RETROSPECTIVE AND PROSPECTIVE STUDY TO ANALYSE OUTCOME OF SURGICAL MANAGEMENT
OF PATIENTS TREATED FOR MULTISEGMENTAL LUMBAR CANAL STENOSIS
Dissertation submitted to
THE TAMIL NADU DR.M.G.R MEDICAL UNIVERSITY CHENNAI- TAMIL NADU
In partial fulfilment of the requirements for M.S. DEGREE
BRANCH -II ORTHOPAEDIC SURGERY
MADRAS MEDICAL COLLEGE
INSTITUTE OF ORTHOPAEDICS AND TRAUMATOLOGY RAJIV GANDHI GOVERNMENT GENERAL HOSPITAL,
CHENNAI-3.
MAY 2020
CERTIFICATE
This is to certify that this dissertation titled “RETROSPECTIVE AND PROSPECTIVE STUDY TO ANALYSE OUTCOME OF SURGICAL MANAGEMENT OF PATIENTS TREATED FOR MULTISEGMENTAL LUMBAR CANAL STENOSIS” is a bonafide record work done by DR.
ADITYA THAKUR , during the period of his Post graduate study from May 2017 to May 2020 under guidance and supervision in the INSTITUTE OF ORTHOPAEDICS AND TRAUMATOLOGY, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai-600003, in parital fulfilment of the requirement for M.S. ORTHOPAEDIC SURGERY degree Examination of The Tamilnadu Dr. M.G.R. Medical University to be held in May 2020.
Prof.Dr.R.Jayanthi MD., FRCP(Glasg).,
Dean,
Rajiv Gandhi Government General Hospital, Madras Medical College, Chennai - 600 003.
Prof.N.Deen Muhammad Ismail
M.S.Ortho, D.Ortho.
Director & Professor, Institute of Orthopaedics &
Traumatology,
Madras Medical College, Chennai.
DECLARATION
I declare that the dissertation entitled “RETROSPECTIVE AND PROSPECTIVE STUDY TO ANALYSE OUTCOME OF SURGICAL MANAGEMENT OF PATIENTS TREATED FOR MULTISEGMENTAL LUMBAR CANAL STENOSIS” submitted by me for the degree of M.S. is the record work carried out by me during the period of June 2017 - October 2019 under the guidance of PROF B PASUPATHY M.S. ORTHO., D.N.B. ORTHO, D. ORTHO, MNAMS.
Professor of Orthopaedics, Institute of Orthopaedics and Traumatology, Madras Medical College , Chennai. This dissertation is submitted to the Tamil Nadu Dr.M.G.R. Medical university , chennai in partial fulfillment of the University regulations for the award of degree of M.S. ORTHOPAEDICS (BRANCH -II) examination to be held in May 2020.
Signature of the candidate Place :
Date :
Dr. Aditya Thakur Signature of the Guide
Prof B Pasupathy, M.S.Ortho, D.N.B Ortho, D.Ortho, MNAMS Professor of Orthopaedics
Institute Of Orthopaedics and Traumatology Madras Medical College, Chennai.
ACKNOWLEDGEMENT
I express my thanks and gratitude to our respected Dean Prof.Dr.R.JAYANTHI M.D. FRCS (Glasg)., Madras Medical College, Chennai – 3 for having given permission for conducting this study and utilize the clinical materials of this hospital.
I would like to express my sincere thanks and gratitude to our beloved Prof.N.DEEN MUHAMMAD ISMAIL M.S., Ortho, D.Ortho., Director, Professor of orthopaedics, Institute of Orthopaedics and Traumatology, for his valuable advice throughout this study.
My sincere thanks and gratitude to Prof.B.PASUPATHY, M.S.Ortho., D.Ortho., DNB Ortho., Professor, Institute Of Orthopaedics and Traumatology, for his guidance and constant advice provided throughout this study.
My sincere thanks to Prof.V.SINGARAVADIVELU, M.S.Ortho., D.Ortho., Ph.D., Professor, Institute Of Orthopaedics and Traumatology, for his valuable advice and support.
I am very much grateful to Prof.A.PANDISELVAN M.S. Ortho., D.Ortho., for his unrestricted help and advice throughout the study period.
I sincerely thank Prof.NALLI R.UVARAJ, M.S.Ortho., D.Ortho., for his advice, guidance and unrelenting support during the study.
I am very much grateful to Prof.K.VELMURUGAN, M.S.Ortho, D.N.B.
Ortho for his valuable guidance and advise from the beginning of the study.
I am deeply indebted to my beloved co-guide Dr.JVAGHAR JILL, M.S.Ortho., who has guided me in every aspect of this study.
I also thank Dr.A.Saravanan, Dr.R.Rajganesh, Dr.A.N.Sarathbabu, Dr.S.Senthil Sailesh, Dr.P.Kannan, Dr.Nalli R.Gopinath,, Dr.P.Kingsly, Dr.N.Muthalagan, Dr.G.Hementhakumar, Dr.G.Karthick Dr.G.Kaliraj, Dr.Suresh Anandan Dr.P.R.Dhanasekaran, Dr.Balasubramanium, Dr.P.L.Srinivasan, Dr.Jeffery Assistant Professors of this department for their valuable suggestions and help during this study.
I thank all anaesthetists and staff members of the theatre and wards for their help during this study.
I am grateful to all my post graduate colleagues for helping in this study. Last but not least, my sincere thanks to all our patients, without whom this study would not have been possible.
ABBREVIATIONS
AP : Antero-Posterior
BADL : Basic Activities of Daily Living
CT : Computed Tomography
CTM : CT Myelography
DM : Distraction Manipulation DSA : Dural Sac Area
DSEP : Dermatomal Somatosensory Evoked Potential EBM : Evidence-Based Medicine
EMG : Electromyelography
ESI : Epidural Steroid Injection ETT : Exercise Treadmill Test
FPVCT : Flat Panel Volumetric Computed Tomography HN : Herniated Nucleus Pulposus
MSCT : Multislice CT Myelography
MSPQ : Modified Somatic Perception Questionnaire NASS : North American Spine Society
NCS : Nerve Conduction Studies
NIC : Neurogenic Intermittent Claudication
NM : Neural Mobilization
NSAIDs : Nonsteroidal Anti-Inflammatory Drugs QALY : Quality Adjusted Life Years
RCT : Randomized Controlled Trial SLR : Straight Leg Raise
SSEP : Somatosensory Evoked Potentials
JOA : Japanese Orthopaedic Association LSO : Lumbosacral Orthosis
mCSA : Minimum Cross-Sectional Area MEP : Motor Evoked Potentials
MEPLT : MEP Latency
MR : Magnetic Resonance
MRI : Magnetic Resonance Imaging MRM : Magnetic Resonance Myelography SWT : Shuttle Walking Test
TENS : Transcutaneous Electrical Nerve Stimula- VAS : Visual Analog Scale
TABLE OF CONTENTS
S.NO CONTENTS PAGE
1 INTRODUCTION 1
2 AIM OF THE STUDY 3
3 REVIEW OF LITERATURE 4
4 NATURAL HISTORY 6
5 CLASSIFICATION 16
6 CLINICAL PRESENTATION 23
7 METHODOLOGY 45
8 FOLLOW UP & OBSERVATIONS 49
9 DISCUSSION 65
10 CONCLUSION 70
11 CASE ILLUSTRATIONS 71
12 BIBLOGRAPHY
13 ANNEXURES
Ethical Clearance Certificate Anti Plagiarism Certificate Proforma
Patient Consent Form Master Chart
INTRODUCTION
Lumbar canal stenosis describes a condition in which there is diminished space available for the neural and vascular elements in the lumbar Spine secondary to degenerative changes in the spinal canal. When symptomatic, this cause a variable clinical syndrome of gluteal and /or lower extremity pain and /or which may occur with or without back pain . Symptomatic Lumbar spinal stenosis has certain characteristic provocative and palliative features. Provocative feature include upright exercise such as walking or positionally- induced neurogenic claudication. Palliative features commonly include symptomatic relief with forward flexion, sitting and/or recumbency.
Spinal stenosis is one of the most common conditions in the elderly. The term was 1st described by verbiest and its associated narrowing of the spinal canal.
Narrowing of the spine can occur in the central canal, lateral recess or foramen leading to compression of the neural elements in those locations . The symptoms produced depends upon the location of the neural compression. Patient who are symptomatic describes low back pain radiating into bilateral legs typically associated with heaviness and weakness in their legs that worsens with movements. The variable presentation of the lumbar canal stenosis is not fully understood. Usually patients with central canal stenosis complain of neurogenic claudication where as patients with lateral recess and foraminal stenosis complains of radicular pain.
Patients in whom symptoms do not improve after a course of non surgical treatment may benefit from surgical treatment . For patients in whom surgery is indicated, several factors must be considered when selecting the appropriate procedure , including the pathology itself as well as patient specific goals and overall functional status . The mainstay of surgical treatment of lumbar spinal stenosis is decompression laminectomy. Patients with concomitant spondylolisthesis or instability, spinal deformity or concerns for iatrogenic postoperative instability should be considered for decompression with fusion.
In our study we analyse the outcome of surgical management of patients with multisegmental lumbar canal stenosis.
AIM AND OBJECTIVE
- To analyse surgical intervention in the management of multisegemental lumbar canal stenosis
- To assess the neurological and functional outcome of surgical procedure done .
REVIEW OF LITERATURE
1. In 1954 Verbiest H describes the 1st description of Canal stenosis in A radicular syndrome from developmental narrowing of the lumbar vertebral canal.In 1956, they Further explains their experiences on pathologic influence of a developmental stenosis of the lumbar vertebral canal. In 1963 Verbiest H reported about Spondylolisthesis : The value of radicular signs and symptoms. In 1966 Verbiest H explained about Pathomorphic aspects of developmental lumbar stenosis. In 1968 they reports of Unilateral lumbo-sacral radicular symptoms due to sequestrated disc material in the spinal canal. 1n 1973 Verbiest H explains about Neurogenic intermittent claudication in cases with absolute and relative stenosis of the lumbar vertebral canal (ASLC and RSLC), in cases with narrow lumbar intervertebral foramina, and in cases with both entities.
In 1974 Kirkaldy-Willis WH, Paine KWE, Cauchoix J, et al came up with further ideas and refined the existing understanding of Lumbar spinal stenosis.
Describing the synergistic effect of different degenerative changes causing stenosis of the spinal canal.
1n 1977 Verbiest H , published the results of surgical treatment of idiopathic developmental stenosis of the lumbar vertebral canal.
In 1978 Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al : Pathology and pathogenesis of lumbar spondylosis and stenosis. On autopsy specimen they find out that progressive degenerative changes in the posterior joints lead to marked
destruction and instability. They also commented on potential aetiology such as Spondylolisthesis , Paget’s disease and fluorosis.
In 1982 Kirkaldy-Willis WH explained about the Lumbar spinal nerve entrapment.1984 Kirkaldy-Willis WH : The relationship of structural pathology to the nerve root. In 1985 Kirkaldy-Willis WH : Presidential symposium on instability of the lumbar spine, there they describe about three phases of degeneration i.e. 1) Dysfunction 2) Instability 3) Restabilisation
In 1990 Boden SD, Davis DO, Dina TS, et al : Abnormal magnetic- imaging scans of the lumbar spine in asymptomatic subjects: A prospective investigation in which they describe the prevalence of abnormal findings on MRI scans of the lumbar spine in people without back pain.
In 1994 Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al : Magnetic resonance imaging of the lumbar spine in people without back pain. They describe the MRI of degenerative disc disease
In 1993 Deyo RA, Ciol MA, Cherkin DC, et al : Lumbar spinal fusion: a cohort study of complications, reoperations, and resource use in the Medicare population. They followup 27,111 patients and describe about indications for fusion among the older patients .
In 1999 Hillabrand AS, R and N: in degenerative lumbar stenosis: Diagnosis and management.They reported 85% success rate in surgical methods . But they also
caution about inadequate decompression, inadequate stabilization or medical comorbidities.
In 2005 Deyo RA, Gray DT, Kreuter W, et al : United States trends in lumbar fusion surgery for degenerative conditions. They did the retrospective cohort study to determine the rate of increase in lumbar spine fusion. They discussed about the indication , efficacy and various fusion techniques
In 2008 Watters WC III, Baisden J, Gilbert TJ, et al : Degenerative lumbar spinal stenosis: an evidence based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis. Evidence-based guidelines produced by North American Spine Society regarding diagnosis and treatment of patients with lumbar spinal stenosis.
In 2008 Weinstein JN, Tosteson TD, Lurie JD, et al: Surgical versus nonsurgical therapy for lumbar spinal stenosis. A large prospective study evaluating outcomes of lumbar spinal stenosis patients treated with surgical versus nonsurgical treatment. They concluded that surgery showed significantly more improvement in all primary outcomes than did patients who were treated non surgically.
NATURAL HISTORY
[1]Spinal stenosis which is defined as a condition in which there is decrease in the spinal canal space for vascular and neural elements leading to variable clinical syndrome of gluteal and lower extremity pain and fatigue which may or
may not be associated with low back pain. [2]Etymologically Stenosis is derived from the Greek word “ stenos” meaning Narrow , this condition was 1st described by Antonine Portal in 1803. The credit for term “Spinal Stenosis” goes to Verbiest[2], he also describes narrowing of the spinal canal as its potential cause of the symptoms. Later on [3] Kirkaldy- Wills describes the degenerative process as the cause of altered anatomy and altered physiology in spinal canal leading to symptomatic spinal stenosis.
It is very common condition in the elderly and its very important to differentiate between three types of stenosis i.e. Central Stenosis, Lateral Stenosis and Root canal Stenosis. Many a times there can be combination of these types. These may be associated with degenerative spondylolisthesis. Other causes of spinal stenosis includes Paget’s disease, secondary spinal stenosis which may be due to Osteoporotic fracture or may be due to tumour compressing the cord ,mostly from metastasis . In unusual circumstances iatrogenic stenosis can occur as a late complication of previous spine surgery . In these kind of scenario stenosis may occur due to so called Adjacent segment problem after fusion surgery or may be the part of scoliosis or kyphotic deformity .
The most common cause of Spinal stenosis is due to degenerative changes . Changes like these can cause symptoms but sometimes the so called stenotic images are symptom less. Relationship between degenerative lesion , abnormal imaging and patients symptoms are unclear. [4]Symptoms are usually insidious in onset and may be precipitated by the heavy activities or by trauma. Patients typically presents with low back pain radiating into bilateral legs which is
associated heaviness and weakness in the legs after prolong walk or exacerbation . Pain is relieved with forward leaning or rest. Pain is progressive in nature. In natural history of Lumbar canal stenosis with mild to moderate degenerative variant may show favourable for 33-50% of the cases.[5] Clinical course of the symptoms generally remains constant and progression to catastrophic neurological decline is rare . Medical treatment applied in the treatment did not significantly alter the symptoms and those with severe symptoms with significant loss of daily activity of living can be managed surgical with application of proper surgical principles.
DEFINITION
Lumbar spinal stenosis can be described as “Buttock or lower extremity pain , which may occur with or without low back pain, associated with diminished space for the neural and vascular elements in the lumbar spine ” may be associated with Paresthesia and weakness of the lower limb.
[6]Radiologically lumbar canal Stenosis is defined as the narrowing of the nerve root canal with decrease in dural sac area (DSA) < 75mm square or decrease Sagittal plane spinal cord diameter < 10 mm as absolute stenosis and 10-13 mm as relative stenosis[7].
Clinic o-radiological association in many a times cannot be established .
Multi-segmental Lumbar canal stenosis is defined as stenosis at two or more intra discal level
REGIONAL ANATOMY
[8]The lumbar region of vertebral column consists of five vertebra , first four vertebrae are similar in structure.Last lumbar vertebrae has structural adaptations for sacral articulation.Typical lumbar vertebrae consist of Body, Arches, Laminae, Zygapophyseal Articular processes, Transverse process, Spinous process, Vertebral Foramen, lumbosacral articulation and Intervertebral Discs.
ZYGAPOPHYSEAL ARTICULAR PROCESSES
They are encapsulated structures Superior and Inferior Zygapophyseal facets vary considerably in shape and orientation. They are oriented 90 degrees in the Sagittal plane 45 degrees anterior in the coronal plane . Superior articular facets is concave and faces medially and dorsally. Inferior facets face anteriorly laterally and vertical and convex.
With disc degeneration and narrowing , stress across the facet joints. This causes facet joint degeneration , hypertrophic and osteophyte formation.
Figure 1 : Sagittal cross section demonstrating D) disc desiccation, S) endplates sclerosis, O) Osteophyte formation, LF) hypertrophy and buckling of the ligamentum flavum, NR) Nerve root compromise within the foramen.
INTERVERTEBRAL DISCS
[9]At the time of birth disc have 50% of nucleus pulposus and annulus. With time collagen content increase and distinction between nucleus and annulus decreases. They have specific regional variation in lumbar segment i.e. the collagen fibres are oriented in 120 degrees opposite to each other . These configuration helps to resist tensile forces in nearly all direction .[10] Disc is the 1st step of spine degeneration , during this water content decreases to 70%.
Ability to handle mechanical load decreases in the dehydrated desiccated disc.
Figure 2 : Drawing showing neural organisation within the thecal sac at the L4- L5 and L5-S1 disc levels. M) motor components , S) sensory components.
VERTEBRAL FORAMEN :
There are three variations in shape of spinal canal which may be circular, oval or trefoil
[11]The foramen is usually larger than ganglion and the nerve it contains It also has fat and loose areolar tissue . Anteriorly it is bounded by vertebral body and disc, posteriorly by lateral aspect of facet and the ligamentum flavum . Superiorly and inferiorly bounded by pedicles of the vertebral bodies corresponding to that segment. During degenerative process , hypertrophy of facet joint causes posterior compression of neural element . Anterior compression can be due to endplates osteophytes.
There is well developed lateral recess due to transitional vertebra i.e. L5 and L4.
The normal canal dimensions in sagittal plane can varies from 15 to 25 mm.
A - Spinal Canal, B - Nerve Canal, C - Intervertebral Foramen . LIGAMENTS
Anterior and Posterior Longitudinal Ligaments are inter body ligaments .
[12]Anterior longitudinal Ligament traverses from C2 to sacrum along the anterior and lateral surface of the vertebral bodies. It is well developed in the lordotic segments of vertebral column . The tensile strength is highest at the Lumbar region and it is twice as strong as the posterior longitudinal ligament.
It becomes stretched in extension and compressed in flexion.
Posterior longitudinal Ligament lies within the vertebral canal . It traverses from C2 to sacrum and it forms ventral border of the vertebral canal. It is only one -sixth of Anterior Longitudinal Ligament and it provides axial tension in the Lumbar area.
It becomes stretched in flexion and slacked in extension.
LIGMANETUM FLAVUM
It forms the posterior surface of the vertebral canal and it traverses from C2 to sacrum.
Ligamentum flavum is strongest in the lower thoracic and weakest in the mid cervical region. This ligament got stretched during flexion and it is in highest strain during flexion.
The ligament is under constant tension even when the spine is in neutral position, because of its elastic nature . This nature of ligamentum flavum provides continuous compressive forces on the disc , which causes intradiscal pressure to remain high , raised pressure in the disc makes the discs stiffer. This elastic nature is advantageous because the ligament will not buckle on itself during movement .
INTERSPINOUS LIGAMENT
It connects spinous processes of adjacent vertebra. It is innervated by medial branches of the dorsal rami . Functionally it provides spine stability and its degenerates with aging.
SUPRASPINOUS LIGAMENT
It traverses from seventh cervical vertebra to L3 or L4, its like cordlike structure that connects the tip of the spinous processes.
THE MOTION SEGMENT
[13]Functional unit of spinal column , its a combination of the both bony and soft tissue structures like intervertebral disc, intervertebral foramen , superior and inferior facets, interlaminar space , Ligamentum flavum,Inter and Supraspinoous ligament along with intervertebral disc and facet joints one on each side of the midline . Functional spinal unit allow for motion in flexion, extension,side bending and rotation at the level of the motion segment .
BIOMECHANICS
[14]Lumbar spine movements are complex because of balancing act of stability and mobility in same moment. The motion segment provides lateral bending in the upper lumbar motion segment whereas in lower lumbar spine and lower sacral region flexion and extension . The anterior column of spine supports a most of the body weight in the upright position. Posterior elements support about 1/7th of the axial load .Intervertebral disc is loaded in the sitting and upright position. On lateral bending the annulus part of disc bulges toward the direction of motion whereas the nucleus component of disc moves away from the pressure . During degenerative process, water content in the nucleus gradually reduces thus the volume of the nucleus decreases. Therefore the load borne by the annulus increases and its subjected to weakening and tearing . The end result of these results in decreased disc height , irregular bony end plates of the vertebra and bone spur formation . These process can lead to increased instability i.e.
Spondylolisthesis in some and restricted painful movement in others . Facets joint in the lumbar region are oriented in the sagittal plane and are positioned to resist rotation and allow flexion and translation.
The concept of Motion segment also helps in formulating concepts of Decompression procedure . The spinous process and the associated ligaments are preserved and only the pathological segments are addressed.
CLASSIFICATION OF SPINAL STENOSIS
[15][2]Broadly into 3 categories:
1. Congenital/ Developmental 1. Idiopathic
2. Achondroplastic 3. Osteopetrosis 2. Acquired
1.Degenerative
A. Central
B. Lateral Recess C. Foraminal 2. Iatrogenic
A. Post laminectomy B. Adjacent to fusion
C. Malposition of Hardware in the canal D. Post procedure epidural hematoma
3. Miscellaneous disorders
A. Acromegaly B. Paget’s C. Fluorosis
D . Ankylosing Spondylitis 4. Traumatic
3. Combined
Any Combination of congenital/developmental or acquired stenosis.
Degenerative type is the most common type of Spinal canal stenosis.
Anatomically on the basis of neural compression it has been further classified as Central , Lateral recess and forminal type.
CENTRAL CANAL STENOSIS
As with degeneration the axial height of the disc and facet joint decreases , their is protrusion of disc in the spinal canal.[16] The dimensions of the canal are further decreased by Posterior Impingement from enlarged facets and the hypertrophied ligamentum flavum. With degeneration their is hypertrophy of the soft tissues which is responsible for 40% of Spinal stenosis.
On extension of the truck the hypertrophied ligamentum flavum buckles centrally in the central canal and further reduces the dimensions of the canal . Thats why these extension will cause worsening of the symptoms.
LATERAL RECESS STENOSIS
It occurs when there is posterior disc protrusion in combination with superior articular facet hypertrophy .[17] It presents with Lumbar Radiculopathy and its incidence ranges from 8 to 11%. The symptoms have dermatomal distribution.
FORAMINAL STENOSIS
It occurs when there is loss of disc height, vertebral endplates osteophytes, facet osteophytes, Spondylolisthesis and disc herniation . [18]It characteristically causes compression of the exiting nerve root and ganglion and also lumbar radiculopathy. Foraminal stenosis mostly occur in the lower lumbar segment with L5 nerve root most commonly involved . As similar to central canal stenosis symptoms of foraminal stenosis worse on extension of the lumbar
PATHOPHYSIOLOGY
It’s a cord dysfunction elicited by mechanical compression and degenerative instability . [19]During degenerative process intervertebral disc degenerates and collapse which leads to spur formation. This results in relative decrease in spinal motion at the level of spur formation with concomitant increase in spinal motion at the level above the spur formation. The increased stress is tackled with bone growth at the superior and inferior margins of osteophytes .[20] Formation can
occur anteriorly or posteriorly. Posterior osteophytes formation leads to narrow intra spinal diameter and lateral recess stenosis . This is also accompanied by ligamentum flavum hypertrophy leading to further canal volume loss . In the natural course of these pathological process there is Disc desiccation and degenerative discs disease resulting from reduced disc height causing segmental instability . These instability incites vertebral body and facet joint hypertrophy.[21] These changes are accompanied by further loss of canal volume from Herniated Nucleus Pulposus , Ligamentum flavum hypertrophy and disc space narrowing . From repetitive dynamic injury, cord is damaged and leads to
radicular pain.
Caudal vertebral body superior articulating process contributes to lateral recess and forminal stenosis.
FLOW CHART OF PATHOGENESIS [21]
Disc Desiccation and Degenerative Disc Disease
↓
Leads to narrow disc height
↓
Permitting the caudal superior articulating process to sublux anterosuperiorly
↓
Subluxation decreases foraminal space and biochemical disruption
↓
Provokes osteophytosis and ligamentum flavum hypertrophy
↓
Compromising foraminal volume
Dynamic foraminal stenosis implies
↓
Intermittent lumbar extension- provoked nerve root impingement from HNP, osteophytosis and vertebral body slippage
[21]Neurogenic claudication pathogenesis Cauda equina microvascular ischemia
↓
Venous congestion
↓ Axonal injury
↓
Intraneural fibrosis
[22]According to Ooi and colleagues On neurogenic claudication:
↓
Ambulation-provoked cauda equine
↓
Blood vessel dilation
↓
Circulatory stagnation
↓
Dilation of epidural venous plexus
↓
increased epidural and intrathecal pressure
↓
Compromise micro circulation
↓ Causes Pain
LUMBAR RADICULOPATHY
[23]It’s defined as a condition affecting one or more nerve roots of the lumbar spine typically caused by a Lumbar disc herniation.
Radiculopathy can be divided into : Pain and nerve dysfunction.
Pain is typically sharp and/or burning quality and follows the nerve root(s) area of sensory innervation in the Lower extremity.
Nerve dysfunction can be loss of motor and/or sensory modalities causing muscles weakness and/or atrophy and sensory disturbances
PATHOPHYSIOLOGY
Pressure + Chemical factors
Pressure
↓
Circulatory compromise
↓
Decreased transport of nutrients
↓
Resulting in Neuro-ischemia
CHEMICAL FACTORS [24] Olmarker et all (1993)
They found that Nucleus Pulpous applied to nerve root and its dorsal root ganglion (DRG) did not induce changes in thresholds for mechanical or thermal stimuli. But combination of mechanical deformation and Nucleus Pulpous exposure of nerve root induced pain .
The Nucleus pulpous acts to sensitive the nerve root to produce pain upon mechanical deformation and/or pressure .
[25]At sub cellular , the application of Nucleus Pulpous to a Dorsal Root Ganglion induces changes in expression of different ion channels in the Dorsal Root Ganglion like Acid sensing ion channel 3 (ASIC3) and other voltage-gated sodium channels.
These modulation of ion channels contribute to hyper-excitability and thus sensitisation of the nerve roots.
[26] Application of Nucleus Pulpous to the DRG in the rat has shown to affect the expression of different 5-HT receptor subtypes . Direct application of 5-HT to. DRG induces nociceptive behaviour
Role of pro-inflammatory cytokines such as TNF, IL-1B, IL-6, INF-Y acts to sensitise the nerve root is significant. Their derangement contribute to nerve dysfunction and radicular pain.
CLINICAL PRESENTATION
Most commonly patient with lumbar spinal stenosis present with leg pain with or without back pain.
The leg pain can be of either neurogenic claudication or radicular pain.
[27] Neurogenic Claudication characterises by : - Symptoms arises from compression of thecal sac
- feeling of Pain, Heaviness, Numbness , Cramping, burning or weakness
- Symptoms typically start from the back or the buttocks and bilaterally radiate down below the knees.
- Usually do not follow the dermatomal pattern and are related to activities .
- Typically worsening of symptoms by extension of lumbar spine during walking or prolonged standing
- Weakness appears in the form of ankle dorsiflexion weakness
- Symptoms relief from flexing the lumbar spine by leaning forward, sitting or lying down
RADICULAR PAIN CHARACTERISES BY:
- Symptoms arises from compression of a particular nerve root in the lateral recess or the neural foramen.
- Pain is described in a specific dermatomal pattern corresponding to the compressed nerve root .
- Along with numbness , weakness can be seen . Eg L5 distribution pain with weakness in Extensor Hallucis longus and Tibialis anterior muscle groups .
Severe spinal stenosis can be associated with - Bowel and bladder incontinence
- Profound weakness
- Urinary dysfunction like perianal sensory disturbance , longer duration of symptoms.
In addition the affected age group can also have - preexisting arterial occlusive disease - Hip arthritis
- Multiple sclerosis
- Neuropathy
Arterial occlusive disease will have characteristics Vascular claudication will is very similar to. Neurogenic claudication in symptoms. It’s essential to differentiate between these .
Characters Neurogenic claudication Vascular claudication Pain
Type Vague cramping , aching , sharp burning in lower extremities
Tightness, cramping (usually in calf)
Location Back, Buttock, lower limb Calf
Radiation Proximal to distal Localised to lower extremities
Exacerbation Withstanding particularly with trunk extended
With walking and bicycling (activities involving lower extremities )
Relieving factor With Sitting , flexion and squatting
With sitting and cessation of muscular activity
Time to relief Prolonged Rapid
Walking uphill More or less pain Pain full Walking downhill Pain with lumbar extension Pain full
Back pain Common Uncommon
Limitation of spinal movements
Common Uncommon
Physical finding Neurological examination
Occasionally deficit, asymmetrical
Findings are rare
Characters Neurogenic claudication Vascular claudication Straight leg rising
test
Usually negative Negative
Femoral stretch test
Usually negative Negative
Pulses Present or symmetrically diminished
Diminished or absent often asymmetrical
Skin Normal Loss of Hair, Atrophy
Bicycle test Positive with lumbar hyperextension
Positive with the spine in any position
Patients in the concerned age group are also prone for Lumbar disc herniation.
It’s is very important to differentiate between the two or find whether the two entities concomitant exist .
Lumbar canal Stenosis Vs Lumbar Disc Herniation
Characteristics Lumbar Canal Stenosis Lumbar Disc Herniation
Onset Insidious Acute
Pain Reffered Radicular
Provocative factors Standing/ Walking Sitting
Palliative factors Sitting Standing
Neurological weakness Occasionally Occasionally more Sensory changes Occasionally Occasionally more
Tension sign Rare Present
CLINICAL EXAMINATION
[28] Most the patient belongs > 5th decade of life or if earlier often associated with inflammatory pathology .
Attitude:
- Sitting flexed forward on a chair
- Flex forward the trunk while standing and ambulating.
- Decreased forward flexion in the daily activity .
- Lying sideways is more comfortable than lying flat .
- Simian stance.
ON EXAMINATION
- Often increased thoracic kyphosis and decrease lumbar lordosis
- Non specific reduced mobility,extension more limited than flexion.
- Hamstring tightness can be observed,
NEUROLOGICAL EXAMINATION
- Typically normal findings, signs may be increased immediately after patient performs symptomatic exercises.
SPORT STUDY[29]
- Absent or decreased ankle reflexes frequently found in older patients.
- Asymmetrical reflexes were noted in 26%
- Motor weakness was noted in 28%
- Sensory deficit in 29%
- Radicular pain , usually unilateral
- Often pain more at night which is increased by the Valsalva manoeuver.
- Pain exacerbated with lumbar extension to the painful side (KEMP’s TEST)[30]
- Straight leg Rising Test or Lasegue Test is positive in 40%.[30]
PERFORMED IN TWO STEPS
1st step includes a Passive straight-leg -raising test, positive if pain is elicited on
<45%
2nd step includes “Verification “ manoeuver , in which the leg is again raised but with the knee flexion. The first step will produce back and/or leg pain in the presence of low back pathology, the second step can be performed without the production of pain.
The test is said to be positive with the production of pain long the distribution of lumbosacral roots on straight-leg raising and disappearance of pain knee flexion.
BRAGAAD’S TEST
The pain will be exaggerated with the dorsiflexion of the foot on point of maximum pain by straight leg raising test.
BOWSTRING TEST
By flexing the knee the buttock pain will get relieved and this would restore by pressing on the lateral popliteal nerve.
Abnormal Romberg test
DIAGNOSTIC STUDIES
RADIOGRAPHY
Standard anteroposterior and lateral radiographs along with flexion and extension views should be taken to assess static and dynamic stability .
[31] CHARACTERISTICS FRACTURES IN RADIOGRAPH :
- Spondylotic changes, look for degenerative Scoliosis and Spondylolisthesis
- Narrowing of the neural foramen and inferred narrowing of the Spinal canal from the location and extent of degenerated structures .
- Ossification of ligamentous structure.
- Ankylosis of the Spine .
- Erosion of disc space.
COMPUTED TOMOGRAPHY :
[32]It’s poor modality for diagnosis of soft tissue pathology . Diagnostic utility of the can be improved by combining it with myelography. Dye in the cerebrospinal fluid during myelogram provides good contrast between the thecal sac and the surrounding soft tissue and bony pathology.
CHARACTERISTICS CT FEATURES
- Hypertrophied posterior articular processes.
- Osteoarthritis of apophyseal joints.
- Osseous proliferation of non articular aspects of superior apophyseal joint
- Osseous proliferation of non articular aspects of Inferior apophyseal joint.
- Calcification of Posterior longitudinal ligament , Yellow ligament , supra Spinal ligament
- Anteroposterior and Transverse diameter of Spinal canal.
- AP diameter normal >15mm
- Relative stenosis = 10 to 12 mm - Spinal Stenosis = <10 mm
MAGNETIC RESONANCE IMAGING :
[33]It’s the diagnostic modality of choice in patient with lumbar canal stenosis.
It provide details information about bony as well as soft tissue anatomy.
Characteristics features of MRI finding are : - Facet arthropathy
- Ligamentum Hypertrophy
- Disc Bulges or Disc Herniation .
- Sagittal sections shows waist -like narrowing of dural tube at the level of facet joint
OTHER DIAGNOSTIC TEST
- Electromyography (EMG)
- Nerve Condition studies (NCS)
- Somatosensory Evoked Potentials (SSEPs).
ELECTROMYOGRAPHY
- It evaluates the effect of nerve function through recording the electrical activity of muscles at rest and stimulation[34].
- It identifies motor neuron dysfunction only.
- It is useful in differentiating chronic changes from active ongoing denervation.
DISADVANTAGE
- Significant incidence of false negative electromyography in patients with spinal stenosis.
- More common abnormalities are not evaluated (Neurogenic Claudication : Sensory neuron)
- Does not differentiate between symptomatic and asymptomatic patients.
NERVE CONDITION STUDIES
It measures the speed with which impulses travels down an axon.
[35]It’s advantageous in differentiating Neuropathy from Radiculopathy.
SOMATOSENSORY EVOKED POTENTIALS (SSEPS)
- It evaluates the electrical transmission of sensory stimulation starting from the peripheral nerves and going through the spinal cord and brain.
- Peripheral nerve lesion will prolong the latency response.
- Lesions of the root and cord will cause changes in the waveform.
DISADVANTAGE
- Higher incidences of false negatives and false positives.
[36] These electro diagnostic studies are to be used if the diagnosis of the neurological symptoms are uncertain in patients with multiple co morbidities .
MANAGEMENT OF LUMBAR CANAL STENOSIS
NONOPERATIVE MANAGEMENT
1st line of management in the patients with lumbar canal stenosis.
It includes : Drug Therapy, Physical Therapy, Epidural Corticosteroid injection.
DRUG THERAPY
- [37]American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) have recommended Acetaminophen A’s initial therapy.
Dose of Acetaminophen : 4 g daily
- For Patients with co- morbidities (hypertension, cardiovascular disease, diabetes) OPIOIDS considering the fact inflammation is not felt to play a central role.
- Long term adverse effects of Opioid therapy includes Cognitive Impairment and Sedation.
- Anticonvulsant and analgesic agent improves walking distances, improves pain scores and recovery of sensory deficits
- Other drugs to treat neuropathic pain syndromes : Pregabalin, Tricyclic antidepressant , duloxetine.
- Tricyclics have potential cardiovascular toxicity, it should be used with caution in the population.
- [38]Calcitonin is reported to have both anti-inflammatory and analgesic properties. Intramuscular and subcutaneous administration has reported to improve walking distance and pain .
PHYSICAL THERAPY
[39] The goal of physical therapy is to decrease lumbar lordosis and extension forces on the spine . It also aim to improve abdominal “core” strength .
They should be tailored to the individual circumstances and optimised for better compliance.
Passive modalities such as
- Bracing or corsets - Manipulation
- Transcutaneous electrical nerve stimulation - Acupuncture.
EPIDURAL STEROID INJECTION
[40] In principle it is directed at treatment of the presumed inflammatory reaction and oedema present at the stenotic segment.
Under Fluoroscopic guidance caudal, inter-laminar or transforminal injection are recommended.
Multiple injection protocol are having better improved pain scores and walking tolerance.
OPERATIVE MANAGEMENT
Indication for surgery
- Stenosis occurring secondary to spondylotic changes at facet joint , instability or congenital small canal.
- Pathological changes affect the central vertebral canal , lateral recess and neural foramina.
- Stenosis at lateral recess from spondylotic changes from the superior articular process of caudal vertebra compressing the traversing nerve root, leading to neurogenic claudication.
- Failure of conservative therapy with activity modification, physical therapy, medication and steroids.
- Acute onset cauda equina syndrome .
- Rapidly deteriorating neurological deficits.
IDEAL CANDIDATE FOR SURGERY
- Patients with neurogenic claudication including
- Pain
- Numbness
- Paresthesia in posterolateral aspect of legs and thigh
- Patient with greater relief from Selective nerve root block
PRINCIPLES OF SURGICAL INTERVENTION
[41] Decompressive laminectomy is the modality of choice . Their are three components of successful decompression : Central Laminectomy or Bilateral Hemilaminotomy, lateral recess decompression and foraminotmy .
Central laminectomy is performed side-to-side manner from pedicle to pedicle . Lateral recess is decompressed by removing bony components from medial part of the facet joint complex along with ligamentum flavum.
Foraminotomies are performed as appropriately to achieve full decompression of the exiting and traversing nerve root.
[42] It must be bear in mind to preserve most of the facet joint and at least 8mm of the pars interarticularis
Over zealous decompression can result in the iatrogenic disruption of facet joint or pars interarticularis which will accelerates degeneration or Spondylolisthesis.
Decompression can be achieved in multiple ways. Following spinal segment fusion can be achieved by two ways :
- Spinal fusion with trans foraminal/ posterior lumbar interbody fusion (IBF) with anterior reconstruction.
- Spinal fusion with posterolateral fusion (PLF).
INSTUMENTATION
INTRA OPERATIVE IMAGES
VARIOUS MODALITIES OF DECOMPRESSION - Laminectomy
- Hemi laminectomy - Wide fenestration
- Spinous process Osteotomy decompression - Lumbar spinous process splitting decompression COMPLICATIONS OF SURGICAL INTERVENTIONS - Intra-operative
- Post operative complications.
INTRA-OPERATIVE COMPLICATION - Inadequate neural decompression.
- Recurrent stenosis . - Incidental dural tear.
- Neural injury.
- Epidural hematoma - Vascular injury.
POST OPERATIVE COMPLICATIONS
- Post operative instability.
- Neural compression .
FUNCTIONAL EVALUATION
- Modified Japanese Orthopaedic Association Score (JOA score ) - JOA recovery rate (Hirabayashi formula).
- Visual Analog Scale (VAS).
METHODOLOGY
AIM OF THE STUDY
This is Retrospective and prospective study to analyse the surgical management of patients with multi-segmental lumbar canal stenosis. Study focuses on
- To analyse surgical intervention in the management of multi-segmental lumbar canal stenosis .
- To assess the neurological and functional outcome of surgical procedure done .
STUDY DESIGN
Retrospective and Prospective analytical study.
MATERIALS AND METHODS
Patients satisfying inclusion criteria were included in the study after obtaining written informed consent . 25 patients with multi-segmental lumbar canal stenosis were recruited and under went surgical intervention.
INCLUSION CRITERIA
- Adult patient with back pain, sciatica, neurogenic claudication
- Radiograph of lumbo-sacral spine with instability/deformity .
- MRI finding suggestive of lumbar canal stenosis
- absolute stenosis (mid sagittal diameter of the canal < 10cm)
- Relative stenosis (mid sagittal diameter of the canal 10mm - 13mm ) - Multiple level canal stenosis (two or more level )
EXCLUSION CRITERIA
- Congenital lumbar canal stenosis.
- MRI suggestive of Lumbar Canal stenosis nut patient symtomatically normal.
PREOPERATIVE EVALUATION
- Patient history and neurological examination.
- Preoperative clinical evaluation of the patients was made by
- Modified Japanese Orthopaedic Association (JOA) score
- Visual analogue score for back and neurogenic Claudication (VAS).
RADIOGRAPHY OF THE LUMBOSACRAL SPINE
- Standard Anteroposterior View.
- Lateral View .
- Dynamic Flexion-extension lateral view - MRI of lumbosacral spine .
SURGICAL TECHNIQUE
For all the procedure, patient under Endotracheal tube General Anaesthesia with knee chest position in Hall’s Frame. Thorough standard Posterior Midline Approach
POSTERIOR MIDLINE APPROACH
- Skin incision centring the stenotic area given in standard posterior midline approach, length of the incision varies with the level involved.
- Skin, subcutaneous tissue , para vertebrae facia incised .
- Para spinal muscles were elevated sub-periosteally from the spinous process and lamina .
- Spinous Process ,transverse process , facet joint identified .
- Through Roy Camille approach posterior stabilisation done
- Decompression achieved by removal of lamina , ligamentum flavum done - Removal of the lamina upto medial border of the pedicle done
- Adequacy of the decompression assessed.
- Discectomy done.
- Some cases instrumented inter-body fusion done along with bone graft
- Paraspinal muscles closed in layers with absorbable sutures and the subcutaneous tissue and skin were closed.
INTRA OPERATIVE ASSESSMENT - Operative time
- Blood loss and transfusion
- Through inspection of neural elements .
POSTOPERATIVE PROTOCOL
- Immediately after extubation neurological assessment done.
- Patients were kept on suction drain and was removed after 2 days.
- Patients were kept on lumbosacral belt.
- Patients were encouraged to walk as soon as is comfortable.
- Sutures were removed after 12th day of surgery .
- Neurological charting was done after 2 weeks of surgery along JOA score and VAS score .
- Patients were followed - up regularly every month during the first 3 months and thereafter every 3 months upto 12 months .
OBSERVATION AND RESULTS
DEMOGRAPHICS
Study sample size was 25 .
25 participants of Indian ethnicity were included in the study .
In our study 14 participants were of male gender and 11 were of female gender .
56%
44%
Male Female
AGE:
Mean age of the participants was 46 yrs (33yrs - 60 yrs ).
Mean age of presentation in male group was 42.21 yrs (34- 60) Mean age of presentation in female group was 43.90 yrs (31 -60)
0 2 4 6 8
male female
SPINAL SEGMENT INVOLVEMENT
Most common level involvement was seen in the L4 L5 ,L5 S1 disc level in 14 subjects
Most common level involved in male and female was L4 L5,L5 S1 disc level 7 and 7 subjects respectively
0 1.75 3.5 5.25 7
L2L3 L3L4
L3L4 L4L5
L3L4 L4L5
L5S1 L4L5 L5S1
Male Female
FUNCTIONAL EVALUATION
Modified Japanese Orthopaedic Association score
Mean Modified JOA score preoperative was 8.625 (5-11)
Mean Modified JOA score preoperative for men was 9.71 (8-11) Mean Modified JOA score preoperative for women was 7.54 (5-10)
0 2.5 5 7.5 10
Male Female
VISUAL ANALOGUE SCORE
Mean Visual Analog Score was 7.615 (6-9)
Mean Visual Analog score for Men preoperative was 7.51 (6-9) Mean Visual Analog score for women was 7.72 (6-9)
6 8
Male Female
25 patients were followed with mean followup of 12 months .
Data of 12 Patients (8 men & 4 women) in the Decompression with Instrumented Inter-body fusion group and 13 patients (6 men & 7 women) Decompression without instrumented inter-body fusion .
The mean age was 44.08(33-54) yrs in Decompression with instrumented inter- body group and 46 (31-60) yrs in Decompression without instrumented inter- body fusion.
Mean number of decompressed level was 2 for Instrumented inter-body fusion group with 2 patients having 2 level of instrumentation . Where as mean number of decompressed level was 2.3 for without instrumented inter body fusion.
PREOPERATIVE PARAMETERS
S.
No.
Contents
Decompression with instrumented Interbody fusion
Decompression with out instrumented interbody
fusion
1 No. Of Patients 12 13
2 Avg age 44.08 46
3 Male : Female 8:4 6:7
4 Mean no. Of Spinal level decompressed
2 2.3
5 Average duration of follow up
25 months 9.23 months
INTRAOPERATIVE PARAMETERS
S.
No
Contents
Decompression with instrumented interbody fusion
Decompression without instrumented
interbody fusion
1 Average duration of surgery
3 hrs 2.5 hrs
2 Average blood loss 200 ml 200 ml
3 No. Of Transfusion 1 1
4 Dural Tear 1 2
5 Iatrogenic Neurologic Deficit
1 1
POSTOPERATIVE PARAMETERS
S.
No
Parameter
Decompression with instrumented interbody
fusion
Decompression without instrumented interbody
fusion
1 Wound infections 1 2
2 Instability Nil Nil
3 Urinary tract infections
Nil Nil
4 Lower respiratory tract infection s
Nil Nil
COMPLICATIONS
Dura tear : 2 (8%)
Managed by Dura repair and Tablet Acetazolamide 500mg bd.
Infection : 3 (12%)
Managed by wound debridement and wash Neurological deficit : 2(8%)
One patient who had undergone Decompression with Posterior stabilisation with anterior reconstruction encountered iatrogenic nerve injury and recovered by Physiotherapy in 3 months .
Other patient who had undergone Decompression with Posterior stabilisation only had Intraoperative injury is on recovery phase .
FUNCTIONAL OUTCOME SCORES
MODIFIED JAPANESE ORTHOPAEDIC ASSOCIATION SCORE
In our study population the Pre op modified JOA score was 8.76 it improved to in the last follow up.Demographically Male gender group had mean Pre op modified JOA of 9.71 with mean improvement of 13.64 in the last follow. Male group had the mean recovery rate of 75.64%. In female group had mean preop modified JOA of 7.54 with mean improvement of 13.27 in the last follow up.
Recovery rate observed in female group was 76.25%.
In the group with Decompression Posterior stabilization with Anterior Reconstruction with fusion prep JOA was 14.75 in 12 months follow up the where as it was 13.46 in the group with Decompression with Posterolateral fusion.
0 3.5 7 10.5 14 17.5
Preop JOA Postop JOA
JOA Score
Statistical analysis of our results , with Paired T Test T(stat) = - 4.94
T(critical) = - 2.060 T(stat) < T(critical) It implies that Alpha 0.05 so, P < 0.005
so the change in the JOA score pre and Post operatively showed statistically significant results.
VISUAL ANALOGUE SCALE
In our series of 25 patients mean Pre-op VAS was 7.4 and it reduced to mean post op VAS of 1.06.
Demographically Male group had Pre-op VAS of 7.2 and it reduced to 0.85 in the last follow up. In female group Pre-op VAS was 7.54 and it reduced to 1.27 in the last follow up.
In group with Decompression with instrumented interbody fusion Pre-op VAS was 8.0, which reduced to mean of 0.58 in the last follow up. In the group with Decompression with posterolateral fusion Pre-op VAS was 7.53 which was reduced to mean of 1.38 in the last followup.
In 2wks , 1 month and 3 months follow up post operatively patients with instrumented interbody fusion had lower score when compared to patients with only posterolateral fusion.
VAS for Laminectomy with posterolateral fusion only.
0 1.5 3 4.5 6 7.5
2wks 1month 3rd month
36m 45m 48m 50m 60f 60m 50f
38f 31f 41f 45m 41m 54f
VAS for decompressive laminectomy with instrumented interbody fusion
0 1.25 2.5 3.75 5 6.25
2wks 1month 3rd month
45m 40m 45m 50f 54m 53m
45m 34m 42f 33f 34f 54m
Parameter
Decompression with Extended Posterolateral
fusion with anterior reconstruction
(Group A)
Decompression with Posterolateral fusion
only (Group B)
Number 12 13
Preop JOA score 9 8.58
JOA score at last follow up
13.58 13.46
JOA recovery rate 76.55% 75%
Pre-Op VAS 8.0 7.53
Post-Op VAS 0.58 1.38
0 2.25 4.5 6.75 9 11.25
Preop Postop
VAS
In statistical evaluation of two methods by ANOVA one way test F(stat) = 0.0960
F(critical) = 7.88 F(critical) > F(stat) So alpha > 0.005 P > 0.005
Results are statistically insignificant.
DISCUSSION
This study was conducted in the Government run tertiary level hospital in Southern part of India with 25 participants, 14 male and 11 female, in a ratio of 1.27 : 1 .
The most common age of presentation was in 4th decade of life in males i.e 40%
(n=10) and 5 th decade in females 45%(n=5) ,this was similar to other relevant studies [44,45,46].
All our patients had symptomatic features of Lumbar Canal Stenosis for a minimum period of 3yrs with low back pain and associated claudicatory pain .This was comparable with the study reported by [47] Amundsen et all who in their series had patients with complaint of back pain in 95% and neurogenic claudication in 91% .
We had the most mobile lumbar levels at L4 L5 & L5 S1 predominantly involved. 24% of our population had established EHL / FHL weakness with complaints of Paresthesia. All patients in our series had undergone conservative treatment in the form of pain relieving medication and Physiotherapy. Some had even underwent epidural steroid injection and has reported intermittent period of pain relief.
The options of surgical decompression was offered to patients who had an unsatisfactory response to conservative management . The goal of the surgery was to achieve complete decompression and to attain solid fusion of the involved
segments. Though decompression was done to the same extent in all the patients , the surgical methodology for fusion was divided into two groups . One group of patients underwent inter transverse fusion, also called as posterolateral fusion (PLF) and the other group underwent an trans foraminal / posterior lumbar interbody fusion (IBF) with an additional cage being placed between the vertebral bodies . Patients were randomly distributed among two expert surgical team, in which one team exclusively did IBF and other did exclusively PLF 12 patients in Group A had decompression with anterior interbody fusion (IBF) and --- patients in Group B had Decompression with Posterolateral fusion (PLF).
Pre-op protocol were same for all the patients including Pre-op Neurology charting , Modified JOA score , VAS . Both the group were followed up similarly.
In group A (IBF), 2 patients underwent double level instrumented inter-body fusion and in group B (PLF), 2 patients underwent 3 levels of instrumented Posterolateral fusion. All other patients underwent only a single level instrumented fusion (PLF/IBF).
In sum , 8% (n=2) had iatrogenic nerve injury (one in each group). In Group A (IBF) the patient had full neurological recovery after 3 months, where as in Group B (PLF)the patient had partial recovery. Post operatively all our patients had complete relief of neurogenic claudication.
Group A(IBF) patients had a significant improvement in Visual Analogue pain Score (VAS ) over Group B (PLF) at time intervals of 2wks, 1 month and 3rd month. This may be attributed to the restoration of discal height and the additional structural stability attained in patients who underwent interbody fusion with cage . At the end of one year both the group had comparable pain scores .
Ganz et al (1990) in their series of 33 patients 86% show good outcome . Nath et all (2012) reported 64% patients with excellent and 28% showed good outcome at one year follow up in series of 32 patient . In our series ,at one year of follow up ( Modified JOA score) In Group A (IBF) 66.6 % had excellent outcome while in group B 76.92% patients had excellent outcome . In sum ,72% (n=18) had
“excellent” clinical outcome and 28% responded with “good” clinical outcome.
Which is statistically significant as measured by paired T Test with P value
<0.05.
.Modified JOA Outcome Ganz et all (1990) R Nath et all (2012) Our study
Excellent 14% 64% 72%
Good 86% 32% 28%
Poor NiL NiL NiL
Nath et al (2012) in their series with 62.5% had no pain, 37.5% had occasional mild pain , 96.87% had no leg pain .[48] Herron et all (1991) concluded similar results with average improvement of leg pain in 82% and improvement of back pain in 71%.
Preoperatively 88% had continuous severe back pain , 8% had occasional severe low back pain and 4% had mild low back pain . With 24% patients have associated stress paresthesia. At one year of followup 24% had low back pain on heavy work (VAS =2), 56% has occasionally mild low back pain on extremes of heavy work (VAS =1) and 20% had no pain. No patient in our series had occasional severe or continuous severe low back pain. Postoperatively 83.3%
patient have improved paresthesia at 1 year follow up only 1 patient who underwent PLF had residual symptoms.
VAS R Nath et all (2012) Our study
Occasional severe Low Back Ache
Nil Nil
Mild Low Back Ache Nil 24%
Occasional pain 37.5% 56%
No Pain 62.5% 20%
Multicentric SPORT study by Weinstein et all (2010) of 654 patients reports significant improvement of pain and function through 4 years who underwent surgical intervention when compared to those who were managed conservatively.
Similarly literature review by [50]Moon Soo Park et all (2015) ,concluded that Decompressive surgery is the Gold standard for the treatment of central or lumbar canal stenosis .
In our series all 25 patients after surgical intervention improved from leg pain neurogenic claudication, this could be attributed to the fact that all were operated after clinico- radiological correlation and 6 months trial of non surgical management was given to every patient..
Decompression laminectomy done at 2 level in 88% and 3 levels in 3 patients these all were supplemented by posterolateral fusion . Additional 12 patient had instrumented interbody fusion.
[51] Farzad Omidi - Kashani et all (2014) in their update review reported that fusion can stabilise the unstable lumbar vertebrae and also eradicate the source of pain originating from the diseased Intervertebral disc or facet joints.
Group A (IBF) had earlier functional recovery when compare to Group B alone which was evident by VAS at 2wks ,1 month and 3rd month and Modified JOA score . At 1 year follow up all had similar VAS and Modified JOA , these comparable results were supported by statistical test in form of ANOVA one way test which was insignificant statistically.
But these study is limited by the time duration and sample size . So as to clearly define the difference in two of the technique is out of the bound in our series .
CONCLUSION
1. Surgical management of multisegmental lumbar canal stenosis yields better result than conservative management.
2. Adequate Decompression laminectomy with instrumental stabilisation of the effected segment is a key to pain relief .
3. Decompression with extended posterolateral fusion with anterior reconstruction with cage heals early with improved functional outcome and it helps in early mobilisation.
LIMITATION OF THE STUDY - Short duration of Follow up.
- Small Sample size.
CASE ILLUSTRATIONS CASE-1
Mrs P 50/F, C/O Low Back Pain for 3 yrs with neurogenic claudication for 4 months.
Diagnosis: L3, L4, L5, S1 Disc Disease.
Procedure done: Decompression with posterolateral fusion.
Pre Op JOA Score-10, VAS Score-7 Post Op JOA Score-13, VAS Score-1
PRE OPERATIVE X-RAY & MRI
POST OPERATIVE X-RAY AT 3 MONTHS
3 MONTHS FOLLOW UP
