Plexopathy is a disorder affecting nerve networks like the brachial or lumbosacral plexus. Symptoms include pain, motor control loss, and sensory deficits. It is usually caused by localized trauma or compression. Brachial plexopathy specifically affects the network of nerves from the cervical spine to the shoulder, arm, and hand. Lumbosacral plexopathy affects the network of nerves from the lumbar spine and sacral spine. Diabetic plexopathy commonly affects the lumbosacral plexus and causes anterior thigh pain and proximal leg muscle weakness.

2. Plexopathy is a disorder affecting a network of
nerves, blood vessels, or lymph vessels.
The region of nerves it affects are at the brachial
or lumbosacral plexus.
Symptoms include pain, loss of motor
control, and sensory deficits.

3. There are two main types of plexopathy; Brachial plexopathy and
Lumbosacral Plexopathy. They are usually caused from some sort of
localized trauma such as a dislocated shoulder. The disorder can also
be caused secondary to a compression, co-morbid vascular disease,
infection, or may be idiopathic with an unknown cause.

5. The brachial plexus is a
network of nerves that
conducts signals from the
spinal cord, which is
housed in the spinal canal
of the vertebral column (or
spine), to the shoulder, arm
and hand.
These nerves originate in
the fifth, sixth, seventh and
eighth cervical (C5-C8), and Diagram illustrates basic anatomy of
first thoracic (T1) spinal brachial plexus. Brachial plexus is
nerves, and innervate the formed by anterior rami of C5-T1 nerve
muscles and skin of the roots. Roots are located in neural
foramina and trunks between scalene
chest, shoulder, arm and
muscles. Divisions are posterior to
hand. clavicle, and cords are inferior to it. LC
Brachial plexus injuries, or = lateral cord, PC = posterior cord, MC
lesions, are caused by = middle cord.
damage to those nerves.

6. Brachial plexus injuries, or lesions, can occur as a result of
shoulder trauma, tumours, or inflammation. The rare
Parsonage-Turner Syndrome causes brachial plexus
inflammation without obvious injury, but with nevertheless
disabling symptoms. But in general, brachial plexus lesions
can be classified as:
i) Obstetric injuries may occur from mechanical injury involving shoulder
dystocia during difficult childbirth.
The baby's shoulders may become impacted during the birth process
causing the brachial plexus nerves to stretch or tear.
The excessive stretch results in incomplete sensory and/or motor function
of the injured nerve.
ii) Traumatic injury may arise from several causes.
(Sports, high-velocity motor vehicle accidents, falls from a height on to the
side of the head and shoulder, whereby the nerves of the plexus are
violently stretched, injury from a direct blow to the lateral side of the
scapula, direct violence or gunshot wounds, by violent traction on the arm,
or by efforts at reducing a dislocation of the shoulder joint“)

7. Causes
In most cases the nerve roots are stretched or torn
from their origin, since the meningeal coverings of
the nerve roots are thinner than the sheaths enclosing
the peripheral nerves. The epineurium of the
peripheral nerve is contiguous with the dura
mater, providing extra support to the peripheral
nerves.
Brachial plexus lesions typically result from
•excessive stretching;
•rupture injury where the nerve is torn but not at the
spinal cord;
•avulsion injuries, where the nerve is torn from its
attachment at the spinal cord.
•build-up of scar tissue around a brachial plexus
injury site (put pressure on the injured
nerve, disrupting innervation of the muscles)

8. Brachial plexus lesions can be divided into two types:
1) An upper brachial plexus lesion, which occurs from
excessive lateral neck flexion away from the shoulder. Most
commonly, falling on the neck at an angle causes upper
plexus lesions leading to Erb's palsy. This type of injury
produces a very characteristic sign called Waiter's tip deformity
due to loss of the lateral rotators of the shoulder, arm flexors,
and hand extensor muscles.
2) Much less frequently, sudden upward pulling on an abducted
arm (as when someone breaks a fall by grasping a tree branch)
produces a lower brachial plexus lesion, in which the eighth
cervical (C8) and first thoracic (T1) nerves are injured "either
before or after they have joined to form the lower trunk. The
subsequent paralysis affects, principally, the intrinsic muscles
of the hand and the flexors of the wrist and fingers". This
results in a form of paralysis known as Klumpke's paralysis.

9. Injury Classification
The severity of brachial plexus injury is determined by the type of
nerve damage.There are several different classification systems
for grading the severity of peripheral nerve and brachial plexus
injuries. Most systems attempt to correlate the degree of injury
with symptoms, pathology and prognosis.
A more recent and commonly used system described by the late
Sir Sydney Sunderland, divides nerve injuries into five degrees:
•first degree or neurapraxia, following on from Seddon, in which
the insulation around the nerve called myelin is damaged but the
nerve itself is spared,
•second through fifth degree, which denotes increasing severity
of injury
•fifth degree injuries, the nerve is completely divided

10. Seddon's classification (based on three main types of nerve fiber
injury, and whether there is continuity of the nerve)
1) Neurapraxia: The mildest form of nerve injury. It involves an
interruption of the nerve conduction without loss of continuity of the
axon. Recovery takes place without wallerian degeneration.
2) Axonotmesis: Involves axonal degeneration, with loss of the relative
continuity of the axon and its covering of myelin, but preservation of
the connective tissue framework of the nerve (the encapsulating
tissue, the epineurium and perineurium, are preserved).
3) Neurotmesis: The most severe form of nerve injury, in which the
nerve is completely disrupted by contusion, traction or laceration. Not
only the axon, but the encapsulating connective tissue lose their
continuity. The most extreme degree of neurotmesis is
transsection, although most neurotmetic injuries do not produce gross
loss of continuity of the nerve but rather, internal disruption of the
nerve architecture sufficient to involve perineurium and
endoneurium as well as axons and their covering. It requires
surgery, with unpredictable recovery.

11. Presentation (Signs and Symptoms)
Signs and Symptoms may include a limp or paralyzed arm, lack of
muscle control in the arm, hand, or wrist, and lack of feeling or sensation
in the arm or hand. Although several mechanisms account for brachial
plexus injuries, the most common is nerve compression or stretch. The
most severe form of injury is nerve root avulsion, which results in
complete weakness in corresponding muscles. This usually accompanies
high-velocity impacts that occurs during motor vehicle or bicycle
accidents.
The cardinal signs of brachial plexus injury then, are weakness in the arm,
diminished reflexes, and corresponding sensory deficits.
Erb's palsy. "The position of the limb, under such conditions, is characteristic: the
arm hangs by the side and is rotated medially; the forearm is extended and
pronated. The arm cannot be raised from the side; all power of flexion of the elbow
is lost, as is also supination of the forearm".
In Klumpke's paralysis, a form of paralysis involving the muscles of the forearm
and hand, a characteristic sign is the clawed hand, due to loss of function of the
ulnar nerve and the intrinsic muscles of the hand it supplies.

13. Diagnosis
The diagnosis may be
confirmed by an EMG
examination in 5 to 7
days. The evidence of
denervation will be
evident. If there is no
nerve conduction 72
hours after the
injury, then avulsion is
most likely.

14. Treatment
Treatment for brachial plexus injuries includes occupational or
physical therapy and, in some cases, surgery. Some brachial
plexus injuries may heal without treatment.
Many infants improve or recover within 6 months, but those that
do not have a very poor outlook and will need further surgery to
try to compensate for the nerve deficits. The ability to bend the
elbow (biceps function) by the third month of life is considered an
indicator of probable recovery, with additional upward
movement of the wrist, as well as straightening of thumb and
fingers an even stronger indicator of excellent spontaneous
improvement.
Gentle range of motion exercises performed by
parents, accompanied by repeated examinations by a
physician, may be all that is necessary for patients with strong
indicators of recovery.

15. Prognosis
The site and type of brachial plexus injury
determine the prognosis. Avulsion and rupture
injuries require timely surgical intervention for any
chance of recovery. For milder injuries involving
build-up of scar tissue and for neurapraxia, the
potential for improvement varies, but there is a fair
prognosis for spontaneous recovery, with a 90 -
100% return of function.

17. The anterior divisions of the lumbar nerve, sacral nerve, and
coccygeal nerves form the lumbosacral plexus, the first
lumbar nerve being frequently joined by a branch from the
twelfth thoracic.
For descriptive purposes this plexus is usually divided into
three parts:
1. lumbar plexus
2. sacral plexus
3. pudendal plexus

19. The lumbosacral plexus is
situated within the relative
protection of the axial
skeleton, making blunt trauma
a relatively uncommon cause
of injury. The most common
causes of a lumbosacral
plexopathy are usually by
direct compression, diabetic
neuropathy, complications of
pelvic surgery, or parturition.
Separating a plexopathy from
other neurological effects of
other spinal-related problems
is often a diagnostic challenge.

20. Diabetic plexopathy
Diabetic plexopathy typically affects the lumbosacral plexus more than a
brachial. It is distinguished from a peripheral polyneuropathy of long-
standing diabetes by its predominantly proximal symptoms. The majority
of patients are in their sixth and seventh decade and also have documented
distal peripheral polyneuropathy. Most frequent clinical presentation of a
diabetic lumbosacral plexopathy is anterior thigh pain, with secondary
proximal leg muscle weakness. The muscle weakness is most pronounced
in the quadriceps muscles. Sensory loss is generally less pronounced,
although patellar reflexes typically are absent or sluggish. With
progression, noticeable muscle wasting occurs, resulting in significant
atrophy and weight loss. There is a trend for progression from unilateral to
bilateral lower-extremity involvement.
Diagnosis is therefore based on presentation, presence of diabetes, and the
presence of acute electrodiagnostic findings to be discussed later.
Therapy is ultimately focused on the control of the hyperglycemia. Most
patients who achieve glucose control typically have significant, but
incomplete, recovery of muscle strength. Maximal improvement can
require more than one year. After control of the hyperglycemia,
rehabilitation strategies address pain management, maintenance of range of
motion, and compensatory mechanisms for knee extensor weakness.

21. Traumatic Plexopathy
Traumatic plexopathy of the lumbosacral plexus typically must be
sufficient to produce an unstable, vertical fracture of the pelvic
region since the plexus is other-vise well protected from direct
impact. Fractures to the sacroiliac joint usually involve the
intralateral lumbosacral trunk with impairment clinically seen at the
L5 and S1 levels. Fractures or dislocations of the hip joint can
produce traction injuries to the lumbosacral plexus. Treatment:
Surgical intervention is imminent and requires initial periods of
immobilization post-operatively. The initial lesions can slowly
recover during the post-operative rehabilitation.
Prognosis: Poor recovery

22. Hemorrhagic Plexopathy
Hemorrhagic plexopathy is usually caused in the retroperitoneal
region, which can compress on the plexus as it passes through either the
iliac or psoas muscles. An expanding hematoma within the more
laterally located iliopsoas muscle can cause local compression of the
femoral nerve at the point along its course from its origin to the inguinal
ligament.
Clinical presentation:
1) Compression (Diffuse) in psoas muscle
Weakness: Obturator & femoral nerve territory
Pain: Mild or none
Mass: None palpable
2) Compression of femoral nerve in iliacus muscle
Pain: In groin or iliac fossa
Radiates to anteromedial thigh & medial lower leg
Weakness: Quadriceps
Sensory: Reduced in anteromedial thigh & saphenous distribution
Reflex loss: Knee
Mass: May be palpable in groin

23. Psoas hematoma (arrow): CT scan

24. Radiation-Induced Lumbosacral Plexopathy
Radiation-induced lumbosacral plexopathy is similar to that affecting the
brachial plexus. Onset is difficult to determine, occurring from one to 31
years after radiation. Patients receiving an external beam or internal cavity
radiation are equally susceptible. Patients generally present with slowly
progressive, bilateral lower extremity weakness that tends to affect the distal
muscles more. Paresthesia and numbness are less frequently reported in the
initial symptoms. Symptom progression can eventually stabilize. Patients are
usually severely disabled by that time. Therefore, early diagnosis or proper
follow up by the oncologist/family physician is essential.
Weakness: Distal legs
Latency: Months to years
Progression: Slow
Pain: Late; Not disabling
Cancer type: Gynecological; Testicular
Predisposing treatment : High radiation dose: > 55 Gy
Chemotherapy
NOT hormonal
Electrodiagnostic : EMG: Myokymia
NCV: Absent late reflexes
Imaging: Multifocal fibrosis

25. Iatrogenic trauma plexopathy
Iatrogenic trauma to the lumbosacral plexus can occur during
surgical, gynecological, or anesthetic procedures. The mechanisms include
compression, traction, and vascular insult. Proper clinical and electrodiagnostic
differentiation is important with such plexopathies since the prognosis depends
on the cause and location.
Surgical laceration injuries are rare, but among the most severe, since the
progress to recovery is not possible. It is most likely to occur during a deep
pelvic procedure, such as a prostatic resection or a hysterectomy.
Blunt trauma from surgical retraction or during forceps delivery is more
common. The femoral and obturator nerves are the most frequently injured. The
lumbosacral trunk, lateral cutaneous nerve, and the sciatic nerves follow.
Arthroplasty of the hip results in a significant number of
femoral, obturator, and sciatic injuries through direct trauma, stretch, or the
effects of heat from cement polymerization. The chiropractor may be more apt to
see such a plexopathy resulting from an epidural anesthesia procedure. An
epidural may cause a rectoperitoneal hemorrhage that may result in a
diffuse, extensive, and neuropathic injury.
Another rare cause of iatrogenic lumbar plexopathy may be due to a pre-
existing atherosclerosis, intraoperative hypotension, or coagulopathy, which
may initiate a spinal artery syndrome. A spinal artery syndrome should always
be considered in the case of unexplained postoperative weakness, particularly in
the elderly population.

26. Neoplastic Plexopathy
Neoplastic plexopathy lesions originating in the pubic regions can
invade the lumbosacral plexus by direct expansion. The most
common is a colorectal carcinoma. However, uterine, prostatic, and
ovarian tumors can be locally invasive as well. Metastatic invasions
of the retroperitoneum and the lumbosacral plexus by breast,
thyroid, testicular cancers, lymphomas, myelomas, and melanomas
are also well known. Patients with neurofibromatosis can develop
grossly huge tumors involving any compartment of the plexus.
Neoplastic plexopathies generally present with unilateral pelvic pain
and, when progressive, show lower motor neuron signs. Weakness:
Proximal
Unilateral; Asymmetric
Progression: Rapid
Pain: Often severe
Mass: Palpable rectal
Cancer type: Colon; Prostate; Sarcoma
Imaging: Focal mass

27. Extrinsic tumor. STIR MR image in a patient with carcinoma of the cervix
showing an extensive soft tissue mass surrounding and infiltrating the entire
pelvis and the sacral plexus bilaterally (arrow) that is enlarged with loss of fat
planes and normal fascicular architecture. Note the hyperintense signal
consistent with extensive marrow infiltration by the mass lesion.

28. Immune (vasculopathy) plexopathy
Onset: Late-age
Clinical features : Sensory Pain: Variable; Occasionally severe
Sensory Loss: Distal; Often asymmetric
Weakness : Asymmetric,
Proximal, Distal or Both
Bilateral
Course: Progression over weeks to months
Association: Diabetes
Laboratory : EMG: Denervation in limbs & paraspinous muscles
Nerve biopsy
Inflammatory cells around small epineurial blood vessels
Differential fascicular loss of axons
High sedimentation rate
Prognosis: Recovery with treatment
Over months to years
Treatment: Corticosteroids
Intravenous Ig

29. Ischemic Lumbosacral plexopathy
Blood supply of lumbar & sacral plexus: Branches of the internal iliac artery
Clinical: Symptoms & Signs mostly after exercise
Exacerbated walking uphill
No effect of bicycle exercise
Distribution: Unilateral or bilateral
Exercise provocation: Walking uphill; Riding a bicycle
Examination at rest often normal
Sensory Pain: Gluteal region after exercise; 85% Paresthesias
Sensory Loss: Pan-modal; Not dermatomal; Distal or Proximal
Weakness: Distal ± Proximal Leg
Tendon reflexes: May be reduced after exercise
Electrodiagnostic: EMG & NCV often normal
Pelvic arteriography
Bilateral stenoses of the internal iliac arteries (75%)
Other stenosis
Distal abdominal aorta + bilateral common iliac artery
Ipsilateral internal & common iliac artery
Treatment: Percutaneous transluminal angioplasty; Stents

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