Lumbosacral plexus injuries …

Christopher Doughty MD

General Neurology

Updated 08.13.2024
Released 03.21.2002
Expires For CME 08.13.2027

Lumbosacral plexus injuries

Author: Christopher Doughty MD

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Editor: Randolph W Evans MD

Lumbosacral plexus injuries

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Introduction

Overview

Lumbosacral plexopathy should be suspected when motor and sensory deficits occur in the territory of multiple nerves and multiple spinal nerve roots in one leg. It can be challenging to differentiate lumbosacral plexopathy from lumbar polyradiculopathy or injury to multiple peripheral nerves. Some causes of lumbosacral plexopathy lead to bilateral involvement, further complicating the diagnostic process. Certain etiologies, referred to as radiculoplexus neuropathies, can even affect both the plexus and the spinal nerve roots. Carefully neurologic examination and proper use of electrodiagnostic testing and/or imaging, however, can accurately localize to the plexus and guide the etiologic work-up. Important causes include neoplasm, prior radiation therapy, compression, diabetes, and ischemia. Traumatic causes are uncommon and are mainly due to fractures of the pelvic ring or acetabulum.

Key points

	• 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.
	• MRI of the lumbosacral plexus and EMG/NCS are important diagnostic tools. CT or PET can be additive in certain cases.
	• Because most traumatic plexopathies improve spontaneously, at least to some extent, they usually are treated conservatively.

Historical note and terminology

The lumbosacral plexus comprises two 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 trunk. The lumbar plexus is primarily derived from branches of the T12-L4 nerve roots and takes shape in the retroperitoneum, below and within the psoas muscle. It should, thus, come as no surprise that pathology within the retroperitoneum (eg, hematoma, abscess) is a frequent cause of lumbar plexopathy. The predominantly sensory iliohypogastric (L1), ilioinguinal (L1), genitofemoral (L1-2), and lateral cutaneous nerve of the thigh (L2-3) arise from lumbar plexus. Contributions from L2-L4 also split into anterior and posterior divisions; the anterior division forms the obturator nerve, and the posterior division forms the femoral nerve. The obturator nerve innervates the adductor muscles of the thigh and the skin of the medial thigh. The femoral nerve innervates the psoas muscle and the iliacus muscle proximally. Once it passes under the inguinal ligament, it innervates the quadriceps muscles and provides sensation to the medial thigh and lower leg via medial and intermediate cutaneous nerves of the thigh and saphenous nerves, respectively.

The caudally located sacral plexus is formed by the lumbosacral trunk (L4-5) and branches from S1-S4. The lumbosacral trunk crosses over the pelvic brim near the sacroiliac joint and is vulnerable to compression in this location. The largest branch of the sacral plexus is the sciatic nerve (L4-5, S1-3), which is comprised of tibial and peroneal divisions. These innervate 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), posterior femoral cutaneous nerve (S1-3), and pudendal nerve (S2-4) all also arise from the sacral plexus.

Strictly speaking, a lumbosacral plexopathy should affect only those nerve fibers within the plexus itself. Certain pathological processes, however, can extend beyond the plexus to the level of the spinal nerve roots and/or the peripheral nerves. When this occurs, the term radiculoplexus neuropathy is most appropriate. This distinction can be helpful when seeking an etiologic explanation, as inflammatory and infiltrative disorders are especially prone to extending beyond a “pure” plexopathy in this manner.

Clinical manifestations

Presentation and course

Lumbosacral plexopathy presents with weakness and/or sensory loss within the distribution of those nerves that are damaged. Clinically, a plexopathy is suspected when neurologic deficits involve the territory of more than one peripheral nerve and more than one spinal nerve root. It can be very challenging in a routine neurologic examination, however, to distinguish between a polyradiculopathy, lumbosacral plexopathy, lumbosacral radiculoplexus neuropathy, or a mononeuropathy multiplex affecting multiple lower extremity nerves on clinical grounds alone, as these can produce overlapping deficits.

Many injuries of the lumbosacral plexus are misdiagnosed as femoral nerve injuries, and many sacral plexus injuries are misdiagnosed as sciatic or common peroneal nerve injuries (56). Accurate localization is especially 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. Electrodiagnostic studies or imaging are often required to establish a definitive anatomic localization.

Pain is prominent with many, but not all, causes of lumbosacral plexopathy. It usually involves the distribution of the involved sensory nerves. Some patients describe pain that worsens when lying down and improves with getting up and walking (48). Severe lower back or hip pain is often the initial presenting complaint in patients with lumbosacral plexopathy caused by a compressive or infiltrative neoplasm, with muscle weakness and sensory deficits appearing later. By contrast, post-radiation plexopathy is frequently painless (15). Patients with the onset of symptoms within 6 months of radiation may more commonly have pain, have a monophasic course, and may even have symptom improvement with steroid treatment (53). Acute onset of unilateral lower back or flank pain can be seen with ischemic etiologies, though weakness of the respective lower extremity follows soon thereafter (21).

Recurrent hip subluxation has been purported to be a rare symptom of lumbosacral plexopathy. Kumar and colleagues have reported two 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 (36).

Prognosis and complications

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.

Biological basis

Etiology and pathogenesis

Lumbosacral plexopathy can result from numerous possible etiologies (see table 1). In most reported series, neoplasm—either directly or as a secondary effect of treatment—is the most common etiology. For example, in one series of 86 patients with lumbosacral plexopathy, 50% were related to neoplasm. By contrast, only 6% were traumatic (40). In another series of 60 sacral plexopathies (specifically excluding upper lumbar plexopathies), 33% were cancer-related, either directly or indirectly (eg, post-radiation plexopathy) (59). In 19% of cases in this series, trauma was the second most common etiology. Seventeen percent were idiopathic, 14% were iatrogenic (inclusive of ischemic causes after vascular or cardiac surgeries), and 8% were intrapartum. Intrapartum injuries are discussed further in section 16.

Lumbosacral plexopathy related to cancer can occur either from direct spread of the primary tumor enveloping the plexus or by metastatic deposits within the plexus (47). About 75% of cases are due to direct invasion, and 25% are from metastatic disease (30). Perineural spread of tumor from its primary site is possible; for example, prostate cancer can invade the inferior hypogastric plexus around the prostate and then travel along the splanchnic nerves to the plexus (04). It is also possible for tumor to track along nerves intradurally to involve spinal nerve roots or distally into the peripheral nerves proper. This is especially true of neurolymphomatosis.

Colorectal cancer is the most common cancer to locally involve the lumbosacral plexus, whereas breast cancer is the most frequent tumor to metastasize to the lumbosacral plexus (31). Sarcoma, lymphoma, and cervical cancer are also frequently encountered. The lower plexus (L4-S1 components) is most commonly involved in neoplastic cases (51% of cases). The upper plexus (L1-L4) is involved in 31%, and 18% present as a pan-plexopathy. Pain is near-universal and an early symptom in neoplastic plexopathy; it may involve the inguinal or perianal area before the legs (39). The presence of unilateral leg edema may be an additional etiologic clue.

Radiation-induced lumbosacral plexopathy can occur anywhere from a few months to many years following radiation therapy to the pelvis. Onset of symptoms is most frequent between 1 and 5 years, but a delay as long as 31 years has been reported (32). Most commonly, affected patients present with progressive painless weakness. Sensory symptoms and pain, when present, typically occur later in the course. Involvement is also frequently bilateral (yet asymmetric), which together with a lack of pain can help distinguish from neoplastic cases (15). Patients with the onset of symptoms within 6 months of radiation may more commonly have pain, have a monophasic course, and may even have symptom improvement with steroid treatment (53). Imaging is usually performed to exclude recurrence of cancer, however. Higher total doses of radiation increase the incidence of this complication; pre-existing neuropathy and/or concurrent chemotherapy may also influence the risk. Injury to the plexus likely relates to both compression of the nerves from fibrosis of surrounding tissue as well as microvascular injury.

Traumatic 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. Traumatic lumbosacral plexus injuries are less common than brachial plexopathies. Closed injury is a more frequent cause of lumbosacral plexopathy than open injuries (such as gunshot wounds or low-velocity puncture wounds) (66). Gunshot wounds more commonly result in injuries to the upper portions of the plexus, probably due to the shielding effect of the pelvic bone protecting the lower plexus (11). The lower plexus is at higher risk for injury from motor vehicle accidents and falls because these injuries result in fractures of the sacroiliac joint and sciatic notch.

Most lumbosacral plexopathies due to trauma are from very violent injuries such as auto-pedestrian accidents, high-speed car accidents, or falls from heights. Both open and closed traumatic lumbosacral plexopathies are typically associated with damage to other internal organs, blood vessels, and bony structures, especially the pelvic ring. Trauma that results in fractures of the pelvic ring and acetabulum, dislocations of the sacroiliac joint, or sacral fractures are more likely to result in nerve injury (29; 38). Fractures of the posterolateral two-thirds of the pelvis are especially unstable and often displaced, which can cause injury to the adjacent structures including the lumbosacral plexus. Sacral fractures, may carry the highest risk; in particular, transverse sacral fractures or injuries that result in longitudinal displacement (at least 10 mm) at the sacrum or sacroiliac joint are associated with higher risk for lumbosacral plexus (or spinal nerve root) injury (38; 58).

Strictly speaking, fractures of the acetabulum may injure the sciatic nerve or other specific peripheral nerves rather than the plexus proper (38; 10). Overall, the sciatic nerve is the most frequently injured component of the lumbar plexus, likely because of the proximity of the lumbosacral trunk to the sacroiliac joint. In a series of 22 traumatic plexopathies, the peroneal division of the sciatic nerve was injured in 96% of cases and the tibial division was injured in 86% (38). Likewise, severe traction injury can lead to avulsion of lumbosacral spinal nerve roots rather than injury to the plexus itself (26).

Histological examination of autopsied specimens by Huittinen offer insight into the specific mechanisms of nerve injury (29). In addition to direct compression by injured and displaced structures, traction injuries were seen. Histologic study revealed intraneural, perineural, and epineural hemorrhages and ruptures, as well as rupture of nerve fibers. Traction can lead to avulsion at the nerve root level, as well. 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 can also lead to root (29).

Iatrogenic injury to the lumbosacral plexus is also possible. Sometimes traction injury to the plexus can occur following hip arthroplasty. Overall rates of nerve palsy are low, however, and when injury does occur, it is typically to individual peripheral nerves (52; 24). The lateral transpsoas approach for lumbar interbody fusion surgery carries some risk for lumbosacral plexus injury (13; 28; 03). The femoral and obturator nerves are at greatest risk due to their origin within the psoas muscle (02). The rate of postoperative plexopathy was as high as 37.8% in one published series, though 64.6% reportedly resolved by about 1 year (70). More levels fused and increased surgical duration were associated with persistent symptoms. An oblique approach that avoids dissection through the psoas muscle may be associated with fewer plexus injuries (33). Lumbosacral plexopathy is an exceedingly rare complication after major gynecologic surgery; two cases out of 1210 patients were noted in one series (07).

Vascular malformations, including aneurysms of the distal aorta and the iliac arteries, can either compress the lumbosacral plexus or lead to ischemic nerve injury. Aorto-iliac occlusive disease or aortic dissection can rarely present as acute flaccid paraparesis due to lumbosacral plexopathy (09; 27). Aneurysmal rupture can lead to a compressive hematoma (06; 69). Aorto-iliac intervention, whether open surgical or endovascular, is associated with a rare risk of ischemic injury to the lumbosacral plexus due to internal iliac artery occlusion (01; 17). Cases of lumbosacral plexopathy have been reported after pelvic vessel embolization for postpartum hemorrhage, but this also appears quite rare (44; 50).

Iliopsoas or iliacus hematoma can present with lumbar plexopathy or isolated femoral neuropathy (12). It can be secondary to coagulopathy (hemophilia or other disorders), anticoagulation, trauma, surgery, and other etiologies (64; 41; 45; 43).

Psoas muscle abscess or perirectal abscess, endometriosis, or foci of extramedullary hematopoiesis are additional rare compressive considerations (47; 21).

Diabetic lumbosacral radiculoplexus neuropathy (DLRPN) typically presents with subacute, asymmetric proximal leg pain followed by ipsilateral leg weakness within days (22; 61). It is less common than the typical distal symmetric polyneuropathy associated with diabetes but leads to significant morbidity due its propensity for causing leg extension weakness that interferes with ambulation. Development of diabetic lumbosacral radiculoplexus neuropathy is not associated with disease duration or control and is frequently encountered in patients with mild diabetes; it may even be the first sign of the disease. Concurrent weight loss is common. Although diabetes is the strongest risk factor for development of this disorder, a near-identical idiopathic form of lumbosacral radiculoplexus neuropathy (LRPN) also occurs (46). In diabetic and nondiabetic cases, about one third of cases are bilateral. The underlying pathophysiology of this disorder appears to be a microvasculitis (19; 20). This is a monophasic illness. Symptoms abate after several months, with most patients showing some improvement over 1 to 2 years.

Sarcoidosis can cause an inflammatory lumbosacral plexopathy (05). Spinal nerve roots and more distal peripheral nerves can also be involved (35). Positive sensory symptoms tend to predominate. Autoimmune or paraneoplastic CRMP5 neuropathy can present as an asymmetric polyradiculoneuropathy, as well (18).

Table 1. Possible Etiologies of Lumbosacral Plexopathy

	• Neoplastic
		- Direct local spread – bladder, cervical, colon, ovarian, or prostate cancer - Metastatic disease involving pelvic and/or retroperitoneal lymph nodes - Neurolymphomatosis - Peripheral nerve sheath tumor or other benign tumors
	• Other compressive causes
		- Hematoma - Retroperitoneal or perirectal abscess
	• Mechanical injury
		- High velocity trauma (eg, motor vehicle accident) - Penetrating trauma (eg, gunshot wound) - Postoperative - Childbirth
	• Radiation
	• Inflammatory
		- Diabetic lumbosacral radiculoplexus neuropathy (“diabetic amyotrophy”) - Idiopathic lumbosacral radiculoplexus neuropathy - Sarcoidosis
	• Infiltrative
		- Amyloidosis
	• Ischemic
		- Aortic or iliac occlusion/surgery

Differential diagnosis

Confusing conditions

Although brain and spinal cord lesions can produce neurologic deficits confined to a single limb, they can typically be identified through the pattern of weakness, accentuation of the muscle stretch reflexes, differential involvement of the posterior columns versus spinothalamic tracts, and/or presence of other upper motor neuron signs. The most important alternative considerations in the differential diagnosis are lumbosacral radiculopathy and injury to one or more peripheral nerves outside of the plexus itself. Establishing clinical concern for a plexopathy accordingly requires demonstration of a pattern of weakness, sensory loss, and/or reflex change that spans multiple peripheral nerves and multiple spinal nerve roots. For example, femoral neuropathy may be suspected in a patient presenting with severe hip flexion and knee extension weakness. Demonstrating concurrent weakness of hip adduction (obturator nerve, L2-L4) and ankle dorsiflexion (peroneal nerve, L4-L5) would instead invoke suspicion of a plexopathy because these deficits span multiple peripheral nerves and nerve roots. In this context, however, it remains difficult to exclude lumbar polyradiculopathy or injury to the relevant individual nerves. Definitive localization often requires electrodiagnostic testing and/or imaging.

Occasionally, causes of mononeuropathy multiplex—for example, vasculitic neuropathy or the multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) variant of chronic inflammatory demyelinating polyradiculoneuropathy—can begin in a single limb, mimicking a plexopathy. As mentioned prior, certain causes of lumbosacral plexopathy can affect both legs concurrently (eg, radiation, diabetic lumbosacral radiculoplexus neuropathy), but consideration of mononeuropathy multiplex is especially important in these cases. In cases of bilateral involvement, it is also important to carefully exclude myelopathy.

Diagnostic workup

Accurate anatomic localization is helpful for guiding the work-up to identify a specific etiology. For example, radiculoplexus neuropathy is frequently associated with diabetes as discussed above. A lumbar puncture may be prioritized after identification of a polyradiculopathy without a structural cause, whereas CSF analysis is typically not required if confident localization to the plexus can be made.

Electrodiagnostic studies nerve conduction studies (NCS) and electromyography can at times narrow the localization and offer helpful prognostic information when plexopathy is suspected (57). Sensory nerve conduction studies can be helpful in distinguishing between spinal root and plexus lesions. Sensory nerve action potentials (SNAPs) typically remain normal in preganglionic (ie, nerve root) lesions but can be affected in postganglionic lesions (ie, plexus or peripheral nerves). Identification of denervation changes within lumbar paraspinal muscles on EMG has particular localizing value, as well. The paraspinal muscles are innervated by the dorsal rami, which branch off the spinal nerves before the plexus is formed. These abnormalities are, therefore, only seen in lesions that involve the nerve root(s).

Motor nerve conduction studies are frequently abnormal in lumbosacral plexopathy and can help define the extent of the injury, but this is not helpful in discriminating between nerve root and peripheral nerve injuries. Compound motor action potential (CMAP) amplitude is reduced when motor axon loss results from damage to either nerve roots or peripheral nerve components. The CMAP amplitude may have prognostic value in femoral nerve injuries. Similar to the bedside examination, needle EMG should reveal denervation changes in different muscles that are innervated by the lumbosacral plexus but not in the territory of a single nerve or a single spinal nerve root. EMG can be especially useful when pain limits accurate bedside assessment of strength or in cases when the limb is immobilized after bony trauma.

Thus, the typical electrodiagnostic hallmark of plexopathy is the combination of abnormal SNAPs in the affected limb, normal needle EMG of lumbar paraspinal muscles, and abnormal EMG suggestive of denervation in muscles innervated by different peripheral nerves and different nerve roots. Radiculoplexus neuropathy is suspected when abnormal SNAPs and signs of denervation in the lumbar paraspinal muscles are seen concurrently, as this indicates both preganglionic and postganglionic involvement. Finally, findings on NCS/EMG can occasionally have etiologic relevance. Myokymic discharges are seen in about 60% of cases of postradiation plexopathy, for example (51).

There are important additional limitations to the electrodiagnostic evaluation of suspected lumbosacral plexopathy. Confounding factors often limit the usefulness of key findings. The presence of an underlying polyneuropathy or advanced age can affect SNAP amplitudes, for example, and prior lumbar spinal surgery or history of radiculopathy can confound assessment of the lumbar paraspinal muscles. Moreover, multiple lesions are always possible, especially in cases of trauma. Identification of signs of radiculopathy on EMG, for example, cannot fully exclude concurrent injury to the plexus. Finally, not all portions of the lumbosacral plexus are readily accessible for study; for example, the inferior sacral plexus (S2-S4) can only be assessed by needle EMG of the anal sphincter muscles which is not performed in most laboratories. A study by Tavee and colleagues exemplifies the challenges faced during electrodiagnostic assessment (59). Out of 171 cases referred for suspected sacral plexopathy, localization remained indeterminate in 111; confounding factors typically prevented definitive localization.

Timing can also affect the electrodiagnostic findings. Even in cases of severe axonal injury, distal nerve conduction studies often remain normal in the hyperacute period because insufficient time has passed for Wallerian degeneration to occur. It typically takes 4 to 5 days for the CMAP amplitude to reach its nadir, and up to 10 days for the SNAP amplitude to reach its nadir (08). Similarly, some findings on needle EMG that indicate axon loss may not appear for 2 to 4 weeks after onset of injury. Obtaining nerve conduction studies/EMG after approximately three weeks will, therefore, offer more accurate information about the extent and severity of the injury, but in acute trauma, a more urgent understanding of the nature may be necessary to guide surgical planning.

Imaging is often required to secure localization to the plexus and to better delineate the underlying cause. In most cases, dedicated MRI of the lumbosacral plexus is the optimal imaging modality (54; 49; 23). Affected nerve segments may appear enlarged, show increased T2 signal, or enhancement. If localization remains ambiguous as discussed above, MRI of the lumbar spine may also be required. In cases of severe trauma, for example, avulsion of nerve roots is possible, and ensuring nerve continuity is important (26). On imaging, nerve root avulsion is typically identified by the presence of pseudomeningocele with the absence of nerve roots visible within it (62). Imaging may also be helpful for directing a biopsy to try to establish a definitive etiology when an inflammatory or infiltrative cause is suspected (68).

In certain situations, CT or PET imaging may be additive. CT may be useful in traumatic cases, for example, to quickly establish the associated bony pathology. PET imaging may be considered in a patient with known malignancy elsewhere. If MRI is contraindicated, a CT scan of the abdomen and pelvis may still offer etiologic information; mass lesions arising from viscera or pelvic organs or compression from a hematoma or abscess should be identifiable (63). In cases where MRI contraindicated and nerve root avulsion is a concern, CT myelogram can be used.

Management

Management of lumbosacral plexopathy varies depending on the underlying etiology and severity of the injury. Most traumatic lumbosacral plexopathies are treated conservatively, as neurapraxic injuries improve spontaneously over time (66). Surgical intervention in these cases is often guided by the extent of bony and vascular injury. Neoplastic plexopathy may be treated with radiotherapy and sometimes concurrent chemotherapy. Symptomatic improvement after treatment has varied widely in reported series, from 35% to 85% (30; 60). Radiation-induced plexopathy is typically irreversible, without any proven therapies. Due to promising results from an earlier observational study (14), a randomized, placebo-controlled clinical trial combining pentoxifylline-tocopherol and clodronate was completed in patients with radiation-induced brachial plexopathy. This failed to show any beneficial effect, though enrolled patients had already had neurologic symptoms for 5 ± 5 years (16).

Pain management and physical therapy are helpful in most cases, irrespective of etiology. 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 (55).

Outcomes

The prognosis of lumbosacral plexopathy varies depending on the etiology and the degree of axonal damage suffered. Some mild traumatic or compressive cases lead to neuropraxia, in which axons remain intact and no Wallerian degeneration occurs. Instead, focal demyelination leads to conduction block. Prognosis in such cases is good, as remyelination of the injured nerve segment will lead to resolution of any weakness or sensory loss. A common example is intrapartum compression of components of the plexus. Typically, these injuries result in conduction block and, thus, patients experience complete recovery over several weeks to months (34). Most other causes of lumbosacral plexopathy lead to axon loss, however (59). In one series of 85 cases of cancer-associated lumbosacral plexopathy, only 17% of patients experienced improvement on neurologic examination even with treatment of the cancer (30).

Findings on nerve conduction studies and EMG can inform prognosis for recovery because they can elucidate the underlying pathophysiology of the injury. Although it did not specifically evaluate patients with plexopathy, a study of patients with femoral nerve injury demonstrated that side-to-side comparison of the femoral nerve CMAP offered the best prognostic value. If the femoral nerve CMAP amplitude was reduced to less than 50% of the amplitude of the contralateral response, less than 50% of such patients recovered over the next year. In contrast, if the compound muscle action potential amplitude was more than 50% of the amplitude of the contralateral response, all patients recovered in a 1-year period (37).

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Christopher Doughty MD

Dr. Doughty of Brigham and Women's Hospital received an honorarium from UCB as a Scientific Advisory Board member, clinical trial funding from AstraZeneca as a co-investigator, an honorarium from TD Cowen as a panel speaker, and a consulting fee from Neurometrix.
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Editor

Randolph W Evans MD

Dr. Evans of Baylor College of Medicine received honorariums from Abbvie, Amgen, Biohaven, Impel, Lilly, and Teva for speaking engagements.
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Former Authors

Anil Nanda MD FACS
Donald Smith MD
Prasad Vannemreddy MD
Anthony H Sin MD
Parveen Athar MD
Shade' Moody MD
Duaa Jabari MD
Muhammad Haroon Shahid MD
Sameera Salman Ghauri MBBS
Ali Reza Shoraka MD
Kazim Sheikh MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Injury of lumbosacral plexus: S34.4
ICD-11: Post-radiation lumbosacral plexopathy: 8B92.0

Vasculitic lumbosacral plexopathy: 8B92.1

Diabetic lumbosacral plexopathy: 8B92.2

Lumbosacral radiculoplexopathy: 8B92.3

Other specified lumbosacral plexus disorders: 8B92.Y

Lumbosacral plexus disorders, unspecified: 8B92.Z

Injury of lumbosacral plexus: NB73

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Lumbosacral plexus injuries

Differential Diagnosis

peripheral nerve lesions (eg, pseudomeningocele, pelvic mass lesion, retroperitoneal mass)
femoral nerve injury
sciatic nerve injury
spinal root injury

Also Relevant

Nerve plexus metastases
Pregnancy: neuromuscular complications
Radiation plexopathy

Lumbosacral plexus injuries …

Lumbosacral plexus injuries

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 1. Possible Etiologies of Lumbosacral Plexopathy

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Primary headache associated with sexual activity

Toxic and nutritional deficiency optic neuropathies

Nystagmus

Third nerve palsy

Brain death/death by neurologic criteria

Lumbosacral plexus injuries

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 1. Possible Etiologies of Lumbosacral Plexopathy

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Primary headache associated with sexual activity

Toxic and nutritional deficiency optic neuropathies

Nystagmus

Third nerve palsy

Brain death/death by neurologic criteria

This is an article preview.
Start a Free Account
to access the full version.