This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
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Neurologic signs of lumbosacral plexus injuries consist of motor deficit with flaccid paralysis associated with sensory deficits to all types of stimulation in the territory of the damaged nerve roots: a lower motor neuron paralysis. Nonstructural causes include radiation therapy, diabetes, vasculitis, and perivasculitis. Traumatic causes are mainly due to fractures of the pelvic ring or acetabulum and hip joint replacements. In this article, the authors provide a systemic review of lumbosacral plexus injuries from the published literature. They have included background information about the historical notes, clinical manifestations, etiology, epidemiology, pathogenesis and pathophysiology, prevention, differential diagnosis, diagnostic work-up, prognosis and complications, and management. In this update, the authors added discussion of the preventive measures that can be considered during spine surgery to lower the risk of lumbar plexus injury.
• Symptoms of lumbosacral plexus injury include varying degrees of lower extremity weakness, sensation changes, pain, and diminished reflexes.
• Most lumbosacral plexopathies due to trauma are from very violent injuries, such as automobile-pedestrian accidents, high-speed car accidents, or falls from heights, and are often associated with damage to internal organs, blood vessels, and bony structures, especially the pelvic ring.
• CT for evaluation of bony injuries, MRI, and EMG/NCS are important diagnostic tools.
• Because most traumatic plexopathies improve spontaneously, at least to some extent, they usually are treated conservatively, but when surgical repair is attempted, it tends to yield better results.
Involvement of the lumbosacral plexus appears in history in its congenital form, most often described as myelomeningocele. Hippocrates and Arabic physicians described this condition with its devastating clinical problems. Aristotle proposed infanticide to resolve this social problem. Even with modern technological advances, lumbosacral plexus injury is not easy to describe. Books on the subject of trauma make only a brief mention of this entity (22).
The lumbosacral plexus comprises 2 distinct portions: the lumbar plexus and the sacral plexus, each innervating a different part of the lower limb. The lumbar plexus connects with the sacral plexus via the lumbosacral cord. The lumbar plexus is formed by the ventral primary rami of L1-3 with contributions from the ventral rami of L4 and T12, which separates into anterior and posterior divisions. The lumbosacral plexus sends muscular branches to the quadratus lumburom (T12, L1-4), psoas minor (L1), psoas major (L2-3), and iliacus (L2-3). The anterior rami (L2-4) form the obturator nerve that innervates the adductor muscles of the thigh and the skin of the medial thigh. The posterior rami (L2-4) form the femoral nerve, which innervates the quadriceps femoris muscle, the anterior thigh, and the medial side of the leg via medial and intermediate cutaneous nerves of the thigh and saphenous nerves, respectively. The predominantly sensory iliohypogastric (L1), ilioinguinal (L1), genitofemoral (L1-2), and lateral cutaneous nerve of the thigh (L2-3) also arise from lumbar plexus. The caudally located sacral plexus is formed by the lumbosacral cord (L4-5) and the ventral rami of S1-3 and part of S4. The main branch is the sciatic nerve (L4-5, S1-3), and its 3 main branches (the peroneal, tibial, and sural nerves) supply the hamstring muscles, all the muscles below the knee, and all the skin below the knee except the area supplied by the saphenous nerve. The superior gluteal nerve (L4-5, S1; innervates the gluteus medius and minimus), inferior gluteal nerve (L5, S1-2; innervates gluteus maximus), and the nerve to piriformis (S1-2) directly arise from the sacral plexus. The posterior femoral cutaneous (S1-3) and pudendal (S2-4) nerves also arise from sacral plexus.
Neurologic signs consist of lower motor neuron type and sensory deficits within the distribution of the damaged nerve roots or nerves arising from lumbosacral plexus. Pain is commonly present in the distribution of the sensory neural structures involved in the injury. Severe lower back or hip pain is the initial presenting complaint in patients with lumbosacral plexopathy caused by the neoplastic process. Muscle weakness and sensory deficits in these patients appear long after the initial pain symptoms. Although the symptoms of lumbosacral plexopathy linked to the vascular disease comprise of an acute onset of unilateral lower back or flank pain, they are soon followed by the weakness of the respective lower extremity (16). Recurrent hip subluxation has been purported to be a rare symptom of lumbosacral plexopathy. Kumar and colleagues have reported 2 cases of recurrent hip subluxation following fixation of acetabular fractures, which is thought to be a complication of lumbosacral plexopathy and associated inadequate hip muscle tension (29).
In routine neurologic examination, many injuries of the lumbosacral plexus are misdiagnosed as femoral nerve injuries, and many sacral plexus injuries as sciatic or common peroneal nerve injuries (47). Accurate localization to the lumbosacral roots, lumbosacral plexus, or nerves derived from the plexus, is extremely difficult in patients with pelvic bony injuries, which severely limits both motor and sensory exams. In postoperative cases, a high level of clinical suspicion is important in diagnosis because pain can be a major factor that limits accurate clinical localization. Differentiating root avulsion from compressive plexus injury can be difficult by cross-sectional clinical or electrodiagnostic testing. Good quality multiplanar imaging is helpful in the diagnosis of avulsion (19).
The peripheral nerve injury associated with pelvic fractures varies from simple neurapraxia through axonotmesis to neurotmesis, just like elsewhere in the body. Signs of spontaneous remission and of permanent disability have been described in the literature. Huittinen performed repeat examinations in a selected group of patients and did not find any signs of remission over an observation period of 1 to 5 years.
Traumatic lumbosacral plexus injuries are less common than brachial plexopathies. Traumatic closed injuries of the lumbosacral plexus are rare because of the high degree of protection provided by the surrounding muscle and bone and because the nerve fibers aren’t near highly mobile structures. Most lumbosacral plexopathies due to trauma are from very violent injuries such as auto-pedestrian accidents, high-speed car accidents, or falls from heights. Traumatic open injuries are less common than the closed type and are often due to gunshot and low-velocity puncture wounds (58). Both open and closed traumatic lumbosacral plexopathies are typically associated with damage to internal organs, blood vessels, and bony structures, especially the pelvic ring. The fractures of the posterolateral two thirds of the pelvis, which connects the trunk to the lower limbs and transmits weight, are often unstable and displaced, causing injury to the adjacent structures including the lumbosacral plexus. Sacral fractures, especially in transverse direction, increase the probability of associated intraspinal and intraforaminal injury to the nerve roots.
Traumatic causes are mainly due to fractures of the pelvic ring and acetabulum, dislocations of the sacroiliac joint, and hip joint replacements. The incidence of lumbosacral plexus injuries varies widely in different series and depends on the location, severity, and type of injury. One series reported neurologic injury secondary to severe pelvic fractures in 22% to 52% of patients. The main type of injury is lumbosacral plexus injury (49). Sugimoto and colleagues assessed risk factors for lumbosacral plexus injury that could be evaluated during the acute injury phase. They found that the incidence of lumbosacral plexus injury was higher when the patient had a longitudinal displacement (at least 10 mm) at the sacrum or sacroiliac joint, had a sacral transverse fracture, or had made a suicide attempt. Gunshot wounds are being described with increasing frequency, and they also have differences in the localization compared to motor vehicle accidents. The upper plexus is injured more often by gunshot wounds compared with motor vehicle accidents, probably due to the shielding effect of the pelvic bone protecting the lower plexus. The lower plexus is at high risk for injury from motor vehicle accidents and falls because these injuries result in fractures of the sacroiliac joint and sciatic notch. Chiou-Tan and colleagues reported that 90% of lumbosacral plexus injuries in their series were from motor vehicle accidents with involvement of 3 or more quadrants of the plexus, the lower quadrants being more affected (11).
Other structural causes include psoas muscle abscess; perirectal abscess (in HIV patients) (16); abdominal aortic aneurysms; common iliac artery aneurysms (05; 60); trauma; and infiltrative, metastatic, or compressive neoplasms. Iliopsoas hematoma can present as femoral neuropathy or even complete lumbar plexopathy (12). It can be secondary to coagulopathy (hemophilia or other disorders), anticoagulation, trauma, surgery, and other etiologies (56; 36; 39; 37). Also, Lee and colleagues described a case of right lumbosacral plexopathy, which was later found to have multiple intramural and subserosal uterine myomas that replaced the uterus (32). It was postulated that the large uterine myomatous lesions caused compressive injury to the lumbosacral plexus during prolonged anesthesia for knee surgery. The patient did improve clinically and electrodiagnostically after total hysterectomy.
In some patients with history of prostate cancer, the perineural spread along the lumbosacral plexus has been described based on anatomical relationships. The tumor cells invade the inferior hypogastric plexus around the prostate and spread to the lumbosacral plexus using the pelvic and sacral splanchnic nerves. From here, the perineural spread can extend distally to the arborizing nerves or proximally to the spinal nerves (03).
Capek and colleagues report a case of bilateral lumbosacral plexopathy in a patient with history of prostate cancer, which can be elucidated as the continuation of the same process (07). They advocate that transmedian dural spread allows the tumor cells to extend from 1 side of the body to the contralateral side.
Also rarely, endometriosis and extramedullary hematopoiesis affecting the lumbosacral plexus can occur (40). Paradoxical nodular hypertrophy of the sciatic nerve and lumbosacral plexus in young patients after lower-limb, above-knee amputations has been reported (40). Iatrogenic injury can be seen as a result of ischemia during vascular surgeries such as abdominal aortic aneurysm repairs. Aorto-iliac occlusive disease can rarely present as acute flaccid paraparesis due to lumbosacral plexopathy, which can be clinically confused with an acute cauda equine syndrome (09). The overall neurologic risk for abdominal aortic surgery ranges from 0% to 1% and includes central cord lesions as well as lumbosacral and peripheral nerve lesions (01; 14). Iatrogenic injuries are also observed following major gynecological pelvic operations, including embolization procedures for postpartum hemorrhage (38). Pelvic vessel embolization is a very rare cause of lumbosacral plexopathy. In this context, Rohilla and colleagues reported 2 rare cases that developed coexisting uterine necrosis and lumbosacral plexopathy after pelvic vessels embolization following postpartum hemorrhage (43). More common mechanisms are direct surgical trauma, stretch injury, suture entrapment, or retractor-related injury (08).
Anterior lumbar spine approach puts the lumbar plexus at risk. Lateral approach was used to avoid the neurologic injury. A cadaveric study of 18 specimens showed that even with the lateral approach, the lumbar plexus is still at risk at L4-L5 disc level due to the proximity of the neural elements to the disc (13). Similar conclusion was reached after a larger cadaveric study done by Guerin and colleagues showed that the anatomical relationships between the lumbar plexus and the intervertebral disc make the lateral approach particularly risky at L4-L5. Lumbar plexopathy has been reported as a complication of transforaminal interbody fusion (L5- S1) in patients with spondylolisthesis. If a patient develops symptoms that do not correlate well to the level of spinal surgery, then the possibility of plexopathy should be considered and appropriately investigated (28). Alternative techniques, such as posterior lumbar interbody fusion or anterior interbody fusion, should be used at this level (21). There is a case report by Tulloch and colleagues about contralateral lumbosacral plexopathy that developed 2 days after a lumbar microdiscectomy (52).
A typical syndrome of obstetric or intrapartum lumbosacral plexopathy occurs in relatively small primi gravida, when carrying a relatively large baby with prolonged labor, malpresentation, and midforceps rotation after transverse arrest. Typically pain is the initial symptom followed by motor symptoms, with foot drop being the most characteristic. Pain quickly resolves after delivery whereas motor features can be more persistent (18; 24).
Nonstructural causes include radiation therapy, diabetes, vasculitis, and perivasculitis. Radiation therapy can cause a relatively mild, reversible lumbosacral plexopathy within a few months of therapy or a severe delayed plexopathy. Delayed plexopathy presents with asymmetric bilateral lower extremity weakness with an L5-S1 predominance, atrophy, fasciculations, areflexia, and sensation changes in one-third of patients (15). Rarely postradiation plexopathy can present with predominant sensory symptoms such as severe pain and hyperesthesia. Komatsu and colleagues described a radiation-induced lumbosacral plexopathy patient who presented with severe burning pain and hyperesthesia (27). The patient was exposed to radiation for cervical cancer 17 years earlier.
Diabetic lumbosacral radiculoplexus neuropathy (DLRPN) affects approximately 1% of diabetics. DLRPN usually affects those with mild diabetes and presents as subacute, asymmetric proximal leg pain (17; 51). It is not the most common diabetic neuropathy, but it undoubtedly causes major suffering among those affected. An interesting fact is that many of these patients also have significant weight loss associated with the neuropathy. Diabetic lumbosacral plexopathy is a monophasic illness exacerbating for a few months, followed by slow recovery (16).
Another rare clinical entity is idiopathic lumbosacral plexopathy (ILSP), which is also known as lumbosacral plexitis. It typically starts with severe asymmetrical leg pain, and patients gradually develop weakness and atrophy of the muscles along with sensory disturbances, including paresthesias and hyperesthesia. Autonomic dysfunction can also be seen in some patients with idiopathic lumbosacral plexopathy. Pathology of distal cutaneous nerves is indicative of an inflammatory microvasculitis and ischemic damage of the nerves. The disease course is monophasic, lasting a few weeks to months; some patients improve gradually without any specific treatment, but recovery is often incomplete. There are no evidence-based recommendations for the treatment of idiopathic lumbosacral plexopathy (54).
Lumbosacral plexopathies, particularly those associated with trauma, are almost always due to axon injury or loss. Nerve fibers of all sizes are affected to a variable extent. Rarely, lumbosacral plexus lesions could be secondary to focal demyelination or conduction block, such as that seen with mild traction or intrapartum injuries.
The highest incidence of nerve damage has been reported with sacral fractures (22). Kutsy and colleagues have shown that sacral fractures have a significantly higher incidence of lumbosacral plexus injury compared to trauma patients in general (30). Chiodo reported that the typical neurologic injury in patients with pelvic trauma was a lumbosacral plexus injury, present in 71% of the cases in his retrospective study (10). Nerve lesions in acetabular fractures occur more often with multiple nerve involvements, rather than plexus injury itself, similar to a fracture of the femur (30). Nine of 10 patients with acetabular fractures in Chiodo’s study had sciatic nerve injuries (10). Histological examination of autopsied specimens by Huittinen confirmed traction injuries and compression injuries (22). The histology revealed intraneural, perineural, and epineural hemorrhages and ruptures of nerve fibers. Relating these autopsy findings, Huittinen postulated different mechanisms for the nerve injury. Sudden movement of a dislocated hemipelvis at the moment of injury places tension on the lumbosacral nerve trunks and secondarily tears the corresponding intradural roots. Indirect forces from the dislocated vertebrae also produce root rupture, as noted at autopsy by Huittinen. Because several forces act simultaneously with high-energy impact, it is difficult to evaluate the effect exerted on the lumbosacral roots by spinal injury at higher levels. A clear correlation between the type of skeletal injury and the occurrence of intradural lumbosacral root lesion may not exist.
Avulsion of the lumbar plexus results from abrupt traction on the nerve roots. In multitrauma cases, the mechanisms are varied and difficult to determine. Laterally rotated, hyperextended thigh or hyperflexion and abduction of the thigh with existent fractured pelvis can produce traction on the plexus. The primary mechanism of lumbosacral plexus injury in motor vehicle accidents is thought to be traction that usually recovers satisfactorily (47). Hematomas or displaced bone following trauma can also damage the plexus secondary to compression, but this is uncommonly reported (11). A correlation is seen in the occurrence of lumbosacral plexus injury and different types of pelvic fractures. The highest incidence of lumbosacral plexopathy was seen in unstable pelvic fractures completely disrupting the sacroiliac complex.
Sometimes traction injury to the plexus can occur following a hip joint replacement surgery. High velocity, high impact injuries may produce traction of the roots tearing the arachnoid and dura with leakage of CSF into the surrounding tissue planes, resulting in a pseudomeningocele. The posttraumatic pseudomeningocele forms in 2 stages. Stage 1 has torn meninges and a collection of cerebrospinal fluid in the perispinal tissues maintained by continued leakage. In the second stage, the arachnoid sheath is fragile and expands as the fluid collection increases; it compresses or erodes into the vertebral body or the intervertebral foramina.
In intrapartum injuries, the lumbosacral cord, and sometimes the superior gluteal and obturator nerves, is compressed at the pelvic brim after protracted, cephalopelvic disproportion or midpelvic forceps delivery (40; 58). The pathophysiology of these lesions is demyelinating conduction block with variable degrees of axonal injury.
Lumbosacral plexus injury can also occur from malignant processes due to direct spread of the primary tumor enveloping the plexus and metastatic deposits in the surrounding structures and by deposits to the plexus itself (40). Presacral recurrence of colon cancer has been reported to cause plexopathy by the involvement of lumbosacral plexus, which can be confused with degenerative spine disease (23). Vascular malformations, such as aneurysmal dilatation of the distal aorta and the iliac arteries, can also compress the lumbosacral plexus in addition to being the source of ischemic nerve injury.
Patients with lumbosacral nerve injury are typically young and have usually sustained a violent injury in a road traffic accident (33). Wilbourn suggests that nontraumatic causes, especially neoplasms, are the most common causes of lumbosacral plexopathies (58). This was demonstrated in a report of 86 cases of lumbar plexopathies in which less than 6% were due to trauma, but more than 50% were due to neoplasms (35). Many posttraumatic cases remain undiagnosed due to the high mortality of the multitrauma patients. This is especially true in patients with pelvic trauma, who may have an incomplete work-up to diagnose the injury to the pelvic nerves. Huittinen performed an autopsy study on 42 cases of fatal trauma and reported that 20 out of 42 (48%) sustained lumbosacral plexus injury (22). Kutsy and colleagues found that 0.7% of almost 3000 patients with pelvic and acetabular fractures developed lumbosacral plexus injury, identical to the report by Lam in 1936, with a 0.75% occurrence of nerve injuries among 1,889 patients with pelvic fractures (30).
Stoehr expressed that complete, or more often an incomplete, paresis of lumbosacral plexus occurs more frequently than commonly believed after an operation or trauma (47). A 9% incidence of lumbosacral plexus injury in fractures of the pelvis is recorded by Lam (31), and Patterson and Morton estimated a 3.5% incidence of neurologic complications in fractures of the pelvis (22). Statistics from Finland disclosed a 9% to 12% incidence of lumbosacral nerve injury in patients with fractures of the pelvis.
The incidence of intrapartum lumbosacral plexopathy may be as high as 1 in 2000 deliveries (18). A retrospective survey of over 6000 women following delivery of a live-born infant showed 0.92% incidence for new nerve injury (59). The authors discussed the direct relation between the duration of prolonged second-stage labor and the incidents. Some patients have reported lumbosacral plexus injuries following major gynecological pelvic operations as well. A retrospective review of 1210 patients over 6 years noted that 1.9% of patients develop postoperative neuropathy (08).
An extensive study from Louisiana State University in New Orleans reviewed 119 surgically treated femoral nerve lesions in intrapelvic and high-thigh regions from 1967 to 2000 (25). The most common cause was iatrogenic (44%) from medical procedures followed by traumatic etiology (31%). Thirty cases represented tumor or cystic lesions. Most of the patients did well with neurolysis and grafts.
The best method of prevention is control of the etiological factors. The motor vehicular crash injuries and gun-related violence may decrease with proper preventive public awareness campaigning. Most iatrogenic injuries can be avoided by acknowledging the possibility of these injuries, while managing pelvic injuries and trauma to and around the hip joint. Manipulation of pelvic injuries with traction must be carried out with proper neurologic assessment at all times. In a high-risk obstetric population, preventive measures must be offered in terms of releasing incisions (episiotomy) or properly timed cesarean section (18). Prevention by careful positioning on the operating table, avoidance of retractor pressure or stretching and anatomically sensitive incision and suture techniques will reduce the risk of injury for the most part. The best preventive measure for a surgical complication is the thorough knowledge of anatomical relationships and careful execution. An anatomical cadaver study demonstrated courses of iliohypogastric and ilioinguinal nerves to map from their lateral emergence on the anterior abdominal wall to their midline termination in reference to fixed bony landmarks. This study pertained mostly to transabdominal surgical approaches utilizing low transverse incisions. The authors concluded that any abdominal wall surgical sites below the level of the anterior superior iliac spine have the potential for ilioinguinal or iliohypogastric injury (Whiteside 2003).
EMG monitoring during lumbar fusion was recommended to avoid lumbar plexus injury. The monitoring was performed through screw stimulation. It was found to be reliable in the detection of perforations in pedicle screw placement (06). Glassman and colleagues concluded that a stimulation threshold greater than 15 mA reliably indicates adequate screw position. A stimulation threshold between 10 and 15 mA was generally associated with adequate screw position, but exploration of the pedicle was recommended. A stimulation threshold less than 10 mA was associated with a significant cortical perforation in most instances (20). Rodgers and colleagues used this technique to study and improve the safety of extremely lateral interbody fusion, a 90-degree off midline approach (42). They concluded that 5 key steps can make the extremely lateral interbody fusion a safe, simple, and efficacious procedure:
(1) Careful patient positioning
(2) Gentle retroperitoneal dissection
(3) Meticulous psoas traverse during exploration by using neurologic monitoring
(4) Discectomy and fusion site preparation
(5) Interbody implant placement
Utilizing preoperative systemic steroids in rat sciatic nerve injury model showed better improvement following 2 weeks post-injury during the observation period (02). The authors injected the experimental group with betamethasone (2mg/kg body weight/day) preoperatively prior to the injury creation on the sciatic nerve and continued for first 24 hours. Although the study was based on animal injury model, the authors strongly recommended pre- and peri-operative systemic steroid injections in surgical cases with possible nerve manipulation. The caveat of steroid use in surgical patients is that it could affect wound healing.
Peripheral nerve lesions are at times difficult to differentiate from the plexus injuries. Both may have the same etiological factors and temporal sequences. Thorough clinical examination along with electrophysiological studies may not be enough to differentiate these two. As described below, good multiplanar imaging of the plexus in light of suspected lumbosacral plexus injury can reasonably make a diagnosis of plexus injury. Pseudomeningocele can mimic a mass lesion and careful historical evaluation and correlation with temporal events are essential. A pelvic mass lesion or a bony pathology of the spine or retroperitoneal mass can be easily identified using modern imaging modalities such as the MRI or CT, with or without a contrast agent administration. It may not be possible, however, to differentiate a peripheral lesion superimposed on a severe plexus injury. A lumbar plexus lesion may mimic a femoral nerve injury, whereas sacral plexus involvement can be mistaken for sciatic nerve injury. A combined peripheral nerve lesion with lumbosacral plexus injury may be clinically difficult to separate, especially with a multiple trauma background.
Baublitz-Brenenborg and colleagues reported a case of spinal root injury mimicking a lumbosacral plexopathy (04). The patient was a 51-year-old female who developed lumbar pain and left anterolateral thigh, anterior leg, and plantar foot pain along with dorsal foot paresthesias after falling from a ladder. She had left dorsiflexion, knee extension, hip flexion, hip abduction, and great toe extension weakness. Her nerve conduction study was notable for abnormal sensory nerve action potentials, suggesting a lesion at or distal to the dorsal root ganglion (DRG). However, her magnetic resonance imaging demonstrated evidence of a lateral extrusion of the L4-L5 disc effacing the left L4 and displacement of the left L5 nerve root. This case illustrates the fact that with trauma, the plexus and spinal roots can be affected by different mechanisms, and correlation of clinical, electrodiagnostic, and imaging may allow recognition of plexus and superimposed spinal root or peripheral nerve injuries.
The initial clinical evaluation and the profile of the existing injuries must be able to guide the physician toward the most appropriate method of diagnostic imaging. Conventional radiographs of the injured parts, especially the pelvis and the hip joint show the associated bony pathology. Disjunction of the pelvis and fractures of vertebral bodies can be identified.
The diagnosis of a nerve root avulsion is based on the presence of pseudomeningocele with the absence of nerve roots visible within it (53). It is also noteworthy that an avulsion can exist without formation of pseudomeningocele.
Myelography distinguishes traumatic pseudomeningoceles from spinal meningeal cysts. The former have a wider neck and fill rapidly on myelography, and characteristically there is absence of visualization of the nerve root at the level of the lesion. Spinal cysts (Type I) are extradural and have associated dural defects that sometimes do not fill with the contrast. Type II cysts are multiple and often arise in the sacrococcygeal region. Type III spinal cysts are intradural and occur anywhere along the posterior subarachnoid space demonstrating intradural defects, sometimes with a valve-like communication with the subarachnoid space. Additionally, there is no history of trauma in the spinal cysts (33).
A plain CT scan helps to identify the associated bony lesions and the erosion of vertebral bodies with a long-standing pseudomeningocele. Contrast examination aids in visualization of the pseudomeningocele, though it is not easy to identify the roots within the sac. A CT scan can readily differentiate between plexopathies caused by mass lesions arising from viscera or pelvic organs (55). In the absence of a tumor, a diagnosis of noncompressive disease must be investigated further (diabetic, or traumatic, or radiation-induced).
MRI has several advantages over myelography in evaluation of the lumbar plexus injuries. Intrathecal contrast injection is not necessary; patients with polytrauma need not be mobilized into different positions; and with a single examination, multiplanar imaging can be obtained with safe repetitions of the procedure. MRI would disclose the pseudomeningocele identical to the CSF intensity. It also shows the pathology around the psoas muscle or the conus medullaris (like hematomas, abscess, pelvic masses and atrophy of muscles). MRI also has the unique capability of demonstrating hemorrhage that can be evaluated on repeat examinations (19). With the advent of MRI, myelography is almost out of use in current practice (34).
Magnetic resonance (MR) neurography can potentially be used in noninvasive characterization of the location, extent, and type of lumbosacral plexus involvement. Higher magnet size, appropriate torso and/or endorectal coils, and imaging sequences could improve spatial resolution and soft tissue contrast, thus increasing the diagnostic yield (45; 03; 41). MR neurography may provide anatomic information that could lead to surgical intervention (45; 41).
The electrodiagnostic testing of the lumbar plexus is often suboptimal because of a lack of reliably obtainable sensory nerve conduction studies. Also, the few muscles that receive innervation from the lumbar plexus receive intermediate innervation from the femoral nerve and are proximally located, making them more likely to have been reinnervated in the interim between injury and electrodiagnostic testing in all but the most severe axonal lesions. The superior sacral plexus (L4-S1 and minimal S2) can be adequately assessed by electrodiagnostic studies (58); however, such studies are often hampered by patient age, prior surgery to the lumbar spine, polyneuropathy, and age of the lesion (50). Electrodiagnostic studies of the inferior portion of the sacral plexus (S2-S4) often cannot be performed with the exception of electromyography of the anal sphincter muscles.
The electrodiagnostic features supporting the diagnosis of lumbosacral plexus injury include denervation changes in different muscles that are not in the territory of a single nerve originating from the lumbosacral plexus. Sensory studies can be helpful in distinguishing between spinal root and plexus lesions. Sensory nerve action potentials (sural, superficial peroneal, saphenous) are usually not affected by spinal root (typically preganglionic) lesions but can be affected in postganglionic lesions such as those in the plexus. The distal CMAP amplitude is probably the single most important prognostic factor in the electrodiagnostic evaluation of plexopathies because CMAP amplitude reflects the degree of axonal loss. Also in evaluating the lumbosacral plexus, sensory nerve action potential (SNAP) parameters derived from the lateral cutaneous nerve of thigh (L2 to L3), saphenous (L4), superficial peroneal (L5), and sural (S1) conductions can be used to assess a significant sensory portion of the lumbosacral plexus, especially when compared with the contralateral asymptomatic side (48). It is worth emphasizing that most EMG laboratories do not routinely perform lateral cutaneous nerve of thigh, saphenous, and superficial peroneal sensory nerve conductions due to technical reproducibility.
The electrodiagnostic abnormalities, in the lumbar plexus show low or absent femoral motor NCS responses in the symptomatic limbs and denervation, on needle EMG, in the obturator and femoral nerve-innervated thigh muscles. The needle EMG is particularly useful in these patients. The presence of fibrillation potentials and decrease MUP recruitment in the thigh adductor muscles in addition to quadriceps muscles allows localization to be made to the lumbar plexopathy rather than femoral neuropathy (58).
In intrapartum maternal lumbosacral plexopathies, electrodiagnostic examination typically reveals a conduction block located proximal to the popliteal fossa; the needle EMG shows abnormalities in an L5 distribution in the limb. With radiation-induced lumbosacral plexopathies, needle EMG shows fibrillation potentials and often fasciculation potentials and myokymic discharges (58).
It is important that the diagnostic methods utilized give reasonable grounds for further management. Most studies state that CT myelography and MRI myelography are superior to routine x-ray myelography or electrophysiological studies. Myelography tends to underestimate the extent of injury mainly due to the traction injury without discontinuity of nerve. The diagnosis of root avulsion based on these studies makes a lumbar laminectomy unnecessary because an avulsion may not be amenable to surgical repair. Spontaneous resolution is most often expected in the majority of cases.
Surgical exploration is indicated if there is any evidence of enlargement of the pseudomeningocele that has a ball valve mechanism causing the cyst to expand. This progressive enlargement of the meningocele causes displacement and then compression of the dural sac, increasing the neurologic deficit. Surgical exploration and decompression is to be offered in these cases of progressive cauda equina syndrome.
A flail, anesthetic limb secondary to the lumbosacral plexus injury may be managed by protective conservative measures, or an above-knee amputation, or may be considered for reconstructive surgery provided that a sufficient amount of the proximal root is preserved (26).
Sensory symptoms may be controlled by analgesics, phenytoin, carbamazepine, or low doses of tricyclic antidepressants. In some patients with neoplastic lumbosacral plexopathy, the pain can be resistant to conventional treatments, thus severely affecting the quality of life. The dorsal root rhizotomy can be an effective treatment for the intractable pain for some patients with lumbosacral plexopathy and pelvic cancer in their terminal stages. Son and colleagues report their experience with dorsal root rhizotomy in 6 patients in whom neuropathic pain from the lumbosacral plexus involvement with pelvic cancer had been refractory to other conventional therapies (46). Results of their study indicated a substantial reduction in subjective pain ratings as well as significant reduction of daily narcotic use.
In patients with motor weakness, physiotherapy maintains the tone and allows safe mobility as nerve regeneration occurs.
At 3 months, clinical and electromyography evidence of functional return may be observed following trauma. When healing is not evident, in selected cases, surgical exploration with external neurolysis or release of entrapment may be indicated.
In most cases, surgical correction is not indicated because the lesions are not surgically accessible for repair. The functional prognosis may not be favorable in ruptures of intradural roots (44). Because most traumatic plexopathies improve spontaneously, at least to some extent, they usually are treated conservatively (58). When surgical repair is attempted, it tends to yield better results with lumbar, as opposed to sacral, plexus lesions (58).
Pregnancy and childbirth are closely associated with lumbosacral plexus injuries. However, the management of the injury may not be influenced by pregnancy specifically, nor if the disease process shows any changes with the continued pregnancy. Because demyelinating conduction block is often responsible for the symptoms, intrapartum maternal lumbosacral plexopathy is usually treated conservatively (58). Caution must be exercised in prescribing drugs for paraesthesias or myalgia or other causes of intractable pain.
The surgical corrective procedures are performed under general anesthesia with short acting muscle relaxants. Anesthesia and analgesia must allow proper electrophysiological monitoring during surgical treatment and manipulations.
Randolph W Evans MD
Dr. Evans of Baylor College of Medicine received honorariums from Allergan, Amgen and Novartis, Biohaven, Lilly, and Teva for speaking engagements.See Profile
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Apr. 09, 2021