cially if the pain is chronic.

Bowel and
bladder incontinence should be explored
because it could indicate a significant neu-
rologic disorder such as cauda equina syn-
A nonsurgical approach to drome. One should document the patient’s
current functional level and the level at
low back pain which the patient is pain free. Finally, the
goals of the patient are extremely impor-
tant, such as walking, sleeping, or even
RICHARD T. JERMYN, DO 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
Low back pain, a leading cause of disability in the United States, has a significant (SF-MPQ), Western Ontario and McMas-
economic impact not only on lost productivity but also on healthcare expendi- ter Universities Osteoarthritis Index, and
tures. Approximately a fifth of patients will see multiple physicians in their quest for various behavioral and physiologic testing
relief of low back pain. Primary care physicians therefore play a crucial role in the instruments.9(pp20,21) The Visual Analog
initial approach to these patients. A thorough history and physical examination Scale is probably the most used and sim-
directed toward the neurologic, orthopedic, and osteopathic evaluation are essential. ple tool for pain evaluation. It is a simple
This article reviews the diagnosis and assessment of pain levels and a triad system analog scale that measures pain perception
of therapy involving cortical, spinal, and peripheral levels. Options include antide- on a scale from 0 to 10, where “0” is
pressants, neuroleptics, neurostimulants, and osteopathic manipulative treatment graded as “no pain” and “10” is graded
(OMT) (cortical level); opiates, tramadol hydrochloride, and transcutaneous elec- “as bad as it gets.” Patients place a mark
trical nerve stimulators (spinal level); and nonsteroidal anti-inflammatory drugs, epidu- between the 0 and 10 (100-mm) line that
ral injections, spinal blocks, antispasmodics, physical therapy, muscle relaxants, corresponds to the level of pain they are
exercise, and OMT (peripheral level), By choosing a modality directed at each experiencing. Studies show that a change
level, the clinician may provide the patient with a pain management program that of 13 mm or more can be considered sta-
will maximize the chosen mode of therapy and restore function and mobility. tistically important and clinically rele-
(Key words: low back pain, neuromusculoskeletal examination, sacroiliac vant.8 The shortcoming of the Visual Ana-
dysfunction, hip dysfunction, lumbosacral strain, lumbosacral sprain, radiculopathy, log Scale is that it does not account for
myopathy, neuropathy, sciatica, pain control, physical therapy, osteopathic evalu- function, depression, or different types of
ation, osteopathic manipulative treatment) pain symptoms.

Physical examination

L ow back pain is the second most com-

mon cause of absence from the work-
place 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 Unit-
ed States.2 Pain is responsible for 50 million
lost work days each year, with a staggering
economic impact of $50 billion spent annu-
ally 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: chi-
ropractors, orthopedic surgeons, neuro-
Dr Jermyn is an assistant professor of physical
medicine and rehabilitation, and Director, Uni-
versity Back Pain Center, University of Medicine
and Dentistry of New Jersey–School of Osteo-
pathic Medicine, Stratford, NJ, He is also Direc-
tor, Comprehensive Back Pain Center,
Voorhees, NJ.
Correspondence to Richard T. Jermyn, DO,
42 Laurel Rd E, Suite 1200, Stratford, NJ 08084-
1504.
E-mail: jermynrt@umdnj.edu
surgeons, physiatrists, rheumatologists,
and physical therapists. The cost of see-
ing multiple healthcare specialists is gen-
erally four times the cost of seeing one pri-
mary 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 eco-
nomic environment, the role of the pri-
mary care physician in the diagnosis, treat-
ment, and prevention of low back pain is
imperative.
Patient history
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 impor-
tant to ascertain whether the pain is chron-
ic or acute because the diagnosis and treat-
ment may vary. The patient should be
screened and treated for depression, espe-
The physical examination begins with
examination of the neuromuscular, vas-
cular, orthopedic, and osteopathic sys-
tems (Figure 2).
The foundation of any neuromuscu-
loskeletal examination begins with a
detailed evaluation of the upper motor
neuron and the lower motor neuron. The
upper motor neuron is generally consid-
ered to be the brain and the spinal cord.
The lower motor neuron begins at the
alpha motor neuron and includes the dor-
sal and ventral roots, the spinal nerve, the
peripheral nerve, the neuromuscular junc-
tion, and the muscle fiber complex. Phys-
ical findings that correspond with a patho-
logic process in the upper motor neuron
system are increased deep tendon reflex-
es, spasticity, Hoffmann’s sign or Babin-
ski’s reflex, and frontal release signs if
there is a frontal lobe pathologic lesion.
Ataxia, tremor, and dysmetria will be pre-
sent if a pathologic process exists in the
cerebellum or posterior fossa. When eval-
uating low back pain, the superficial cre-

S6 • JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 Jermyn • A nonsurgical approach to low back pain
 No pain
1 2 3 4 5 6
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 cor-
related with head and spine magnetic res-
onance imaging (MRI) or computed
tomography (CT) scans.
A lower motor neuron pathologic pro-
cess will present with decreased reflexes
and weakness on physical examination.
The triceps surae reflex, or Achilles tendon
reflex, corresponds to the first and sec-
ond sacral level; the patellar reflex corre-
sponds to the third and fourth lumbar
segment; the medial hamstring reflex cor-
responds 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 flex-
ion, indicating irritation of the sciatic
nerve.11(pp59-90) Studies show that the test
is very sensitive to lumbar disk hernia-
tion but not highly specific.12 Nonneuro-
logic etiologies of a positive SLT include
tight hamstrings, muscle spasms, and
sprained posterior longitudinal ligament
sprain.
Manual muscle testing can be extreme-
ly helpful in determining weakness corre-
sponding 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 com-
ponent of the lower motor neuron is com-
pressed, there will be a corresponding sen-
sory abnormality in that sensory
dermatome. Sensory abnormalities include
hypoesthesia, burning, electrical sensa-
tions, or allodynia (a painful sensation to
a nonpainful mechanical stimulation such
as clothing or bed covers).
Jermyn • A nonsurgical approach to low back pain
7 8 9 10
(100 mm)
Worst pain
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 pre-
sents 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 sit-
ting or forward flexion of the lumbar
spine.11(p31)
The orthopedic evaluation of the low
back includes gait, posture, standing bal-
ance, 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, seg-
mental and intersegmental somatic dys-
functions, sacroiliac dysfunctions, and
sources of referred pain from the abdomen
and viscera. Each lumbar and sacral seg-
ment should be palpated for tenderness.
Mobility of the spine should be evaluated
in flexion, extension, sidebending, and rota-
tion. The patient should be evaluated sitting,
standing, supine, and prone. Patrick’s test,
consisting of flexion, abduction, and exter-
nal rotation of the hip, can evaluate both
hip and sacroiliac dysfunction.
Causes of low back pain
Causes of low back pain are listed in Fig-
ure 3. Metabolic abnormalities are the
most common clinical finding associated
with global deep tendon hyperreflexia
and upper motor neuron findings. Syn-
dromes 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-occu-
pying lesions should always be consid-
ered, especially if there is a history of can-
cer. Cerebrovascular accidents (CVAs)
can present with both neck and low back
JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 • S7


✔ 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 sec-
ondary 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 dis-
ease processes such as the human immun-
odeficiency virus (HIV) infection. Diag-
nosis 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 com-
plex accounts for the majority of true
“sciatica.” Although no definition of sci-
atica is universally agreed on, most prac-
titioners consider it a neuropathic injury to
the sciatic or proximal tibial nerve. If neu-
ropathic injury is involved, proximal tib-
ial nerve neuropathy is probably more
appropriate nomenclature. Disk hernia-
tion is a common cause of sciatica; how-
ever, not all disk herniations result in a
painful process. It has been demonstrated
that 20% to 30% of healthy, asymp-
tomatic patients have CT- or MRI-evi-
dent herniated disks.13 The most com-
mon symptoms of radiculopathy are pain,
reflex loss, sensory changes, and weak-
ness. Computed tomography or MRI can
be diagnostic if disk disease is present.
Electromyography (EMG) and nerve con-
duction 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 dis-
ease or bony stenosis.
Myopathy is an abnormal breakdown
of muscle and may present as pain involv-
ing 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 rec-
ommended that serum creatine kinase
levels be measured. Diagnosis can be made
with EMG and NCS or muscle biopsy.
Spinal stenosis, cauda equina syn-
drome, and multiple sclerosis should be
considered when a patient has a combi-
nation of mixed upper and lower motor
neuron findings on physical examination.
By definition, spinal stenosis is a narrow-
ing 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 congeni-
tally narrow spinal canal or foramen.
Many times, the patient will have nor-
mal 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 dys-
function, 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 syn-
drome 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 non-
radicular back pain. They describe general
S8 • JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2
✔
NEUROLOGIC
Checklist

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 hyper-
ostosis
 Ankylosing spondylitis
OSTEOPATHIC
 Somatic dysfunctions
 Posture
 Piriformis syndrome
 Referred pain
Figure 3. Causes of low back pain.
or point tenderness in the low back. Phys-
ical activity usually makes the pain worse,
and rest relieves it. The examination will
demonstrate a decreased lumbar lordo-
sis, paraspinal tenderness, and spasm.
Diagnosis can be made with a plain x-
ray 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 but-
tocks which is made worse by extension
and rotation of the lumbar spine. Radio-
logic studies may demonstrate facet arthri-
tis but most likely will show no abnor-
mality.
Lumbar spondylolisthesis is a slippage
Jermyn • A nonsurgical approach to low back pain
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 postulat-
ed as the cause.11(p92) Imaging studies usu-
ally show no abnormality.
Lumbar spinal fractures are usually
the result of trauma occurring mostly in
osteoporotic patients or patients with pro-
longed 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 deter-
mine the acuity of the fracture.
Diffuse idiopathic skeletal hyperosto-
sis 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, non-
radicular 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 pro-
gresses. X-ray films will show sclerosis of
the sacroiliac joint and bridging syndesmo-
phytes 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 longi-
tudinal 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 exam-
ination 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-
dinal ligament, the interspinous ligaments,
the nerve roots and dural coverings, the
facet joints, and the deep muscles.15
Osteopathic lesions may be the pri-
mary cause or a result of low back injury,
both acute and chronic. Somatic dys-
functions, both segmental and interseg-
mental, may result in significant pain.
Physical examination will demonstrate
decreased mobility at that segment and
resultant paraspinal tenderness. Evalua-
tion of posture should be part of every
osteopathic evaluation. According to Cail-
liet,15 80% to 90% of low back pain is
related to poor posture. Piriformis syn-
drome is a compression of the sciatic nerve
as it courses under or through the piri-
formis muscle. Patients complain of gluteal
and hip pain that is exacerbated with flex-
ion, 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 viscero-
somatic 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 symp-
toms, 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-diam-
eter and fast-conducting myelinated A
delta fibers and slow-conducting unmyeli-
nated 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 ) mod-
ulate 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, nore-
pinephrine, -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
Jermyn • A nonsurgical approach to low back pain
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 orig-
inated. In the example of the person who
stubbed a toe, the mechanoreceptors and
quick A delta fibers are stimulated, quick-
ly resulting in a reflex to move the foot.
The slow C fibers go through the modu-
lation 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 experi-
ence pain, stimulation must occur at the
periphery, spinal cord, and cortex. Treat-
ment options can be geared toward those
that affect the periphery, spinal cord, and
cortex, that is, the pain triad. When treat-
ing 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 ther-
apy modalities, osteopathic manipulation,
and physical exercise are current treat-
ment 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 neu-
rostimulants 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 inhibit-
ing 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 cyclooxy-
genase-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-
JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 • S9
dose corticosteroid can also be used in
acute, significant inflammatory processes.
Muscle relaxants such as cyclobenza-
prine 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 med-
ications 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 effec-
tive in about 66% of selected patients
with low back pain.17 Patients with sus-
pected nerve root inflammation due to
disk disease or lumbar stenosis may ben-
efit. Although no clear criterion exists,
patients who respond best are those who
have not improved after 4 weeks of con-
servative 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 piri-
formis pain has been proven beneficial in
relieving pain15 in both acute and chron-
ic 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 recov-
ery of patients to restore flexibility,
motion, and improved function. Stretch-
es to increase flexibility of the hip flex-
ors, 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. Even-
tually, patients should progress to more
taxing exercises to strengthen the abdom-
inal musculature and improve pelvic sta-
bility. An integral part of rehabilitating
and preventing future injuries is instruct-
ing the patient on proper lifting techniques
that emphasize lifting with the large mus-
cle groups of the lower extremity, as
 opposed to the weak paraspinal stabiliz-
ing musculature. Physical therapy modal-
ities such as application of heat and cold
Cortical 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 pro-
vide temporary relief in the acute pain
Spinal setting, but prolonged use can promote
muscular weakness and even atrophy due
to disuse.

Osteopathic manipulation is a treat-
ment for both acute and chronic low back
pain. Manual muscle techniques are crit-
ical in enhancing segmental hypomobili-
ty, thus allowing uniform segmental
motion and functional balance.11(pp59-90
Manual techniques have been used in
Peripheral most diagnoses of both acute and chron-
Nerve ic pain syndromes. High-velocity tech-
niques should be used with caution on
patients who have an upper motor neuron
pathologic process or when bone metastat-
ic disease is known or suspected. Osteo-
pathic manipulative medicine is the only
treatment modality that has effects at all
three treatment levels, having effects on
Figure 4. Diagram demonstrating the neurophysiologic pain pathway when a person peripheral, spinal, and cortical regions.
stubs a toe.
Spinal level
Modes of treatment geared at the spinal
Antidepressants level are to dampen or impede pain from
Neuroleptics ascending to the brain. In addition to
Cortical
Neurostimulants osteopathic manipulative medicine, opioid
OMT analgesics and TENS units have effect
here. According to the World Health
Organization analgesic ladder,19 opioids
Opiates
are appropriate for moderate and severe
Spinal Tramadol
pain. In patients with mild pain, adjunc-
TENS
tive analgesics are the mainstay of phar-
macologic therapy; these agents include

NSAIDs, acetaminophen, neuroleptics,
NSAIDs and antidepressants. Opiates work at the
Epidural Injection spinal level by binding to opiate recep-
tors at the interneuron level in the dorsal
horn as mentioned earlier. There are two
Spinal Blocks
classes of opioid analgesics: agonists and
agonist-antagonists. The pure opioid ago-
Peripheral Physical Therapy nists include oxycodone, hydrocodone,
Nerve Antispasmotics and codeine. Stronger opioid agonists
Muscle Relaxants include morphine in both an immediate-
release formulation (morphine sulfate
immediate release, MSIR) with effects
Exercise lasting 3 to 4 hours, and a sustained-
OMT release form (OcyContin, MS Contin,
Roxanol SR), which provides 12 hours
of relief. It is recommended to start with
Figure 5. Illustration of trilevel pain management program for low back pain. the lowest possible dose and titrate as
OMT  osteopathic manipulative treatment; TENS  transcutaneous electrical needed. Never prescribe opioids on an
nerve stimulator; NSAIDs  nonsteroidal anti-inflammatory drugs. as-needed basis but as a scheduled dose.

S10 • JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 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-act-
ing agents with rescue doses of immediate-
release medication for breakthrough pain
to augment the sustained-release drugs.
This decreases the euphoria usually asso-
ciated 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 cen-
tral nervous system and prevents reup-
take 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 stim-
ulators 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 Melza-
ck and Wall.20 Generally, a TENS unit
works only when on and may provide
significant improvement in pain and mus-
cle spasm. Patients can be given their own
unit and simply master its use. Although
no clear criterion exists for surgical place-
ment 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 med-
ications 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 anal-
gesic effects of the opioids and help to
alleviate depression that is commonly seen
in patients with chronic pain. Common-
ly used tricyclic antidepressants (TCAs)
include amitriptyline hydrochloride (Elav-
il), 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-
Jermyn • A nonsurgical approach to low back pain
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 (Neu-
rontin), 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 opi-
oid medications and be powerful mood-
stabilizing agents. Other treatment modal-
ities that are effective in pain control at the
cortical level include tramadol, which has
been previously mentioned. Although no
published studies exist, osteopathic manip-
ulative 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 cat-
egorized into a triad system involving
peripheral, spinal cord, and cortical levels.
The clinician can choose a modality direct-
ed at each level to provide the patient
with a pain management program that
will maximize the chosen mode of thera-
py and restore function and mobility to
the patient with low back pain.
References
1. Taylor H, Curran NM. The Nuprin Pain Report. New
York, NY: Louis Harris & Associates; 1985. Cited in: Raj
P. Pain Management: A Comprehensive Review. Los
Angeles, Calif: Mosby; 1996; p 406.
2. Deyo RA. The role of the primary care physician in
reducing work absenteeism and costs due to back
pain. Occup Med 1988;3(1):17-30.
3. Weber BS, Snook SH. The cost of compensable
low back pain. J Occup Med 1990;32:13-15.
4. Louis Harris & Associates. 1999 National Pain Sur-
vey. New York, NY; January 1999. Cited in: Katz W.
Pain Management in Rheumatologic Disorders: A
Guide for Clinicians. Drugsmartz Pub; 2000; p 14.
JAOA • Vol 101 • No 4 • Supplement to April 2001 Part 2 • S11
5. Louis Harris & Associates. Pain and absenteeism in
the workplace. New York, June, 1996. Cited in: Katz W:
Pain Management in Rheumatologic Disorders: A Guide
for Clinicians. Drugsmartz Pub; 2000; p 14.
6. Carey TS, Garrett JM, Jackman A, Hadler N. Recur-
rence and care seeking after acute back pain: results of
a long-term follow-up study. North Carolina Back Pain
Project. Med Care 1999;37:157-164.
7. Sundararajan V, Konrad TR, Garrett J, Carey T.
Patterns and determinants of multiple provider use in
patients with acute back pain. J Gen Intern Med
1998;13:528-533.
8. Gordon M, Greenfield E, Marvin J, Hester C, Lauter-
bach S. Use of pain assessment tools: is there a pref-
erence? J Burn Care Rehabil 1998;19:451-454.
9. Katz W. Pain Management in Rheumatologic Dis-
orders: A Guide for Clinicians. Drugsmartz Pub; 2000;
pp 1-11, 14, 20-21, 110.
10. Hoppenfeld S. Physical Examination of the Spine
Extremities. Norwalk, Conn: Appleton & Lange; 1976;
pp 237-263.
11. Cole A, Herring S. The Low Back Pain Handbook:
A Practical Guide for the Primary Care Clinician.
Philadelphia, Pa: Handley & Belfus, Inc; 1997; pp 31, 39,
59-90, 92.
12. Kosteljanetz M, Espersen JO, Halaburt H, Miletic T.
Predictive value of clinical and surgical findings in
patients with lumbago-sciatica. A prospective study
(Part I). Acta Neurochir (Wien) 1984;73(1-2):67-76.
13. Bozzao A, Gallucci M, Masciocchi C, Aprile I, Bar-
ile A, Passariello R. Lumbar disk herniation: MR imag-
ing assessment of natural history in patients treated
without surgery. Radiology 1992;185:135-141.
14. Cohen BA. HIV/AIDS management in office prac-
tice. Primary Care: Clinics in Office Practice September
1997; Volume 24, Number 3.
15. Cailliet R. Low back pain. In Cailliet R, ed: Soft Tis-
sue Pain and Disability. Philadelphia, Pa: FA Davis;
1977.
16. Raj P. Pain Management: A Comprehensive
Review. Los Angeles, Calif: Mosby; 1996: pp 12-23.
17. Benzon HT. Epidural steroid injections for low back
pain and lumbosacral radiculopathy. Pain 1986;24:277-
295,
18. Sauser DD, Neumann M: Facet block. In: Raj PP,
ed. The Practical Management of Pain, ed 2. St Louis,
Mo: Mosby; 1992.
19. World Health Organization. Cancer Pain Relief, ed
2, With a Guide to Opioid Availability. Geneva, Switzer-
land: World Health Organization; 1996.
20. Melzack R, Wall PD. Pain mechanisms: A new
theory. Science 1965;150:971-979..
21. North RB, Ewend MG, Lawton MT, Piantadosi S.
Spinal cord stimulation for chronic, intractable pain:
Superiority of “multi-channel” devices. Pain 1991;44:119-
130.
22. Mellick GA, Mellicy LB, Mellick LB. Gabapentin in the
management of reflex sympathetic dystrophy. J Pain
Symptom Manage 1995:10:265-266.