Cancer Rehabilitation
K. Rao Poduri in Geriatric Rehabilitation, 2017
Brachial plexopathy has also been commonly associated with breast cancer treatment, as well as has been induced by radiation treatments for other malignancies occurring in proximity to the brachial plexus.126 Radiation plexopathy presents with upper extremity weakness without pain, originating within the upper trunk of the brachial plexus. Lymphedema is often secondary in onset, with most patients developing these symptoms within 3 years of radiotherapy, although later presentations may occur.127 Physical examination will initially reveal shoulder girdle weakness and then subsequent involvement of the entire arm as the disorder progresses.128 Management of radiation-induced brachial plexopathy is largely supportive. Pain should be controlled, and weakness mediated with bracing.129 Neoplastic brachial plexopathy presents with sensory loss and pain that originates in the lower trunk and progresses to the entire plexus. The presence and severity of the pain help distinguish this particular condition from radiation-induced plexopathy.116 MRI and electrodiagnostic studies may also help differentiate between neoplastic and radiation-induced plexopathy. For instance, myokymic discharges on electromyography are suggestive of radiation plexopathy, though its presence does not rule out tumor recurrence.130 Neoplastic brachial plexopathy is best managed by treating the underlying malignancy with radiation and chemotherapy.116
Pain in cancer survivors
Nigel Sykes, Michael I Bennett, Chun-Su Yuan in Clinical Pain Management, 2008
Rarely, BPN occurs concomitantly or soon after radiotherapy,108 yet most radiation-induced plexopathy occurs more than six months after treatment. Higher doses have a reduced latency for BPN.106 Progressive forelimb weakness characterizes this plexopathy with variable deficits of sensation and pain. Pain is much more common in tumor-related plexopathy,102, 109 although pain has been described as anything from a rare symptom110 to almost a universal one in radiation-induced BPN.111
Pathogenesis of normal tissue side effects
Michael C. Joiner, Albert J. van der Kogel in Basic Clinical Radiobiology, 2018
The brachial plexus is often included in treatments of the axillary and supraclavicular nodes in breast cancer patients. Clinically, plexopathy is characterized by mixed sensory and motor deficits, developing after a latent period ranging from 6 months to several years. The pathogenesis involves progressive vascular degeneration, fibrosis and demyelination with loss of nerve fibres.
Two-year toxicity of hypofractionated breast cancer radiotherapy in five fractions
Published in Acta Oncologica, 2020
Hans Van Hulle, Vincent Vakaet, Kathleen Deckmyn, Chris Monten, Leen Paelinck, Annick Van Greveling, Giselle Post, Max Schoepen, Arthur Fonteyne, Bruno Speleers, Pieter Deseyne, Marc Mareel, Wilfried De Neve, Liv Veldeman
About one-third of patients received LNI. None of the patients reported symptoms of brachial plexopathy, but longer follow-up is needed to rule out the possibility of plexopathy. In contrast to our data, the UK FAST trial observed no differences in 3-year rates of toxicity between 28.5 and 50 Gy [3]. The FAST trial only reported on moderate to marked toxicity, while we report on presence of any toxicity, including mild toxicity. This explains the higher rates of breast retraction and fibrosis in our cohort. An approach comparable to the FAST trial was not possible with our dataset due to different toxicity scoring systems. Other differences between the FAST trial and this study are the number of patients receiving a boost and patient age. In the FAST trial no boost was administered, while 90% of our patients received a boost. The mean age of the FAST group was 63 years compared to 73 years in our HF5 group. However, it was only 65 years in the HF15 group.
The evolution and rise of stereotactic body radiotherapy (SBRT) for spinal metastases
Published in Expert Review of Anticancer Therapy, 2018
Balamurugan A. Vellayappan, Samuel T. Chao, Matthew Foote, Matthias Guckenberger, Kristin J. Redmond, Eric L. Chang, Nina A. Mayr, Arjun Sahgal, Simon S. Lo
Re-irradiation using cEBRT is technically challenging. In order to limit the cumulative dose to the spinal cord, the treatment dose for the second course of cEBRT is often lower than the first (e.g. 20–25 Gy in 10 fractions). As such, even the palliative benefits are expected to be limited, as the disease has proven itself to be relatively radio-resistant. The effectiveness of a lower dose of radiation is expected to be confined to temporary partial pain relief with little chance of tumor control. Based on a RCT which included, but was not limited to, spine the rates of partial pain relief and complete pain relief at 2 months was about 20% and 8% respectively [12]. As such, in the setting of re-irradiation, there was room for improvement, which is likely to be achieved by higher doses to the tumor. SBRT allows a higher BED to the tumor, than the first course of radiotherapy, and thereby addressing any radio-resistant clones. Ultimately, the aim of re-irradiation is still durable lifelong palliation. Data from selected retrospective series report local control rates ranging from 66% to 93%. A prospective study of 59 patients, using doses of 30 Gy in 5 fractions or 27 Gy in 3 fractions, corroborates the 1-year local control rate of about 76%, and significant improvements in pain control [76]. There were only two patients who developed a Grade 3 toxicity of lumbar plexopathy.
Diabetic lumbosacral plexopathy: an unpredictable clinical entity
Published in Disability and Rehabilitation, 2023
Muhammad Faraz Jeddi, Roger Zebaze, Isabelle Urbano, Sarah Skinner, Vinamra Jain, Marc Budge
Diabetic plexopathy is the result of an acute to subacute, unilateral assault of the nerves that is most likely the result of an inflammatory process [6]. When the lumbosacral plexus is involved, it typically presents with acute, asymmetrical pain in the back, hip, or thighs accompanied by pelvic and femoral muscle wasting and weakness; thus, the term diabetic lumbosacral plexopathy (DLSP) [7,8]. Sensory impairment may be present but is usually minimal, and in the cutaneous distribution sharing the same root (or peripheral) nerve as the affected musculature [9]. The pathogenesis of DLSP is thought to involve micro-vasculitis and secondary ischemic injury to the lumbosacral roots, plexus and/or peripheral nerves not metabolic dysfunction as observed in diabetic neuropathy [7–10].
Related Knowledge Centers
- Nerve
- Brachial Plexus
- Lumbosacral Plexus
- Brachial Plexus Injury
- Injury
- Dislocated Shoulder
- Erb'S Palsy
- Diabetes
- Cancer
- Infection