Download A nonsurgical approach to low back pain

A nonsurgical approach to
low back pain
RICHARD T. JERMYN, DO
Low back pain, a leading cause of disability in the United States, has a significant
economic impact not only on lost productivity but also on healthcare expenditures. Approximately a fifth of patients will see multiple physicians in their quest for
relief of low back pain. Primary care physicians therefore play a crucial role in the
initial approach to these patients. A thorough history and physical examination
directed toward the neurologic, orthopedic, and osteopathic evaluation are essential.
This article reviews the diagnosis and assessment of pain levels and a triad system
of therapy involving cortical, spinal, and peripheral levels. Options include antidepressants, neuroleptics, neurostimulants, and osteopathic manipulative treatment
(OMT) (cortical level); opiates, tramadol hydrochloride, and transcutaneous electrical nerve stimulators (spinal level); and nonsteroidal anti-inflammatory drugs, epidural injections, spinal blocks, antispasmodics, physical therapy, muscle relaxants,
exercise, and OMT (peripheral level), By choosing a modality directed at each
level, the clinician may provide the patient with a pain management program that
will maximize the chosen mode of therapy and restore function and mobility.
(Key words: low back pain, neuromusculoskeletal examination, sacroiliac
dysfunction, hip dysfunction, lumbosacral strain, lumbosacral sprain, radiculopathy,
myopathy, neuropathy, sciatica, pain control, physical therapy, osteopathic evaluation, osteopathic manipulative treatment)
cially if the pain is chronic. Bowel and
bladder incontinence should be explored
because it could indicate a significant neurologic disorder such as cauda equina syndrome. One should document the patient’s
current functional level and the level at
which the patient is pain free. Finally, the
goals of the patient are extremely important, such as walking, sleeping, or even
competitive running.
Several pain assessment tools have been
established to objectify pain. These tools
include the Visual Analog Scale (Figure
1),8 McGill Pain Questionnaire (MPQ),
Short-Form McGill Pain Questionnaire
(SF-MPQ), Western Ontario and McMaster Universities Osteoarthritis Index, and
various behavioral and physiologic testing
instruments.9(pp20,21) The Visual Analog
Scale is probably the most used and simple tool for pain evaluation. It is a simple
analog scale that measures pain perception
on a scale from 0 to 10, where “0” is
graded as “no pain” and “10” is graded
“as bad as it gets.” Patients place a mark
between the 0 and 10 (100-mm) line that
corresponds to the level of pain they are
experiencing. Studies show that a change
of 13 mm or more can be considered statistically important and clinically relevant.8 The shortcoming of the Visual Analog Scale is that it does not account for
function, depression, or different types of
pain symptoms.
Physical examination
L
ow back pain is the second most common cause of absence from the workplace among people younger than 55 years,
second only to the common cold.1 Among
people younger than 35 years, back pain is
the leading cause of disability in the United States.2 Pain is responsible for 50 million
lost work days each year, with a staggering
economic impact of $50 billion spent annually in the United States.2-5 In a recent
study,6 79% of patients with acute low
back pain will see one physician and 21%
will see multiple physicians including: chiropractors, orthopedic surgeons, neuro-
Patient history
Dr Jermyn is an assistant professor of physical
medicine and rehabilitation, and Director, University Back Pain Center, University of Medicine
and Dentistry of New Jersey–School of Osteopathic Medicine, Stratford, NJ, He is also Director, Comprehensive Back Pain Center,
Voorhees, NJ.
Correspondence to Richard T. Jermyn, DO,
42 Laurel Rd E, Suite 1200, Stratford, NJ 080841504.
E-mail: [email protected]
The evaluation of the patient with low
back pain begins with a thorough history
and physical examination. History
includes the onset, intensity, duration,
quality, frequency, radiation, severity,
associated symptoms, and factors that
relieve and intensify the pain. It is important to ascertain whether the pain is chronic or acute because the diagnosis and treatment may vary. The patient should be
screened and treated for depression, espe-
surgeons, physiatrists, rheumatologists,
and physical therapists. The cost of seeing multiple healthcare specialists is generally four times the cost of seeing one primary care physician.7 By the 3-month
interval of continued low back pain, 54%
of patients will seek out multiple healthcare
specialists.8 In the current healthcare economic environment, the role of the primary care physician in the diagnosis, treatment, and prevention of low back pain is
imperative.
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The physical examination begins with
examination of the neuromuscular, vascular, orthopedic, and osteopathic systems (Figure 2).
The foundation of any neuromusculoskeletal examination begins with a
detailed evaluation of the upper motor
neuron and the lower motor neuron. The
upper motor neuron is generally considered to be the brain and the spinal cord.
The lower motor neuron begins at the
alpha motor neuron and includes the dorsal and ventral roots, the spinal nerve, the
peripheral nerve, the neuromuscular junction, and the muscle fiber complex. Physical findings that correspond with a pathologic process in the upper motor neuron
system are increased deep tendon reflexes, spasticity, Hoffmann’s sign or Babinski’s reflex, and frontal release signs if
there is a frontal lobe pathologic lesion.
Ataxia, tremor, and dysmetria will be present if a pathologic process exists in the
cerebellum or posterior fossa. When evaluating low back pain, the superficial cre-
Jermyn • A nonsurgical approach to low back pain
1
2
3
4
5
6
7
8
9
10
(100 mm)
No pain
Worst pain
Figure 1. Visual Analog Scale for patient’s self-assessment of level of pain.
masteric reflex and the superficial anal
reflex can indicate a significant upper
motor neuron lesion corresponding to
L1,L2 and S2,S3,S4, respectively.10 The
finding of an unexplained upper motor
neuron pathologic process on physical
examination should be immediately correlated with head and spine magnetic resonance imaging (MRI) or computed
tomography (CT) scans.
A lower motor neuron pathologic process will present with decreased reflexes
and weakness on physical examination.
The triceps surae reflex, or Achilles tendon
reflex, corresponds to the first and second sacral level; the patellar reflex corresponds to the third and fourth lumbar
segment; the medial hamstring reflex corresponds to the fifth lumbar and the first
and second sacral segment.10
Dural tension test, or Lasègues’s test, is
a classical test to indicate a proximal nerve
impingement. The straight-leg test (SLT)
is performed with the patient supine, and
the lower extremity is slowly raised. With
a positive test, radicular symptoms will
be present at less than 70 degrees of flexion, indicating irritation of the sciatic
nerve.11(pp59-90) Studies show that the test
is very sensitive to lumbar disk herniation but not highly specific.12 Nonneurologic etiologies of a positive SLT include
tight hamstrings, muscle spasms, and
sprained posterior longitudinal ligament
sprain.
Manual muscle testing can be extremely helpful in determining weakness corresponding to a neurologic level. Weakness
of great toe dorsiflexion corresponds to the
fifth lumbar segment. Weakness of ankle
plantar flexion corresponds to the first
sacral segment.10 If the dorsal root component of the lower motor neuron is compressed, there will be a corresponding sensory abnormality in that sensory
dermatome. Sensory abnormalities include
hypoesthesia, burning, electrical sensations, or allodynia (a painful sensation to
a nonpainful mechanical stimulation such
as clothing or bed covers).
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The evaluation of the vascular system
of the patient with low back pain includes
detection of any ischemic changes in the
lower extremity. Palpation of the pulses in
the lower extremity should be a routine
part of the evaluation of the patient with
low back pain. Vascular claudication presents as bilateral leg pain that begins at a
fixed distance when ambulating and is
relieved by standing. Pseudoclaudication,
or neurogenic claudication (associated
with spinal stenosis), is relieved only by sitting or forward flexion of the lumbar
spine.11(p31)
The orthopedic evaluation of the low
back includes gait, posture, standing balance, crouching, range of motion, SLT,
and fabere (flexion, abduction, external
rotation, extension) sign (Patrick’s test). A
complete osteopathic evaluation includes
evaluation of leg-length discrepancies, segmental and intersegmental somatic dysfunctions, sacroiliac dysfunctions, and
sources of referred pain from the abdomen
and viscera. Each lumbar and sacral segment should be palpated for tenderness.
Mobility of the spine should be evaluated
in flexion, extension, sidebending, and rotation. The patient should be evaluated sitting,
standing, supine, and prone. Patrick’s test,
consisting of flexion, abduction, and external rotation of the hip, can evaluate both
hip and sacroiliac dysfunction.
Causes of low back pain
Causes of low back pain are listed in Figure 3. Metabolic abnormalities are the
most common clinical finding associated
with global deep tendon hyperreflexia
and upper motor neuron findings. Syndromes include a thyroid pathologic
lesion, electrolyte imbalances, and drug
toxicities. Parkinson’s disease can present
with low back pain and leg pain. Physical
findings are increased tone and shuffling
gait. Primary or metastatic space-occupying lesions should always be considered, especially if there is a history of cancer. Cerebrovascular accidents (CVAs)
can present with both neck and low back
✔
Checklist
Neurolologic
Deep tendon reflexes
Manual muscle testing
Sensory dermatomes and
peripheral nerve testing
Muscle tone and spasticity
Hoffmann’s sign and Babinski’s
reflex
Straight-leg test
Vascular
Arterial pulses
Evaluation for claudication
Orthopedic
Spinal mobility
Gait
Patrick’s test
Osteopathic
Somatic dysfunctions
Referred pain
Figure 2. Components of examination
of low back pain.
pain. Pain associated with CVAs is secondary to increased tone or even pain
syndromes such as complex regional pain
syndromes or hand-shoulder syndrome.
Myelopathy, both cervical and lumbar,
can result from central disk herniations
and severe spinal stenosis or chronic disease processes such as the human immunodeficiency virus (HIV) infection. Diagnosis can be made with CT or MRI.
The conditions that will present with
lower motor neuron symptoms are
impingement syndrome of the proximal
nerve root (radiculopathy), neuropathy,
and myopathy. Impingement syndrome
resulting from dorsal root compression
of the proximal lower motor neuron complex accounts for the majority of true
“sciatica.” Although no definition of sciatica is universally agreed on, most practitioners consider it a neuropathic injury to
the sciatic or proximal tibial nerve. If neuropathic injury is involved, proximal tibial nerve neuropathy is probably more
appropriate nomenclature. Disk herniation is a common cause of sciatica; however, not all disk herniations result in a
painful process. It has been demonstrated
that 20% to 30% of healthy, asymptomatic patients have CT- or MRI-evident herniated disks.13 The most common symptoms of radiculopathy are pain,
JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 • S7
reflex loss, sensory changes, and weakness. Computed tomography or MRI can
be diagnostic if disk disease is present.
Electromyography (EMG) and nerve conduction studies (NCS) may be helpful in
determining chronicity and recovery of
the nerve or detection of an injury at the
nerve root that is not related to disk disease or bony stenosis.
Myopathy is an abnormal breakdown
of muscle and may present as pain involving the back and proximal region of the
leg. It is usually bilateral and involves the
proximal muscle groups. It also can be
associated with decreased reflexes and
pain in a myotomal distribution. Causes
include disuse myopathy, inflammatory
processes (that is, dermatomyositis,
polymyositis, hepatitis, or HIV,14 and side
effects of pharmacotherapy (“statin”
drugs). If myopathy is suspected, it is recommended that serum creatine kinase
levels be measured. Diagnosis can be made
with EMG and NCS or muscle biopsy.
Spinal stenosis, cauda equina syndrome, and multiple sclerosis should be
considered when a patient has a combination of mixed upper and lower motor
neuron findings on physical examination.
By definition, spinal stenosis is a narrowing of the spinal canal or foramen (or
both). Patients with central canal stenosis
will have bilateral neurologic symptoms,
whereas patients with foraminal stenosis
will have unilateral symptoms. Causes
include discogenic disease, degenerative
arthritis, spondylolisthesis, or a congenitally narrow spinal canal or foramen.
Many times, the patient will have normal findings on neurologic examination
but the history will point to pain with
walking which radiates to the buttocks
and legs and is relieved only by bending or
sitting, that is, neurogenic claudication.
Symptoms progress slowly over a course
of years. Sudden onset of symptoms with
urinary retention may indicate an acute
cauda equina syndrome. Other symptoms
include bowel incontinence, sexual dysfunction, bilateral lower extremity pain,
and diminished perineal sensation. Fifty
percent of acute cauda equina syndromes
are due to tumors causing central canal
stenosis.11(p39) Acute cauda equina syndrome is considered a surgical emergency.
Diagnosis can be made with MRI or CT.
Orthopedic causes of low back pain
are mechanical alterations in the spine.
Patients with lumbar spondylosis or
degenerative disk disease will have nonradicular back pain. They describe general
✔
Checklist
NEUROLOGIC
Upper motor neuron
Metabolic
Space-occupying lesions
Parkinson’s disease
Cerebrovascular accident
Central disk herniations
Myelopathy
Congenital: Spina bifida
Lower motor neuron
Disk herniation: posterolateral
Neuropathy
Lumbar foraminal stenosis
Myopathy
Mixed upper and lower motor
neuron disease
Cauda equina syndrome
Multiple sclerosis
Lumbar spinal stenosis
VASCULAR
Claudication
ORTHOPEDIC
Lumbar sprain/strain
Lumbar spondylosis
Vertebral fracture
Coccygodynia
Diffuse idiopathic skeletal hyperostosis
Ankylosing spondylitis
OSTEOPATHIC
Somatic dysfunctions
Posture
Piriformis syndrome
Referred pain
Figure 3. Causes of low back pain.
or point tenderness in the low back. Physical activity usually makes the pain worse,
and rest relieves it. The examination will
demonstrate a decreased lumbar lordosis, paraspinal tenderness, and spasm.
Diagnosis can be made with a plain xray film. Facet (zygapophyseal) joint pain
may account for up to 15% to 40% of
low back pain.11(pp56-90) Patients have low
back pain that may radiate to the buttocks which is made worse by extension
and rotation of the lumbar spine. Radiologic studies may demonstrate facet arthritis but most likely will show no abnormality.
Lumbar spondylolisthesis is a slippage
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usually of the fifth lumbar segment due to
a fracture of the pars interarticularis, and
those affected have low back pain that
radiates to the coccyx or lateral aspect of
the leg.9(p14) Plain x-ray films are all that
are usually needed to make the diagnosis.
Coccygodynia is the complaint of pain at
the base of the spine; etiology is unknown.
Trauma, intraosseous lipoma, chordoma,
and giant cell tumor have been postulated as the cause.11(p92) Imaging studies usually show no abnormality.
Lumbar spinal fractures are usually
the result of trauma occurring mostly in
osteoporotic patients or patients with prolonged corticosteroid use. In younger
patients without a history of trauma,
malignancies such as multiple myeloma or
metastatic disease should be considered.
Pain is localized to the involved vertebrae
and made worse with flexion. Plain x-ray
films are usually diagnostic, but a bone
scan may prove more beneficial to determine the acuity of the fracture.
Diffuse idiopathic skeletal hyperostosis is a hypercalcification of the anterior
and posterior longitudinal ligament and is
found in middle-aged men. X-ray films
will demonstrate large bone spurs and
syndesmophytes that fuse regions of the
spine. Patients complain of diffuse, nonradicular back pain. Younger male
patients with ankylosing spondylitis will
have gradual sacral pain that ascends to
the low back. It is usually worse in the
morning and improves as the day progresses. X-ray films will show sclerosis of
the sacroiliac joint and bridging syndesmophytes that will eventually take on the
form of a “bamboo” spine.
Lumbosacral sprain and strain is the
most common diagnosis of low back pain.
The etiology is not completely understood,
but this condition is associated with an
increased mechanical load through the
low back. The abnormal forces can result
in microtrauma to the ligamentous and
muscular structures. The posterior longitudinal ligament and interligamentous
structures are heavily innervated with pain
fibers, and overstretching or tearing them
can cause pain. The patient describes pain
localized in the low back and may have
some symptoms of radicular pain but no
numbness or tingling. The physical examination will demonstrate paraspinal spasm,
decreased lumbar lordosis, and pain with
increased flexion but no neurologic
deficits. X-ray films may show a decreased
lumbar lordosis. Overall, the main sites of
low back pain are the posterior longitu-
Jermyn • A nonsurgical approach to low back pain
dinal ligament, the interspinous ligaments,
the nerve roots and dural coverings, the
facet joints, and the deep muscles.15
Osteopathic lesions may be the primary cause or a result of low back injury,
both acute and chronic. Somatic dysfunctions, both segmental and intersegmental, may result in significant pain.
Physical examination will demonstrate
decreased mobility at that segment and
resultant paraspinal tenderness. Evaluation of posture should be part of every
osteopathic evaluation. According to Cailliet,15 80% to 90% of low back pain is
related to poor posture. Piriformis syndrome is a compression of the sciatic nerve
as it courses under or through the piriformis muscle. Patients complain of gluteal
and hip pain that is exacerbated with flexion, adduction, and internal rotation of the
hip, that is, piriformis stretch. Finally, low
back pain can be the result of referred
pain from the viscera, known as viscerosomatic reflexes. These reflexes can be
seen with pathologic lesions in the
prostate, stomach, colon, uterus, kidney,
urinary bladder, liver, and spleen.
Understanding the pain complex
To understand how to treat pain symptoms, it is important to understand the
pain pathway. Figure 4 is a simplification
of the pain process that demonstrates the
neurophysiologic pain pathway when a
person stubs a toe. At the site of injury,
inflammatory precursors are released, as
well as free nerve-ending stimulation.
Nociceptors in the toe are stimulated and
ascend to the spinal cord via large-diameter and fast-conducting myelinated A
delta fibers and slow-conducting unmyelinated C fibers. At the level of the dorsal
horn of the spinal cord, neurotransmission
occurs via a complex array of interneurons
before ascending to the brain. Here is
where opiate receptors (, , and ) modulate or dampen the transmission of pain,
forming a gate. If enough pain stimulation
has occurred to overwhelm the system,
the gate will open and pain will ascend to
the brain via the spinothalamic tract to
the medulla and thalamus of the brain
and eventually on to the cerebral cortex.
At the cortical level, modulation occurs
again to dampen the effect of pain before
descending back to the spinal cord. Here,
the neurotransmitters serotonin, norepinephrine, -aminobutyric acid (GABA),
dopamine, and opioids again work to
dampen the effect of pain at the cortex,
thalamus, and medulla.9(pp1-11),16 If there is
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enough pain stimulation to overwhelm
the cortical modulation process, the pain
will descend back to the spinal cord and
back to the peripheral nerve where it originated. In the example of the person who
stubbed a toe, the mechanoreceptors and
quick A delta fibers are stimulated, quickly resulting in a reflex to move the foot.
The slow C fibers go through the modulation at the spinal cord and the cortex
and eventually will transmit back to the
foot, accounting for that millisecond delay
that is experienced after banging the toe.
Treatment strategies for low
back pain: the pain triad
As previously outlined, for one to experience pain, stimulation must occur at the
periphery, spinal cord, and cortex. Treatment options can be geared toward those
that affect the periphery, spinal cord, and
cortex, that is, the pain triad. When treating pain, especially chronic, the clinician
can choose modalities from each level,
giving the patient a more efficient pain
management program. Figure 5 illustrates
the trilevel pain management program
for low back pain.
At the level of the peripheral nerve,
NSAIDs and muscle relaxers, epidural
and nerve and spinal blocks, physical therapy modalities, osteopathic manipulation,
and physical exercise are current treatment options. At the level of the spinal
cord, opiate analgesics and transcutaneous
electrical nerve stimulators (TENS) have
efficacy. And finally, control of pain at
the cortical level can be achieved with
antidepressants, neuroleptics, and neurostimulants as well as opiate analgesics
and osteopathic spinal manipulation.
Peripheral pain control
NSAIDs are the most common analgesic
medication used to treat low back pain. It
is most beneficial where inflammatory
processes are evident. It works by inhibiting prostaglandin synthesis, primarily
through the cyclooxygenase pathway,
which occurs in response to injury of the
cell membrane. Two broad categories of
NSAIDs exist:
traditional NSAIDs, which inhibit
cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and
selective COX-2.
COX-2 inhibitors are reported not to
interfere with protective prostaglandins
in the gastric mucosa and should be used
for patients who have a history of or risk
factors for peptic ulcerative disease. Oral-
dose corticosteroid can also be used in
acute, significant inflammatory processes.
Muscle relaxants such as cyclobenzaprine hydrochloride, methocarbamol,
baclofen, and tizanidine (Zanaflex) can
relieve muscle spasm. The purpose of these
medications is to allow increased range
of motion and improved tolerance for
physical exercise. Side effects of these medications are extreme sedation; they should
be used judicially. The long-term effects of
continued use of these agents are still
unknown, and they should be used only
for short periods.
Epidural steroid injections are effective in about 66% of selected patients
with low back pain.17 Patients with suspected nerve root inflammation due to
disk disease or lumbar stenosis may benefit. Although no clear criterion exists,
patients who respond best are those who
have not improved after 4 weeks of conservative care and those who have an
acute flair of a chronic condition.
Other blocks include paravertebral,
sacroiliac, and facet joint nerve blocks.
Facet joint blocks can be both diagnostic
and therapeutic in the treatment of low
back pain18; as mentioned previously,
radiologic studies most likely will show
absolutely no abnormality in patients with
facet joint–mediated pain. Injections into
trigger points in isolated muscle spasm
locations can be beneficial in decreasing
pain symptoms. Injections are usually
given with a local anesthetic. Injections
into trigger points in patients with piriformis pain has been proven beneficial in
relieving pain15 in both acute and chronic low back pain. Chemical neurolytic
agents such as botulinum toxin are also
being used, but long-term studies are still
on going.
Physical therapy is critical to the recovery of patients to restore flexibility,
motion, and improved function. Stretches to increase flexibility of the hip flexors, hip extensors, and hamstrings should
be taught to patients, even those with
acute pain. Patients with tight hamstrings
will not have adequate hip range of
motion and may sprain the lumbar spine
with relatively minimal hip flexion. Eventually, patients should progress to more
taxing exercises to strengthen the abdominal musculature and improve pelvic stability. An integral part of rehabilitating
and preventing future injuries is instructing the patient on proper lifting techniques
that emphasize lifting with the large muscle groups of the lower extremity, as
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Cortical
Spinal
Peripheral
Nerve
Figure 4. Diagram demonstrating the neurophysiologic pain pathway when a person
stubs a toe.
opposed to the weak paraspinal stabilizing musculature. Physical therapy modalities such as application of heat and cold
can provide strong anti-inflammatory and
analgesic effects. Patients should be
instructed to heat, perform stretches, and
to ice afterward. The use of low back
bracing remains controversial. It may provide temporary relief in the acute pain
setting, but prolonged use can promote
muscular weakness and even atrophy due
to disuse.
Osteopathic manipulation is a treatment for both acute and chronic low back
pain. Manual muscle techniques are critical in enhancing segmental hypomobility, thus allowing uniform segmental
motion and functional balance.11(pp59-90
Manual techniques have been used in
most diagnoses of both acute and chronic pain syndromes. High-velocity techniques should be used with caution on
patients who have an upper motor neuron
pathologic process or when bone metastatic disease is known or suspected. Osteopathic manipulative medicine is the only
treatment modality that has effects at all
three treatment levels, having effects on
peripheral, spinal, and cortical regions.
Spinal level
Cortical
Antidepressants
Neuroleptics
Neurostimulants
OMT
Spinal
Opiates
Tramadol
TENS
NSAIDs
Epidural Injection
Spinal Blocks
Peripheral
Nerve
Physical Therapy
Antispasmotics
Muscle Relaxants
Exercise
OMT
Figure 5. Illustration of trilevel pain management program for low back pain.
OMT osteopathic manipulative treatment; TENS transcutaneous electrical
nerve stimulator; NSAIDs nonsteroidal anti-inflammatory drugs.
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Modes of treatment geared at the spinal
level are to dampen or impede pain from
ascending to the brain. In addition to
osteopathic manipulative medicine, opioid
analgesics and TENS units have effect
here. According to the World Health
Organization analgesic ladder,19 opioids
are appropriate for moderate and severe
pain. In patients with mild pain, adjunctive analgesics are the mainstay of pharmacologic therapy; these agents include
NSAIDs, acetaminophen, neuroleptics,
and antidepressants. Opiates work at the
spinal level by binding to opiate receptors at the interneuron level in the dorsal
horn as mentioned earlier. There are two
classes of opioid analgesics: agonists and
agonist-antagonists. The pure opioid agonists include oxycodone, hydrocodone,
and codeine. Stronger opioid agonists
include morphine in both an immediaterelease formulation (morphine sulfate
immediate release, MSIR) with effects
lasting 3 to 4 hours, and a sustainedrelease form (OcyContin, MS Contin,
Roxanol SR), which provides 12 hours
of relief. It is recommended to start with
the lowest possible dose and titrate as
needed. Never prescribe opioids on an
as-needed basis but as a scheduled dose.
Jermyn • A nonsurgical approach to low back pain
Be aware of the development of physical
tolerance after prolonged use of an opioid.
To decrease the risk of addictive behavior,
the patient should be placed on long-acting agents with rescue doses of immediaterelease medication for breakthrough pain
to augment the sustained-release drugs.
This decreases the euphoria usually associated with shorter-acting agents that are
thought to contribute to drug-seeking
behavior. Tramadol hydrochloride
(Ultram) is a nonnarcotic medication that
also works on opioid receptors in the central nervous system and prevents reuptake of the neurotransmitters serotonin
and nerepinephrine. Tramadol is a unique
agent in that it can work both on the
spinal and cortical levels in the pain triad.
Transcutaneous electrical nerve stimulators and dorsal column stimulators
work at the spinal level by inhibition of the
A delta and C fibers by utilizing A alpha
or beta neural input, according to Melzack and Wall.20 Generally, a TENS unit
works only when on and may provide
significant improvement in pain and muscle spasm. Patients can be given their own
unit and simply master its use. Although
no clear criterion exists for surgical placement of dorsal column stimulators, they
have been helpful in some patients who
have failed to respond to conservative
treatment and are not candidates for low
back surgery.21
Cortical level
Antidepressant and anticonvulsant medications are adjunctive analgesics that
work cortically to dampen pain before
descending from the cortex to the spinal
cord. Antidepressant medications work
on both serotonergic and noradrenergic
pathways in the cortical pain centers of the
brain. They can also potentiate the analgesic effects of the opioids and help to
alleviate depression that is commonly seen
in patients with chronic pain. Commonly used tricyclic antidepressants (TCAs)
include amitriptyline hydrochloride (Elavil), nortriptyline (Pamelor), imipramine
hydrochloride (Tofranil), desipramine
hydrochloride (Norpramin), and doxepin
hydrochloride (Sinequan). Although not
studied as extensively as the TCAs, other
classes of antidepressants such as tra-
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zodone hydrochloride (Desyrel) as well
as serotonin-specific reuptake inhibitors
(SSRIs) such as fluoxetine hydrochloride
(Prozac), paroxetine hydrochloride (Paxil),
and sertraline hydrochloride (Zoloft) are
also used for adjunctive pain control with
some clinical success.
Medications originally designed to treat
seizure disorders, such as carbamazepine
(Atretol, Tegretol) and gabapentin (Neurontin), have been shown to be helpful
in the treatment of neuropathic and other
types of pain.22 These medications also
use neurotransmitters such as GABA, in
the case of gabapentin, to dampen the
pain before its descent to the spinal cord.
These agents also can potentiate the opioid medications and be powerful moodstabilizing agents. Other treatment modalities that are effective in pain control at the
cortical level include tramadol, which has
been previously mentioned. Although no
published studies exist, osteopathic manipulative treatment with such techniques as
craniosacral manipulation has also been
reported to have effects at the cortical
level.
Comment
The approach to the patient with low
back pain begins with a thorough history
and physical examination. The physical
examination should be geared toward the
neurologic, orthopedic, and osteopathic
evaluation. Modes of therapy can be categorized into a triad system involving
peripheral, spinal cord, and cortical levels.
The clinician can choose a modality directed at each level to provide the patient
with a pain management program that
will maximize the chosen mode of therapy and restore function and mobility to
the patient with low back pain.
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