Diabetic amyotrophy is typically a lumbosacral radiculoplexus neuropathy resulting in weakness, muscle wasting, and pain (1). Brachial plexus involvement has been occasionally described with lumbosacral radiculoplexus neuropathy (2–6), but isolated diabetic brachial plexopathy has been described only in a patient with diabetic ketoacidosis (7). We describe a patient with well-controlled type 2 diabetes who developed isolated bibrachial diabetic plexopathy.
A 56-year-old African-American man with a 13-year history of well-controlled diabetes (total glycohemoglobin 6.2%, normal 3.9–6.3%), on insulin for 5 years and having no other major medical illness, developed left shoulder pain that extended to the hand over a few weeks and right shoulder, extending into the right hand 3 months later.
Pain was dull with intermittent shooting and sharp pains. He denied sensory symptoms in the arms. Progressive left arm weakness evolved >3 months after the onset of pain and stabilized thereafter. Right arm weakness developed over the preceding 3 months and has continued to progress. He denied leg symptoms. He reported a 60-lb weight loss in the preceding year. Examination revealed strength as follows: MRC (Medical Research Council) grade 1–5 (3 in bilateral deltoid and biceps; 5 in right triceps, bilateral finger abduction, and right finger extension; and 4 in left triceps, bilateral wrist extension, and left finger extension). Strength was normal in the legs. Reflexes were absent in bilateral brachioradialis and biceps muscles but were normal in other areas. Babinski's sign was absent.
Electromyography and nerve conduction studies revealed bilateral upper-trunk brachial plexopathy; fibrillation potentials in upper-trunk innvervated muscles (biceps, deltoid, infraspinatus, and brachioradialis); and sparing of triceps, pronator teres, first dorsal interroseus and abductor pollicis brevis, and cervical paraspinal muscles. Radial, ulnar, and median sensory nerve action potential amplitudes were reduced. (Only the reduction in median sensory nerve action potentials could be accounted for by median nerve entrapment at the wrist.)
Despite treatment with prednisone, gabapentin, and narcotics, pain and weakness are still prominent 2 years after initiation of symptoms. However, the patient's weight increased to baseline.
Brachial plexopathy in this patient was likely related to his diabetes because there was no other obvious etiology; pain and weakness were prominent with relative paucity of sensory symptoms, and there was preceding weight loss, both characteristic features of lumbosacral radiculoplexus neuropathy.
In conclusion, isolated lumbosacral radiculoplexus neuropathy can occur as the initial complication of diabetes, even with good glycemic control. Thus, it is likely due to microvasculitis-causing nerve infarction rather than metabolic abnormalities in diabetes (1). Efficacy of immunosuppressive treatments is unproven and is being evaluated in clinical trials.
