British Journal of Radiology (2006) 79, e45-e49
© 2006 British Institute of Radiology
doi: 10.1259/bjr/16265478
Radiation myelopathy after radioactive iodine therapy for spine metastasis
H Murakami, MD
1
N Kawahara, MD
1
T Yahata, MD
1
K Yokoyama, MD
2
K Komai, MD
3 and
K Tomita, MD
1
Department of 1Orthopaedic Surgery 2Nuclear Medicine 3Neurology and Neurobiology of Aging, Kanazawa University, Kanazawa, Japan
Correspondence: Norio Kawahara, Department of Orthopaedic Surgery, Kanazawa University, 13-1 Takaramachi, Kanazawa, 920-8641, Japan
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Abstract
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A case of radiation myelopathy after radioactive iodine therapy is reported. This is the first report to describe radiation myelopathy after I-131 therapy. A 62-year-old female with spinal metastasis of T10 received I-131 therapy. She presented with radiation myelopathy 34 months after the irradiation. We need to recognize the possibility of this serious complication even in the case of I-131 therapy. There is a risk of radiation myelopathy even after I-131 therapy, especially in cases with spinal cord compression such as this.
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Introduction
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Radiation therapy is commonly applied as a primary or adjuvant therapy for malignancies. One of the most serious complications following radiation therapy is myelopathy, particularly in long-term surviving patients. Post-radiation myelopathy occurs when the spinal cord is included within the radiation field in cases of high total radiation doses, or for high radiation doses per fractionation. The myelopathy may result in chronic progressive symptoms months or years after radiotherapy and no treatment has proved satisfactory. Radioactive iodine (I-131) therapy is a type of radiotherapy and has an important role in the treatment of thyroid cancer and its metastasis. However, there are no previous reports describing myelopathy after I-131 therapy. We report on the first case of radiation myelopathy due to I-131 administration in a case of thyroid cancer metastasis.
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Case report
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A 62-year-old female underwent a total thyroidectomy for follicular thyroid carcinoma and a partial lobectomy for solitary lung metastasis in March 1999. At that time, spine metastasis of T10 was detected (Figure 1
) and I-131 therapy was done three times (7.6 GBq each time) from September 1999 to March 2000. The patient received a total of 22.8 GBq of radioiodine, the routine amount for bone metastasis. In January 2003, she felt hypesthesia on her left lower extremity without any apparent trauma. Then, muscle weakness in her right lower extremity appeared and she was transferred to our hospital for further examination.
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Figure 1. On axialT2 weighted image taken in 1999, the tumour extended to the right vertebral body, right pedicle, and right lamina of T10.
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Upon neurological examination, she had hypothermia and hypoalgesia in her left lower limb, and muscle weakness (3-4/5) and pyramidal signs in her right lower limb. That is, right side injured type Brown-Sequard syndrome was present. All laboratory data were within normal range. Plain X-ray film revealed a right pedicle sign and CT scans demonstrated an osteolytic lesion of T10. MRI demonstrated a tumour lesion with abnormally low signal intensity on T1 weighted images and high signal intensity on the T2 weighted images on the right side of the T10 vertebral body without clear enhancement after intravenous gadolinium (Gd) injection. In addition, it showed an appearance of high signal intensity from T10 to T5 on the T2 weighted images on the spinal cord (Figure 2a). On axial images of the MRI, the tumour extended to the right vertebral body, right pedicle and right lamina of T10 (Figure 2b). The size of the tumour at T10 had not changed since I-131 therapy in 1999. A technetium-99m bone scan showed a cold spot at the right side of T10, and positron emission tomography (PET) also demonstrated no increased uptake. It meant that the I-131 therapy had a sufficient effect on the T10 tumour and there were no other metastatic lesions. Although there was no cord compression by the tumour as seen on the MRI, the spinal canal was narrow due to ossification of the yellow ligament (OYL), as seen on the CT (Figure 3a), and the cord was severely compressed by the OYL as seen on the MRI (Figure 3b) at the level of T10/11. At first, we diagnosed this as Brown-Sequard syndrome due to the OYL on T10/11, rather than the metastatic tumour of T10 based on imaging studies.
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Figure 2. MRI demonstrating abnormal intensity at T10.(a) Sagittal T2 weighted image showing high signal intensity on the spinal cord. (b) Axial T2 weighted image.
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To improve her paralysis, an excision of the OYL was performed after laminectomies of T9, 10 and 11 in March 2003. During the surgery, extensive fibrous scar tissue existed around the dural matter (Figure 4). Simultaneously, curettage of the T10 vertebral tumour from the posterior approach to evaluate the viability of the tumour and spinal instrumentation was performed. Histological examination of the excised material (vertebral tumour) showed fibrous tissue and necrotic tissue (total necrosis), and no tumour cells (Figure 5).
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Figure 5. Low-power photomicrograph of the specimen from excised materials of T10 tumour. Haematoxylin and eosin x120.
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Her sensory and motor disturbance improved (4-5/5 from 3-4/5) immediately after the operation. Her gait exercise was started 6 days after surgery and her post-operative course was uneventful for a week. However, she gradually felt muscle weakness (2-3/5) in her right leg without any apparent trauma about 10 days after the surgery. In spite of intravenous corticosteroid injections for a few days, motor paralysis in the right leg progressed and was complete 24 days after the surgery. Furthermore, muscle weakness (2-3/5) in her left leg and sensory disturbance in her right leg, which was not seen before the operation, appeared simultaneously. Then, sensory disturbance of her left leg, which had improved immediately after the surgery, progressed rapidly. She also had difficulty with urination. Her symptoms did not improve at all and her paralysis was completed 35 days after the surgery. During the progression of paralysis, an MRI was performed several times and the follow-up MRI showed adequate decompression from the OYL with no other lesions around the spinal cord such as haematoma or tumour. The high intensity area of the spinal cord on T2 weighted images, which was detected before the surgery, was seen to remain at the same size and level without any changes on the MRI (Figure 6).
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Figure 6. Post-operative MRI. A sagittal T2 weighted image showing high signal intensity on the spinal cord.
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Discussion
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From the patient's clinical and imaging studies, we diagnosed radiation myelopathy developing after I-131 therapy. Although it is difficult to diagnose radiation myelopathy definitively in the absence of pathological evidence from the spinal cord, three criteria for the diagnosis of radiation myelopathy have been established [1]:
- The spinal cord must have been included in the radiation field.
- The neurological deficit must correspond to the cord segment that was irradiated.
- Metastases or other primary spinal cord lesions must be ruled out.
The clinical and imaging features in this case met the three criteria. This patient received I-131 therapy for a metastatic tumour of T10 from 1999 to 2000. An extensive fibrous scar around the dural matter at T10, which was seen in surgery, is usually seen after external irradiation. It proves that the spinal cord was certainly irradiated at this level (criteria 1). The neurological deficit level of Brown-Sequard syndrome in this case corresponded to T10 tumour level (criteria 2). The post-operative MRI in this patient showed no cord compression by the metastatic tumour or the OYL. There was no intradural invading tumour. Furthermore, her clinical findings, clinical course and imaging findings were completely different from those of other spinal cord lesions such as spinal cord infarction, multiple sclerosis, or myelitis. Damage to the cord during this surgery was not a cause of myelopathy, since her neurological deficit improved immediately after the surgery. Her paralysis progressed although no other causes of paralysis were apparent (criteria 3). In addition to the three criteria, the MRI findings in this case were also consistent with those of radiation myelopathy. The MRI features of radiation myelopathy are characterized as an area of high signal intensity within the spinal cord detected on T2 weighted images [2–4]. In this case, the high intensity area of the spinal cord on T2 weighted images from T5 to T10, which was not seen when I-131 therapy started in 1999, is compatible with findings of radiation myelopathy. Another reason to diagnose radiation myelopathy, not Brown-Sequard syndrome due to the OYL, is the characteristic neurological findings. Despite the spinal cord compression by the OYL in the same degrees bilaterally, on the tumour side (right side) injured Brown-Sequard syndrome was seen. The definite diagnosis in this case must be radiation myelopathy. There are no previous reports describing radiation myelopathy due to I-131 therapy in the literature. We need to recognize the possibility of this serious complication even in the practice of I-131 therapy.
Radiation-induced myelopathy is the most serious complication associated with radiotherapy. Many cases have been reported since Ahlbom [5] first published on radiation myelopathy after external radiotherapy in 1941. The latent period between termination of irradiation and onset of neurological symptoms has varied between 3–5.5 months and 30–41 months, but in the majority of cases was 9–20 months [6]. In this case, it was 34 months. Higher radiation doses, larger doses per fraction and previous exposure to radiation could be associated with a higher probability of developing radiation myelopathy [7, 8]. Based on animal and human data, the 5% likelihood of the complication after external radiotherapy at 5 years and 50% likelihood of the complication at 5 years for a 10 cm length of spinal cord are 57–61 Gy and 68–73 Gy in 2 Gy fractions, respectively [9]. Radiotherapy is often administered to end-stage patients with metastatic spinal tumours. There would be many cases in which the patients died before the appearance of myelopathy. The incidence of myelopathy in long-term surviving patients is estimated to be higher than the incidence reported in the literature. The pathogenesis of radiation myelopathy is reported to involve damage to the vascular endothelium with secondary permeability disorders of the blood–brain barrier [10–13]. Once radiation myelopathy occurs, there is no known effective treatment for radiation myelopathy and the symptoms, in general, are irreversible.
Because it is primarily concentrated in thyroid tissue, I-131 can be used in the treatment of thyroid cancer, and lung or bone metastasis of thyroid cancer. Bone metastases typically have little or no response to I-131 therapy [14]. However, some authors have found that I-131 therapy can be used with curative intent in patients with bone metastases [15]. Thyroid cancer cells that have spread to other parts of the body are killed when they absorb I-131, which has a physical half-life of 8.05 days. It decays by high energy gamma photon and particulate emissions (beta particle). The beta particle will deposit the majority of its energy within 2 mm of its site of origin [16]. The patient reported on here received a total of 22.8 GBq of radioiodine. This amount of radioiodine is equivalent to about 20–30 Gy in external radiotherapy and should be within the safety margin for the spinal cord. However, especially in cases with spinal cord compression such as in this case, there is a risk of radiation myelopathy after I-131 therapy even if it is the amount generally used, since the tumour is attached to the spinal cord.
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Acknowledgments
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The authors thank William C Hutton, DSc for his kind criticism and advice.
Received for publication June 20, 2005.
Revision received August 15, 2005.
Accepted for publication August 17, 2005.
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Abstract
Introduction
