03 February 2009
Lumbosacral plexus neuropathies are rare syndromes, which are caused by damage to the nerve bundles in the lumbosacral plexuses. After establishing the existence of a plexus lesion nerve by demonstrating that symptoms cannot be explained by a lesion of a single nerve root or peripheral nerve the underlying pathology needs to be unravelled. Most frequently, the lumbosacral plexus is damaged: in diabetics, by direct or indirect pelvic trauma, by compression, or obstetric complications. Tumours, aneurysms and idiopathic or hereditary neuropathies are more infrequent causes of a lumbosacral plexopathy. Treatment, course and prognosis largely depend on the underlying disorder.
B.G.M. van Engelen, M.D., Ph.D., Professor of Neuromuscular Diseases
N. van Alfen, M.D., Ph.D.
Lumbosacral plexus neuropathies are relatively rare, and fairly unknown clinical syndromes, which are caused by damage to the nerve bundles in the lumbosacral plexuses.
One of the main causes for a lumbosacral plexus neuropathy is the so-called 'diabetic amyotrophy'. Another cause is the idiopathic form of lumbosacral plexus neuropathy, the lower-extremity counterpart of the more well-known Parsonage-Turner syndrome or neuralgic amyotrophy, which usually affects the brachial plexus(-es). Locally invasive tumour-growth in the pelvic region can be another cause of a lumbosacral plexopathy.
The clinical features of a lumbosacral plexopathy depend on two things: the exact parts of the plexus and nerves that are involved, and the underlying etiology. As localisation of a lesion is the first objective of any neurological evaluation, and from then on a possible etiology can be inferred, the anatomical features will first be discussed.
The lumbosacral plexus (see picture) consists of the interwoven nerves bundles coming from the 3rd, 4th and 5th lumbar nerve roots, and the 1st, 2nd and 3rd sacral nerve roots, with small additions from the 2nd lumbar and the 4rd sacral nerve root as well. Actually, the plexus consists of two separate parts, the lumbar and the sacral plexuses, that are connected by the so-called lumbosacral trunk. The lumbar part of the plexus mainly lies embedded between and in the paraspinal quadratus lumborum and psoas muscles, making it vulnerable to local trauma or compression (e.g. by a hematoma). On the other hand, the sacral plexus lies in the pelvis, with the lumbosacral trunk crossing the pelvic brim, making it vulnerable to intrapelvic pathology.
Clinically, the patient's symptoms can be attributed to a plexopathy if they are localised to the peripheral nervous system, but neither fit the distribution of one nerve root or one single peripheral nerve. For this conclusion, a careful and detailed neurological examination is required. If the symptoms are attributable to a plexus lesion, they must be further devided in mainly lumbar, mainly sacral or diffuse or patchy lesions of the whole plexus. This localisation will then aid the question of 'how' did the nerves get damaged (see: differential diagnosis).
For the patient, the symptoms of a lumbosacral plexopathy can be that of any other peripheral nerve lesion: neuropathic (severe, shooting, burning or stabbing) pains, tingling, numbness of certain skin areas or, conversely, areas that are very hypersensitive to the touch, and weakness and wasting of certain muscles in the thigh, buttock and leg region. Usually, when a lesion is acute, pain will be a marked symptom, followed by weakness and wasting. More slowly progressive lesions usually start with sensory symptoms such as numbness and tingling and increasing pain, or sometimes just slowly increasing muscle weakness.
Natural course and prognosis
Not surprisingly, the course and prognosis will largely depend on the underlying disorder causing the lumbosacral plexopathy, and especially on whether a treatable cause can be demonstrated (see Therapy section). Once a fixed plexus deficit has been established, recovery of sensory and motor function can take months to years, depending on the degree of axonal damage and the length new nerve fibers have to grow to reinnervate the affected muscles or skin parts. Unfortunately, complete functional recovery is not always the rule, and many patients remain with functional impairments, hindering daily activities such as walking or cycling.
There are no data on the incidence or prevalence of lumbosacral plexopathies in the general population. For diabetics, the prevalence of a proximal diabetic neuropathy is estimated at 8 per 1000 (type I and II diabetics combined); the prevalence of type II diabetes alone in the general population is about 3% (± 500.000 people in the Netherlands). In trauma's, the incidence of a lumbosacral plexus lesion with a sacral fracture is about 2%, in other types of pelvic fractures it's about 0.8%. After major gynaecologic pelvic surgery, the incidence of lumbosacral plexus lesions was 0.16% in a series of 1200 patients. The incidence of obstetric lumbosacral trunk lesions is estimated at 1 per 2000 - 6000 deliveries. In coagulopathies, either during anticoagulant therapy or in hemophiliacs, the occurrence of an iliopsoas hematoma compressing the lumbar plexus is rare, but does occur, especially after invasive procedures. Idiopathic lumbosacral plexus neuropathy is a rare disorder, with a few hundred cases known in literature.
The most important aspect in the differential diagnosis is establishing the existence of a plexus lesion, by demonstrating symptoms that cannot be explained by a lesion of a single nerve root or peripheral nerve. However, there are some disorders that can mimic this clinical picture. For example, a lumbar spinal stenosis can cause compressive lesions of multiple nerve roots, which causes pain, sensory symptoms and sometimes paresis in a 'plexus' distribution. Usually, the additional symptoms of lower back pain and provocation of symptoms by certain activities (e.g. walking) give a clue to this diagnosis, and when in doubt, imaging of the lower spine should be performed. Read more
Depending on whether there's an obvious or plausible cause for the lumbosacral plexopathy, there will be a need for limited or more extensive ancillary investigations.
Imaging studies are warranted whenever any structural cause of the plexopathy is suspected.
If there is a direct or indirect trauma to the plexus, imaging of the region by CT or MRI scanning, sometimes by abdominal or pelvic ultrasound, will help to clarify the extent of the lesion and identify treatable causes (such as a hematoma).
An electrophysiological examination, including needle examination (EMG) and nerve conduction studies (ENG) can help to confirm the clinical diagnosis of a plexopathy, and identify the nerve structures involved. Read more
For space-occupying lesions, relieving the compression of the plexus by tumour debulking or irradiation, hematoma evacuation or abscess drainage, should be the first goal of therapy. For diabetic and idiopathic lumbosacral plexopathy, an early treatment with high-dose corticosteroids could be helpful, by mitigating the inflammatory response in the nerves. Ofcourse, when an infectious process is suspected, treatment should be aimed at eradicating that infection, e.g. by antibiotics for Borrelia, or aciclovir in case of a Herpes infection. Read more