LOW BACK PAIN

SEM 101

Respectfully submitted by:

PRINCESS EDELWEISS M. CORPUZ
WENDY PEARN F. CASTAÑEDA
ANDRE KAIEN S. CORPUZ
BSPT IV-B

Respectfully submitted to:

MARILOU J. RAVAL, MSPT, PTRP
MARY AUDREY D. VILORIA, PTRP
 LOW BACK PAIN (LBP)
DEFINITION

 Pain in the lower back area that can relate to problems with the lumbar spine, the discs
between the vertebrae, the ligaments around the spine and discs, the spinal cord and
nerves, muscles of the low back, internal organs of the pelvis and abdomen, or the skin
covering the lumbar
 Pain between the costal margin and the gluteal folds. It is a symptom, not a disease, and
has many causes and it is a common musculoskeletal symptom that may be either acute
or chronic. It is also often accompanied by sciatica, which is pain that involves the sciatic
nerve and is felt in the lower back, the buttocks, and the backs of the thighs.
(Braddom et al, 2011)

EPIDEMIOLOGY
LBP is generally described as pain between the costal margin and the gluteal folds. It is
extremely common. About 40% of people say that they have had low back pain within the past 6
months. Studies have shown a lifetime prevalence as high as 84%. Onset usually begins in the
teens to early 40s. Most patients have short attacks of pain that are mild to moderate and do not
limit activities, but these tend to recur over many years. Most episodes resolve with or without
treatment. The median time off work for a back injury is 7 days, and many people with low back
pain never alter their activity. A small percentage of low back pain becomes chronic, however,
and causes significant disability. In most studies about half of the sick days used for back pain
are accountable for by the 15% of people who are home from work for more than 1 month.
Between 80% and 90% of the health care and social costs of back pain are for the 10% who
develop chronic low back pain and disability. Just over 1% of adults in the US are permanently
disabled by back pain, and another 1% are temporarily disabled.
The percentage of patients disabled by back pain, as well as the cost of low back pain,
has steadily increased during the past 30 years. This appears to be more from social causes
than from a change in the conditions that cause low back pain. The two most commonly cited
factors are the increasing societal acceptance of back pain as a reason to become disabled,
and changes in the social system that pay benefits to patients with back pain. (Braddom et al,
2011)

ETIOLOGY
Various disease entities can cause low back pain. The causes of low back pain are
many, most of which can be categorized according to the classification provided below. Some of
the entities are listed with each classification.

Cause Common disease

1. Degenerative Degenerative joint disease (DJD), osteoarthritis, lumbar spondylolysis,
Facet joint disease, facet (DJD),
Degenerative spondylolisthesis,
Degenerative disc disease,
Diffuse idiopathic skeletal hyperostosis

2.Inflammatory Spondyloarthropathies (ankylosing spondylitis)

(non-infectious) Rheumatoid arthritis

3. Infectious Pyogenic vertebral spondylitis

Intervertebral disc infection
Epidural abscess

Osteoporosis or osteopenia
4. Metabolic Pagets disease of bone

Benign
-Spinal (benign bony tumors of spine)
-Intraspinal (meningiomas, neurofibromas, neurilemomas,low grade
ependymomas)

5. Neoplastic Malignant
-Spinal (malignant bony or soft tissue tumors, metastasis)
-Intraspinal (metastasis, high-grade ependymomas, astrocytomas,
meningeal carcinomatosis)

6. Traumatic Fractures or dislocations

Sprains (lumbar, lumbosacral, sacroiliac)

7. Congenital or Dysplastic spondylolisthesis

developmental Scoliosis

8. Musculoskeletal Acute or chronic lumbar strain

Mechanical low back pain
Myofascial pain syndrome
Fibromyalgia, tension myalgia
Tension myalgia of the pelvic floor, coccygodynia
Postural abnormalities, pregnancy

9. Viscrerogenic Upper genitourinary disorders

Retroperitoneal disorders (often neoplastic)

10. Vascular Abdominal aortic aneurysm or dissection

Renal artery thrombosis or dissection
Stagnation of venous blood (nocturnal back pain of pregnancy)

11. Psychogenic Compensation neurosis

Conversion disorder

12. Postoperative
and multiply
operated on back
 (Braddom et al, 2011)
PATHOPHYSIOLOGY
The Degenerative Spine Cascade
Although the post zygapophyseal joints (facets) and the ant intervertebral disks are
separated anatomically, forces and lesions affecting one certainly alter and affect the other.
For example, axial compressing injuries can damage the vertebral end plates, which can
lead to degenerative disk disease, which eventually stresses the post joints, leading to the
common degenerative changes seen in them over time. Torsional stress can injure the post
joints and the disks, which in turn leads to increase stress on both elements, resulting in further
degenerative changes over time. When a degenerative changes affect one level, such as L4 –
L5, a chain reaction occurs, placing stress on the levels above and below the currently affected
level, and eventually resulting in more generalize multi-level spondylotic changes.
The degenerative changes that occur in the Z joints from aging and repetitive
microtrauma are similar to those that occur in the appendicular skeletal joints. The process
begins with synovial hypertrophy, which eventually results in cartilage degeneration and
destruction. With joint instability and repetitive abnormal joints motion, the bony joint
hypertrophies which narrows the central canal and lateral recesses, potentially impinging nerve
roots.
A similar process occurs anteriorly at the disk level from repetitive microtrauma of
primarily shearing forces. Tears in the annulus are thought to be the first anatomic sign of
degenerative wear. Where the annulus is weakened enough, typically posterolaterally, the
internal nucleus pulposus can herniated. Internal disk disruption can occur without herniation,
however, because age and repeated stress acting on the spine cause the gelatinous nucleus to
become more fibrous over time. Tears in the annulus can progress to tears in the fibrous disk
material, resulting in “internal disk disruption” without frank herniation. All this result in loss of
disk height, which causes instability as well as lateral recess and foraminal narrowing and
potential nerve root impingement. The loss of disk height also places new stresses on the
posterior elements, resulting in degeneration and nerve root impingement.
The Degenerative Spine Cascade Theory offers an explanation as to how the spine
ages, it is unclear why there is such a marked disconnect between anatomic changes in the
spine associated with aging and back pain. Because many patients still suffer from back pain
and occasionally disabling pain even though they have a normal spine anatomy, and many
patients with marked degenerative changes on imaging are nearly or fully pain free.

Radiculitis and Radiculopathy

Studies have shown that disk herniation can cause an inflammatory response. The
mechanism stems from the fact the nucleus pulposus is highly antigenic as a result of being in
an immunoprotected setting in nonpathologic states. When the fluid of the nucleus pulposus is
exposed to the neural tissue of the spinal canal and neuroforamen through a defect in the
annular fibers, an autoimmune-mediated inflammatory cascade begins the inflammatory
mediators generated can cause swelling of the nerves. This can alter their electrophysiologic
function, sensitizing these neurons and enhancing pain generation without specific mechanical
compression.
 The mechanism of mechanical compression of the nerve roots has been studied as well.
Compression of nerve roots can induce structural and vascular changes as well as
inflammation. Neural compression can result in impairment of intraneural blood flow,
subsequently decreased nutrient supply to the neural tissue, local ischemia, and information of
intraneural edema. This can set off an inflammatory cascade similar to that described above.
Mechanical stimulation of lumbar nerve roots has also been shown to stimulate production of
substance P, the neuropeptide known to modulate sensory nociceptive feedback. With these
biochemical reactions, the local structural effects of mechanical compression just compound the
symptomatic response.
Pain of Spinal Stenosis
 Venous engorgement theory
The spinal veins of patients with stenosis dilate, causing venous congestion and
stagnanting blood flow. This pooling of blood in the spinal veins increases epidural and
intrathecal pressure, leading to a microcirculatory, neuroischemic insult, which in turn leads to
the typical neurogenic claudication symptoms of stenosis.

 Arterial insufficiency theory

It is based on the arterial dilation of the lumbar radicular vessels during lower limb
exercise to provide increased blood flow and nourishment to the nerve roots. In patients with
spinal stenosis, this reflex dilation might be defective. Because patients with spinal stenosis are
typically elderly they are also at higher rise for atherosclerosis, which in turn just amplifies the
arterial insufficiency.

Pain Generators of Lumbar Spine

Innervated Structures: o Muscle and fascia
o Bone: Vertebrae o Nerve root
o Joints: Zygapopgyseal
o Disk: Only the external annulus and Noninnervated:
potentially diseased disk o Ligamentum flavum
o Ligaments: ALL, PLL, interspinous o Internal annulus
ligament o Disk: nucleus pulposus

Most common pain generators

o Segmental dysfunction

A segment encompasses the disk, the vertebrae on each side of the disk, and
the muscles and the ligaments that act across this area. A segmental dysfunction occur
when either a segments is too stiff or too mobile.
o Muscular imbalances and Neural Procession Problems

There appear to be consistent muscular problems in patients with chronic low

back pain. Some of these factors might exist pre- injury and make the spine more
susceptible to injury, and some are adaptations to injury. Studies have shown abnormal
firing patterns in the deep stabilizers of the spine and transverses abdominus with
activities such as limb movements, accepting a heavy load, and responding to balance
 challenges. Other research have found strength ratio abnormalities and endurance
deficits in patient with low back pain.
o Psychological Factors and LBP
o Depression, Anxiety, and Anger
o Patient Beliefs About Pain and Pain Cognition

Centralization and Pain

Pain processing begins in the spinal cord and continues extensively in the brain, and
ultimate pain that someone experiences is the sum of multiple descending and ascending
facilitatory and inhibitory pathways. Extensive evidence now supports the theory that persistent
pain might be caused by central sensitization, which could help explain why often no pain
generator is found in chronic low back pain.
(Braddom et al, 2011)
CLASSIFICATIONS
 Acute pain- low back pain present for up to six weeks. It may be experienced as aching,
burning, stabbing, sharp or dull, well-defined, or vague.
 Sub-acute pain - pain lasts up to 6 to 12 weeks.
 Chronic pain - it has been present for longer than three months and it may originate from
an injury, disease or stresses on different structures of the body.
 Neuropathic pain - all signs of the original injury are usually gone and the pain that one
feels is unrelated to an observable injury or condition and there is certain nerves
continue to send pain messages to the brain even though there is no ongoing tissue
damage; it was different to musculoskeletal pain and is often described with the following
terms: severe, sharp, lancinating, lightning-like, stabbing, burning, cold, and/or ongoing
numbness, tingling or weakness.

TYPES
1) Mechanical low back pain
 Common cause of low back pain. It includes poor muscle, recruitment; emotional
stress, and changes associated with aging and injury such as disk generation,
arthritis, and ligamentous hypertrophy.
2) Spondylosis
 Osteoarthritis of the spine.
3) Spondylolysis
 Is a defect of the pars interarticularis and is a common cause of back pain in
children and adolescents. It is a repetitive hyperextension loading in the
immature spine, and is commonly reported in adolescent gymnasts and football
linemen.
4) Spondylolisthesis
 Refer to a forward slippage of one vertebra upon the one below it, it can result
from many causes. It is most common adolescent athlete particularly in those
who engage in repetitive extension type activities.
5) Posterior column fractures
 This is transverse process and spinous process fractures. These are stable
fracture.
6) Anterior column fractures
 These are compression fractures and generally are caused by flexion injuries.
 These fractures usually do not cause neurologic deficit and do not require
energy.
7) Spondyloarthropaties
 Group of disease associated with the HLA-B27 allele.
8) Ankylosing spondylitis
 Is the prototype for the spondylarthroses. It is a chronic, progressive
inflammatory disorder of undetermined cause. It is common in rheumatoid
disorders. It is 3x more common in men than in women. Symptoms begins in the
late tens or 20s.
9) Lumbar disc herniation
 Occurs when the nucleus pulposus herniates through the annulus fibrosus,
leading to irritation or compression of the spinal nerve.
10) Lumbar spinal stenosis
 Narrowing of the spinal canal by either osseous or soft tissue encroachment.
Frequent in older patients due to spinal degeneration.
11) Lumbosacral radiculopathy
 Radicular symptoms can be the result of overt mechanical compression of a
nerve root or a mechanically mediated inflammatory process. The most common
compressing lesion by far is a disk protrusion.
12) Cauda equina syndrome
 Mechanical compression of the lower lumbar and sacral nerve roots as they pass
through the spinal canal in the cauda equina bundle.
13) Vertebral osteomyelitis
 Infection in the vertebra caused by bacteria, fungi, mycobacteria, spirochetes, or
parasites.
14) Osteoporosis
 Common metabolic disorder to produce low back pain. It is caused by a loss of
bone mass despite a normal bone mineral to matrix ratio and is most common in
older women.

Other types:
1) Low back pain in pregnancy
LBP is a common problem in pregnancy. Multiple studies have estimated the
prevalence of low back pain in pregnancy at 49% to 76%. Risk factors include a
history of previous back pain, previous pregnancy related back pain and low back
pain during menses. It can begin at any time during the pregnancy and generally
reaches a peak at 36 weeks.

2) Pediatric low back pain

In a subset of studies more than 300 children each, the prevalence of back pain
was cited between 30% and 51%. Severe back pain, which is either relapsing or
permanent, was reported in 3% to 15%. Other studies demonstrate that the
prevalence of low back pain has the greatest increase during puberty and the
time of the maximum growth spurt. The risk factors for pediatric LBP population
include increase in age, female gender, parents with low back pain, hyperlordotic
posture, history of spinal trauma, participation in competitive sports, a high level
of physical activity, and depression. Sitting appears to be the main exacerbating
factors of low back pain in the pediatric population.
(Braddom et al, 2011)
CLINICAL SIGNS AND SYMPTOMS
Symptoms that can be associated with low back pain include:

 dull ache
 numbness
 tingling
 sharp pain
 pulsating pain
 pain with movement of the spine
 pins and needles sensation
 muscle spasm
 tenderness
 sciatica with shooting pain down one or both lower extremities
 rash, and
 Loss of continence of bowel or bladder

DIFFERENTIAL DIAGNOSIS
DIAGNOSIS AGE LOCATION QUALITY AGGRAVATING SIGNS
/ ALLEVIATING
Mechanical 20 to 40 Low back, Acute, Increased with Local
back strain buttock, spasm activity or tenderness,
posterior bending limited spinal
thigh motion
Acute disc 30 to 50 Low back to Sharp, Decreased with (+) Straight leg
herniation lower leg shooting or standing, test,
burning increased with weakness,
pain, bending or asymmetric
paresthesia sitting reflexes
in leg
OA or spinal >50 Low back to Ache, Increased with Mild decrease
stenosis lower leg, shooting walking, in extension of
often bilateral pain, “pins especially up an spine, may
and incline, have
needles” decreased with weakness or
sensation sitting asymmetric
reflexes
Spondylolisth Any age Back, Ache Increased with Exaggeration
esis posterior activity or of the lumbar
thigh bending curve,
palpable “step
off” (defect
between
spinous
processes),
tight
hamstrings
Ankylosing 15 to 40 SI joint, Ache Morning Decreased
spondylitis lumbar spine stiffness back motion,
tenderness
 over SI joint
Infection Any age Lumbar Sharp pain, Varies Fever,
spine, ache percussive
sacrum tenderness;
may have
neurologic
abnormalities
or decreased
motion
Malignancy >50 Affected Dull ache, Increased with May have
bone(s) throbbing recumbency or localized
pain, slowly cough tenderness,
progressive neurologic
signs or fever
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DIAGNOSTIC PROCEDURES
Physical Examination for Low Back Pain
 Observation
 Observation of overall posture
o To determine whether structural abnormality or muscle imbalances are
present.
 Observation of lumbar spine
o To further define muscle imbalance and habitual posture.
 Observation of the skin
o To search for diagnoses such as psoriasis, shingles, or vascular disease
as the cause of pain.
 Observation of gait
o To screen the kinetic chain and determine whether muscular, neurologic,
or joint problems are contributing to symptoms.
 Palpation
 Bones
o To search for bony problems such as infections or fracture.
 Facet joints
o To identify whether specific levels are tender.
 Ligaments and intradiskal spaces
o To determine whether these are tender
 Muscles
o To search for trigger points, muscle spasms, muscle atrophy
 Active Range of Motion
 Forward flexion
 Extension
 Lateral flexion
 Rotation
 Neurologic examination
 Manual muscle testing of L1- S1 myotomes
o To determine weakness
  Pinprick and light touch sensation, L1- S1 dermatomes
o To determine sensory loss
 Reflexes: patellar, hamstring, Achilles
o To test injury to L4, L5, or S1 roots if diminished, upper motor neuron
disease if brisk
 Balance and coordination testing
o Signs of upper motor neuron disease
 Plantar responses
o Signs of upper motor neuron disease
 Straight leg raise
o Neural tension at L5 or S1
 Femoral nerve arch
o Neural tension at L3 or L4
 Orthopaedic special tests
 Abdominal muscle strength
o To determine weakness and deconditioning
 Pelvis stabilizer strength, i.e. gluteus medius, maximus, etc.
o To determine weakness and deconditioning
 Tightness or stiffness of hamstrings, hip flexors, hip rotators
o To determine areas of poor flexibility
 Prone instability test
o Signs of instability
Imaging Studies
 Plain Radiography (X-Ray)
o Initial screening tool for lumbar spine pathology, indicated in trauma to evaluate
for fracture and to look for bony lesions such as tumor when red flags are present
in the history. Oblique views can be obtained to examine for a spondylolysis by
visualizing the pars interarticularis and the “Scottie dog” appearance of the
lumbar spine.
o Have very low sensitivity and specificity.
 Magnetic Resonance Imaging (MRI)
o Well-known imaging method for evaluating degenerative disk disease, disk
herniations, and radiculopathy.
o Very sensitive test, it is not very specific in determining a definite source of pain.
 Computed Tomography (CT Scan)
o Useful in the postsurgical patient with excessive hardware that can obscure
MRIs, and in patients with implants (aneurysm clips or pacemakers) that
preclude MRI.
 Myelography
o Typically reserved as a potential presurgical screening tool but has been used
less with the advancement of MRI.
o Contrast dye is injected into the dural sac and plain radiographs are performed to
produce images of the borders and contents of the dural sac.
 Scintigraphy
o Radionuclear bone scanning is a fairly sensitive but not specific imaging modality
that can be used to detect occult fractures, bony metastases, and infections.
 Electromyography
 o Useful in evaluating radiculopathy because it provides a physiologic measure for
detecting neurogenic changes and denervation with good sensitivity and high
specificity.
o It can also provide information as to which anatomic lesions found in imaging
studies are truly physiologically significant.
Laboratory Studies
Blood tests are rarely used in isolation as a diagnostic strategy for low back pain. Some
blood tests are helpful as an adjunct in diagnosing inflammatory disease of the spine (with such
markers of inflammation as sedimentation rates and C- reactive proteins), as well as some
neoplastic disorders, such as multiple myeloma with a serum protein electrophoresis and urine
protein electrophoresis.
(Braddom et al, 2011)
PROGNOSIS
Prognosis for LBP is difficult to ascertain because it is a symptom caused by a vast
spectrum of pathology, the pain experience is individual and treatment expectations vary, and a
huge body of literature highlights the complex cultural, psychological, social support, and
economic factors that influence pain and rehabilitation.
That being taken into account, the prognosis for low back pain is better defined. The
much quoted view that 90% of cases of acute low back pain will recover within 6 weeks does
not include the entire story of low back pain will recover within 6 weeks does not include the
entire story of LBP, either in clinical practice or in reviews of the scientific literature.
(Braddom et al, 2011)

MANAGEMENT
Treatment of Mechanical Low Back Pain
In treating mechanical low back pain, clinicians use multiple treatments on a particular
patient in the hope that their cumulative effect will provide sufficient pain relief and an
improvement in symptoms.
 Reassurance and patient education
Education should include providing as much of an explanation as patients need
in terms they can understand. Reassurance that there is no serious underlying
pathology, that the patient can stay active and get on with life despite the pain can help
counter negative thoughts and misinformation that the patient might have about back
pain.
 Back schools
The term back school is used for group classes that provide education about
back pain. Studies have found that back schools are effective in reducing disability and
pain for those with chronic low back pain.
 Exercise
 Many practitioners believe that exercise for patients with acute low back pain is
appropriate to prevent deconditioning, to reduce the chance of recurrence of symptoms,
to reduce the risk of the development of chronic pain and disability.
Exercise prescriptions for mechanical low back pain generally begin with the goal
of improving alignment and posture.
 Flexion Exercises
 Extension Exercises
 Aerobic activity
 Aquatic exercises
 Exercise after spine surgery

 Medication
o NSAIDs- provide pain relief for both acute and chronic low back pain.
o Muscle relaxants- used for pain relief (benzodiazepines, nonbenzodiazepine
antispasmodics, antispasticity medication).
o Antidepressants- effective treatment for painful conditions, such as diabetic
neuropathy, postherpetic neuralgia, fibromyalgia and headaches. Studies found
that tricyclics and tetracyclics had significant effects in reducing pain. These
reductions were seen in studies in which depressed patients were excluded, so
the mechanism is independent of any treatment of underlying depression.
o Opioids- used for treatment of acute low back pain (e.g. Tramadol)
o Anticonvulsants- Gabapentin and Pregabalin, both anticonvulsants, are widely
used for neuropathic pain.
o Herbal medicines- herbal medicines, like Capsicum frutescens (cayenne) in a
topical preparation, Salix albab (white willow bark), Harpagophytum procumbens
(devil’s claw), seem to reduce pain.
o Topical treatments- Lidocaine (lignocaine) patches have been found effective by
some patients for treatment of back pain.

 Injections and Needle Therapy

o Myofascial pain and Trigger point injections
o Acupuncture
o Experimental injection procedures
 Botulinum toxin injections are increasingly being used to treat low back
pain.
o Steroid injections

 Manual Mobilization or Manipulation

 Traction
 Lumbar supports
 Massage
 Complementary Movement Therapies
o Yoga- This is both an exercise system and philosophy that promotes relaxation,
acceptance, and breathing techniques while various stretching and strengthening
exercises are done.
o Pilates- This is a form of core-strengthening exercises that stress alignment and
proper form.
 o Alexander technique- This is an educational approach to posture and normalizing
movement patterns.
o Feldenkrais method- This is a combination of classes and hands-on work with
therapeutic exercise to promote natural and comfortable movement patterns and
improve body awareness.
 Multidisciplinary pain treatment programs
 Treatment of comorbidities
Treatment for Spondylosis
 Lifestyle and activity modification include weight control, relative rest, and initially limiting
activities that result in increased pain (e.g. sleeping prone generally is to be avoided).
 Medications used include analgesics such as acetaminophen and NSAIDs.
 Exercise programs are generally designed to decrease the forces acting on the
zygoapophyseal joints.
Treatment for Spondylolysis
 Relative rest for 3 months and avoidance of activities that increase pain (especially
repetitive extension)
Treatment for Spondylolisthesis
 Relative rest for 3 months and avoidance of activities that increase pain (especially
repetitive extension)
 Operative intervention with fusion is generally considered only for recalcitrant pain after
an appropriate rehabilitation program, persistent radiculopathy, or progressive instability.
Treatment for Spinal Fractures
 Calcitonin, TENS, intercostal nerve block- used to decrease pain.
Treatment for Ankylosing Spondylitis
 Exercise
 NSAIDs
Treatment for Lumbar Disc Herniation
 Same treatments with mechanical low back pain, because of the difficulty of definitively
diagnosing this source of low back pain and there are no proven specific treatments yet.
Treatment for Lumbar Spinal Stenosis
 Oral medications
 Epidural steroids
 Comprehensive functional rehabilitation program- flexion- based lumbar stabilization
exercises, strengthening the abdominals, pelvic girdle stabilizers, and gluteals, aerobic
conditioning
 Surgical consideration for patients with intractable pain resistant to nonoperative
management
Treatment for Lumbosacral Radiculopathy
 Neuropathic pain agents- anticonvulsants and tricyclic antidepressants
  Active exercise program potentially with epidural steroid injections.
 Surgical management for those patients who have significant persistent radicular
symptoms despite 6 to 8 weeks of maximized conservative management, neurologic
progression, or cauda equine syndrome.
Treatment for Cauda Equina Syndrome
 Surgery
Treatment for Vertebral Osteomyelitis
 Surgical debridement
 Antibiotics
Treatment for Osteoporosis
 Medication
 Lifestyle modification
 Exercise
(Braddom et al, 2011)
REFERENCES
Braddom, R. L., et al, Physical Medicine and Rehabilitation, 4th ed 2011
Kasper, D.L., et al., eds. Harrison's Principles of Internal Medicine, 19th Ed. United States:
McGraw-Hill Education, 2015
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