lower back and leg pain approaches

Bradly 2016
32: Lower Back and Lower Limb
Pain

ANATOMY AND PHYSIOLOGY
* The lumbosacral spinal cord terminates in the conus medullaris
at the level of the body of the L1 vertebra
* The motor and sensory nerve roots from the lumbosacral cord
form the cauda equina. From there, the motor and sensory
nerve roots unite at the dorsal root ganglion to form the
individual spinal nerves.
* These anastomose in the lumbosacral plexus from which run
the major nerves supplying the leg
* Pain in the lower back can have many origins. A good
beginning for the differential diagnosis is determining whether
the leg also has pain.
* A complicating factor in this consideration is that local
spine pain can be referred—that is, felt at a distance—because
of the common nerve root innervation of the proximal spinal
nerves and peripheral nerves supplying distal parts of the leg.

# Causes of lower back pain without leg pain include:
• Ligamentous strain
• Muscle strain
• Facet pain
• Bony destruction
• Inflammation
# Causes of lower back plus lower limb pain include:
• Radiculopathy
• Plexopathy
# Important causes of leg pain without low back pain include:
• Sciatic neuropathy
• Femoral neuropathy
• Peroneal neuropathy
• Meralgia paresthetica
• Peripheral polyneuropathies

* Isolated tibial neuropathy is uncommon.
* Individual peripheral nerve lesions usually are caused by
local trauma, entrapment by connective tissue, or
involvement with mass lesions.
# Lower back pain caused by non-neurological and
nonskeletal lesions are:
• Urolithiasis
• Ovarian cysts and carcinoma
• Endometriosis
• Bladder or kidney infection
• Abdominal aortic aneurysm
• Visceral ischemia or other aortic ischemic disease.

History and Examination
Focus first on
• Mode of onset
• Character
• Distribution
• Associated motor and sensory symptoms
• Bladder and bowel control
• Exacerbating and remitting factors
• History of predisposing factors (e.g., trauma, cancer,
osteoporosis)
* The acute onset of lower back pain radiating down the leg
suggests a lumbosacral radiculopathy.
* Onset with exertion suggests a herniated disk as a cause of
the radiculopathy.
* Progressive symptom development can be from any expanding
lesion, such as a tumor, infection, or expanding disk extrusion.

# Muscle groups that can be tested include:
1- Hip–girdle muscles:
• Hip flexors (psoas, sartorius)
• Hip extensors (gluteus maximus, semitendinosus, semimembranosus,
biceps femoris)
• Hip adductors (adductor group: longus, brevis, magnus)
• Hip abductors (gluteus medius, gluteus minimus, piriformis)
2- Knee muscles:
• Knee extension (quadriceps)
• Knee flexion (semitendinosus, semimembranosus, biceps femoris)
3- Ankle and foot muscles:
• Foot plantar flexion (gastrocnemius)
• Foot dorsiflexion (tibialis anterior)
• Foot everters (peronei)
• Foot inverters (tibialis posterior)
• Toe extension (extensor digitorum)
• Great toe extension (extensor hallucis longus)
• Toe plantar flexion (flexor digitorum longus)
• Great toe flexion (flexor hallucis longus)

# Sensory examination should include the important nerve
roots and peripheral nerve distributions: the femoral, peroneal,
tibial, and lateral femoral cutaneous, lumbar roots L2– L5,
and sacral root S1.
# Reflexes to be studied include the Achilles, patellar, and
plantar reflexes.
* Exacerbation of pain with some maneuvers also can be
revealing.
* Stretch of damaged nerves results in increased pain by
deforming the axon membrane, thereby increasing membrane
conductance, depolarizing the nerve, and producing
repetitive action potentials.
* Straight leg raising augments pain in a lumbosacral
radiculopathy.
* Hip extension exacerbates pain of upper lumbar radiculopathy
or that due to damage to the upper parts of the lumbar plexus,
such as from carcinomatous infiltration or inflammation.

# Differential Diagnosis of Lower Back and Leg Pain
* Some basic guidelines :
• Pain confined to the lower back generally is caused by a
low back disorder.
• Pain confined to the leg usually is caused by a leg
disorder, although neuropathic pain from lumbar spine
disease can radiate down the leg without back pain in a
minority of patients.
• Pain in both is caused by lumbar radiculopathy or, less
commonly, lumbosacral plexopathy.
• Clinical abnormalities confined to one nerve root
distribution usually are caused by intervertebral disk
disease or lumbosacral spondylosis producing
radiculopathy.

• Clinical abnormalities that involve several nerve
distributions usually are caused by plexus lesions, with
cauda equina lesions being the alternative diagnosis.
• Bilateral lesions suggest proximal damage in the spinal
canal affecting the roots of the cauda equina.
• Impairment of bladder control indicates either a cauda
equina lesion or, less commonly, a bilateral sacral
plexopathy
• Multiple lesions can make the differential diagnosis more
difficult. For example, radiculopathies at two or more levels
may look like a plexopathy or peripheral neuropathic
process.

# Non-neurological causes of lower back pain :
1- Urolithiasis
2- Ovarian cysts
3- Endometriosis
4- Pelvic carcinoma
5- Bladder infection
6- Other retroperitoneal lesions including tumor, abscess,
abdominal aortic aneurysm, visceral ischemia, and hematoma.
* These conditions produce pain that does not radiate unless
neural structures are involved.
* Neural involvement in the abdomen and pelvis can produce
radiating pain that can be clinically differentiated from
radiculopathy only if multiple nerve roots are involved.
* Early involvement of bowel or bladder function together with
abdominal pain suggests one of these non-neurological
conditions.

Evaluation
1- Magnetic Resonance Imaging
* to assess the lumbosacral spine and lumbosacral plexus.
* It also can be used to evaluate the peripheral nerves in
the pelvis and lower limbs.
* Intraspinal disorders that may not be revealed by MRI
without contrast enhancement include neoplastic
meningitis, epidural abscess, diskitis, and some chronic
infectious meningitides
2- Myelography and Postmyelographic Computed
Tomography
* If adequate information is not obtained from noninvasive
studies, myelography occasionally may be indicated.
* Postmyelographic computed tomography (CT) is
performed in most instances.

3- Nerve Conduction Studies and Electromyography
They are performed for four principal purposes:
• Assist localization of the lesion(s)
• Assist in evaluating the severity of the lesion(s)
• Determine whether the lesion is acute, subacute, or
chronic
• Determine whether the lesion is neuropathic, axonal, or
Demyelinating
* Axonal damage seen with radiculopathy or entrapment
neuropathy suggests consideration of surgical
decompression.
* Signs of denervation may not appear on EMG until up to 4
weeks after onset of axonal damage.

* Entrapment neuropathy, or nerve root compression which
can be responsible for lower limb pain, is likely to slow
conduction velocity across the region of compression.
* Conduction velocities proximal and distal to the compression
usually are normal, so conduction across the affected nerve
segment must be studied.
* Radiculopathy typically is associated with normal NCS
findings in the peripheral branches of the nerves but with
slowing of the F-wave.
*Absence of abnormalities on NCSs and EMG does not rule out
the presence of a radiculopathy.
* Mechanical lower back pain is associated with no EMG or
NCS alterations,

4- Radiography
Among the potential findings are degenerative joint
disease, vertebral body collapse, bony erosion,
subluxation, and fracture.
5- Bone Scan
*Bone scan is especially important for examining multiple
bone regions in cases of suspected neoplastic bone
involvement.
* Multifocal involvement makes a neoplastic cause more
likely than an infectious cause for the destruction.

# CLINICAL SYNDROMES
A - Lower Back and Leg Pain
1- Lumbar Spine Stenosis
* affects mainly late middle-aged and older adults.
* The cause is multifactorial,with disk disease, bony hypertrophy,
and thickening of the ligamentum flavum being the most
important.
* Some of the symptoms are undoubtedly caused by direct
pressure of these tissues on the cauda equina and exiting nerve
roots, but a major contributor appears to be compression of the
vascular supply of the nerve roots.
* Standing is associated with extension of the lumbar spine,
which causes anterior bulging of the ligamentum flavum that lies
posteriorly.
* Compression of the vascular supply creates nerve root
ischemia, which can produce severe pain and weakness with
exertion.

* Presents with leg pain that is exacerbated by standing
and walking and relieved promptly by sitting.
* Lying down, especially in the prone position, may
exacerbate the low back pain, again through lumbar
extension, a feature that helps differentiate lumbar spine
stenosis from lumbar radiculopathy.
* This neurogenic pain is called pseudoclaudication or
neurogenic claudication
* Patients suffering from spinal stenosis exhibit a simian
posture ( with a forward-flexed trunk and slightly bent
knees when walking, to decrease the symptoms)
*Extension of the spine may cause an increase in
symptoms.
* Weakness and lack of coordination in the affected
extremity may be noted.

* Patients often have a positive stoop test for spinal
stenosis.
*Decreased sensation, weakness, and reflex changes are
demonstrated on physical examination.
* Occasionally, patients suffering from spinal stenosis
experience compression of the lumbar spinal nerve roots
and cauda equina, with resulting lumbar myelopathy or
cauda equina syndrome.
* These patients experience varying degrees of lower
extremity weakness and bowel and bladder symptoms
(neurosurgical emergency)
* Mimics of spinal stenosis include low back strain,
lumbar bursitis, lumbar fibromyositis, inflammatory
arthritis, and disorders of the lumbar spinal cord, roots,
plexus, and nerves, including diabetic femoral neuropathy.

Figure 78-4 Acquired degenerative
spinal stenosis. A and B, Sagittal
T2- and T1-weighted magnetic
resonance imaging (MRI)
demonstrates severe disk
degeneration at L3-4 and L4-5,
with disk desiccation, disk space
narrowing, irregularity of the
adjacent vertebral end plates, and
posterior bulging disks. The
nerve roots of the cauda equina
have an undulating or wavy
appearance because of the
marked constriction at L3-4. C and
D, On axial T2-weighted MRI,
the combination of posterior
bulging disks, facet hypertrophy,
and thickened ligamenta flava
causes severe spinal canal
stenosis at L3-4 and moderate
stenosis at L4-5. Also note severe
compromise of the lateral recesses
at L3-4 bilaterally.

* EMG can also distinguish plexopathy from radiculopathy
and can identify a coexistent entrapment neuropathy that
may confuse the diagnosis.
* MRI or CT of the lumbar spine shows obliteration of the
subarachnoid space at the level of the lesion.
* The hypertrophied ligamentum flavum and osteophyte
formation usually are evident on these studies.
* If doubt about the diagnosis exists, myelography with
postmyelographic CT scanning can be performed.
*Weakness of the legs or sphincter disturbance indicates a need
for decompression.
* If the diagnosis is in question, send for CBC, ESR, antinuclear
antibody testing, human leukocyte antigen (HLA)-B27 antigen
screening, and automated blood chemistry should be performed
to rule out other causes of the patient's pain.

* Treatment:
* Physical therapy, combined with nonsteroidal
antiinflammatory drugs and skeletal muscle relaxants
* If necessary, caudal or lumbar epidural nerve blocks
can be added.
* Caudal epidural blocks with local anesthetic and steroid
are extremely effective in the treatment of spinal stenosis.
* Underlying sleep disturbance and depression are best
treated with a tricyclic antidepressant such as
nortriptyline, which can be started at a single bedtime
dose of 25 mg.

2- Cauda Equina Syndrome and Conus Medullaris
Syndrome
* Lesions of the lumbar spine can result in damage to the
conus medullaris, cauda equina, or both.
Cauda equina syndrome
*is compression of the nerve roots below the termination of
the spinal cord.
* Nerve root dysfunction is due to direct compression by
surrounding structures.
* Important causes include acute trauma, chronic
degenerative bony disease with retropulsion of fragments
into the spinal canal, lumbar disk disease, infections
such as abscess, intraspinal and meningeal tumor, and
intraspinal hematoma.

* This syndrome can be a rare complication of minor and
major spinal procedures
* Cauda equina syndrome usually develops as an insidious
chronic process unless due to acute trauma.
* Symptoms can include back pain, leg pain, and weakness
and cramps in the legs.
* Sensory symptoms can be sensory loss as well as
neuropathic pain.
* Sphincter disturbance is common, especially with
progression.

Conus medullaris syndrome
* is due to damage to the terminus of the spinal cord
above most of the cauda equina and therefore at a higher
spinal level.
* Etiology can be compression from all the conditions listed
above plus occasional infiltrating lesions of the conus
medullaris itself, especially by tumor.
* Conus medullaris syndrome is usually more rapidly
progressive, associated with earlier back pain and
sphincter disturbance, and is more likely to be associated
with preservation of some lower extremity reflexes, usually
patellar.
*If MRI cannot be performed, many causes of both
syndromes can be identified on CT of the spine but contrast
may be required.

3- Lumbosacral Radiculopathy (sciatica)
*Lumbar radiculopathy is a constellation of symptoms
including neurogenic back and lower extremity pain
emanating from the lumbar nerve roots.
* Causes : herniated disk, foraminal stenosis, tumor,
osteophyte formation, and, rarely, infection.
* Herniated disk is more common in young patients;
osteophyte formation is more common in older patients.
* Signs and Symptoms:
* pain, numbness, tingling, and paresthesias in the
distribution of the affected nerve root or roots
* Patients may also note weakness and lack of coordination
in the affected extremity.
* Muscle spasms and back pain, as well as pain referred
into the buttocks, are common.

* Decreased sensation, weakness, and reflex changes
* They may experience a reflex shifting of the trunk to one side,
called list
* Lasègue's straight leg raising sign is almost always positive
* Occasionally,patients suffering from lumbar radiculopathy
experience compression of the lumbar spinal nerve roots
and cauda equina that results in lumbar myelopathy or cauda
equina syndrome; if so, they experience varying degrees of
lower extremity weakness and bowel and bladder symptoms.

Testing:
1- MRI , CT or MYelography
2- Diskography may also help clarify the diagnosis in
difficult cases
3- Radionuclide bone scanning and plain radiography are
indicated if fracture or a bony abnormality, such as
metastatic disease, is being considered.
4- EMG and nerve conduction velocity testing provide
neurophysiologic information about the actual status of
each individual nerve root and the lumbar plexus.
* EMG can also distinguish plexopathy from radiculopathy
and can identify a coexistent entrapment neuropathy,
such as tarsal tunnel syndrome, which may confuse the
diagnosis.

* NCS findings usually are normal in patients with lumbosacral
radiculopathy, although F-waves may be delayed in the affected
root.
* EMG can reveal evidence of denervation in a nerve root
distribution and usually can differentiate peripheral neuropathic
processes from radiculopathy.
* This study also can determine whether denervation is present
with
radiculopathy.
5- other lab tests as for lumbar spinal stenosis
Management : as for lumbar spinal stenosis
* Surgery indications: intractable pain refractory to conservative
care; when weakness is prominent, especially if it is
unresponsive to conservative management; and when sphincter
disturbance is present.
* Sphincter disturbance caused by lumbar disk disease or
spondylosis necessitates consideration of urgent surgery.

4- Arachnoiditis
* is inflammation of the arachnoid membranes surrounding
the spinal cord.
* The inflammation can be caused by a number of
processes including trauma to the spinal canal by injury or
surgery, chronic compression of spinal nerves, chemicals
such as intrathecal chemotherapy or contrast agents, blood
products from subarachnoid hemorrhage, infections, or
neoplasms.
* There is chronic inflammation of the motor and sensory
nerve roots.
* The inflammation results in fibrinous adhesions between
the membranes and nerve roots and between adjacent
nerve roots.

* Common symptoms include pain in the back and legs
which typically has a neuropathic character.
* Sensory symptoms can be loss of sensation or
dysesthesias.
* Muscle symptoms can include twitching and cramps, and
in severe cases, weakness or even paralysis can develop.
* Diagnosis of arachnoiditis is suspected in patients with
low back and leg pain who have radiological studies which
suggest the diagnosis;
* arachnoiditis is seldom a diagnosis of first consideration
during initial evaluation.
* MRI shows thickened and clumped nerve roots.
* Careful examination of the imaging shows nerve roots
adherent to each other and to the dura.
* myelography can show the same overall appearance.

* EMG can identify denervation spanning single root
distributions and document motor dysfunction, but no EMG
findings are specific for arachnoiditis.
* CSF analysis is performed if the differential diagnosis
includes meningeal infection or tumor.
* Treatment of arachnoiditis is usually symptomatic since
the underlying cause is either remote or unknown.
*Preventing this disorder is the best approach and can be
achieved by avoiding injury and sometimes by
administering steroids with intrathecal medications.

5- Plexopathy
One: Neoplastic Lumbosacral Plexopathy
* Neoplasms affecting the lumbosacral plexus can be solid
or infiltrating.
* Both can produce severe neuropathic pain affecting one
or both sides of the lumbosacral plexus.
* Diagnosis is suspected when a patient with known cancer
presents with pain and often weakness of one or both legs.
* Diagnosis might be stumbled upon if there is no known
cancer, with paravertebral tumor identified on lumbar spine
MRI or other scan of the abdomen and pelvis.
* The differential diagnosis might include radiation
plexopathy, EMG can be helpful with that differentiation

* MRI is diagnostic
* Treatment depends on the tumor type and stage:
-- If there is no known cancer diagnosis then biopsy with or
without excision is usually performed.
-- Complete excision of some solid tumors is possible.
-- Otherwise, radiation therapy is given initially.
* Pain often is relieved shortly after the radiation therapy
has begun. During initial treatment, anticonvulsants can be
used to relieve the neuropathic pain. Pure analgesics also
may be used and sustained-release opiate formulations are
effective in treating this condition.

Two :Plexus Injury from Retroperitoneal Abscess
* is caused by peritonitis from gastrointestinal neoplasms or
following surgery.
* Retroperitoneal abscess can affect the lumbosacral
plexus.
*Patients present with abdominal and flank pain, often with
overt signs of systemic infection, with fever, malaise,
elevated white blood cell counts, and elevated C-reactive
protein (CRP) concentration.
* The diagnosis is confirmed by CT of the abdomen.
* Management typically begins with surgical drainage
followed by prolonged antibiotic treatment.
* Narcotics usually are needed for the pain of
retroperitoneal abscess.

Three :Plexus Injury from Retroperitoneal Hematoma.
*is caused by a bleeding disorder, a pelvic fracture, or abdominal
surgery.
* Occasionally, bleeding from the site of arteriography puncture
can result in tracking of blood into the region of the lumbosacral
plexus, especially after thrombolytic therapy or anticoagulation.
* Hematoma has also been described in patients after lumbar
plexus block and may be delayed
* This diagnosis should be suspected in patients with leg
motor and sensory symptoms who are at risk for intraabdominal
hemorrhage; abdomen and leg pain are common.
* Confirmation of the diagnosis is by CT of the abdomen, which
can show blood in the region of the plexus.
* Treatment of plexus hematoma is supportive.
* Evacuation of the hematoma is seldom needed, and surgery
commonly is reserved for patients with continued blood loss,
which must be arrested.

B- Leg Pain without Lower Back Pain
1- Peripheral Nerve Syndromes
* is commonly the result of sustained compression.
* Peroneal palsy is the most common lower extremity
syndrome, usually caused by pressure at the fibular neck.
* Femoral neuropathy commonly results from intraabdominal
causes and can be difficult to differentiate from upper lumbar
plexopathy.
* The diagnosis of peripheral nerve palsy is clinical, with
symptoms and signs confined to one neural distribution.
* Patients usually present with neuropathic pain and sensory
loss.
* Dysesthesias and paresthesias in the affected distribution
are common.
*Reflex abnormalities depend on the individual nerves affected.

* Definitive treatment of peripheral nerve entrapment is surgical
release.
* Tumor compression of peripheral nerves can be treated
surgically, but radiation therapy can shrink the tumor, thereby
relieving pain.
One: Femoral Neuropathy: The femoral nerve usually is
injured in the pelvis as it passes beneath the inguinal ligament or
in the leg.
* Intra-abdominal disorders including mass lesions and
hematoma are commonly implicated.
* Femoral artery puncture for angiography also may be a cause,
either directly or via resultant hematoma.
* Patients present with weakness that is most easily detected in
the psoas, because the quadriceps are so strong.
* Sensory loss is over the anterior thigh and medial aspect of the
calf and has a saphenous nerve distribution (the terminal
sensory branch of the femoral nerve).

* This distribution of sensory loss is helpful to differentiate
femoral neuropathy from lumbar radiculopathy.
* The patellar reflex usually is depressed.
* The diagnosis can be supported by EMG evidence of
denervation in the quadriceps but not in the lower leg or
posterior thigh muscles.
* The adductors are especially important to test because
they are innervated by the same nerve roots that supply the
femoral nerve but instead are innervated by the
obturator nerve.
* Normal EMG findings cannot rule out this diagnosis,
because many patients do not have active or chronic
denervation.
* NCS of the femoral nerve is difficult, especially in large
patients, who are predisposed to development of
femoral neuropathy.

** Treatment is seldom surgical, except for the removal of a
massive psoas or iliacus hematoma or mass lesion.
** Weight loss and avoidance of marked hip flexion can
reduce the chance of persistent damage.
** Physical therapy will aid recovery of motor power.
Femoral neuropathy in the absence of marked damage
usually resolves.

Two: Meralgia Paresthetica: Dysfunction of the lateral
femoral cutaneous nerve commonly is caused by
compression as it passes beneath the inguinal ligament.
* Obesity and pregnancy predispose to this disorder, as
does intra-abdominal surgery of a variety of types.
* Meralgia paresthetica is the sensory syndrome of pain
and sensory loss on the lateral thigh.
* Patients present with numbness and often pain on the
lateral thigh.
* Motor deficits are not a feature.
* Meralgia paresthetica is differentiated from femoral
neuropathy by the lateral distribution of the sensory findings
and the absence of motor and reflex abnormalities.

* Nerve conduction testing of the lateral femoral cutaneous
nerve, although feasible, is technically difficult even in the
best circumstances. It is even more difficult in obese
patients, who are at particular risk for entrapment of the
nerve.
* Treatment is conservative. Weight loss usually is effective
in preventing recurrence.
* Medications and blocks for neuropathic pain are
sometimes helpful.

Three: Sciatic Neuropathy:
* The sciatic nerve is most likely to be injured as it leaves the
sciatic notch and descends into the upper leg.
* Compression can occur in patients in prolonged coma,
especially those who are very thin.
* The sciatic nerve also is susceptible to injury from pelvic and
sacral fractures, hip surgery or dislocation, needle injection
injuries, and any penetrating injury.
* Patients present with pain that usually is localized close to
the level of the sciatic nerve lesion, although substantial
radiation of the pain may be a feature.
* Loss of sensation is prominent below the knee, sparing the
medial lower leg (the territory of the saphenous branch of the
femoral nerve).
*Weakness can affect all muscles of the lower leg, but peroneal-
innervated muscles are more likely to demonstrate weakness for
two reasons.

* First, tibial-innervated foot extensors are so strong that
substantial weakness would have to be present for weakness
to be evident on examination.
* Second, the peroneal division of the sciatic nerve is more
susceptible to compression injury than the tibial division, even
high in the thigh.
* Sciatic neuropathy is usually diagnosed clinically but can be
supported by EMG evidence of denervation in sciatic innervated
muscles; signs of denervation may not be seen until 4 weeks
after injury.
* Treatment of sciatic compression is supportive, with avoidance
of recurrent compression. Medications for neuropathic
pain are often used. Surgical exploration and decompression
are performed only in patients with clear evidence of a structural
lesion.

Four: Piriformis Syndrome:
* is an uncommon
* the sciatic nerve is compressed by the piriformis muscle in
the posterior gluteal area (sciatic notch)
* The piriformis muscle's primary function is to rotate the
femur externally at the hip joint; this muscle is innervated
by the sacral plexus.
*With internal rotation of the femur, the tendinous insertion
and belly of the muscle can compress the sciatic nerve; if
this compression persists, it can cause entrapment of the
nerve.
* * Hypertrophy of the piriformis muscle and other
anatomical variants predispose affected persons to
development of the syndrome.

The pain of piriformis syndrome
can be exacerbated by lifting.

* This condition may affect not only the main sciatic trunk
but also the superior gluteal nerve.
* Patients present with pain in the buttock that radiates
down the leg and foot and is exacerbated by adduction
and flexion of the hip.
* Pain tends to be aggravated by prolonged sitting, climbing
steps, and other maneuvers that irritate the piriformis
muscle.
* Patients suffering from piriformis syndrome may develop
an altered gait, leading to coexistent sacroiliac, back, and
hip pain that confuses the clinical picture.
* Physical findings include tenderness over the sciatic
notch. Palpation of the piriformis muscle reveals
tenderness and a swollen, indurated muscle belly.
* A positive Tinel sign over the sciatic nerve as it passes
beneath the piriformis muscle is often present.

* A positive straight leg raising test result suggests
sciatic nerve entrapment.
* Lifting or bending at the waist and hips increases the pain
in most patients suffering from piriformis syndrome
* Weakness of the affected gluteal muscles and lower
extremity and, ultimately, muscle wasting are seen in
patients with advanced, untreated cases of piriformis
syndrome.
* (EMG) can distinguish lumbar radiculopathy from
piriformis syndrome.
* Plain radiographs of the back, hip, and pelvis are
indicated in all patients who present with piriformis
syndrome, to rule out occult bony disorders.
* additional testing including a complete blood count, uric
acid level, erythrocyte sedimentation rate, and antinuclear
antibody testing.

* It is a clinical diagnosis.
* A patient with symptoms of sciatic neuropathy has no
signs of radiculopathy or spinal stenosis on imaging.
* MRI neurography may show the lesion in many patients
## Differential Diagnosis
* Lumbar radiculopathy
* primary hip disease; radiographs of the hip and EMG
can make the distinction.
- In addition, most patients with lumbar radiculopathy have
back pain associated with reflex, motor, and sensory
changes, whereas patients with piriformis syndrome
have only secondary back pain and no reflex changes.
## Lumbar radiculopathy and sciatic nerve entrapment may
coexist as the double-crush syndrome.

* it is managed with anti-inflammatory agents and
sometimes local injections of steroids.
* The local application of heat and cold may also be
beneficial.
* If the patient sleeps on his or her side, placing a pillow
between the legs may be helpful.
* If the patient is suffering from significant paresthesias,
gabapentin may be added.
* For patients who do not respond to these treatment
modalities, injection of local anesthetic and
methylprednisolone in the region of the sciatic nerve at the
level of the piriformis muscle is a reasonable next step.
* Surgical treatment is rarely performed

Five: Peroneal (Fibular) Neuropathy
* Peroneal neuropathy commonly is caused by compression of
the nerve as it passes from the popliteal fossa across the fibular
neck into the anterior compartment of the lower leg.
* Patients often present with foot drop from weakness of the
tibialis anterior muscle.
* The diagnosis is confirmed by NCS and EMG, with slowing of
peroneal nerve conduction across the region of entrapment,
usually
across the fibular neck.
* The EMG shows evidence of active and chronic denervation in
many patients, in keeping with the axonal damage indicated by
the foot drop
* Peroneal neuropathy can develop in a variety of conditions
which predispose to mechanical compression such as prolonged
bed rest, hyperflexion of the knee, sitting with crossed legs, and
lower leg cast.
* Peroneal neuropathy is of increased incidence in patients with
peripheral neuropathy, those with a neurofibrous band attached
to the peroneus longus, and ballet dancers

Six: Polyneuropathy:
* Peripheral neuropathy is a common cause of lower-
extremity pain.
* Among the most important causes are diabetes mellitus,
familial neuropathy, metabolic neuropathies, and vasculitis.
* Pain is the presenting manifestation and differs in
character according to the type of neuropathy.
* Small-fiber neuropathies manifest with burning pain that
often is worse in the evening.
* Large-fiber neuropathies manifest with dysesthesias and
paresthesias, often with electric shock-like pains.
* Diagnosis usually is confirmed by NCS and EMG.
* Axonal neuropathy is more common than demyelinating
neuropathy.
* Occasionally, patients with a predominantly small-fiber
sensory neuropathy have normal NCS findings.

* Treatment is with tricyclic antidepressants or
anticonvulsants. Amitriptyline commonly is used for patients
with smallfiber neuropathic pain.
* Anticonvulsants are used predominantly for patients with
large-fiber neuropathic pain.
* When patients have symptoms of both, treatment with
gabapentin, pregabalin, or oxcarbazepine can be helpful.
* Combination therapy with a tricyclic and anticonvulsant
may be beneficial.
* Pure analgesics occasionally are used on a nightly basis
to assist with sleep

3- Plexopathy
One: Lumbosacral Plexitis
* It is similar to brachial plexitis, a presumed autoimmune
process, but is less common.
* This entity is differentiated from radiculitis, which can be an
inflammatory disorder of autoimmune or infectious origin
* Management of idiopathic lumbosacral plexitis is supportive,
with no medical intervention known to alter the course of the
disease.
* Anticonvulsants commonly are used for pain management.
* Corticosteroids and high-dose intravenous immunoglobulin
also are used occasionally, although it is not clear that their
benefits outweigh the risks.
* The relatively short duration of the pain makes opiates
appropriate for some patients if needed.

Two: Diabetic Amyotrophy:
* Diabetic amyotrophy is lumbosacral plexopathy occurring in persons
with diabetes mellitus.
* The disorder is thought to be an inflammatory vasculopathy, with
damage that probably is immune mediated.
* Patients present with pain in the hip and thigh associated with
weakness of
the quadriceps, psoas, and adductors.
* The plexopathy is more often unilateral than bilateral.
* Diagnosis is suspected by proximal pain and weakness of a leg in a
patient with known diabetes.
* This disorder must be differentiated from lumbar radiculopathy and
other structural lesions in the region of the plexus.
* NCSs and EMG show coexistent peripheral polyneuropathy plus
denervation in proximal muscles including quadriceps, psoas, and
adductors.
* MRI and CT do not show a structural lesion.
* Treatment is symptomatic. Immune-modulating treatments have
been tried but are not standard. Most patients improve, although
recovery is usually incomplete. The pain abates before recovery of
muscle strength.

4- Herpes Zoster
* pain in a single nerve root distribution.
* In most patients, a vesicular rash develops in the same
cutaneous distribution usually several days after the onset
of the
pain.
* When the rash crusts over, there is commonly pigmentary
changes of variable duration.
* The pain abates as the inflammation recedes, although
the patient may be left with sensory or motor deficit.
* Weakness can be evident in muscles innervated
predominantly by the single nerve root.
* Diagnosis is clinical, and with a typical presentation
including
rash, structural imaging usually is not necessary.

* EMG and imaging are usually considered if the diagnosis
is uncertain or with prolonged deficit.
*The differential diagnosis is broader in scope before
development of the rash.
* Treatment with antiviral agents such as acyclovir or
famciclovir should begin within 72 hours of symptom onset.
* Early treatment may help hasten recovery and reduce the
incidence of postherpetic neuralgia.
* Corticosteroids are often used in immuno-competent
patients and especially for zoster ophthalmicus.

5-Claudication of Leg Arteries
* Arterial claudication is an important element in the differential
diagnosis of spinal stenosis.
* Vascular disease of the iliac arteries and terminal branches
results in marginal perfusion of lower limb muscles.
* Walking and other moderate activities exacerbate the
ischemia, producing pain and weakness with exertion.
* The clinical picture may resemble that of spinal stenosis,
but differentiating features include the lack of back pain, lack of
exacerbation of leg pain with recumbent lumbar extension, and
vascular changes in the leg.
* Claudication is diagnosed by vascular imaging.
*Ultrasound examination can be a good screening test but
angiography can provide a definitive diagnosis and in some
patients can be the means for definitive treatment by
angioplasty.

C- Lower Back Pain without Leg Pain
1- Mechanical Lower Back Pain
* Mechanical lower back pain usually is caused by strain of
paraspinal muscles and ligaments with local inflammation.
* Muscle tears also may cause acute lower back pain.
Therefore, mechanical lower back pain usually is a
combination of bone, muscular, and connective tissue pain.
* Patients present with pain in the lower back without
radicular symptoms and show no motor, sensory, or reflex
abnormalities on examination.
* Any weakness or gait disturbance is due to pain and not
neurological deficit.

* Diagnosis is based on the clinical features and exclusion
of other causes.
* In the absence of objective neurological deficits, imaging
including spinal MRI usually is not needed initially.
* In the absence of signs of bony or neural destruction,
conservative management may begin.
* If the patient does not respond to initial treatment, MRI
may be indicated.
* Mechanical lower back pain usually is treated by an initial
period of rest of approximately 2 days, followed by an
increase in activity including physical therapy.
* Muscle relaxants and anti-inflammatories are often used.
* Surgery and repetitive nerve blocks are seldom indicated
for mechanical back pain.

2- Sacroiliac Joint Inflammation (Sacroilitis)
* presents with pain isolated to the back and just lateral
to the spine in the region of the SI joint.
* This is often a component of more generalized arthritic
conditions including ankylosing spondylitis but can also be
seen in psoriatic and autoimmune arthritides
* Diagnosis is suspected with the local pain without
radiation. MRI can show the inflammatory change
* While a primary inflammatory or degenerative lesion
is most common, in some cases infections and destructive
processes can produce similar symptoms

3- Facet Joint Pain Syndrome
* Pain from the facet joints of the lumbosacral spine usually is
not an isolated entity but rather a component of mechanical.
back pain.
* Pain results from long-term degenerative changes in the facet
joints, usually caused by strain. Repetitive strenuous activity,
excessive weight, and abnormal posture may predispose
affected persons to the development of facet pain.
* Acute trauma to the back may produce active joint
inflammation
that can be self-limited.
* Diagnosis is suspected with pain usually lateral to the spine
which is exacerbated by spine extension or bending toward the
affected side.
* Facet pain often is bilateral. Pain can be exacerbated by
prolonged sitting or walking up steps, as well as retaining one
position for a prolonged time.

* Patients present with pain without motor, sensory, or
reflex deficit unless radiculopathy or spinal stenosis is also
present.
* Imaging may show chronic degenerative changes or be
normal.
* Facet pain usually is treated with anti-inflammatory
agents, physical therapy, and avoidance of precipitating
activities.
*Facet blocks are usually not necessary, and effectiveness
in terms of long-term relief is controversial

4- Lumbar Spine Osteomyelitis
* Vertebral osteomyelitis is infection of the vertebrae,
usually due to Staphylococcus aureus.
* This is most common in the lumbar region and may
develop as a sequela of trauma or systemic infection.
* Adjacent structures are often affected with diskitis often
resulting from this, although the route of infection can be
from infected disk to vertebra.
* Diagnosis is suspected by lower back pain associated
with
systemic signs of infection—fever, elevated CRP, ESR,
WBC
* Helpful clinical features include pain with percussion over
the spine, marked limitation of motion of the spine, and
tightness of paraspinal muscles which is more marked than
usually seen with mechanical pain.

* MRI shows changes in the vertebral body and often in
disk
and adjacent psoas muscle.
* Radiographs show degeneration of the disk margin of the
vertebral body and disk space narrowing.
* Needle biopsy can reveal the causative organism in
most cases.
* The diagnosis can easily be missed initially, since it can
occur in patients with pre-existing lumbar spine pain,
and inflammatory signs may not be marked early on
* Treatment is with antibiotics and bed rest. Surgical
debridement is needed in patients who do not respond to
antibiotics.

5- Lumbar Spine Compression
* Compression of the lumbar vertebral bodies occurs in the
setting of acute trauma, osteoporosis, infection, or tumor.
* Compression with minimal trauma is especially of concern
for advanced osteoporosis or tumor.
* Patients present with severe lower back pain, usually without
radicular symptoms.
* If the collapse results in impingement on nerve roots, radicular
pain may develop.
* Compression of the cauda equina can result in weakness of
the legs and sphincter disturbance.
* The diagnosis of lumbar spine compression is suggested by
a clinical presentation of lower back pain that is exacerbated
by movement, jarring, or certain postures such as bending or
twisting.
*Imaging of almost any type shows the bone deformation
or destruction.

* MRI or bone scan may be needed to help differentiate
tumor or infection from degenerative causes.
* Treatment consists of immobilization of the fracture site,
which may include bracing. Pure analgesics often are
needed, especially at night.
* Corticosteroids should be avoided if the cause is
osteoporotic but can be very helpful for malignant vertebral
collapse.
* Vertebroplasty can be very helpful.
* Surgery may be needed for unstable lesions or if there is
spinal or neural compression.
* Radiation therapy is used for malignant collapse

6- Lumbar Diskitis
* Diskitis is an inflammatory process affecting the intervertebral
disks of any level, often occurring in the lumbar spine.
* The organism is dependent on the infectious source, with
Staphylococcus aureus and mycobacteria being among the
most important causes.
* Diskitis associated with recent lumbar surgery is likely to be
caused by resistant bacteria.
* In children, extraspinal manifestations of infection are less
likely
* Patients present with lower back pain with marked restriction
of flexion of the spine.
* Patients with postoperative diskitis usually have systemic
inflammatory markers, but overt signs of infection with fever and
chills may be absent.

* A diagnosis of lumbar diskitis is suggested by the presence of
severe lower back pain without a radicular component, often
with tenderness and spasm of the paravertebral muscles
associated with willingness of the patient to flex the hips but not
the spine
* ESR and CRP concentration are usually increased.
* The diagnosis can be confirmed by MRI, and often shows
changes in the end-plates of the adjacent vertebrae.
* Bone scan shows increased uptake in the region of the
infected disk.
* Biopsy often is needed to identify an organism.
* Treatment begins with bed rest and antibiotics
* Extensive surgery usually is not necessary; even tuberculous
diskitis is successfully treated with antibiotics in more than 80%
of cases
* In some patients, diskectomy with fusion of the adjacent
vertebral bodies may be required for relief of symptoms.

7- Spinal epidural abscess
* Bacterial infection of the epidural space can develop into a spinal
epidural abscess.
* The infectious organisms can spread from adjacent structures, the
skin, or hematogenously.
* There is a triad of fever, back pain, and neurologic deficits; however,
the combination of all three is rarely seen.
* Most patients have limited symptomatology initially.
* Diagnosis is confirmed by MRI but contrast may be needed to reveal
the infection.
* We have even seen cases where the lesion was not initially seen,
but subsequently visualized on repeat scanning.
* Laboratory studies including elevated peripheral blood WBC, CRP,
and ESR are frequently abnormal.
* Treatment usually begins with identification of the organism
from blood or surgery
* An increasing proportion of patients is diagnosed by MRI when the
epidural abscess is quite small. In this case, aspiration rather than
open surgery or even empiric treatment may be appropriate.

PITFALLS
Low Back Pain: Disc, Tumor, Diskitis, or Epidural Abscess
* If the patient initially has signs of neurologic deficit or
clinical/laboratory signs of inflammation then evaluation
without delay is appropriate.
* Contrast-enhanced MRI is more sensitive for looking for acute
inflammatory or neoplastic changes.
* CSF analysis may be needed to look for neoplastic meningitis
which can present with polyradiculopathy, associated with leg as
well as back pain.
* Peripheral blood markers of inflammatory disease, such as
ESR, CRP, and peripheral blood WBC, are often but not
invariably elevated in patients with epidural abscess and spinal
osteomyelitis.

Lower Back Pain from Intra-abdominal and Pelvic
Causes
* Patients with intra-abdominal and pelvic lesions can
present to the neurologist with symptoms of isolated back
pain or even pain which may resemble radiculopathy.
* Neuropathic pain in this case developed from plexus
invasion.
* Abdominal and pelvic disorders which may present with
back pain and/or leg pain are numerous, but include not
only gynecological lesions but also renal, hepatic,
pancreatic, and other gastrointestinal lesions.

Lower Back and Leg Pain from Arterial Insufficiency
* Patients presenting to the neurologist with lower back and leg
pain may be considered for lumbar spine lesion, but a peripheral
arterial process also should be considered.
* Rarely, patients are seen who present with saddle emboli to
the femoral arteries where the clinical presentation can resemble
cauda equina syndrome
* If cauda equina syndrome is suspected, rapid evaluation is
performed and if this does not show a clear reasonable etiology
then peripheral arterial disease as well as other visceral
conditions should be considered.
* On initial exam, clinical signs of ischemia should be considered
for further study even before spine imaging.
* While peripheral ischemia usually produces leg pain without
back pain, back pain can occasionally be manifest and even be
unrelated to the acute leg pain.

lower back and leg pain approaches

lower back and leg pain approaches

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