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Spinal Injury Mimicking Lumbosacral Plexopathy

Baublitz-Brenenborg, Jennie-Corinne DO; DePalma, Michael J. MD; Cifu, David X. MD

American Journal of Physical Medicine & Rehabilitation: May 2007 - Volume 86 - Issue 5 - p 422
doi: 10.1097/PHM.0b013e31804a7bfc
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A 51-yr-old female presented with a chief complaint of left lower-limb pain and weakness after falling from a ladder. She experienced immediate lumbar pain that resolved during the ensuing week. One month later, she experienced an acute onset of stabbing left anterolateral thigh, anterior leg, and plantar foot pain, with dorsal foot paraesthesias. Physical examination revealed diminished sensation over the left first dorsal webspace, 4+/5 left ankle dorsiflexion, knee extension, hip flexion, hip abduction, and 4/5 great toe extension, and a diminished left medial hamstring reflex. Left straight-leg raise to 45 degrees and reverse straight-leg raise to 90 degrees of knee flexion reproduced radicular pain.

Electrodiagnostic evaluation revealed +1 positive sharp waves and fibrillation potentials in the left tensor fascia lata and vastus medialis, +1 positive sharp waves in the tibialis anterior, and peroneus longus with 15-Hz recruitment frequencies of increased duration, normal amplitude motor unit potentials. No abnormalities were noted in distal foot musculature, corresponding right lower-limb musculature, or lumbar paraspinals. The left saphenous sensory nerve action potential amplitude was reduced by approximately 75%, and the left extensor digitorum brevis compound muscle action potential amplitude was 50% attenuated compared with the right. Contralateral nerve-conduction studies were normal.

The electromyogram is an indirect functional representation of the axon, reflecting altered muscle cell membrane physiology.1,2 The sensory nerve action potential can localize the lesion either proximally to the dorsal root ganglion (DRG), such as in lumbosacral radiculopathy, with preserved sensory nerve action potentials, or distally to the DRG, with diminished or absent sensory nerve action potential. In our case, a lesion at or distal to the DRG was suspected on the basis of the electrodiagnostic data. A pelvic magnetic resonance imaging (MRI) did not reveal a structural origin for lumbar plexopathy. Subsequent contrast-enhanced lumbosacral MRI demonstrated a lateral extrusion of the L4–5 disc effacing the left L4 DRG and displacing the left L5 nerve root (Fig. 1). This structural abnormality corroborated both the clinical presentation and the electrophysiologic evidence.



MRI is useful in defining nerve root morphology because it can differentiate between nerve and surrounding soft tissue. However, the morphologic features of DRGs are difficult to evaluate on MRI because of variable position and small size.3 Therefore, MRI studies must be evaluated attentively in a patient with clinical evidence of disc herniation, particularly when DRG involvement is suspected or suggested by electrodiagnostic evaluation.4

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© 2007 Lippincott Williams & Wilkins, Inc.