Review articleNeurologic complications of radiation therapy
Section snippets
Epidemiology
The incidence of radiation-induced nervous system complications varies with the radiation dose, field size, and fractionation scheme; degree of edema; patient age; underlying diseases (malignant and nonmalignant); concomitant treatments; and length of survival after completion of radiation (Table 1). As a rule, incidence increases and latency decreases with higher total doses, higher fraction size, and larger volumes of treated nervous system [2].
Among the acute complications, acute radiation
Clinical characteristics
Radiation-related nervous system injury can affect every level of the nervous system and can occur acutely during the course of treatment or months or years after treatment has been completed. Different syndromes of nervous system injury have been characterized and can be classified anatomically or temporally (Table 2, Table 3). Because the same nervous system structures are susceptible to different radiation-related syndromes occurring at differing times after radiation therapy, a temporally
Differential diagnosis and approach to the patient
In general, the most frequent and most pressing diagnosis competing with radiation-related nervous system injury is recurrent tumor. For specific syndromes, however, other neurologic and non-neurologic conditions may complicate the differential (Table 6).
When new symptoms develop over days or weeks, are mild, or improve over the weekend break from radiation therapy, a presumptive diagnosis of acute radiation encephalopathy and an empirical increase of steroid dose are reasonable. Marked or
Treatment and prevention
No specific intervention for radiation-related fatigue beyond adequate rest and prudent scheduling of activities is generally necessary. When recent or rapid tapering of corticosteroids has taken place, a return to higher doses may be beneficial. Occasionally, stimulant medication (methylphenidate or modafinil) may be considered. Increasing doses of corticosteroids generally ameliorates the symptoms of acute radiation encephalopathy and may hasten improvement in some patients with early delayed
Summary
Injury to the central and peripheral nervous systems is an increasingly frequent consequence of standard radiation treatment protocols for tumors involving or adjacent to nervous system structures. Characteristic temporal, clinical, radiographic, and laboratory features distinguish a number of specific radiation injury syndromes, but meticulous and repeated evaluations over time are often required to establish a diagnosis. These syndromes vary with regard to prognosis and therapeutic options,
References (92)
- et al.
Factors affecting risk of symptomatic temporal lobe necrosis: significance of fractional dose and treatment time
Int J Radiat Oncol Biol Phys
(2002) - et al.
External irradiation followed by interstitial high activity iodine-125 implant “boost” in the initial treatment of malignant gliomas: NCOG study 6G–82–2
Int J Radiat Oncol Biol Phys
(1991) - et al.
Late radiation injury following hyperfractionated craniospinal radiotherapy for primitive neuroectodermal tumor
Int J Radiat Oncol Biol Phys
(1999) - et al.
High incidence of secondary brain tumours after radiotherapy and antimetabolites
Lancet
(1999) - et al.
Analysis of the histopathology of radiation myelopathy
Int J Radiat Oncol Biol Phys
(1988) - et al.
Therapeutic irradiation and brain injury
Int J Radiat Oncol Biol Phys
(1980) - et al.
Radiation-induced brachial plexopathy: neurological follow-up in 161 recurrence-free breast cancer patients
Int J Radiat Oncol Biol Phys
(1993) - et al.
Late temporal lobe necrosis in patients with nasopharyngeal carcinoma: evaluation with combined multi-section diffusion weighted and perfusion weighted imaging
Eur J Radiol
(2001) - et al.
Confusion after antibiotics
Lancet
(2001) - et al.
Magnetic resonance imaging of radiation optic neuropathy
Am J Ophthalmol
(1990)