Brachytherapy: Applications and Technique, 1st Edition

4. Central Nervous System Brachytherapy

 

Arnab Chakravarti

Thomas F. Delaney

Jay S. Loeffler

Brachytherapy for Malignant Gliomas

Introduction

Primary malignant brain tumors are among the most aggressive of all human neoplasms. There have been few significant advances over the past 25 years in the management of malignant gliomas, despite aggressive surgery, radiation, and chemotherapy, which truly represent curative options. The median survival times for patients with glioblastoma multiforme (GBM) remain around 12 to 15 months in most modern series.1,2,3 Significantly, most patients with GBM fail locally within close proximity to the original tumor. Given this pattern of failure, there has been much interest in radiation dose escalation in improving clinical outcomes of this patient population. Radiation dose escalation has taken many forms including conventional radiotherapy, stereotactic radiosurgery (SRS), and brachytherapy. Brachytherapy refers to placement of radioactive sources within or in close proximity to the tumor/tumor bed. Given the ability of brachytherapy to increase central radiation doses within the tumor/tumor cavity, it has been hypothesized that brachytherapy should improve outcomes in patients with newly diagnosed or recurrent malignant gliomas. This chapter comprehensively reviews brachytherapy for malignant gliomas from the radiobiologic, physics, and clinical standpoints.

Radiobiology of Brachytherapy

There are several biologic advantages of brachytherapy over the more conventional teletherapy approaches for malignant gliomas. These pertain to the four “R's” of radiobiology as described by Eric Hall: repair, redistribution, reoxygenation, and repopulation.4 The relatively low dose rates of brachytherapy permit greater repair of deoxyribonucleic acid (DNA) damage in normal tissues, including both sublethal and potentially lethal damage. As tumor cells have less repair capacity compared with their normal cell counterparts, it follows that they should be relatively more sensitive to the effects of brachytherapy. As the proliferating cells are killed, the nonproliferating cells enter the cell cycle and eventually enter the more radiosensitive G2/M phase. As greater numbers of tumor cells are killed by radiation, there is increased oxygenation of remaining tumor cells, also contributing to greater radiation sensitivity. Repopulation can occur if tumor cells reproduce faster than they are killed off. With brachytherapy, continuous administration of radiation is inherent over a given length of time that can in theory minimize such a repopulation effect.

Physics of Brachytherapy

Brachytherapy for tumors of the central nervous system (CNS) is most commonly performed using either temporary high-activity or permanent low-activity iodine 125 (125I) sources (see Chapter 2 for isotope characteristics). There are important differences between the two approaches with regard to both technical detail and indications. Temporary implants have been investigated for both patients with newly diagnosed and recurrent malignant gliomas. Generally, candidate tumors should be supratentorial, but without involvement of the basal ganglia and diencephalon. The procedure entails the placement of a stereotactic head frame, followed by a contrast-enhanced brain computed tomography (CT). Catheter trajectories are then planned, and a dose of 50 Gy is typically prescribed to the margin of the contrast-enhancing tissue. Following the afterloading of the nylon catheters with dummy sources, paired orthogonal films are obtained. Careful dosimetry is subsequently performed. The source positions can be adjusted to reflect the desired dosimetry. The isotope-containing inner catheters are then loaded for the prescribed amount of time to achieve the correct dose. Once this has been accomplished, the catheters are removed and the patient is discharged.

Permanent Implants

The most common indication for implantation with permanent sources is in cases of recurrent GBMs. The neurosurgeon performs as complete a resection as possible. Once this has been completed, low-energy 125I sources are placed along the walls of the resection cavity at 0.5- to 1.0-cm intervals. As these 125I sources can only penetrate limited distances, this technique is most effective for treating microscopic disease. Following implantation, a CT scan is performed to calculate final dosimetry. As demonstrated in Figures 4.1, 4.2 and 4.3, the resulting dose distribution is highly conformal in such cases with sharp dose falloffs, limiting dose to surrounding normal brain.

Figure 4.1 Inferior cut of axial computed tomography scan with isodose lines tightly conforming to 125I seed implantation (Dr Loeffler's teaching file.).

Figure 4.2 Superior axial plane (Dr Loeffler's teaching file).

GliaSite

Another brachytherapy approach is the GliaSite device (Cytyc Corp., Marlboro, MA) (see Fig. 4.4). During the tumor resection, the balloon portion of the GliaSite catheter is placed within the resection cavity (see Figs. 4.5, 4.6, 4.7, 4.8, 4.9 and 4.10). The other end of the catheter serves as the injection port and is fixed on top of the skull and concealed underneath the skin. After the surgery, Iotrex (see Fig. 4.11), which is an 125I liquid source, and saline are injected into the catheter (see Fig. 4.12) and fill the balloon, allowing for size and placement verification of the balloon with a magnetic resonance imaging (MRI) scan. The Iotrex dwells for 3 to 7 days, delivering the prescribed dose of radiation (see Figs. 4.13 and 4.14). At the end of this period, the Iotrex and saline are withdrawn and the balloon catheter is then removed during a brief surgical procedure. Figure 4.15 demonstrates axial and coronal images, before, during, and at follow-up from intracavitary CNS brachytherapy with GliaSite.

Figure 4.3 Coronal computed tomography scan reconstruction confirms tight conformality of implant (Dr Loeffler's teaching file).

Figure 4.4 GliaSite catheter is tested with saline before insertion into tumor cavity. Note the flexible catheter and balloon with central infusion channel (Courtesy of Cytyc Corp., Marlboro, MA).

 

Figure 4.5 Schematic of relationship of intraparenchymal intracavitary balloon with extradural subgaleal infusion port (Courtesy of Cytyc Corp., Marlboro, MA).

Figure 4.6 Intraoperative photograph of GliaSite with saline instillation and partial dural closure (Courtesy of Cytyc Corp., Marlboro, MA).

 

Figure 4.7 Intraoperative photograph of GliaSite with saline instillation and dural window to insure catheter does not kink. Note that the catheter and infusion port are extracranial and subgaleal (Courtesy of Cytyc Corp., Marlboro, MA).

Figure 4.8 Intraoperative photograph demonstrating apposition of intracavitary balloon to brain parenchyma as the dura undergoes partial closure (Courtesy of Dr James W. Welsh, University of Arizona).

 

Figure 4.9 Intraoperative photograph demonstrating calvarial reposition with titanium plates. The GliaSite catheter exits through the burr hole created for the craniotomy. The catheter is gently curled so as not to kink. No retention suture is used (Courtesy of Dr James W. Welsh, University of Arizona).

Figure 4.10 The scalp is primarily closed in the usual way. Note the protruding profile of the infusion port of the GliaSite catheter (Courtesy of Cytyc Corp., Marlboro, MA).

Results of Central Nervous System Brachytherapy

Newly Diagnosed Malignant Gliomas

There have been several retrospective and prospective series examining the efficacy of brachytherapy for patients newly diagnosed with malignant glioma. One of the earliest and largest series on brachytherapy was reported by Loeffler et al.5 This study included patients having supratentorial tumor measuring 5 cm or less in size without involvement of the corpus callosum or ependymal surfaces, and a Karnofsky performance status (KPS) of at least 70. Thirty-three out of the 35 patients underwent surgical debulking, with the remaining two patients undergoing biopsies. Treatment consisted of external beam radiation therapy (EBRT) to a dose of 59.4 Gy at 1.8 Gy fractions followed by brachytherapy. Two weeks following EBRT, brachytherapy was administered using high-activity 125I sources (20 to 50 mCi), which was used to deliver a minimum dose rate of 0.4 Gy per hour for a total of 50 Gy. Survival at 1 year was 87% for the brachytherapy group, compared with 40% for historic controls treated with EBRT (p <0.001). At 2 years, the survival in the brachytherapy group was 57% compared with 13% for the control group. Forty percent of the patients in the brachytherapy group required reoperation. Histologic analysis revealed residual microscopic disease in most specimens, although the viability of these cells was difficult to determine. The acute toxicity rate was 18%. It is of note that patients treated with brachytherapy generally underwent a decline in their KPS from 80 at the time of implantation to 70 at 6 months and 60 at 12 months. After this time, there did not appear to be any further decline of KPS. In an updated report, Loeffler et al. reported a median survival of 18 months in the group treated with both brachytherapy and EBRT compared with 11 months for patients treated primarily with EBRT.6 The reoperation rate was 64% for the brachytherapy group and the median survival improved to 22 months in the patients undergoing reoperation compared with 13 months for those that did not (see Figs. 4.16, 4.17, 4.18 and 4.19).

Figure 4.11 V-vial containing radioactive 125I, Iotrex, for infusion with normal saline into the catheter (Courtesy of Cytyc Corp., Marlboro, MA).

Figure 4.12 After treatment planning the volume of saline within the balloon is withdrawn and an equal amount of 125I solution Iotrex and saline is instilled. Note the shielded syringe to protect the treating physician and staff (Courtesy of Cytyc Corp., Marlboro, MA).

 

Figure 4.13 Idealized radial dose distribution from a GliaSite spherical balloon treatment with 125I Iotrex in solution (Courtesy of Cytyc Corp., Marlboro, MA).

Figure 4.14 Axial magnetic resonance imaging with GliaSite in place in the right parietal lobe with treatment planning isodose lines superimposed. The prescription is at 10 mm from the balloon (Courtesy of Cytyc Corp., Marlboro, MA).

 

Figure 4.15 A clinical vignette following a single patient through therapy. The top row shows axial magnetic resonance imaging, while the bottom shows the coronal image. The left images are pretreatment, the central images are during the GliaSite treatment, and the right images are at follow-up postcatheter removal. Note the excellent conformance of the balloon to the tumor cavity in the middle images (Courtesy of Cytyc Corp., Marlboro, MA).

The results of a single-institution, University of California San Francisco (UCSF), trial appeared to support these findings, with a median survival time of 88 weeks in 34 patients with GBM and 157 weeks in 29 patients with anaplastic astrocytoma (AA).7 It is of note that approximately 40% of patients required a reoperation, with a mortality rate of 0.7% and a morbidity rate of 7.8%. It was determined that there was no benefit for patients with anaplastic astrocytoma, as the survival time was not appreciably different from historic controls, for example, patients treated with external beam involved-field radiotherapy and procarbazine, lomustine, and vincristine (PCV) chemotherapy. It was further determined that patients with GBM who underwent reoperation had significantly longer survival times compared with those that did not. A significant brachytherapy dose–response relationship could be appreciated in this patient population.8 Results for Cox proportional hazards analyses, adjusting for age, KPS, extent of resection, and administration of PCV/hydroxyurea (HU) revealed that minimum brachytherapy tumor dose and biologic effective dose (BED) were significantly associated with freedom from local failure. It is noteworthy that two patients expired and one had severe necrosis requiring hospice care. The deceased patients had received brachytherapy doses of 119 and 66 Gy, respectively, to 95% of the tumor volume and a dose of 60 Gy to 31.9 and 20.0 cm3 of normal brain, respectively. The authors warned, on the basis of this data, that brachytherapy boost doses exceeding 50 to 60 Gy may lead to life-threatening necrosis. They further recommended careful tailoring of the prescription isodose volume to the contrast-enhancing volume, delivery of a minimum brachytherapy dose of 45 to 50 Gy with EBRT, and reoperation for symptomatic necrosis. These encouraging results led to two randomized, phase III studies evaluating the role of brachytherapy in the initial management of malignant glioma patients.9,10 In a study from the University of Toronto,10 140 patients were randomized between 1986 and 1996: 71 to the EBRT plus implant arm and 69 to EBRT only. Implants were performed using temporary stereotactic 125I implants delivering a minimum peripheral tumor dose of 60 Gy. Inclusion criteria was the following: biopsy-proven supratentorial malignant astrocytoma <6 cm in size, not crossing midline or involving the corpus callosum, age 18 to 70, and KPS >70. EBRT was delivered to a dose of 50 Gy in 25 fractions over 5 weeks. It was determined that factors associated with improved survival on univariate analysis included age <50, KPS >90, chemotherapy at recurrence, and reoperation. Median survival in the brachytherapy group was 13.8 months versus 13.2 months in the EBRT group (p = 0.49). Therefore, no survival advantage was found with the addition of brachytherapy in this prospective randomized study (see Figs. 4.20, 4.21 and 4.22).

Figure 4.16 Schematic of temporary 125I catheter–based implants showing transcranial placement by closed stereotactic technique (Dr Loeffler's teaching file).

Figure 4.17 Axial computed tomography scan shows computer-optimized catheter location and isodose pattern (Dr Loeffler's teaching file).

 

Figure 4.18 Coronal computed tomography scan reconstruction of the same case (Dr Loeffler's teaching file).

Figure 4.19 Sagittal computed tomography scan reconstruction of the same case (Dr Loeffler's teaching file).

 

Figure 4.20 Neurosurgeon placing catheter for temporary 125I brachytherapy (Courtesy of Dr Normand Laperierre).

The Brain Tumor Cooperative Group 87-0101 trial was another randomized trial examining the benefits of brachytherapy in patients newly diagnosed with malignant glioma.9 This study compared surgery, EBRT, and BCNU compared to the same with the addition of brachytherapy implant. Until May 1989, all patients received whole-brain radiotherapy to a dose of 43 Gy in 25 fractions, plus a boost for an additional 17.2 Gy delivered in 10 fractions. After May 1989, all patients received 60.2 Gy in 35 fractions to the contrast-enhanced volume plus a 3-cm margin. Interstitial implant was performed using 125I sources. The implants were designed to cover the contrast-enhancing volume with up to a 1-cm margin. A total of 60 Gy was delivered to the tumor perimeter over 5 to 7 days. The median survival for the brachytherapy group was 68.1 weeks, compared with 58.8 weeks for patients treated with EBRT. However, this difference was not found to be statistically significant (p = 0.101). Factors associated with outcome were reported to be age, KPS, and histopathology.

Recurrent Malignant Glioma

The outcomes of patients with recurrent malignant gliomas are known to be especially poor. Although there have not been phase III randomized studies reported on the value of brachytherapy for this patient population, there have been retrospective reports published that suggest potential benefit. Shrieve et al. reported on patients with recurrent malignant gliomas who were either treated with temporary high-activity brachytherapy or radiosurgery.11 The median survivals were found to be comparable in both groups (brachytherapy = 11.5 months vs. 10.2 months for radiosurgery). The risk of reoperation was higher in the brachytherapy group at 64% versus the radiosurgery group at 33%, although the treatment volumes were significantly larger in the brachytherapy group.

Figure 4.21 Axial computed tomography scan after the placement of catheter with dummy markers into right frontal lobe tumor cavity (Courtesy of Dr Normand Laperierre).

Figure 4.22 Axial computed tomography scan after the placement of catheter with dummy markers into left frontotemporal contrast-enhancing recurrent glioblastoma multiforme (Courtesy of Dr Normand Laperierre).

Emerging data suggests that low-activity permanent implants may provide some advantages over high-activity temporary implants with the rates of symptomatic necrosis being lower. Several studies also suggest an improvement in median survival times of patients with recurrent malignant gliomas. Larson et al. reported on the outcomes of permanent low-activity sources in 37 patients with recurrent glioblastoma.12 The dosage administered approached 300 Gy at 5-mm-depth dose, with an initial dose rate of 15 cGy per hour. The median survival of these patients was found to be 52 weeks, with a median time to progression of 16 weeks. Of the 37 tumors, 34 recurred. Given the relatively short time to tumor progression, the UCSF group has recommended options other than brachytherapy for patients with recurrent malignant gliomas.13

Novel Brachytherapy Approaches for Malignant Gliomas

High dose rate stereotactic brachytherapy (HDR-STBT) has also been investigated in cases of newly diagnosed GBM. In one study, 28 patients with GBM were treated using HDR-STBT in combination with surgery and EBRT.14 Eligibility requirements included unifocal lesions, residual tumors <6 cm, supratentorial lesions, tumors not crossing midline and without subependymal spread, and KPS >60. HDR-STBT was administered over 5 consecutive days with 2 fractions per day for a total median dose of 30 Gy. Twenty-eight HDR-STBT GBM patients who were treated with surgery and EBRT alone (without HDR-STBT) served as matched controls. It was determined that the median survival times for the HDR-STBT and the control group were 19.5 and 12.5 months, respectively. The 1- and 2-year survivals were 89% versus 42% and 61% versus 28%, respectively (p = 0.12). On multivariate analysis, age, KPS, and HDR-STBT were significant determinants of survival. It was ultimately found that the survival benefit was most significant for RPA Class V patients, compared with the control group. These findings have yet to be confirmed in larger, prospective studies.

Another interesting brachytherapy approach involves 125I-labeled monoclonal antibodies administered into surgically created resection cavities in patients newly diagnosed with GBM. This approach takes advantage of the molecular characteristics of these tumors. Tenascin, which is an extracellular matrix hexabrachion glycoprotein, has been found to be expressed in high frequencies in high-grade gliomas, but not in normal brain.15 A monoclonal antibody (9mAb) called 81C6 has been developed, which binds to an epitope within the alternatively spliced fibronectin type III region of tenascin, which is expressed in high frequencies in gliomas. In a phase II study from Duke, 120 mCi of 131I-labeled murine 81C6 was directly injected into the resection cavity of 33 patients with high-grade gliomas (GBM = 27; AA = 4; anaplastic oligodendroglioma [AO] = 2). Patients then received EBRT followed by 1 year of alkylator-based chemotherapy. Median survival for all patients was 86.7 weeks and for patients with GBM, in particular, it was 79.4 weeks. There were some patients who had longer-term survival outcomes. In fact, 11 patients remain alive at a median follow-up of 93 weeks. The treatment was generally well tolerated, with nine patients (27%) having developed reversible hematologic toxicity. Histologically confirmed neurotoxicity occurred in five patients (15%). One patient (3%) required reoperation for radio necrosis. The authors concluded that the median survival achieved with 131I-labeled 81C6 exceeded that of historical controls, with significantly lower rates of reoperation.

Summary

Of all human tumors, malignant gliomas are one of the most treatment refractory types. Few therapies have been demonstrated to significantly improve outcome in this disease. Unfortunately, phase III studies have not demonstrated a significant survival benefit for the general population of patients with GBM. However, there appear to be a relatively small, but distinct, subset of patients with GBM who do appear to derive benefit. Perhaps molecular/genetic profiling can identify which patients with GBM would derive the greatest benefit from the addition of brachytherapy into the overall treatment regimen. Novel strategies such as 131I-labeled murine mAbs may in fact improve the therapeutic ratio of brachytherapy through reduction of neurotoxic side effects. As novel therapeutic strategies emerge for patients with GBM, strategies to enhance the safety and efficacy of brachytherapy may be realized in the future.

Dural Plaque Brachytherapy—Massachusetts General Technique

Intraoperative dural brachytherapy by customized iridium or yttrium 90 (90Y) plaques has been investigated at the Massachusetts General Hospital. In the clinical scenario of spinal and paraspinous sarcomas, there was a well-documented dilemma, even with advanced external beam techniques including proton therapy, that because of inability to deliver high dose to the spinal cord the residual burden of microscopic disease after best possible resection was high. A testament to this problem is seen in intraoperative ultrasound measurements that show the very small distances between the dura and spinal cord.

Surgery is the primary treatment for most tumors, but wide margins are very uncommon and tumor cells may remain on the dura. Resection of the dura itself poses risks of contamination of cerebrospinal fluid (CSF) and CSF leak.

Radiation therapy (RT) has historically shown that for sarcoma microscopic residual disease doses of >65 Gy are required. Clearly, these doses are very difficult to achieve with EBRT without exceeding spinal cord tolerance of 45 to 50 Gy. The main problem is one of geometric spacing. The dura and the spinal cord are separated by only 3 to 4 mm of CSF at best.

Supported by an interdisciplinary academic team, an Institutional Review Board (IRB)-approved and National Cancer Institute (NCI)-supported protocol was designed to develop a dural brachytherapy applicator to preferentially treat the dural surface and spare the spinal cord. There was a need to identify the optimal isotope and to characterize its dosimetry before taking the new modality to clinical trial.

Figure 4.23 Polycarbonate dural plaque custom made for intraoperative implantation to spinal dura (Dr DeLaney's teaching file).

Figure 4.24 Sagittal magnetic resonance imaging demonstrating enhancing paraspinous mass with compression of thecal sac around L2-L3 (Dr DeLaney's teaching file).

 

Table 4.1 Number of Plaques Created with 192Ir, 90Y Liquid, and 90Y Foil

192Ir
90Y (liquid)
90Y (foil)

Table 4.2 Comparative Depth Doses

 

192Ir (%)

90Y (%)

2 mm

80

27

4 mm (cord surface)

60

8

8 mm (cord center)

50

0

The comparative depth doses discovered by Gaf chromic film exposure were superior for the 192Ir for the endpoint of better gradient of falloff for the spinal cord.
The 192Ir plaque was loaded in a modified Patterson and Parker distribution. The 90Y liquid plaque was made with a thin 2.5-mm hollow chamber within the plaque that was filled with 90Y in solution. The foil plaque had the 0.05 mm 90Y foil between the inner and outer layers of polycarbonate of 5-mm total thickness. The plaque length was 26 to 30 mm. The plaque covered 152 degrees and the foil covered 136 degrees.

The methodology included the fabrication of a semicylindrical polycarbonate brachytherapy plaque of appropriate size and to test various isotopes in it (see Fig. 4.23). The dural areas at risk were measured on preoperative MRI scan (see Fig. 4.24). A nonradioactive plaque was also made to assess the fit at surgery before temporary installation of the live plaque. The initial plaques were made with 192Ir. Subsequent plaques were made with 90Y because of demonstrated superior dose distribution. (see Tables 4.1 and 4.2)

The treatment protocol included EBRT (conformal/IMRT ± protons) and best resection of vertebral, soft tissue, and/or epidural tumor. Table 4.3 shows the distribution of tumor types. The nonradioactive plaque was fitted to the dura at risk. When the fit was approved, there was an intraoperative brachytherapy boost to dura by placing radioactive dural plaque for between 6 and 40 minutes to deliver an intraoperative radiotherapy (IORT) boost dose of 7.5 to 15 Gy (see Figs. 4.25 and 4.26). The timing of dwell was carefully precalculated to ensure conformance to prescription and written directive and was independently monitored by the authorized user and physicist (see Table 4.4). When the time was up, the plaque was removed and the surgery proceeded to additional vertebral reconstruction and stabilization as indicated by the primary resection. Postoperative chemotherapy was given when clinically indicated.16

Table 4.3 Distribution of Histologic Cell Types of Tumors Treated

Spinal chondrosarcoma

3

Chordoma

1

Osteosarcoma

1

Spindle cell sarcoma

1

Renal cell metastasis

1

Paraspinal Malignant Peripheral Nerve Sheath Tumor (MPNST)

1

There were no acute or late complications from plaque therapy. Local control was achieved in seven out of eight patients at 7 to 31 months. Three out of eight patients were alive without evidence of disease at 7 to 31 months. Four out of eight patients died of disease at 8 to 25 months.
The initial experience was encouraging enough for future development efforts to be focused on 90Y foil plaques and integrating this technology into multidisciplinary management of spinal and paraspinal sarcomas.

 

Figure 4.25 Intraoperative photograph where the paraspinous tumor has been grossly resected and the dura is intact. Harrington rods have been placed for stabilization (Dr DeLaney's teaching file).

Figure 4.26 The radioactive plaque is in situ on the dura and stabilized with gauze packing for the duration of treatment. The radiation physicist carefully manages the timing of the implant (Dr DeLaney's teaching file).

P.111

 

Table 4.4 Intraoperative Doses, Times, Dose Rates for the Various Isotope Systems

Intraoperative dural doses of 7.5 to 15 Gy
6.4–40.1 min
Dose rates
192Ir: 37.4 cGy/min (average)
90Y (liquid): 45.2 cGy/min
90Y (foil): 98.3 cGy/min (average)
Two 90Y patients treated anteriorly and posteriorly
90Y: minimal personnel exposure
External beam radiotherapy doses
16.2–70.2 Gy (median 55 Gy)

Paraspinal Permanent 125I Seed Brachytherapy for Malignant Tumors with Spinal Cord Compression

Rogers et al. reported the follow-up on 24 of 30 patients implanted with 125I permanent implants at the time of spinal cord decompressive surgery. The study group consisted primarily of patients with metastatic disease who were undergoing decompressive surgery. The implant methodology employed 125I seeds in suture strand (Oncura, Inc.) with seed spacing set at 1 cm. The space between the strands was also 1 cm. The average activity per seed was 0.46 mCi, with an average of 20 seeds per implant for an average activity of 13.8 mCi. The mean minimal peripheral dose was 22 Gy (very low dose rate [VLDR]). Most patients received EBRT up to spinal cord tolerance, with a mean of 38 Gy (various fractionations).

Figure 4.27 Radioactive 125I seeds in place at the time of resection of tumor involving the left side of the ninth thoracic vertebral body. Rods, screws, and cage are used to stabilize the spine (Courtesy of Dr C. Leland Rogers).

 

The implant methodology was to fixate seeds in suture to the target area with a combination of methylmethacrylate, staples, suture, Gelfoam, and direct fixation to the implanted reconstructive devices (e.g., screws and rods, cages). The methodology avoided direct placing of seeds on nerve roots or dura, by using a double layer Gelfoam technique. The postoperative implant evaluation was carried out with orthogonal films and later with CT scan dosimetry. Implants were evaluated for dose and also for the risk of seed migration. The 2- and 3-year median local control at median follow-up of 42 months was 87% and 73%, respectively. The functional outcome in this group was closely linked to the pretreatment level. No myelopathy or other adverse radiation events were observed.17 See Figures 4.27 and 4.28 for radiographs of thoracic and cervical spine cases.

Figure 4.28 Radioactive 125I seeds are placed at the time of resection of tumor involving C3-C5 region. Screws and a plate are used to stabilize the spine (Courtesy of Dr C. Leland Rogers).

References

1. Walker MD, Alexander E, Hunt WE. Evaluation of BCNU and/or radiotherapy in the treatment of anaplastic gliomas. J Neurosurg. 1978;49:333–343.

2. Walker MD, Green SB, Byar DP. Randomized comparisons of radiotherapy and nitrosureas for the treatment of malignant gliomas after surgery. N Engl J Med. 1980;303:1323–1329.

3. Stupp R, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 2005;352(10):987–996.

4. Hall EJ. Radiobiology for the radiologist, 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:361–376.

5. Loeffler JS, Alexander A, Wen PY, et al. Results of stereotactic brachytherapy used in the initial management of patients with glioblastoma. J Natl Cancer Inst. 1990;82(24):1918–1921.

6. Wen PY, Alexander A, Black PM, et al. Long term results of stereotactic brachytherapy used in the initial treatment of patients with glioblastomas. Cancer. 1994;73(12):3029–3036.

7. Gutin PH, Prados MD, Phillips TL, et al. External irradiation followed by an 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;21(3):601–606.

8. Sneed PK, et al. Demonstration of brachytherapy boost dose-response relationships in glioblastoma multiforme. Int J Radiat Oncol Biol Phys. 1996;33(1):37–44.

9. Selker RG, et al. The Brain Tumor Cooperative Group NIH Trial 87-01: A randomized comparison of surgery, external radiotherapy, and carmustine versus surgery, interstitial radiotherapy boost, external radiotherapy, and carmustine. Neurosurgery. 2002;51(2):343–357.

10. Laperierre NJ, et al. Randomized study of brachytherapy in the initial management of patients with malignant astrocytoma. Int J Radiat Oncol Biol Phys. 1998;41(5):1005–1011.

11. Shrieve DC, et al. Comparison of stereotactic radiosurgery and brachytherapy in the treatment of recurrent glioblastoma multiforme. Neurosurgery. 1995;36(2):275–282.

12. Larson DA, et al. Permanent iodine 125 brachytherapy in patients with progressive or recurrent glioblastoma multiforme. Neuro-oncol. 2004;6(2):119–126.

13. McDermott MW, et al. Stereotactic radiosurgery and interstitial brachytherapy for glial neoplasms. J Neurooncol. 2004;69:83–100.

14. Chang CN, et al. High-dose-rate stereotactic brachytherapy for patients with newly diagnosed glioblastoma multiforme. J Neurooncol. 2003;61(1):45–55.

15. Reardon DA, et al. Phase II trial of murine (131)I-labeled antitenascin monoclonal antibody 81C6 administered into surgically created resection cavities of patients with newly diagnosed malignant gliomas. J Clin Oncol. 2002;20(5):1389–1397.

16. DeLaney TF, Chen GC, Mauceri T. Intraoperative dural irradiation by customized 192iridium and 90yttrium brachytherapy plaques. Int J Radiat Oncol Biol Phys. 2003;57(1):239–245.

17. Rogers CL, Theodore N, Dickman CA, et al. Surgery and Permanent I-125 seed paraspinal brachytherapy for malignant tumors with spinal cord compression. Int J Radiat Oncol Biol Phys. 2002;54(2):505–512.



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