Anatomy and pathoanatomic of Lumbosacral Plexus

(Article Review)

Oleh:
Rachmad Faisal

Pembimbing:
dr. Rieva Ermawan, Sp.OT(K)

PROGRAM PENDIDIKAN DOKTER SPESIALIS – I

ORTHOPAEDI DAN TRAUMATOLOGI
FAKULTAS KEDOKTERAN UNIVERSITAS SEBELAS MARET /
RSUD DR. MOEWARDI / RSO PROF. DR. R. SOEHARSO
SURAKARTA
2022
 Table of Content

Table of Content.......................................................................................................2
Abstract....................................................................................................................3
Introduction..............................................................................................................4
Anatomy...................................................................................................................4
Structure and Function.........................................................................................4
Embryology........................................................................................................11
Blood Supply and Lymphatics...........................................................................12
Nerves.................................................................................................................12
Muscles...............................................................................................................13
Clinical Significance..........................................................................................14
Epidemiology and Etiology...................................................................................15
Clinical Feature and Pathogenesis.........................................................................16
Tumor or Mass...................................................................................................17
Infection..............................................................................................................18
Trauma................................................................................................................18
Inflammatory and Microvasculitis.....................................................................19
Hematomas and Other Vascular Lesions in the Retroperitoneal and Pelvic Area
............................................................................................................................20
Imaging..................................................................................................................21
Diagnosis................................................................................................................22
Treatment...............................................................................................................24
Non Surgical.......................................................................................................25
Surgical...............................................................................................................25
Prognosis................................................................................................................27
Complication..........................................................................................................27
Conclusion.............................................................................................................28
Reference...............................................................................................................29

2
Abstract
The lumbosacral (LS) plexus is a network of nerves formed by the
anterior rami of the lumbar and sacral spinal cord. LS plexopathy is an injury to
the nerves in the lumbar and/or sacral plexus. LS plexopathy is not an uncommon
condition but can be difficult to diagnose and manage. Due to the diverse
etiologies, the age of presentation and prevalence varies. However, the median
age for diagnosis of LS plexopathy is around 65 years for all causes. LS
plexopathy is more common in women due to the predisposing risk factors of
pregnancy and gynecological cancers. The incidence of diabetic amyotrophy is
4.2 per 100,000 annually and occurs in 0.8 percent of people with diabetes
mellitus (DM).
Lumbosacral plexopathy should be suspected if a patient presents with
weakness, sensory loss, and reflex asymmetry in the lower extremity in a pattern
that involves more than one nerve or nerve root. Many cases of lumbosacral
plexopathy previously thought to be idiopathic have been shown to be caused by
ischemic injury from microvasculitis; despite lack of evidence for efficacy in
improving neurologic deficits.

Keyword: Anatomy of lumbosacral plexus, Lumbosacral Plexopathy,

Microvasculitis

3
Introduction
Lumbal plexus is formed by ventral branches of L1–L4 in musculus psoas
major with a share of Th12 or without it. It is located on internal surface of dorsal
abdominal wall, ventrally from processus transversus of coxal vertebrae. It is
protected with layers of the muscle and bone structures. As well-protected and
safely located structure, it provides better safety to the plexus. Lumbosacral
plexopathies are therefore less frequent peripheral lesion aVecting lower
extremities.1
Sacral plexus is formed by ventral branches of S1–S3 with a share of S4
and very important lumbosacral trunk formed of L4 and L5 roots. It extends above
sacroiliac junction and consequently connects with sacral nerves forming n.
ischiadicus.1
Depending of Th12 root presence, we say on high cranial prefixed plexus
or low caudal one. Boundary root participating in the plexi formation is L4 root,
which in some cases is largerly involved in lumbal plexus formation and sacral in
others. Its proportion in that or the other plexus helps to characterize the whole
plexus as cranial prefixed with a share or caudal post-fixed without a share of
Th12. It is necessary to realize that L4 root does not play, always, the role of
boundary root, sometimes it is L5 root.1
Therefore, in this paper, the author will review more deeply about the
Anatomy, Pathoanatomy, and Biomechanics of The Lumbosacral Plexus.

Anatomy
Structure and Function
The lumbar plexus is formed by anastomosisof the ventral rami of the four
first lumbar nerves.The lumbar plexus lies within the posterior portion of the
musclepsoas. Numerouscollateral and terminal branchesarisefrom the lumbar
plexus.2 The roots of spinal nerves from L1 to L5 emerge in front of the
transverse processes of lumbar vertebra. These roots enter into the part of psoas
major muscle which is in between the muscle fibres taking origin from the bodies
of lumbar vertebra and intervertebral discs and muscle fibres arising from the

4
transverse processes of lumbar vertebra. When traced from body of L1 to lower
lumbar vertebra, the plexus shares the same coronary plane at L1 but when it
comes down, it is more anterior in position. The first four lumbar ventral rami
with a contribution from subcostal nerve form the lumbar plexus.3
The plexus is complex and prone to have variations. The incidence of
variations in lumbar plexus is around 20%. The L1 ventral rami with a branch
from ventral rami of subcostal nerve form a common trunk which divides and
give rise to iliohypogastric and ilioinguinal nerves. L1 ventral ramus gives a
branch which joins with a branch from L2 ventral rami to form genitofemoral
nerve.3
The ventral rami of L2 L3 and L4 spinal nerves divide into ventral and
dorsal divisions. The ventral divisions of L2, L3 and L4 unite to form Obturator
nerve. In 29% of individuals, L3 and L4 ventral divisions form accessory
obturator nerve. The dorsal divisions of L2 and L3 spinal nerves join to form
lateral cutaneous nerve of thigh. Dorsal divisions of L2, L3 and L4 form the
femoral nerve. The L4 ventral rami or the furcal nerve contributes to both lumbar
and sacral plexus. After giving a branch to lumbar plexus, it joins with the ventral
rami of L5 and forms the lumbo sacral trunk which joins the sacral plexus.4
There are six constant branches formed from the lumbar plexus. The
iliohypogastric and ilioinguinal nerves pass through the lateral border. The lateral
cutaneous nerve of thigh and femoral nerve cross the later border in the lower part
of psoas major. The genitofemoral nerve pierces the anterior surface and runs over
the psoas major. The obturator nerve exits psoas major muscle through its medial
border. The inconstant branch, accessory obturator nerve if present exits through
the medial border.4

5
Figure 1. Formation of Lumbar Plexus.3

Iliohypogastric Nerve
It arises from L1 but sometimes from T12 also and emerges from the
upper part of lateral border of psoas major. It lies posterior to medial arcuate
ligament near its exit. It runs over the anterior surface of the quadratus lumborum
where it is related to the lower pole of kidney and reaches the lateral surface of
lower part of anterior abdominal wall. Here, it innervates the posterior fibres of
transversus abdominis near its origin from iliac crest.3

6
After this, it runs anteriorly between transversus abdominis and internal oblique
muscles, supplies them. It also gives a lateral cutaneous branch which supplies the
posterolateral part of gluteal region. It continues medially and pierces internal
oblique anteromedial to anterior superior iliac spine, runs in between internal and
external oblique muscles. It ends by piercing the external oblique above the
superficial inguinal ring and supplies skin over the suprapubic region.3
Ilioinguinal nerve
It takes its origin from L1 but may get communications from T12 or L2
and emerges below the iliohypogastric nerve in the lateral border of psoas major.
Its courses obliquely over the quadratus lumborum and iliacus. After that it
reaches transversus abdominis and pierces it inferomedial to anterior superior iliac
spine. It supplies transversus abdominis and internal oblique before it enters the
inguinal canal where it travels superficial to its contents. It exits the inguinal canal
through superficial inguinal ring and gives cutaneous innervation to the root of the
penis and scrotum in males, mons pubis and labia majora in females and upper
medial part of the thigh in both sexes.3
Lateral femoral cutaneous nerve
It usually arises from dorsal divisions of L2 and L3. It emerges from the
lateral border of psoas major and runs obliquely over the iliacus muscle before it
reaches the anterior superior iliac spine. In the iliac fossa the nerve lies posterior
to caecum in the right side and descending colon in the left side beneath the
parietal peritoneum. It crosses behind inguinal ligament medial to anterior
superior iliac spine and enters the thigh anterior to Sartorius. Here in the thigh it
divides into anterior and posterior branches. The anterior branch innervates skin
over the anterior and lateral part of thigh up to the knee joint and takes part in the
formation of peripatellar plexus. The posterior branch pierces the fascia lata and
supplies skin over the greater trochanter and adjacent gluteal region.3
Femoral nerve
It is formed by dorsal divisions of L2, L3 and L4 and emerges from the
lateral border of psoas major about 4 cm above inguinal ligament. It runs in the
groove between psoas major and iliacus below the inguinal ligament and reaches

7
the thigh lateral to femoral sheath. Here it divides in to anterior and posterior
divisions before supplying the anterior compartment of thigh. It supplies the
muscles of anterior compartment of thigh and skin over the anterior surface of
thigh and medial side of leg and foot.3
Genito femoral nerve
It is formed by L1 and L2 and exits psoas major muscle by piercing its
anterior surface opposite third or fourth lumbar vertebra. It runs beneath the
parietal peritoneum and crosses the ureter before dividing in to genital and
femoral branches. The genital branch crosses external iliac artery and enters the
deep inguinal ring. It traverses behind the contents of inguinal canal and exits
through the superficial inguinal ring where it ends by supplying cremaster muscle
and skin over the external genitalia. The femoral branch runs lateral to external
iliac artery and enters the femoral sheath behind the inguinal ligament and lateral
to femoral artery. It pierces the femoral sheath and ends by supplying the skin
over the femoral triangle.3
Obturator Nerve
It arises from the ventral divisions of L2, L3 and L4 and emerges from the
medial border of psoas major muscle opposite to fifth lumbar vertebra. It runs
behind the common iliac vessels and lateral to internal iliac vessels. It crosses the
pelvis in its lateral wall where it is anterosuperior to obturator vessels before
reaching obturator foramen. After crossing obturator foramen it enters the medial
compartment of thigh where it is divided into anterior and posterior divisions. It
supplies the muscles of adductor compartment of thigh, hip and knee joints.3
Accessory obturator nerve
It is a small and rare branch. It arises from ventral rami of L3 and L4. It
too courses along the medial border of psoas major. When it reaches the superior
pubic ramus it runs posterior to pectineus. It branches out here; one of them
supplies hip joint, the other supplies pectineus. The third branch joins the anterior
division of obturator nerve. But the branching pattern is not constant.3

8
 The sacral plexus innervates the muscles of the buttocks, posterior thigh,
and leg below the knee as well as the skin of the the posterior thigh and leg, lateral
leg, foot, and perineum. It is formed from the lumbosacral trunk and the ventral
rami of S1-S3 (or S4) nerve roots. The anterior primary rami of S2 and S3 nerve
roots carry parasympathetic fibers that mainly control the urinary bladder and anal
spinchters. Triangular in shape, the sacral plexus lies on the anterior surface of the
sacrum in the immediate vicinity of the sacroiliac joint and lateral to the cervix or
prostate. The sacral plexus enters the pelvis at an angle between the psoas major
muscle and the sacral promontory, anterior to the sacral ala and the anterior
surface of the piriformis muscle. The branches of the sacral plexus include the
superior gluteal, inferior gluteal, sciatic (tibial and common peroneal divisions),
pudendal, and posterior cutaneous nerve of the thigh.5

9
 Figure 2. The Sacral Plexus.5

There are three main functions of the lumbar spine. First, the lumbar spine
assists in supporting the upper body. The lumbar vertebrae (L1-L5) are much
larger when compared to other regions of the vertebral column, which allow them
to absorb axial forces delivered from the head, neck, and trunk. The lumbar
vertebrae form a canal that serves to protect the spinal cord and spinal nerves.
This arrangement allows for the communication of information from the central
nervous system to the lower extremities and vice versa. The lumbar spine allows
for diverse types of truncal motion, including flexion, extension, rotation, and side
bending. From a lateral view, the lumbar spine has a concave curvature, referred
to as the lumbar lordosis. This curvature is variable in degree and transfers the
upper body mass over the pelvis to allow for efficient bipedal motion.6

Figure 3 Left: Lumbar vertebrae lateral view; Lumbar region of vertebral

column in T1-weighted MR image in sagittal plane.7
Each lumbar vertebra consists of multiple components. These include the
vertebral body and the dorsal structures termed the posterior elements.
Immediately dorsal to the vertebral body lie two pedicles that attach to the
laminae. The pedicles resist motion and transmit forces from the posterior

10
elements to the vertebral body. From the junction of the two laminae, the spinous
process extends posteriorly. At the junction between the pedicles and laminae,
four articular processes and two transverse processes reside. The transverse
processes extend laterally, serving as attachment points for ligaments and
musculature. The superior and inferior articular processes create the
zygapophyseal joints (aka facet joints). This joint occurs between the superior
articular process of a vertebra and the inferior articular process of the vertebra
immediately cephalad. These joints lie in the sagittal plane and participate in
flexion and extension of the lumbar spine. The pars interarticularis is the location
of the lamina between the superior and inferior articular processes and is prone to
the development of stress fractures (spondylolysis) in the growing spine. 8

Embryology
The development of the lumbar spine begins around the third week of
gestation. The notochord initiates this process by secreting growth factors that
stimulate the ectoderm to transform into the neuroectoderm. The process of
neurulation produces the neural tube, which ultimately develops into the spinal
cord. Errors during neurulation may result in numerous congenital anomalies
ranging from mild (spina bifida) to severe (anencephaly).9
Also occurring around the third week, the paraxial mesoderm develops
into pairs of somites along either side of the neural tube. Each somite
differentiates into a dermomyotome and sclerotome. The sclerotome separates
into cell clusters located caudally and cranially. Neurons from the neural tube
penetrate these clusters to innervate individual myotomes and dermatomes. The
caudally located cell clusters then fuse with the cranially located clusters of the
adjacent sclerotome to create the vertebral body. Between each cell cluster, the
interverbal disc develops. Simultaneously, sclerotome cells migrate around the
neural tube and fuse dorsally, creating the vertebral arch.9
Each vertebra undergoes a process of endochondral ossification, in which
the mesenchymal cells differentiate into cartilage and eventually bone.
Chondrification centers develop around the sixth week and primary ossification
centers in the seventh. These processes are responsible for strengthening the

11
eventual vertebra. Bone remodeling continues throughout the lifespan and is
highly dependent on stress and mechanical loads.10
Blood Supply and Lymphatics
The lumbosacral plexus receives its major blood supply from the internal
iliac artery and its branches, especially the lateral sacral, iliolumbar, and superior
gluteal arteries. Injury or disease involving these vessels, or the common iliac
artery and aorta from which they are derived, may result in malfunction of the
plexus. Some protection from ischemic injury to the plexus from disease of the
internal iliac artery is rpovided by collateral blood flow from the middle sacral,
contralateral internal iliac, mesentric, and deep femoral arteries. The lumbar
plexus is afforded additional protection from ischemia through the rich arterial
collaterals from the psoas muscle in which it is embedded.5
An extensive system of lymphatics in the lumbar region is responsible for
draining lymph from the lower limb and pelvis. These lymph nodes are present
along the inferior vena cava and aorta. The lumbar lymph nodes receive drainage
from the common iliac nodes and deliver this lymph to the thoracic trunk.11
Nerves
Five pairs of mixed spinal nerves emerge from either side of the lumbar
spinal cord, carrying both motor and sensory nerve fibers—the spinal nerves
branch after exiting the neural foramen into ventral and dorsal rami. The dorsal
rami supply motor innervation to the erector spinae musculature and sensation to
the skin over the back. The ventral rami supply motor and sensory fibers to the
remainder of the prevertebral musculature and lower limbs.11
The T12 to L4 ventral rami combine to form a network of nerves called
the lumbar plexus. The lumbar plexus gives rise to the obturator (L2-L4) and
femoral (L2-L4) nerves, respectively. The remaining nerves of the lumbar plexus
include the iliohypogastric (T12-L1), ilioinguinal (L1), genitofemoral (L1-L2),
and lateral femoral cutaneous nerve of the thigh (L2-L3)—the lumbosacral plexus
form from the L4 to S4 ventral rami. The L4 and L5 roots join to form the
lumbosacral trunk, which descends into the pelvis to join to sacral plexus. The
lumbosacral plexus then gives rise to the sciatic nerve (L4-S3), which branches

12
into the common peroneal and tibial nerves. The sacral plexus also includes the
superior gluteal (L4-S1), inferior gluteal (L5-S2), posterior femoral cutaneous of
the thigh (S1-S3), and pudendal nerve (S1-S4).12
Each lumbar spinal nerve exits below its corresponding vertebra—for
example, the L4 nerve exits below the L4 vertebra through the L4-L5 neural
foramen. A majority of lumbar disc herniations occur centrally and do not
compress the exiting nerve root at the level of the disc. The nerve root most
commonly affected exits one level below the herniated disc. For example, an L4-
L5 central disc herniation will most commonly compress the L5 nerve root in the
lateral recess of the spinal canal. However, in the setting of a far lateral disc
herniation, the L4 nerve root is compressed, albeit less commonly. This difference
is due to the more central position of the traversing spinal nerves when compared
to the more lateral position of the exiting spinal nerves.11

Each spinal nerve supplies an area of skin with afferent sensory fibers.
This area of skin is referred to as a dermatome. Each lumbar spinal nerve also
innervates a group of muscles with motor fibers, termed a myotome. Dermatomes
and myotomes trace back to our embryological development. Dermatomes and
myotomes are clinically relevant as they can be used to determine the lumbar
spinal nerve(s) involved in the setting of pathology.11

Muscles
Many muscles use the lumbar vertebrae as attachment points. These
muscles allow for smooth, controlled movement in different functional planes.
These muscles also serve a secondary role in stabilization, protection, and
proprioception. Three major muscle groups originate or insert on the lumbar spine
and aid in movement. First, the extensor group consists of the erector spinae and
the multifidi. This group lies posterior to the lumbar spine. In this region, the
erector spinae muscles include the longissimus thoracis and iliocostalis
lumborum. The contraction of this group results in an extension moment at the
lumbar spine. The flexor group lies anterior to the lumbar spine and allows for
trunk flexion as well as hip flexion. The psoas major originates from the T12-L4

13
transverse processes and joins the iliacus in the thigh to become the iliopsoas
(composite muscle). The iliopsoas plays a key role in hip flexion and also assists
with the arching of the lumbar spine. The abdominal musculature
(internal/external oblique, rectus abdominis) plays a more important role in
truncal flexion. Finally, a concerted effort involving several muscles is required to
create rotation and lateral flexion (side-bending) of the lumbar spine. The
quadratus lumborum, psoas major, abdominal musculature, and multifidi play an
important role in creating these motions.13
Muscle strains in the lumbar region are typically the result of abnormal
tension placed upon a tendon; this can occur from overstretching a muscle,
repetitive use, or muscle tearing from excessive force. Most lumbar muscle strains
will respond to conservative treatment.14
Clinical Significance
The lumbosacral (LS) plexus is a network of nerves formed by the
anterior rami of the lumbar and sacral spinal cord. LS plexopathy is an injury to
the nerves in the lumbar and/or sacral plexus. LS plexopathy is not an uncommon
condition but can be difficult to diagnose and manage. 15 However, it is far less
common than brachial plexopathy. Patients with LS plexopathy usually present
with low back and/or leg pain. They can also experience motor weakness, other
sensory symptoms of numbness, paresthesia, and/or sphincter dysfunction. 16 LS
plexopathy can be caused by multiple etiologies, with diabetes mellitus, traumatic
injury, neoplasms, and pregnancy being a few of the important causes. Treatment
is often limited and varies significantly depending on the underlying pathology.
LS plexopathy can be debilitating, severely affecting a patient's quality of life.
Early identification and management are critical in reducing morbidity and
mortality.17
Lumbosacral plexopathy should be suspected if a patient presents with
weakness, sensory loss, and reflex asymmetry in the lower extremity in a pattern
that involves more than one nerve or nerve root. A plexopathy primarily affecting
the upper roots or lumbar plexus will present with changes in the gluteal and
sciatic nerve distribution. Weaknes may be seen in hip extension, hip abduction,

14
knee flexion, dorsiflexion, and pkantar flexion; change in sensation on the
postertio thigh, anterolateral and posterior leg, and dorsal and plantar surfaces of
the foot; and decreased or absent ankle reflex.

Epidemiology and Etiology

Due to the diverse etiologies, the age of presentation and prevalence
varies. However, the median age for diagnosis of LS plexopathy is around 65
years for all causes. LS plexopathy is more common in women due to the
predisposing risk factors of pregnancy and gynecological cancers. The incidence
of diabetic amyotrophy is 4.2 per 100,000 annually and occurs in 0.8 percent of
people with diabetes mellitus (DM).15,18 The median duration of DM is four years
with a median hemoglobin A1c of 7.5% at the time of diagnosis of diabetic
amyotrophy.19 For neoplastic cases of LS plexopathy, L4-S1 segment is
commonly affected (>50% of cases) followed by L1-L4 segment (31%), and pan-
plexopathy (about 10%). In 73% of cases, a local compression or invasion of an
abdominopelvic malignancy was present. LS plexopathy occurs within one year
of diagnosis in over one-third of patients with primary tumors. In 15% of cases,
LS plexopathy resulted in the diagnosis of cancer. LS plexopathy occurs in
roughly 0.7% of cases following a traumatic pelvic fracture. Incidence increases
to 2% following a sacral fracture. LS plexopathy occurs in an estimated 1 in 2000-
6400 deliveries.19,20
Since LS plexus is present near to abdominal and pelvic organs, various
pathologies and injuries contribute to LS plexopathy, such as :19
1. Direct trauma
a. Posterior hip dislocation
b. Sacral fracture
c. After lumbar plexus block
2. Metabolic, inflammatory, and autoimmune causes
a. Diabetes mellitus (DM) - more likely in those with type II DM
b. Amyloidosis
c. Sarcoidosis 
3. Infections and local abscess

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 a. Vertebral osteomyelitis
b. Chronic infections (e.g. Tuberculosis, fungal infections)
c. Other infections: Lyme disease, HIV/AIDS, Herpes zoster (HZ)
d. Psoas abscess
4. Radiation therapy of the abdominal and pelvic malignancies.
5. Pregnancy-related
a. Mostly occur in the third trimester and after delivery due to birth trauma.
6. Postoperative plexopathy
a. Scar tissue formation and hematomas may occur following gynecological
and other pelvic surgeries.
7. Damage to the vasculature innervating the LS plexus
a. Femoral vessel catheterization
b. Ischemia from direct compression due to arterial pseudoaneurysms, aortic
dissection, retroperitoneal hematoma, etc.).

Clinical Feature and Pathogenesis

Lumbosacral plexopathies arise from various disease processes, such as
neoplasm, infection, trauma, radiation treatment of pelvic neoplasm, hematoma
and other vascular lesions in the retroperitoneal or pelvic areas, mechanical or
stretch injury especially after hip surgery, ischemia, inflammation, infiltration
(amyloid); and idiopathic causes. Often, lumbosacral plexopathies do not occur in
isolation with involvement of only the lumbosacral plexus nerve segment.
Frequently, they occur with involvement of the root, plexus, and nerve (causing
lumbosacral radiculoplexus neuropathies). This is especially true for the
inflammatory or infiltrative varieties. From an electrophysiologic perspective, a
lumbosacral plexopathy is defined as involvement from at least two different root
levels and from at least two different peripheral nerves. For pure lumbosacral
plexopathies, there should not be denervation of the paraspinal muscles, but
paraspinal involvement is present in radiculoplexus neuropathies.21

16
Tumor or Mass
Because of its proximity to many pelvic organs, such as colon, cervix,
ovaries, and urinary bladder, the lumbosacral plexus is often affected by direct
malignant invasion from those adjacent organs. Metastatic deposits from remote
solid organs, such as breast or lung cancer, and hematologic malignancy, such as
lymphoma, can directly infiltrate or cause retroperitoneal lymph node enlargement
and com pression on the lumbosacral plexus. In cases of intraneural
lymphomatosis causing lumbosacral plexopathy, the peripheral nerve and
lumbosacral plexus can act as a safe haven for the lymphoma cells as the
chemotherapeutic agents may not be able to cross the blood nerve barrier. 22
Rarely, perineural spread by prostate cancer causing lumbosacral plexopathy has
been reported. In these cases, the tumor cells spread up the small sacral nerve root
fibers innervating the prostate gland and then grow down the nerves into the
lumbosacral plexus within the perineural lining of the nerve. Neoplasm has been
reported to be the most common cause of non- traumatic lumbosacral
plexopathy.23
Clinically, neoplastic lumbosacral plexopathy presents with subacute onset
of pain located in the lower back, buttock, thigh, or hip, depending on which part
of the lumbo- sacral plexus is involved. Neoplasm in the upper lumbosacral
plexus causes pain in the costovertebral area radiating to the upper thigh, and a
lower lumbosacral plexus lesion causes pain in the iliac crest, buttocks, and the
posterior aspect of the thighs.21
A unique feature of pain arising from neoplastic lumbosacral plexopathy is
that it is exacerbated by lying down but relieved by getting up and walking. Motor
weakness, loss of reflexes, and sensory disturbance develop after the onset of
pain; the distribution of these symptoms and clinical signs depend on the level of
involvement of the plexus. Bilateral involvement can be seen with wide spread
metastatic lesions. A rectal mass found during rectal examination can 4 suggest
neoplasm as a cause.21

17
Infection
Local infection at the psoas muscle or adjacent retroperitoneal space, such
as abscess in the psoas muscle or in the gluteal region, can affect the lumbosacral
plexus. The infection can arise locally from the adjacent organs, such as the
gastrointestinal or urinary tract, or the lumbar spine. Systemic infection such as
tuberculosis (Pott disease) can cause psoas abscess and lumbosacral plexopathy.
Perirectal abscess can cause lumbosacral plexopathy in HIV patients.22
The symptoms can be similar to neoplasm, but there can be symptoms
suggesting infection such as fever, malaise, point tenderness, weight loss, and
night sweats. Neuroimaging studies may show local collections of gases or
abcess.21

Trauma
Traumatic lumbosacral plexopathy occurs much less commonly compared
with traumatic brachial plexopathy. This is because the lumbosacral plexus is
protected and encased within the bony environment of the pelvic brim. Also, the
plexus lies within the retroperitoneal space with minimal mobility. The trauma
that causes traumatic lumbosacral plexopathy is usually severe, involves very high
velocity and energy at the time of impact, and usually is associated with pelvic
fractures.23 Traumatic dislocation of the hip, usually related to high-energy trauma
associated with multiple injuries, can cause lumbosacral plexopathy pre-
dominantly involving its lower portion, particularly at the major branches of the
sciatic nerve (most commonly fibular [peroneal], followed by tibial), and is seen
in up to 20% of cases.24
The symptoms of traumatic lumbosacral plexopathy are typically pain and
limited mobility from trauma to the local tissues, as well as muscle weakness and
sensory loss depending on the extent of the nerves involved. Most commonly,
traumatic lumbosacral plexopathy causes paresis in the distribution of the

18
common fibular (peroneal) nerve, followed by the gluteal, tibial, and obturator
nerve.21

Inflammatory and Microvasculitis

The inflammatory lumbosacral plexopathies present with acute to subacute
onset of spontaneous painful, unilateral or bilateral but asymmetric, lower limb
weakness; sensory loss; and paresthesia involving proximal and distal nerve
segments with the disease process localizing to the lumbosacral plexus. This
category includes several clinical entities, such as diabetic lumbosacral
radiculoplexus neuropathy, nondiabetic lumbosacral radiculoplexus neuropathy,
postsurgical inflammatory neuropathy, and (probably) some cases of intrapartum
lumbosacral plexopathy. Diabetic lumbosacral radiculoplexus neuropathy occurs
typically in patients with mild type 2 diabetes mellitus who often have good
control of glucose.21
Diabetic lumbosacral radiculoplexus neuropathy is clearly distinguished
from a more common distal diabetic sensorimotor neuropathy, where the onset is
insidious and symptoms are typically length dependent and symmetric, affecting
sensory functions only. These differences can be explained by a different
pathogenesis causing each type of diabetic neuropathy, with inflammation and
microvasculitis as the cause of diabetic lumbosacral radiculoplexus neuropathy
and abnor- mal glucose metabolism as the cause of diabetic distal sensorimotor
neurop- athy. Diabetic lumbosacral radiculoplexus neuropathy has been called by
other names, including diabetic amyotrophy, Bruns-Garland syndrome, diabetic
mononeuritis multiplex, diabetic polyradiculopathy, or diabetic proximal
neuropathy.21
Diabetic lumbosacral radiculoplexus neuropathy seems to be a
monophasic illness that worsens for an average of about 6 months and then
gradually improves. Another form of diabetic lumbosacral plexopathy presents as
painless lower limb and motor predominant neuropathy. Patients with this form

19
present more slowly and symmetrically with greater degree of weakness than
typical painful diabetic lumbosacral radiculoplexus neuropathy. There has been
debate as to whether this pain- less diabetic motor neuropathy is best classified as
diabetic chronic inflamma- tory demyelinating polyradiculoneuropathy (CIDP) or
a form of diabetic lumbosacral radiculoplexus neuropathy. A pathologic study of
these patients showed that the pathophysiology is ischemic injury and
microvasculitis and not inflammatory demyelination. Consequently, the painless
motor neuropathy of diabetes mellitus is a form of diabetic lumbosacral
radiculoplexus neuropathy and not diabetic CIDP.25
These patients may induce the attack by deciding to lose weight, start an
exercise program, or tighten their glycemic control. With these measures, they
often lose weight easily. Then, a patient typically has an acute or subacute onset
of severe neuropathic pain, often burning, stabbing, electric shocks, or contact
allodynia, typically of the thigh or leg, followed by motor weakness and sensory
loss. These deficits often begin focally in the thigh or leg but then spread to the
uninvolved segment and then to the contralateral side.21

Hematomas and Other Vascular Lesions in the Retroperitoneal and Pelvic

Area
Structural lesions such as retroperitoneal hematoma or an unruptured
aneurysm of the iliac artery have been reported to cause lumbosacral plexopathy.
Retroperitoneal hematoma affecting the psoas muscle can cause lumbosacral
plexopathy and may have various causes, either traumatic or nontraumatic, such
as hemophilia, anticoagulant use, or hematologic malignancy.21
Retroperitoneal hematoma can cause a compartment syndrome and
compress the lumbosacral plexus. Vascular lesions, such as occlusion of the lower
portion of the aorta and common iliac artery causing ischemia, bleeding from
rupture of a common iliac aneurysm, ischemia following aortoiliac procedures
such as intravascular stents or bypass grafts, or bleeding due to internal iliac artery
pseudoaneurysm, can cause lumbosacral plexopathy. The symptoms of
lumbosacral plexopathy related to vascular diseases or procedures consist of acute

20
onset of unilateral pain in the lower back or flank followed by motor weakness in
the ipsilateral lower limb.21

Imaging
MRI with gadolinium contrast is the best test for the evaluation of the LS
plexus. When there are contraindications to MRI like noncompatible pacemaker,
a computed tomography (CT) scan with contrast can be utilized. MR neurography
is a useful modality compared to traditional MRI in LS plexopathy evaluation.
Neurography helps identify extraspinal injuries responsible for neuropathic leg
pain.19

21
Figure 4. MR imaging appearance of the normal sacral plexus26.

Figure 5. A xial T1-weighted (A) and STIR (B) images through the midportion of
the thigh show the appearance of an abnomal sciatic nerve (arrows).26

In cases of malignancy, it can be challenging to differentiate direct

compression from metastatic disease. Thus advanced imaging is often needed.
MRI is often ordered for the initial evaluation of neoplasm-associated LS
plexopathy. Positron emission tomography (PET) is to determine the full extent of
malignancy. It also helps in the staging of the disease and subsequent treatment
and prognosis. In cases in which the clinical examination does not reveal the
cause of a neuropathy, MR imaging may identify a focal or diffuse nerve
abnormality that may indicate a structural abnormality, such as may be seen with

hereditary hypertrophic neuropathies or an inflammatory pseudotumor of the

nerve. Demonstration of a normal-appearing nerve is also useful because it
narrows the differential diagnosis and may obviate interventional therapy. Not
uncommonly, patients who undergo MR imaging for unexplained plexopathy will
have idiopathic, probably postviral, inflammatory conditions, such as brachial or
lumbosacral plexitis (neuritis).26

Diagnosis
Usually the presence of a lumbosacral plexopathy can be suspected based
on clinical history and neurologic examination. A detailed clinical history and

22
physical examination are crucial for the diagnosis of LS plexopathy. Patients
typically present with low back pain radiating to one side. Pain may be positional,
worse in a supine position. Patients with diabetic LS plexopathy (diabetic
amyotrophy) typically complain of unilateral pain in the proximal thigh. Pain may
be associated with numbness, paresthesias, or dysesthesias of the lower limbs.
These symptoms are usually unilateral. LS plexopathy secondary to radiotherapy
is usually painless. The duration of symptoms may vary from very acute (after
road traffic accident) to chronic (after radiotherapy). In severe cases, muscle
weakness and atrophy may occur. Sphincter disturbances are rare and their
presence should suspect cauda equine syndrome. Fever, chills, night sweats,
fatigue, and weight loss may suggest malignancy or infection. A history of a road
traffic accident, abdominopelvic neoplasm, radiotherapy, abdominal surgery,
diabetes mellitus, bleeding disorders, or recent pregnancy hints towards LS
plexopathy and narrows down the etiology.19
Physical examination may be normal in mild cases. Bruises may be seen in
cases of trauma. A straight leg raise test is positive in more than half of the
patients. Asymmetric lower limb muscle weakness may be seen with
asymmetrically absent or reduced deep tendon reflexes. Knee jerk reflex is
affected in lumbar plexopathy and ankle jerk is affected in sacral plexopathy.
Muscle weakness in hip flexion, knee extension, or adduction suggests a possible
injury to the lumbar plexus. Sensory loss may be present in a dermatomal pattern
in cases of proximal LS plexopathy involving the roots, or in the nerve
distribution. Sensory changes to the medial thigh, anterior thigh, and medial leg
can suggest lumbar plexus involvement; posterior thigh, dorsum of the foot, and
perineum are likely related to sacral plexus involvement. Spinal point tenderness
may be present, especially in cases of sacral fracture or infection. A rectal exam
should be performed to assess rectal tone. Saddle anesthesia and bowel or bladder
incontinence are rare and may be present, making it difficult to differentiate from
cauda equina and conus medullaris syndromes. The inguinal region should also be
palpated for suspected hematomas.19

23
 Accurate localization of lumbosacral plexopathy requires an
electrophysiologic study. The electrophysiologic definition of a lumbosacral
plexopathy is involvement of muscles from at least two lumbosacral root levels
from at least two peripheral nerves. In a pure lumbosacral plexopathy, fibrillation
potentials of the lumbosacral paraspinal muscles are not present, whereas in a
lumbosacral radiculoplexus neuropathy, fibrillation potentials in paraspinal
muscles are present. An electrophysiologic study usually helps differentiate
lumbosacral plexopathy from a more common lumbar radiculopathy, where with
the latter the sensory conduction studies are normal and paraspinal denervation is
usually present.21
Neuroimaging studies, in particular MRI, of the lumbosacral plexus are of
diagnostic importance, particularly when a suspicion of neoplasm,6 traumatic
injury, or compression of the lumbosacral plexus exists. In diabetic lumbosacral
radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, or
postsurgical inflammatory neuropathy causing lumbosacral plexopathy, an MRI
of the lumbosacral plexus may show abnormal images with increased T2 signal in
short time inversion recov ery (STIR) of the involved plexus or a normal
result.27,28
MRI of the lumbosacral plexus is useful for looking for masses or tumors,
such as in perineurioma, sarcoidosis, local malignancies, malignancies through
perineural spread, or amyloidosis. MRI of the lumbosacral plexus is also of value
in distinguishing neoplastic from radiation-induced lumbosacral plexopathy.28,29
A sensory nerve (saphenous, superficial fibular [peroneal], or sural) taken
distally, or targeted fascicular (often sciatic) nerve biopsy taken from the site of
imaging abnormality, is sometimes useful in the diagnosis of lumbosacral
plexopathies, especially when an inflammatory cause (microvasculitis in diabetic
lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy,
or postsurgical inflammatory neuropathy) is suspected. A targeted fascicular nerve
biopsy in selected cases may be mandatory to the diagnosis of the other causes of
lumbosacral plexopathy, such as malignancies, lymphoma, sarcoidosis, or
amyloidosis.21

24
 In cases of inflammatory lumbosacral plexopathy (diabetic lumbosacral
radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, and
postsurgical inflammatory neuropathy), blood tests such as serologic studies or
inflammatory markers are usually nondiagnostic but occasionally may be mildly
positive. CSF is very important in the evaluation of most lumbosacral
plexopathies. In inflammatory lumbosacral plexopathy (diabetic lumbosacral
radiculoplexus neuropathy and lumbosacral radiculoplexus neuropathy), protein is
elevated without elevation of the white cells. In lumbosacral plexopathy from
sarcoidosis, cell count and protein are elevated, and in lumbosacral plexopathy
from lymphoma, cytology may confirm the malignancy.21

Treatment
Treatment of lumbosacral plexopathy is targeted depends upon the
underlying etiology even though pain management and physical therapy remain
the main- stay in many types of lumbosacral plexopathy as pain is usually severe
and causes significant morbidity. The treatment and prognosis of neoplastic
lumbosacral plexopathy depend on the underlying neoplasm. The treatment is
divided into Non surgical and surgical.19
Non Surgical
Symptomatic management with analgesics and muscle relaxants is given.
Analgesics include non-steroidal anti-inflammatory drugs (NSAIDs),
corticosteroid, pregabalin, gabapentin, duloxetine, amitriptyline, and opioids.
Ankle-foot orthoses (AFOs) can be used for the foot drop. Appropriate antibiotics
and antifungals are required for the infection. Diabetic amyotrophy is a transient
condition that usually resolves with good glycemic control. Neuropathic pain
treatments are advised for symptomatic management. In severe unremitting cases,
steroids, intravenous immunoglobulin (IVIG), cyclophosphamide, and even
plasma exchange may be tried.30

In an open trial of IV methylprednisolone in lumbosacral radiculoplexus

neu- ropathy, all patients had improvement on neurologic examination. The dose
and type of corticosteroid varies in practice study. The often use a dose of 1 g of

25
IV methylprednisolone weekly for 12 weeks.31 IV immunoglobulin or plasma
exchange can be considered but have fewer supportive. Immunotherapy should be
reserved for patients thought to be clinically worsening or at least not improving,
particularly when they are evaluated early in the course of disease.21

Radiation plexopathy can often present without pain, only weakness and
sensory changes. Unlike other types of plexopathy, it is usually bilateral and can
occur even years after radiation. There are no known treatments for radiation-
induced plexopathy. Physiotherapy and rehabilitation are the mainstays of
treatment. Further radiotherapy sessions should be discontinued.32

Surgical
In cases of malignancy, the primary tumor should be removed and
accordingly managed. In severe symptomatic cases, a dorsal rhizotomy may be
considered. Rhizotomy was shown to cause a significant reduction in pain and
opioid usage in this population.33 This treatment method is primarily used for
terminal patients. Surgical nerve repair techniques and nerve grafting have helped
improve muscle function in pelvic fractures. 21 The lumbar plexus was reached
through a lateral retro- peritoneal approach and the sacral plexus through the
lower abdomen and peritoneum. The lumbar and sacral roots were exposed
through a standard lumbosacral laminectomy and the origin of the sciatic and the
gluteal nerves were reached by detaching the gluteus maximus either laterally or
medially.34

The most difficult and risky injuries to repair are the intrapelvic lesions of
the sacral plexus. Sedel suggested a transiliac approach with a comfortable view
of the whole lumbosacral plexus after an osteotomy. Another possibility to
explore the sacral plexus and the sciatic nerve at its point of exit from the pelvis is
via a dorsal transsacral approach.35 This approach allows bypass grafts with a
maximal length of 15 cm (L4–5) and a minimal length of 6 cm (S-3). When the
distal stumps of the lumbosacral plexus slide through the foramina to the front of
the sacroiliac area they are dif- ficult to retrieve. An intrapelvic exploration to
retrieve distal stumps has a poor chance of success and the risk is high. A

26
reconnection of the intradural proximal stump with a sural nerve graft to a more
distal part of the nerve or to the sciatic nerve outside the pelvis is recommended in
such cases.36

In the present study new surgical strategies have been developed to reach
inaccessible intrapelvic and intraspinal lesions. A surgical strategy for intraspinal
brachial plexus lesions has been described. In a series of animal experiments it
was demonstrated that functional deficits from ventral root avulsion from the
spinal cord could be corrected by replanting the avulsed root into the spinal cord.
Restored useful function has been reported in patients when reconnection of
avulsed brachial plexus ventral roots to the spinal cord was performed. This
recovery depends on an initial regrowth of new nerve fibers through the central
nervous tissue within the spinal cord. An intraspinal lesion sustained in a
lumbosacral plexus injury is favorable regarding the ventral roots as this injury
occurs within the peripheral nervous system where regeneration and restora- tion
of function is predictable.34

Indication for surgery within the 1st weeks after injury was clear evidence
of a severe lesion, usually with displaced pelvic or lumbosacral spinal fractures.
Plexus reconstruction was performed if possible at the same time as the surgery to
repair the fracture(s). In less severe trauma cases when a neurotmesis could not be
verified or was less probable, that is, a “patchy” neurological deficit or early signs
of recovery, the treatment was initially conservative. When reinnervation did not
occur within 3 to 4 months surgical exploration was then performed. Due to late
referral to our institutions some patients underwent surgery several months after
their injury occurred.21,34 One small study of 10 patients experiencing traumatic
lumbosacral plexopathy, who underwent nerve grafting showed significant
improvement of muscle function at 38 months follow-up.37

Prognosis
Prognosis depends upon the underlying etiology, its response to treatment,
and the timing of therapeutic intervention. Prognosis is good for patients with LS
plexopathy secondary to pregnancy, retroperitoneal hematoma, and diabetic

27
amyotrophy. The majority of patients with pregnancy-related LS plexopathy have
a complete resolution of their symptoms two to six months following delivery.32,38
Progressive neurological deterioration is common in patients with
lumbosacral plexopathy secondary to malignancy. Prognosis is abysmal in
neoplastic instances, with a mean survival of six months. Lymphoma has
demonstrated to be the most responsive tumor to therapy. At 42 month follow-up,
86% of patients diagnosed with LS plexopathy secondary to malignancy had
died.39
Traumatic LS plexopathies are generally considered to have an
unfavorable prognosis but a case-series of 72 patients with traumatic LS
plexopathies demonstrated that more than two-thirds (about 70%) of patients
recovered spontaneously within 18 months.40,41

Complication

Painful lumbosacral plexopathy quite often occurs with certain neuroinfec

tions (herpes simplex and varicella zoster). most common neural symptoms of
Lyme borreliosis, in the form of meningoradiculitis (Bannwarth syndrome). In
this form, the roots are afflicted already in the spinal canal. It is clinically
manifested as meningeal irritation, painful radiculopathy (with both lumbar and
thoracic localization). Paresis is usually severe. After alleviation of pain, gradual
regression of paresis occurs. There is occurrence of mononuclear pleocytosis and
high blood protein, sometimes only with g-globulins. A spontaneous activity
(fibrillation) is noted in the paraspinal muscles. The basic diagnostic method is
detection of antibodies in serum and CSF (first immunoglobulin M enzyme-linked
immunosorbent assay testing and then polymerase chain reaction). Painful
idiopathic LSP afflicts lumbar plexus predomi- nantly, although sacral plexopathy
or complete LSP might also occur, albeit rarely. It is a monophasic disease,
whereas relapses and continuous progression are exceptional.42

For a number of years, radio-chemotherapy has been a treatment of choice

in cervical cancer patients, starting from stage IB2. Radiation induced

28
 Lumbosacral plexophaty (RILP) is a rare but severe complication, its frequency
ranges from 0.3 % to 1.3 %; it is characterized by a latent period between
radiation exposure and the development of symptoms, according to data from the
literature, it may take even 30 years from the end of radiotherapy to occurrence of
neurological symptoms.43

Conclusion

Many pathophysiologic processes, such as neoplastic, traumatic, infec-

tious, radiation, and inflammatory/microvasculitic processes, can affect the
lumbosacral plexus causing lumbosacral plexopathy. The clinical symptoms and
signs depend on the part of the plexus involved and the temporal course.
Management depends on the cause of the lumbosacral plexopathy. Many cases of
lumbosacral plexopathy previously thought to be idiopathic have been shown to
be caused by ischemic injury from microvasculitis; despite lack of evidence for
efficacy in improving neurologic deficits, the authors of this article include
immunotherapy in their management of patients with this condition.

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33