Chapter 43 Overview of Low Back Pain Disorders Flashcards
Pain originating from the spine usually manifests as
pain in the low back and neck, and infrequently as pain in the upper lumbar and mid back areas.
Spinal pain (SP) can
be grouped into three broad categories:
acute pain when the pain duration is between 2 to 4 weeks; subacute pain when the pain persists for up to 12 weeks; chronic pain, when the pain continues for more than 12 weeks
The risk factors associated with SP have been classified into three broad categories:
biomechanical, psychosocial,
and personal.
The biomechanical risk factors of spinal pain
are determined by spinal loading, and typically include parameters such as physical stress and the asymmetry of physical tasks
The psychosocial risk factors of spinal pain
pertain to psychogenic stress and are often related to job satisfaction,
responsibility, and variety
Personal risk factors of spinal pain
have
been acknowledged as physical, familial, anthropometric,
gender, and personality traits
The following risk
factors have been associated with the development of
spinal pain:
- Jobs that are stressful and that require heavy lifting and use of heavy equipment
- Cigarette smoking
- Psychiatric, emotional, and personality issues
- Obesity
- Spinal deformities and endplate injury
- Genetic predisposition
- Peripheral vascular disease
The human vertebral column consists of
7 cervical, 12 thoracic,
5 lumbar, 5 sacral, and 3 to 5 coccygeal vertebrae.
comprise a vertebral motion segment
two adjacent vertebral bodies and an intervening
intervertebral disc
The linear array of adjacent spinal motion segments
forms the continuum of the spinal column that houses dorsally the
neural elements of spinal cord and nerve roots of
the cauda equina.
nerve roots of the cauda equina are encompassed dorsally and laterally by
the neural arch
Components of neural arch
comprised of spinous
processes, spinal laminae and the ligamenta flava posteriorly, and pedicles and intervertebral foraminae laterally.
In addition to the linkage of the vertebral bodies by intervertebral discs, the adjacent vertebral bodies are articulated
dorsally by a pair of synovial joints, the zygapophysial or
facet joints.
The most significant of the spinal ligaments
include
the anterior and posterior longitudinal ligaments
and ligamentum flavum
The incredible forces applied to the spinal column are transmitted to the lower extremities by
two large synovial-fibrous joints, the sacroiliac joints
The vertebral bodies are largely composed of
cancellous bone housed in a thin layer of cortical bone.
*The intervertebral discs (IVDs) are made of
annulus fibrosus (AF), nucleus pulposus (NP), and vertebral endplates.
*Distinction of annulus fibrosus (AF) and nucleus pulposus (NP)
Both the NP and AF are populated by sparsely present cells immersed in abundant intercellular matrix. Cells populating the NP are found in clusters and are chondrocyte-like,
whereas the cells found in AF have fibrocytic features.
*Distinction of annulus fibrosus (AF) and nucleus pulposus (NP) Matrix
NP matrix is jelly-like, and is made of high concentration of water and proteoglycans, whereas matrix constituting AF is high in collagen arranged in the form of interlacing lamellae. These collagenous lamellae are firmly attached to the adjacent vertebral bodies and are most dense anteriorly.
*Although the cancellous vertebral bodies and the spinal canal contents are highly vascular, the IVDs are mostly
avascular and the largest avascular structure in the body. The normal NP and inner third of the AF completely lack any vasculature; moreover, the avascular cartilaginous endplates act as a barrier separating
the vertebral body vasculature from the IVD contents
*Innervation of the IVDs and the neural canal contents is mainly by
nerve plexuses along the anterior and posterior longitudinal ligaments. The nerve plexus along the posterior longitudinal ligament receives its
input mainly from the sinuvertebral nerve and the gray rami communicans, while the plexus along the anterior longitudinal ligament is contributed to mainly by the gray rami communicans
*The sinuvertebral nerve originates from
the segmental spinal nerve as it exits the intervertebral foramen; it re-enters the vertebral canal and contributes mostly to the posterior longitudinal plexus. it also receives contribution from the gray rami communicans.
*The posterior longitudinal ligament plexus innervates
the ventral half of the vertebral column, including the anterior dura and posterior intervertebral discs.
*The gray ramus communicans nerve emerges from
the spinal segmental nerve; soon after, it enters the intervertebral
foramina and runs anteriorly along the inferior third of the
vertebral body.
*The gray ramus communicans nerve connects to the
sympathetic trunk before branching into lateral and anterior branches to innervate the lateral and anterior disc annulus of the disc levels above and below
The posterior primary ramus, soon after its division from the anterior primary ramus, branches into
medial and lateral branches.
The medial branch of the posterior primary ramus supplies
most dorsal spinal column
components, including facet joints, posterior neural arch components, and spinous processes
The annulus fibrosus (AF) of the intervertebral
discs (IVD) has complex innervation from several sources and multiple spinal segments, including contributions from the
sinuvertebral nerves, segmental spinal nerve, gray ramus communicans nerve, and the sympathetic trunk; thus, a normal IVD has rich autonomic connections.
the pain receptors—
mostly mechanoreceptors—are found mainly
in the spinal ligaments, paraspinal muscles, vertebral body periosteum, and the outer third of the AF and facet joints.
The flexibility and remarkable range of motion exhibited by an active spine depend almost entirely on
the cumulative plasticity
exhibited by the individual IVDs.
the plasticity of IVD
The individual IVD is only moderately plastic and the NP, like the vertebral body, is practically incompressible due to its high water content. The compressive forces applied to the IVD are borne by the NP and are distributed equally to
the AF as a tensile force
NP incompressibility is maintained almost exclusively
by the
hydrostatic pressure generated by its proteoglycan content, which is a function of intricate metabolic processes.
Being mostly avascular, IVD obtains metabolic
requirements almost exclusively by
diffusion from capillary
plexuses in adjacent vertebral bodies and the outer AF.
Discal catabolic activities are in addition facilitated by
discal matrix metalloproteinases (MMPs)
Dysfunction and decline in the viable NP cells, enhanced MMP activity, and increased disc cytokines and proinflammatory mediator concentration can start a vicious cycle that can reduce
NP proteoglycan and water content and consequent loss
of disc hydrostatic pressure
The ensuing laxity of the NP
exposes the AF to
direct compressive forces
The
cumulative effect of increased AF stress and collagen loss
may lead to
eventual AF failure with the consequent development
of annular tears and fissures
Structural changes within the IVD alter its biomechanical
properties and cause it to
shrink and become less plastic.
These changes in the IVD dynamics increases stress on
adjacent vertebral motion segment and may propagate
degenerative changes in several contiguous spinal structures.
degenerative changes in several contiguous spinal structures
sclerosis and hypertrophic
new bone formation in adjacent vertebral bodies—Modic changes, accelerated degenerative changes in the
adjacent IVDs, hypertrophy and arthritis of the facet joints, sacroiliac joint dysfunction, and paraspinal myofascial syndrome.
Hypertrophic changes in the discs, facet joints and ligamenta flava may leads to
narrowing of the spinal canal and the intervertebral foraminae. These stenotic
changes may cause symptoms from compression of the spinal cord and the spinal nerve roots
Etiology of Mechanical Spinal Pain
- Herniated discs
- Spondylosis or degenerative disc disease
- Discogenic pain, internal disc disruption, or annular tears
- Spondylolisthesis or displacement of one vertebral body over the other
- Spondylolysis or defect in pars interarticularis without the vertebral slippage
- Spinal instability or anomalous movement between the contiguous vertebral bodies
- Foraminal stenosis or skeletal hypertrophy causing symptoms of nerve root compression
- Spinal canal stenosis or neurogenic claudication or myelopathic symptoms and signs
- Facet arthropathy
- Musculoligamentous strains or sprains
- Myofascial pain syndrome
- Congenital spinal conditions such as kyphosis or scoliosis
Etiology of Nonmechanical Spinal Pain
- Primary and metastatic neoplasms of the spine or its neural contents
- Infections, such as osteomyelitis of the vertebral bodies, septic discitis, paraspinal or epidural abscess
- Noninfectious inflammatory spinal disorders such as ankylosing spondylitis, Reiter’s syndrome, psoriatic spondylitis, and inflammatory bowel disease
- Traumatic or pathologic fractures such as vertebral body compression fractures and dislocations
- Metabolic disorders of the spine such as Paget’s disease
- Miscellaneous conditions such as Scheuermann’s disease or
osteochondrosis, and hemangiomas
Etiology Referred or Visceral Spinal Pain
- Pelvic visceral disorders such as prostatitis, endometriosis, or pelvic inflammatory disease
- Renal disease such as nephrolithiasis, pyelonephritis, or perinephric abscess
- Vascular disease such as abdominal aortic aneurysm
- Gastrointestinal disease such as pancreatitis, cholecystitis, or
perforated bowel
Mechanical SP
is ubiquitous and may be defined as pain emanating from the benign degenerative conditions afflicting the various spinal structures, such as IVDs, facet joints, and the neural
elements, or the immediately adjacent paraspinal structures,
such as muscles, ligaments, periosteum and blood
vessels.
range of terms used to
describe mechanical SP
lumbago, spondylosis,
segmental or somatic dysfunction, ligamentous strain,
subluxation, and facet joint, sacroiliac, or myofascial
syndromes.
A detailed history of SP patient should note the following
- Location and any radiation of pain, especially in the dermatomal distribution
- Characteristics of pain, such as burning, lancinating, or aching quality
- Severity of pain, especially patient’s ability to function and to sleep at night
- Circumstances of onset of pain such as history of trauma
- Factors aggravating and relieving the pain
- Patient’s age
- Presence of any constitutional symptoms such as fever, malaise, or weight loss
- Special pain features such as night pains, bone pain, morning stiffness, and history of claudication
- Neurologic symptoms such as numbness, tingling, and weakness, along with any bowel or bladder dysfunction; especially urinary retention and urinary or fecal incontinence
- History of any previous treatments and their efficacy
- Patient’s detailed past medical and surgical history
- Assessment of social and psychological factors that may affect patient’s pain
- Functional impact of pain on patient’s work and activities of daily living
A comprehensive general physical and a detailed neurologic examination should be performed in all the patients
with SP. Specific spinal examination should include:
l Assessment of gait.
l Range of spinal motion.
l Determination of local spinal and paraspinal tenderness.
l Specific tests for the clinical diagnosis of various SP
syndromes, including those for nerve root irritation, facet syndrome, and sacroiliac joint dysfunction
“Red Flags” in Patient’s Clinical Evaluation
guidelines to recognize clinical features that would signify the presence of conditions such as fractures, tumors, and infections that can pose significant threat to life or neurologic
function
Age50 years
Symptoms over 3 months indicate a less serious
etiology
History of significant traumatic injury, or mild
trauma in an elderly patient or in a patient with a serious medical condition
Presence of constitutional
symptoms: Fever, chills, malaise, night sweats, unexplained weight loss,
History of cancer, recent bacterial infections,
intravenous drug abuse, immunosuppression,
organ transplantation, and corticosteroid use are at higher risk for pathologic fractures, epidural and vertebral body abscesses, and metastasis.
Pain not relieved with rest, supine position, and analgesics suggesting a a serious pathologic conditions
Presence of cauda equina
syndrome
cauda equina syndrome
etiology
Caused by acute compression of the spinal cord or the nerve roots of the cauda equina. caused by massive midline disc herniation or rarely by spinal metastases, hematoma, epidural abscess, traumatic compression, acute transverse myelitis, and abdominal aortic dissection.
cauda equina syndrome symptoms
Symptoms include bilateral, but often unequal, lower extremity radicular pains and weakness, gait disturbances, abdominal discomfort and overflow incontinence.
cauda equina syndrome physical examination
Physical examination
exhibits neurologic dysfunction, saddle anesthesia, diminished anal sphincter tone, and urinary bladder retention. In addition to the positive findings on neurologic examination, the patient’s physical examination typically exhibits saddle
anesthesia—diminished sensation in the buttocks and perineum—diminished anal sphincter tone, and the evidence of urinary bladder retention.
cauda equina syndrome diagnosis and treatment
Due to the possibility
of spinal cord compression at higher levels, dx must be made by imaging the entire spine. Treatment is urgent decompressive surgery in order to reduce permanent neurologic disability
In general, patients with
benign mechanical SP should have pain mainly with
spinal movements such as sitting, bending, lifting, or twisting, and the pain should improve over the course of few days to
weeks.
