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Lumbosacral Radiculopathy
Andrew W. Tarulli, MDa,b,
Elizabeth M. Raynor, MDa,b,*
a
Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
b
Department of Neurology, Beth Israel Deaconess Medical Center,
330 Brookline Avenue, TCC 810, Boston, MA 02215, USA
Epidemiology
Although precise epidemiologic data are difficult to establish, the preva-
lence of lumbosacral radiculopathy is approximately 3% to 5%, distributed
equally in men and women [1,2]. Men are most likely to develop symptoms
in their 40s, whereas women are affected most commonly between ages 50
and 60 [1].
Anatomy
Detailed spinal anatomy is discussed elsewhere in this issue by Devereaux;
however, clinically relevant points are reviewed. There are five moveable
lumbar vertebrae, five fused sacral vertebrae, and four fused coccygeal ver-
tebrae [3] with intervertebral disks sandwiched between each of the lumbar
vertebrae and between the fifth lumbar vertebra and sacrum. The moveable
vertebrae are connected by paired facet joints between the articular processes
of the pedicles and by the anterior and posterior longitudinal ligaments.
The intervertebral foramina are formed by notches in the articular processes
0733-8619/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.ncl.2007.01.008 neurologic.theclinics.com
388 TARULLI & RAYNOR
L2 radiculopathy
Also rarely caused by disk herniation, L2 radiculopathy produces pain,
paresthesias, and sensory loss in the anterolateral thigh. Weakness of hip
flexion may occur; MSRs are normal. Lateral femoral cutaneous neuropa-
thy (meralgia paresthetica) may mimic L2 radiculopathy; the presence of
hip flexor weakness suggests radiculopathy rather than meralgia. Femoral
neuropathy and upper lumbar plexopathy may present similarly.
L3 radiculopathy
Although more common than with higher lumbar roots, disk herniation
is an uncommon cause of L3 radiculopathy. Pain and paresthesias involve
LUMBOSACRAL RADICULOPATHY 391
Table 1
Neurologic examination findings in monoradiculopathies
Root Sensory loss Motor abnormalities Muscle stretch
level Pain (paresthesias) or weakness reflex abnormalities
L1 Inguinal region Inguinal region None None
L2 Groin, anterior Anterolateral Iliopsoas None
thigh thigh
L3 Anterior thigh Medial thigh Quadriceps, Knee jerk
to knee, and knee iliopsoas,
anterior leg hip adductors
L4 Medial foreleg Medial lower leg Tibialis anterior, Knee jerk
quadriceps,
hip adductors
L5 Lateral thigh Lateral lower Toe extensors Internal hamstrings
and lower leg, leg, dorsum and flexors,
dorsum foot foot, great ankle dorsiflexor,
toe everter and
inverter,
hip abductors
S1 Posterior Sole, lateral foot Gastrocnemius, Ankle jerk
thigh, calf, and ankle, hamstrings,
heel lateral two gluteus
toes maximus,
toe flexors
S2-4 Medial Medial buttocks, None unless S1-2 Bulbocavernosus,
buttocks perineal, involved anal wink.
perianal region Ankle jerk
if S1 involved
the medial thigh and knee, with weakness of hip flexors, hip adductors, and
knee extensors; the knee jerk may be depressed or absent. L3 radiculopathy
may be confused with femoral neuropathy, obturator neuropathy, diabetic
amyotrophy, or upper lumbar plexopathy. Combined weakness of hip ad-
duction and hip flexion differentiates L3 radiculopathy from femoral and
obturator mononeuropathies.
L4 radiculopathy
Unlike the higher lumbar levels, L4 radiculopathy is produced most com-
monly by disk herniation. Spinal stenosis frequently involves this nerve root
in conjunction with roots at adjacent spinal levels. Sensory symptoms in-
volve the medial lower leg in the distribution of the saphenous nerve. As
with L3 radiculopathy, knee extension and hip adduction may be weak; ad-
ditionally, foot dorsiflexion weakness uncommonly may be observed. When
present, ankle dorsiflexion weakness generally is less prominent than in L5
radiculopathy. The knee jerk may be depressed or absent. Lumbosacral
plexopathy is the main differential diagnostic consideration; saphenous neu-
ropathy also is a possibility in pure sensory syndromes.
392 TARULLI & RAYNOR
L5 radiculopathy
The most common cause of L5 radiculopathy is intervertebral disk herni-
ation. Foot drop is the salient clinical feature, with associated sensory symp-
toms involving the anterolateral leg and dorsum of the foot. In addition
to weakness of ankle dorsiflexion, L5 radiculopathy commonly produces
weakness of toe extension and flexion, foot inversion and eversion, and
hip abduction. Common peroneal neuropathy closely mimics and must be
distinguished from L5 radiculopathy. Physical examination is helpful in
localization as weakness of foot eversion (mediated by the L5/peroneal-
innervated peroneus muscles) in conjunction with inversion (mediated by
the L5/tibial-innervated tibialis posterior) places the lesion proximal to the
peroneal nerve. Lumbosacral plexopathy and sciatic neuropathy are import-
ant differential diagnostic considerations. The involvement of hip abductors
(gluteus medius and minimus) indicates a lesion proximal to the sciatic nerve
but does not differentiate L5 radiculopathy from lumbosacral plexopathy.
Although there is no classic MSR abnormality associated with L5 radi-
culopathy, an asymmetric internal hamstring reflex can support its presence.
S1 radiculopathy
S1 radiculopathy also is caused commonly by intervertebral disk hernia-
tion, with associated weakness of foot plantar flexion, knee flexion, and hip
extension. Subtle weakness of foot plantar flexion may be demonstrated by
having patients stand or walk on their toes. Sensory symptoms typically in-
volve the lateral foot and sole. The ankle jerk is depressed or absent. Sciatic
neuropathy and lower lumbosacral plexopathy may mimic S1 radiculop-
athy. Both of these conditions, however, also are expected to affect L5-
innervated muscles.
Differential diagnosis
The majority of lesions causing lumbosacral radiculopathy are compres-
sive in nature and result from disk herniation or spondylosis with entrap-
ment of nerve roots. It is important, however, to recognize a variety of
other lesions that may produce lumbosacral radiculopathy, including several
neoplastic, infectious, and inflammatory disorders (see Box 1).
Degenerative spondylosis
After age 50, acute disk herniation is a less common cause of lumbosacral
radiculopathy, and chronic lesions related to degenerative spinal arthropa-
thy predominate [7]. With advancing age, intervertebral disks desiccate
and flatten, transferring increasing axial load to the facet joints, with resul-
tant facet joint hypertrophy, osteophyte formation, and thickening of the
ligamentum flavum [7,10]. These changes contribute to narrowing of the
central spinal canal, lateral recesses, and neural foramina. L4-5 and L5-S1
levels in particular are affected [7]. Chronic radiculopathy may result from
entrapment of nerve roots in the lateral recess, intervertebral foramen, or
central canal, involving single or multiple nerve roots. Clinical syndromes
of radicular pain involving buttock, hip, or posterior thigh and intermittent
neurogenic claudication are more common than back pain [10].
MRI frequently is performed in the evaluation of these lesions, although
bony pathology is demonstrated better by CT. Because degenerative
changes are commonplace in older patients, electrodiagnostic studies fre-
quently are necessary to establish the relevance of neuroimaging abnormal-
ities. Initial management involves pain control with analgesic medications
and physical therapy to strengthen supporting musculature and improve
postural mechanics. Surgical decompression is considered for progressive
or recalcitrant symptoms or worsening neurologic deficits.
Neoplasms
Radiculopathy may result from tumor in various locations within the spi-
nal canal; usually, these lesions are extramedullary. Primary tumors tend to
be intradural, whereas metastatic lesions are extradural. Furthermore, pri-
mary lesions tend to be solitary (neurofibromatosis type 1 being a notable
exception), whereas metastatic lesions frequently are multiple.
Primary tumors
Primary nerve root tumors are a rare cause of lumbosacral radiculop-
athy. Most primary spinal tumors are benign and slow growing, and their
clinical manifestations may be difficult to distinguish from more common
causes of radiculopathy, such as disk herniation [11]. Both are characterized
by back pain; however, the nature of pain related to tumor is distinctive, as
it becomes increasingly severe over time and is worse when lying down,
often interfering with sleep. Primary tumors producing lumbosacral radi-
culopathy most frequently are neurofibromas (often associated with neur-
ofibromatosis type 1) and ependymomas; less common are schwannomas
(in neurofibromatosis type 2), meningiomas, lipomas and dermoids, and
lipomas [11]. Ependymomas and neurofibromas typically affect the filum
terminale, producing a cauda equina syndrome [11]. Diagnosis of primary
tumors is established by MRI, and their definitive treatment is surgical.
LUMBOSACRAL RADICULOPATHY 395
Infections
Herpes zoster
Primary infection with varicella-zoster virus produces chickenpox, usually
in children, after which it lies dormant in dorsal root ganglia and may be
reactivated decades later, producing acute Herpes zoster (HZ) or shingles
[22,23]. A common disorder, it is prevalent especially in immunocompro-
mised and elderly populations. HZ usually affects a single dermatome and
is accompanied by intense neuralgic pain reflecting the level of infection;
pain often precedes the classic vesicular eruption. Ophthalmic and thoracic
dermatomes are affected most commonly, whereas lumbosacral zoster acco-
unts for approximately 20% of cases [23,24]. In the presence of rash, the
diagnosis of HZ is obvious, but a minority of patients may present with zoster
sine herpete, dermatomally distributed pain without rash [25]. Approximately
5% of patients may develop a local neuritis of the spinal nerve, which subse-
quently affects the motor axons, producing a segmental zoster paresis [26].
The pain of acute HZ, frequently overwhelming at the outset, gradually sub-
sides as the vesicles crust over in most patients. Approximately 10% to 15%
suffer from chronic pain, or postherpetic neuralgia (PHN), however, despite
treatment with antiviral agents [27]. Complete resolution of motor deficits
occurs in 50% to 70% of those who have segmental zoster paresis [24].
Tricyclic antidepressants, gabapentin, pregabalin, opioids, and topical
lidocaine patches are effective in the treatment of acute herpetic neuralgia
(grade A evidence) [28]. Amitriptyline usually is effective, in a dosage of
75 to 100 mg per day, in the treatment of pain related to PHN (grade A)
[29]. Gabapentin, in doses between 1800 and 3600 per day, also is effective
in relieving the symptoms of PHN (grade A) [30] and may be preferred to
amitriptyline because of a lower incidence of side effects. If begun within
72 hours of development of the rash, famciclovir, valacyclovir, or acyclovir
reduces the pain of acute HZ but may not be effective in the prevention of
PHN (grade A) [23]. Of these antiviral agents, valacyclovir (1000 mg 3 times
a day for 7 days) is preferred for its more rapid resolution of neuralgia
symptoms, shorter duration of PHN, and smaller pill burden [31]. Cortico-
steroids by themselves do not alter the course of PHN but, in combination
with an antiviral agent, may improve pain [23].
Lyme radiculopathy
Lyme disease is transmitted by the bite of Ixodes ticks infected with the
spirochete Borrelia burgdorferi [42]. The classic rash of erythema migrans
develops in 50% to 90% of patients [43]. In addition to a flu-like illness, he-
matogenous dissemination may affect the heart, joints, and nervous system
[42,43]. Acute Lyme radiculoneuropathy is seen most commonly in the first
398 TARULLI & RAYNOR
Spinal cysts
Cystic lesions in the sacral spine are common, with an incidence ranging
from 4.6% to 17% on imaging studies [52,53]. Most sacral meningeal
cysts are dural diverticula (Tarlov cysts) produced by fluctuations in CSF
pressure [52]. There is little to differentiate the presentation of meningeal
sacral cysts from other causes of lumbosacral radiculopathy [52]. Radicular
pain often is relieved or disappears when patients are recumbent and is
aggravated by Valsalva’s maneuver [52]. Because they are common and
not necessarily the cause of symptoms, establishing a cyst as the cause of
lumbosacral radiculopathy involves eliminating other causes first. MRI is
the diagnostic procedure of choice for demonstrating lumbosacral cysts;
however, clinical relevance of the imaging findings must still be established.
Although analgesic medications may reduce pain, relief of symptoms with
fluoroscopic-guided aspiration and surgical treatment is definitive [52].
Spinal hematomas
Hematomas are uncommon causes of lumbosacral radiculopathy. Epidu-
ral and subdural spinal hematomas occur most frequently in patients who
have coagulopathies, who are taking anticoagulants, or who recently have
undergone epidural injections or instrumentation of the lumbosacral spine
[54–56]. Spinal subarachnoid hemorrhage is uncommon. Unlike its intracra-
nial counterpart, spinal subarachnoid hemorrhage is caused most commonly
by arteriovenous malformation rupture rather than aneurysmal rupture [57].
Hemorrhage into synovial cysts or the ligamentum flavum also may produce
hematomas and lumbosacral radiculopathy [58,59].
401
402 TARULLI & RAYNOR
relevance of imaging findings [69,70]. EMG also can be used to help provide
confirmation of clinically suspected nerve root involvement.
In some cases, further laboratory testing is appropriate based on the his-
tory, physical examination, EMG, or imaging findings. Lumbar puncture
may be indicated to investigate inflammatory or infectious causes. The
direction of the evaluation is guided by patient presentation and subsequent
clinical course. As discussed previously, a basic understanding of the diverse
disorders producing lumbosacral radiculopathy and those who are at risk
for them is the foundation for accurate diagnosis and treatment.
Summary
Lumbosacral radiculopathy is a common neurologic syndrome that is an
important source of disability. Although the most common causes are disk
herniation and chronic spinal arthropathy, physicians should be mindful of
other causes, including neoplasm and infection. Initial evaluation should
focus on localization of lumbosacral radiculopathy and exclusion of disor-
ders that may produce irreversible neurologic compromise. Treatment is
aimed at providing pain relief and preventing neurologic deficits in addition
to appropriate directed therapy based on the underlying cause.
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