Diabetic Lumbosacral Plexopathy Workup
- Author: Divakara Kedlaya, MBBS; Chief Editor: Robert H Meier III, MD more...
Approach Considerations
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.
Go to Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Neuropathy; and Electrophysiology for more information on these topics.
Lab Studies
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.
Imaging Studies
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.[21]
Histologic Findings
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.
Neural Studies
Electromyography (EMG) and nerve conduction studies (NCS) should be performed.[22, 23] 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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