selected patients, surgical intervention has been demonstrated to
provide for improvement in pain, disability and quality of life. Outcomes
seemed less favorable with greater complication rates among patients with
diabetes or obesity. Elderly patients are recommended to be excluded from
surgical intervention for symptomatic LSS.[6]
Pathoanatomy
Ligamentum flavum, the facet
joints and the disk space are the three primary structures that contribute to
spinal stenosis. With degenerative changes, the ligamentum flavum and facet
joints may hypertrophy, secondary to mechanical stresses. The aging process
results in diminished disk height, which if pronounced can allow buckling of
the ligamentum flavum into the spinal canal. Ligament hypertrophy, osteophytes
or disk bulging can all encroach on the spinal canal.[7]
Pathophysiology
The pathophysiological changes of Lumbar spinal stenosis
(LSS) are caused by degenerative changes of the lumbar spine which include
thickening and buckling of ligamentum flavum (LF), osteophyte formation, facet hypertrophy,
and bulging of the intervertebral disk. Consequently, the central spinal canal
is narrowed resulting in compression-induced ischemia of the cauda equine. Venous
congestion is another proposed mechanism of intermittent postural radiculopathy
in lumbar stenosis.6, [8]
Clinical Presentation
Patients classically present with Low Back Pain (LBP) that
may be associated with neurogenic claudication, described as radiating pain
along the lower extremities usually down to the knees or even to the calf muscle
level. The pain is triggered and is worsened as the patient ambulates or stands
and is relieved with flexion of the spine or sitting down. Neurogenic
claudication is believed to be a result of structural narrowing of the spinal
central canal, which impedes venous return thus causing venous hypertension,
resulting in arterial ischemia of the cauda equine.2
Diagnosis
Definitive diagnostic information is most readily obtained
from lumbar spinal MR images and/or CT scans with sagittal reconstructions. These
studies clearly show the size, shape and anatomic relationships of spinal and
neural elements and can demonstrate the relative contribution of developmental
stenosis as well as disk, facet and ligamentous elements of nerve root
compression.6
In addition, MRI usually provides
anatomic information sufficient for surgical planning. Axial MRI scan of
central stenosis typically demonstrates a circumferentially narrowed canal.
Hypertrophic bone appears as a dark region of low signal of T1-weighted and T2-weighted
images, hypertrophic ligamentum flavum as an intermediate signal on T1-weighted
and T2=weighted images, and loss of fat in the epidural space due to prolonged
compression as a loss of high T1 signal. T2 weighted sagittal images are useful
for their myelogram like representation of the thecal sac. Lateral stenosis
appears on axial and sagittal views as bone encroachment and loss of fat signal
(best appreciated on T1-weighted images) surrounding the exiting nerve root.6
Classification
Spinal stenosis is classified as either primary or
secondary. In primary stenosis, the spinal canal is constricted due to a
congenital abnormality or a disorder in postnatal development. Primary stenosis
is extremely rare. However, secondary stenosis is due to degenerative changes
of the vertebral bodies, facet joints and disks.[9]
Treatment
Current treatment options range from conservative management
to invasive spinal surgical decompression and lumbar fusion, with or without
instrumentation.
Conservative Therapy
VS Surgery
Conservative methods of therapy may be of use in early and
moderately severe cases; it is certainly useful and appropriate to initially
pursue nonsurgical measures. Conservative measures usually include bed rest,
non-steroidal anti-inflammatory drug, acetaminophen, exercise program, aerobic
fitness and epidural steroid injections. Once patients progress past the point
of moderate symptom severity, conservative methods may become ineffective or
unrealistic. Surgical decompression has been helpful in about two-thirds of
patients, but is associated with considerable morbidities. Patients who delay
surgery have similar outcomes to patients who proceed immediately with surgery.
Thus, the consideration of proceeding with surgery should await evaluation of comorbidities
as well as assessing the patient’s response to conservative therapy.2
Weight loss is recommended for obese patients. to reduce
symptoms, including pain, patients are generally advised to avoid activities
that place mechanical stress on the lower back, particularly those that place
the spine in extension. When oral drugs and physical therapy fail to provide
relief of symptoms, epidural steroid injections may be used on the assumption
that symptoms result from inflammation at the interface between the nerve root
and compressing tissues. The goal of surgery is to decompress the central
spinal canal and neural foramina to eliminate pressure on nerve roots.
Alternatively, a minimally invasive laminectomy can be done using several
smaller incisions.
Complications
Although lumbar spinal stenosis is not life-threatening, it
can cause chronic and substantial pain and can severely limit patient activity.
Discussion
Lumbar spinal stenosis has a high prevalence in older adults
and a strong negative influence on quality of life, preventing many older
adults from maintaining an active independent life.1 Surgery is
superior to nonsurgical treatment for improving pain and function. Symptoms may
recur with either approach.1 The chief complaint of patients with
symptomatic spinal stenosis is claudication, an intense pain brought on by
walking and usually felt in one or both lower extremities.9
Knutsson et al in 2015 described the experience of being a
person with LSS and how life and suffering were managed under the influence of
their disease. Being a patient with LSS included suffering. Both physicians and
patients needed to work towards salutogenic perspective, focusing on resources
to improve care, making it more comprehensible, manageable and meaningful.[10]
K. Kato et al, 2014 conducted LSS support tool project in
1657 hospitals and evaluated the diagnostic accuracy of the Self-administered,
Self-reported History Questionnaire in Japan. They concluded the improved
version can be used for LSS screening and its use may improve the quality of
LSS diagnostic practice in Japanese primary care settings.[11]
Yaldiz et al, 2015 retrospectively, demographically and
clinically investigated the causes of postoperative infection in patients with
lumbar spinal stenosis who underwent posterior stabilization. Implant-related
infections (IRIs) still appeared to be a major problem in spinal surgery, even
though the infection rate has been reported to be around 1%. However, PSI rate
increased upto 2.1% to 8% as the frequently performed spine surgeries such as
laminectomies and discectomies with plantation increased. Dead space in the
surgical field, foreign bodies, necrotic tissue and prolonged surgical
procedures are among the factors that increase the risk of IRI. Implant use in
spinal surgery increased the risk of infection about 3 fold.[12] Beyer et al in 2015 studied the
influence of spinopelvic parameters on non-operative treatment of lumbar spinal
stenosis.[13]
Kim et al, 2015displayed patients with high pain sensitivity
may display less improvement in back pain, leg pain, and disability after
surgery for LSS compared with patients with low pain sensitivity. Furthermore,
the Pain Sensitivity Questionnaire (PSQ) can be used to predict surgical
outcomes after spine surgery for LSS.[14]
Shamji et al, in 2015 systematically reviewed the
effectiveness of lumbar spinal surgery for symptomatic LSS in elderly patients
(over age 65 years). They revealed that the majority of elderly patients
exhibited significant symptomatic improvement. Outcomes seem less favorable
with greater complication rates among patients with diabetes or obesity. They
recommended that elderly patients should not be excluded from surgical
intervention for symptomatic LSS.[15]
Ulrich in 2015 concluded the patients 80 years or older can
expect a clinically meaningful improvement after lumbar decompression for
symptomatic DLSS and the patients showed significant positive development in
quality of life in the short and long term follow ups.[16] Ferrari et al, 2015 investigated the
clinical validity of clinical tests for the diagnosis of lumbar instability.
They suggested Passive Lumbar Extension (PLE) test was the most appropriate
test to detect lumbar instability in specific LBP.[17]
LBP is a growing health problem in the industrialized world.
Despite the high medical expenses required for its management, the prevalence
of LBP is increasing. LBP is a heterogeneous condition, and the identification
of different sub-groups could help the management decisions.14
Lurie et al, 2015 compared 8-year outcomes of surgery with
non-operative care for symptomatic LSS. They concluded symptomatic spinal
stenosed patients showed diminishing benefits of surgery in as-treated analyses
of the randomized group between 4 and 8 years, whereas outcomes in the
observational group remained stable.[18]
Dahal et al (2012) noticed most common spinal pathology in
patients with low back ache was degenerative changes of the spine. MRI, though
expensive was beneficial in early diagnosis and management of lumbar spine
abnormalities.[20] Markman and Nandigam (2015) assessed
changes in spine segment biomechanics due to laminotomy and laminectomy.[21]
Segar et al (2015) also investigated that obesity might be
associated with clinical diagnosis of LSS but not lumbar disc herniation or
degenerative spondylolisthesis.[22] Burton et al (1981) noticed 800
Failed Back Surgery Syndrom (FBSS) and stated FBSS is actually a spectrum of
organic disease processes complicated by secondary financial gain and learned
chronic pain behavior. While many of the patients can be salvaged to varying
degrees by comprehensive rehabilitation programs, it is uncommon to achieve
complete pain relief by any combination of therapeutic measures. This is due in
part to the great difficulty in quantitating pain and associated psychologic
occupational, social, monetary, intellectual, motivational and education
factors.[23]
Atlas et al (1996) resulted the patients with severe LSS who
were treated surgically had greater improvement than patients treated
non-surgically.[24]They again assessed outcomes till 4
year and concluded for severe LSS, surgical treatment was associated with
greater improvement in patient-reported outcomes than non-surgical treatment.
The relative benefit of surgery declined over time but remained superior to
non-surgical treatment.[25] Atlas et al (2005) again completed
follow-up for 8 to 10 years and concluded LBP relief, predominant symptom
improvement and satisfaction with the current state were similar in patients
initially treated surgically or non-surgically. These results support a shared
decision-making approach among physicians and patients when considering
treatment options for LSS.[26]
Kuslich (1991) defined the tissue origin of low back pain
and sciatica. He took 193 patients who had surgery for herniated discs, spinal
stenosis, or both.[27] Pasqualini et al. (2012) concluded
there was no correlation between the degree of stenosis and the Oswestry index and MRI in cases and
controls.[28] Paine et al (1974) defined LSS as a
condition in which the A-P and lateral diameters of the bony canal are narrower
than normal and/or in which the shape of the canal in cross section is often
abnormal.[29]
DA Chad (2007) also stated LSS may
be congenital or acquired. A classic clinical presentation is described as
neurogenic claudication. Physical signs of sensory loss, weakness and
attenuation of reflexes often are mild and limited in distribution.[30] Bowen et al (1978) reviewed LSS as a
condition not only affecting the middle-aged and elderly but young adults may
produce symptoms.[31] J Englund (2007) stated LSS is a
clinical syndrome first described in the 1950s. It is defined as narrowing of
the spinal canal with cord or nerve root impingement resulting in symptoms of
radiculopathy or pseudoclaudication.[32]
Conclusion
In summary, LBP resulting from degenerative disease of the
lumbosacral spine is a major cause of morbidity, disability, and lost
productivity. So, rapid diagnosis and treatment are essential if patients are
to be returned to their previous levels of activity.
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