Background
Although radiation therapy is used in the treatment of a myriad of neoplastic diseases, it has potentially adverse effects on several organs and systems that are exposed during treatment. Radiation-induced neurotoxicity can involve the central and peripheral nervous systems. Radiation-induced brachial plexopathy can occur when radiotherapy is directed at the chest, axillary region, thoracic outlet, or neck.
Results from the English National Cancer Survivorship initiative, which includes a study on the consequences of treatment in adult cancer, such as radiation-induced brachial plexopathy, suggest that patients benefit significantly when the prevention, detection, and treatment of some of these consequences are approached systematically. [1]
Pathophysiology
When treating the axillary and supraclavicular lymph nodes with radiation therapy, it is impossible to avoid irradiating normal tissues, including the brachial plexus. While dosing regimens are designed to limit damage to healthy tissue, radiation-induced neuropathy may occur. The radiation dose; treatment technique; concomitant use of chemotherapy; surgical lymph node dissection; and underlying comorbidities such as diabetes, hypertension, obesity, and vascular disease all demonstrate significant association with the development of radiation injury to the brachial plexus. [2, 3] The mechanism is believed to be a combination of failure of cellular proliferation and localized ischemia. The net result is fibrosis of the neural and perineural soft tissues secondary to microvascular insufficiency. This, in turn, leads to ischemic damage to the axons and Schwann cells. [4]
Epidemiology
Frequency
United States
The frequency of radiation-induced brachial plexopathy has declined over the past 60 years and depends significantly on both the radiation dose and the proximity of the radiation volume to the underlying plexus. In the 1950s, the incidence was as high as 66% after 60-Gy total dosing to the axillary and supraclavicular area using 5 Gy/fraction. The current incidence is 1-2% in patients receiving a typical dose of less than 55 Gy. [5] Breast carcinoma accounts for 40-75% of reported cases, followed by lung carcinoma and lymphoma. [6, 7]
International
No satisfactory data have been reported.
Mortality/Morbidity
The natural course of radiation injury to the brachial plexus varies. Most commonly, the plexopathy develops months to years after radiation therapy and demonstrates a relatively stable course over months to years with a gradual worsening of paresthesias and pain. One third of patients deteriorate rapidly and exhibit significant weakness, lymphedema, and pain. Rarely, the disorder presents as a mild and relatively reversible set of symptoms. [8] No present studies quantify the degree of disability experienced by patients with this disorder.
Race
No sources in the literature have examined the racial or ethnic distribution of patients with radiation-induced brachial plexopathy.
Sex
Given that breast cancer often is treated with radiation therapy, women experience a greater incidence and prevalence of radiation-induced brachial plexopathy than men. [9]
Age
Advanced age may be a risk factor for the development of brachial plexopathy after radiation treatment. [10] Otherwise, the age range closely parallels that of patients with breast cancer.
Tables
Feature |
Tumor Infiltration |
Radiation Fibrosis |
Transient Radiation Injury |
Acute Ischemic Injury |
Incidence of pain |
80% |
18% |
40% |
Painless |
Location of pain |
Shoulder, upper arm, elbow, fourth and fifth fingers |
Shoulder, wrist, hand |
Hand, forearm |
Hand, forearm |
Nature of pain |
Dull ache in shoulder, lancinating pains in elbow and ulnar aspect of hand; occasional paresthesias and dysesthesias |
Ache in shoulder; prominent paresthesias in C-5/C-6 distribution of hand and arm |
Ache in shoulder; prominent paresthesias in C-5/C-6 distribution of hand and arm |
Paresthesias in C-5/C-6 distribution of hand and arm |
Severity |
Moderate to severe (severe in 98%) |
Usually mild to moderate (severe in 20-35%) |
Mild |
Mild |
Course |
Progressive neurologic dysfunction; atrophy and weakness in C-7/T-1 distribution, persistent pain; occasional Horner syndrome |
Progressive weakness; panplexus or upper plexus distribution; Horner syndrome uncommon |
Translate weakness with complete resolution |
Acute nonprogressive weakness and sensory loss |
Study findings |
|
|
|
|
Magnetic resonance imaging |
High signal intensity on T2-weighted images; may enhance with gadolinium |
Low signal intensity on T2-weighted images; generally nonenhancing with gadolinium |
No data |
Normal |
Computed tomography |
Mass; circumscribed or diffuse tissue infiltration |
Diffuse tissue infiltration |
Normal |
Angiography demonstrates subclavian artery segmental obstruction |
Electromyography |
Segmental slowing |
Diffuse myokymia |
Segmental slowing |
Segmental slowing |
