American Journal of Physical Medicine & Rehabilitation:
From the Department of Physical Medicine and Rehabilitation, University of Pittsburgh, Pennsylvania.
All correspondence and requests for reprints should be addressed to Patrick Kortebein, MD, Novartis Pharmaceuticals Corporation, One Health Plaza (Bldg 125/3097A), East Hanover NJ 07936.
Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.
A 35-yr-old right-handed male dishwasher was referred to the authors’ electrodiagnostic laboratory for evaluation of left shoulder weakness and atrophy. The patient reported the insidious onset of a sharp, “stinging” pain of his left shoulder region 6 mos before evaluation. This pain lasted approximately 10 days and gradually subsided after initiation of ibuprofen prescribed 1 wk after onset. He denied any preceding systemic illness or trauma, associated neck or radicular pain, and no weakness or numbness/tingling. A few weeks after resolution of the shoulder pain, he noted progressive weakness and decreasing muscle bulk of his left shoulder. His medical history was otherwise unremarkable, and he was taking no medications.
Upper extremity inspection revealed significant atrophy of the entire left deltoid (see Fig. 1) with otherwise normal upper extremity muscle bulk. The findings from the neurologic examination were normal except for slightly weak shoulder abduction and flexion on the left with diminished sensation of a small area overlying the left deltoid.
Magnetic resonance arthrogram of the left shoulder showed significant atrophy and edema of the left deltoid muscle (see Fig. 2) as well as a superior labral tear and minimal undersurface fraying of the rotator cuff.
The findings from the patient’s electrodiagnostic study were markedly abnormal. The left axillary motor response had a prolonged distal latency with CMAP amplitude 90% lower than the normal right response. The findings from sensory studies, including medial/lateral antebrachial cutaneous, were normal. Concentric needle examination showed marked active denervating changes (i.e., fibrillation potentials, positive sharp waves, and polyphasic motor units) of the left deltoid, with all other muscles examined, including C5–6 root/axillary nerve innervated, being normal. The patient was diagnosed with neuralgic amyotrophy with severe involvement of the left axillary nerve.
Neuralgic amyotrophy (also known as Parsonage-Turner syndrome) is a neurologic syndrome affecting the brachial plexus.1 Clinically, it is characterized by the acute onset of intense pain with resolution in 1–2 wks followed by weakness and atrophy of the arm/shoulder girdle muscles. Sensory loss in the axillary nerve distribution is common. Neuralgic amyotrophy may have an antecedent triggering event, such as a viral illness, immunization, pregnancy, or surgery; however, as in this case, an inciting etiology is frequently not identified. Although most cases present with unilateral findings, bilateral involvement may occur. Discrete mononeuropathies (e.g., suprascapular, long thoracic, or axillary nerve) are relatively common (6%–41%).2–4 Recovery may require up to 2–3 yrs.1,4
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3. Tjoumakaris FP, Anakwenze OA, Kancherla V, et al.: Neuralgic amyotrophy (Parsonage-Turner syndrome). J Am Acad Orthop Surg. 2012; 20: 443–9
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