Radiation-induced lumbar plexopathy (RILP) or radiation-induced lumbosacral plexopathy (RILSP) is nerve damage in the pelvis and lower spine area caused by therapeutic radiation treatments. RILP is a rare side effect of external beam radiation therapy and both interstitial and intracavity brachytherapy radiation implants. RILP is a Pelvic Radiation Disease symptom. In general terms, such nerve damage may present in stages, earlier as demyelination and later as complications of chronic radiation fibrosis. RILP occurs as a result of radiation therapy administered to treat lymphoma or cancers within the abdomen or pelvic area such as cervical, ovarian, bladder, kidney, pancreatic, prostate, testicular, colorectal, colon, rectal or anal cancer. The lumbosacral plexus area is radiosensitive and radiation plexopathy can occur after exposure to mean or maximum radiation levels of 50-60 Gray with a significant rate difference noted within that range.
Signs and symptoms Lumbosacral plexopathy is characterized by any of the following symptoms; usually bi-lateral and symmetrical, though unilateral is known.
Lower limb dysaesthesia, abnormal sensations of touch or feeling Lower limb weakness Lower limb numbness Lower limb paresthesia, e.g., foot drop, muscle atrophy Lower limb neuropathic pain Symptoms are typically a step-wise progression with periods of stability in between, weakness often appearing years later. Weakness frequently presents in the lower leg muscle groups. Symptoms are usually irreversible. Initial onset of symptoms may occur as early as 2 to 3 months after radiotherapy. The median onset is approximately 5 years, but can be highly variable, 2-3 decades after radiation therapy. One case study recorded the initial onset occurring 36 years post treatment.
Cause The treatment's ionizing radiation is an activation mechanism for apoptosis (cell death) within the targeted cancer, but it can also impact nearby healthy radiosensitive tissues, like the lumbosacral plexus. Plexopathy and neuropathic pain occurring after radiation is associated with ischemic demyelination and perineural fibrosis. The occurrence and severity of RILP is related to the magnitude of ionizing radiation and the peripheral nerves' radiosensitivity and may be further aggravated if combined with chemotherapy consisting of taxanes and platinum drugs.
Pathophysiology The pathophysiological process behind radiation's RILP nerve damage has been discussed since the 1960s and is still without a precise definition. Consensus does exist on a progression of RILP symptoms, with a stepping (a time delay) between two periods of plexopathy onset, the first from radiation injury and the later from fibrosis. Proposed mechanisms of the early nerve damage include microvascular damage (ischemia) supplying the myelin, radiation damage of the myelin, and oxygen free radical cell damage. Some plexopathies arising within the first year post-RT respond to corticosteroids and may recover. This variation is presumed to be from radiation injury of the Schwann cells forming the myelin sheaths and demyelination (loss of axon insulation). Later delayed nerve damage is attributed to compression neuropathy and a late fibro-atrophic ischemia from retractile fibrosis.
Diagnosis The more common source of lumbar plexopathy is a direct or secondary tumor involvement of the plexus with MRI being the typical confirmation tool. Tumors typically present with enhancement of nerve roots and T2-weighted hyperintensity. The differential consideration of RILP requires taking a medical history and neurologic examination. RILP's neurological symptoms can mimic other nerve disorders. People may present with pure lower motor neuron syndrome, a symptom of amyotrophic lateral sclerosis (ALS). RILP may also be misdiagnosed as leptomeningeal metastasis often showing nodular MRI enhancement of the cauda equina nerve roots or having increased CSF protein content. Other differential diagnoses to consider are Chronic Inflammatory Demyelinating Polyradiculoneuropathy, neoplastic lumbosacral plexopathy, paraneoplastic neuronopathy, diabetic lumbosacral plexopathy, degenerative disk disease (osteoporosis of the spine), Osteoarthritis of the spine, Lumbar Spinal Stenosis, post-infectious plexopathy, carcinomatous meningitis (CM), mononeuritis multiplex, and chemotherapy-induced plexopathy. The testing to resolve a RILP diagnosis involves blood serum analysis, X-rays, EMG, MRI and cerebrospinal fluid analysis.
Prevention Since RILP's neurological changes are typically irreversible and a curative strategy has yet to be defined, prevention is the best approach. Treating the primary cancer remains an obvious requirement, but lower levels of lumbar plexus radiation dosing will minimize or eliminate RILP. One method to reduce the lumbosacral plexus' dosing is to include it with other at-risk organs that get spared from radiation, albeit the lumbosacral plexus it is not generally recognized as an organ at risk (OAR). Key to prevention is resolving the lack of clinical evidence between radiation treatments and the onset of neurological problems. That relationship is hidden by RILP's low toxicity rate, the lack of a large monitored population size and the lack of data pooling across multiple institutions.
Management Treatment of RILP is primarily supportive with mental, physiological and social aspects and consideration of any aggravating (synergistic) neurological factors. To prevent compounding existing RILP symptoms and to minimize further progression
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