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Published on: November 29, 2015
Clinical, Neurophysiologic, and Pathologic Features in Patients With Early-Onset Postradiation Neuropathy
Michael Skolka1, Shahar Shelly1, Marcus V Pinto1
1From the Department of Neurology (M.S., M.V.P., D.D., T.O., J.H.U., A.S., N.P.S., P.J.B.D., C.E.R., C.J.K.), Mayo Clinic, Rochester, MN; Department of Neurology (S.S.), Rambam Health Care Clinic, Haifa, Israel; Department of Neurosurgery (R.J.S.); and Department of Laboratory Medicine and Pathology (C.J.K.), Mayo Clinic, Rochester, MN.
Objectives:
The objective of this study was to study early-onset radiation-induced neuropathy reviewing neurologic course, steroid response, and available nerve biopsies.
Methods:
Patients coded with radiation-induced neuropathy within 6 months of radiation were reviewed from January 1,1999, to August 31, 2022. Patients had to have electrodiagnostically confirmed neuropathy localized within or distal to radiation fields. Neurologic course and nerve biopsies were reviewed.
Results:
Twenty-eight patients (16 male and 12 female patients, mean age 63.8 years) were identified. The average radiation dose was 4,659 cGy (range 1,000-7,208). Tumor infiltration was not observed on MRI and PET. Postradiation onsets averaged 2 months (range 0-5). Localizations included brachial (n = 4) plexopathies, lumbosacral (n = 12) plexopathies, radiculopathies (n = 10), and mononeuropathies (n = 2). Neuropathic pain (n = 25) and weakness (n = 25) were typical. The clinical courses were subacute monophasic (n = 14), chronic progressive (n = 8), or static (n = 1), and 5 were without follow-up. Nerve biopsies (n = 8) showed an inflammatory ischemic process with perivascular inflammatory infiltrates (n = 7) or microvasculitis (n = 2). Nine patients, 7 with monophasic courses, received steroid burst therapy with symptom improvement in 8. No patients recovered entirely back to baseline.
Discussion:
In contrast to chronic radiation-induced neuropathy, early-onset patients most commonly have painful monophasic courses with residual deficits, possibly steroid responsive. An ischemic inflammatory pathogenesis is suggested.
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