Diabetic Lumbosacral Plexopathy Workup
- Author: Divakara Kedlaya, MBBS; Chief Editor: Robert H Meier, III, MD more...
In evaluating suspected diabetic lumbosacral plexopathy, neural and electrophysiologic studies are generally helpful. Laboratory tests used to diagnose or assess control of diabetes mellitus (eg, fasting blood glucose, hemoglobin A1C) should be performed. Imaging studies may help in differentiating other causes.
In addition to tests performed to evaluate or diagnose diabetes, lumbar puncture results may show elevated cerebrospinal fluid (CSF) proteins, sometimes more than 1 g. Additional laboratory studies to rule out other causes of neuropathy, as well as cancer and bleeding diathesis, are also important.
Lumbar spine and pelvic radiographs should be performed to evaluate for other causes of the plexopathy. Computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the lumbosacral spine and pelvis may be indicated in some cases to rule out mass lesions.
A study by Matsuda et al of a patient with diabetic lumbosacral radiculoplexus neuropathy found that on T2-weighted MRI scans of the skeletal muscles, high signal intensities could be seen in the bilateral hamstrings and the adductor magnus and right tensor fasciae latae, as well as in the extensor muscles of the lower legs. Another study, which used short tau inversion recovery (STIR) MRI sequences to examine 17 patients with lower limb neuropathies, found that MRI-assessed amyotrophy was significantly greater in patients with severe, chronic, or proximal neuropathy.
Biopsies are rarely indicated in patients with diabetic lumbosacral plexopathy, and systematic studies are lacking in the literature. Early in the disease course, epineurial and perivascular inflammation around the small vessels may be caused by infiltration by mononuclear cells, with or without polymorphonuclear cells. Endoneurium and subperineurial space immunoglobulin-M (IgM) deposition should be expected. Activated complement (C5b-9) deposition in the endothelium of small vessels is also common. Reduced numbers of myelinated and unmyelinated axons may be observed, and differential fascicular loss of axons is also characteristic.
In an autopsy study of a patient with diabetic lumbosacral radiculoplexus neuropathy, Younger found that small blood vessels of the epineurium of the sciatic nerve were surrounded by perivascular chronic inflammation. In another case report, by Tracy et al, a superficial peroneal nerve biopsy revealed evidence of active axonal degeneration, microvasculitis, and ischemic injury in a patient with diabetic lumbosacral radiculoplexus neuropathy.
Electromyography (EMG) and nerve conduction studies (NCS) should be performed.[27, 28] In patients without distal symmetrical polyneuropathy (DSPN), needle EMG usually shows positive sharp waves and fibrillation potentials in the iliopsoas, hip adductors, and quadriceps, but other muscles may also be involved.
In patients with underlying DSPN, in addition to the above findings, sural sensory nerve action potential (SNAP) is usually absent, and amplitudes in peroneal and tibial compound motor action potential (CMAP) are reduced.
Femoral nerve motor conduction studies may show asymmetrical amplitudes, and paraspinal muscle needle EMG may show fibrillations and positive sharp waves, but the results are usually within the reference range.
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