PLEXOPATHIESBy:

Stacy Arvinna Binti JamarunGroup 3

4th Year 1st Sem

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.

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.

BRACHIALPLEXOPATH

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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 first thoracic (T1) spinal nerves, and innervate the muscles and skin of the chest, shoulder, arm and hand.

Brachial plexus injuries, or lesions, are caused by damage to those nerves.

Diagram illustrates basic anatomy of brachial plexus. Brachial plexus is formed by anterior rami of C5-T1 nerve roots. Roots are located in neural foramina and trunks between scalene muscles. Divisions are posterior to clavicle, and cords are inferior to it. LC = lateral cord, PC = posterior cord, MC = middle cord.

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“)

CausesIn 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)

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.

Injury ClassificationThe 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

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.

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.

DiagnosisThe 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.

TreatmentTreatment 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.

PrognosisThe 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.

LUMBOSACRALPLEXOPATHY

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 plexus2. sacral plexus3. pudendal plexus

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.

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.

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

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

Psoas hematoma (arrow): CT scan

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

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.

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

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.

Immune (vasculopathy) plexopathyOnset: 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

Ischemic Lumbosacral plexopathyBlood 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

THANK YOUFOR YOUR ATTENTION

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