First 1,000 cases of gamma knife surgery for various intracranial disorders in LSU health-Shreveport: radiological and clinical outcome.
Radiosurgeries including gamma knife radiosurgery (GKRS), linear accelerators and cyclotrons have emerged as important treatment options for the management of variousdisorders. (1-3) Numerous studies, including retrospective and prospective series, reported the safety and efficacy of GKRS alone or as an adjunct therapy with microsurgery or conventional radiotherapy. (4-6) GKRS delivers a high single procedural radiation dose to a target volume of tumor or vascular malformation and provides various beneficial effects including excellent control of local tumor or nidus growth, shorter hospital stay, lower cost, lower mortality and morbidity, minimum invasiveness, and wide access of GKRS for repeated treatments. (7-8) GKRS can successfully treat the patients with various intracranial tumors including metastatic brain tumors (MBTs), meningiomas, vestibular schwannomas (VS), astrocytomas and pituitary adenomas etc. (1,9,10) Similarly, GKRS can be used to treat intracranial vascular disorder such as arteriovenous malformation (AVM), arteriovenous fistulas and cavernous malformation. (11-13) In addition, GKRS can also be an important treatment option for other miscellaneous disorders including trigeminal neuralgia (TGN), epilepsy and tremor. (14-16) However, there is no summarized information in existing literature about the effect of GKRS in the above mentioned diseases. In the present study, we retrospectively reviewed our experience in the management, outcome and complications of first 1,017 GKRS in various disorders.
MATERIALS AND METHODS
This study was done after approval by the Institutional Review Board at LSU Health-Shreveport, Louisiana. Information related to clinical history, microsurgery, radiotherapy, GKRS, neuroimaging including MRI, and outcomes of the patients with various intracranial lesions between 2000 and 2013 were collected retrospectively by review of the patients' case reports and follow-up charts.
PATIENTS AND TUMOR CHARACTERISTICS
There were 1,017 GKRSs in 911 patients with various disorders. The patients' characteristics and distribution of different disorders among the patients are described in Table 1.
GKRS was performed using the Leksell stereotactic unit; model "C" with automatic positioning system, manufactured in Atlanta, Georgia. The Leksell head frame was placed on the patient's head while the patient was under IV sedation and local anesthesia. The patient was then transferred to the MRI suite for imaging. High resolution contrast enhanced axial pictures of the brain were taken in the 3-D SPGR sequence. The imaging data was then transferred to the gamma knife planning computer via the ethernet. The Leksell Gamma Plan software version 5.34 was used to perform the dose planning. A management team including neurosurgeon, medical physicist and radiation oncologist performed dose selection and planning.
DOSING PLAN OF THE GKRS FOR VARIOUS INTRACRANIAL LESIONS
The median marginal dose to the schwannoma was 13Gy (range 8-20), maximum dose to the schwannoma was 24Gy (range 16-40), and median 50% isodose line was 50% (range 15-100). Median radiation exposure time was 36 minutes (range 4-98).
The median marginal dose to the meningioma was 14Gy (range 12-30), maximum dose to the meningioma was 28Gy (range 24-60), and the median 50% isodose line was 50% (range 50-80). Median radiation exposure time was 35 minutes (range 4-94).
The median marginal dose to the MBTs was 16Gy (range 7-22), maximum dose to the MBTs was 32Gy (range 14-44), and the median 50% isodose line was 50% (range 40-70). Median radiation exposure time was 29 minutes (range 4-95).
The median marginal dose to the astrocytomas was 14Gy (range 10-20), maximum dose to the astrocytomas was 28Gy (range 20-40), and the median 50% isodose line was 50% (range 40-50). Median radiation exposure time was 30 minutes (range 4-56).
The median marginal dose to the pituitary adenomas was 15Gy (range 8-20), maximum dose to the pituitary adenomas was 30Gy (range 16-40), and the median 50% isodose line was 50% (range 30-54). Median radiation exposure time was 45 minutes (range 4-94).
The median marginal dose to the AVM was 18Gy (range 14-25), maximum dose to the AVM was 36Gy (range 28-50), and the median 50% isodose line was 50% (range 50-60). Median radiation exposure time was 32 minutes (range 12-82).
The median maximum dose to the TGN was 80Gy (range 60-90), and median 100% isodose line was 100%. Median radiation exposure time was 44 minutes (range 24-90).
Preoperative and follow-up data were collected from the patients in this study from patient's notes and follow-up charts. Follow-up was performed at three month intervals in the first year of the GKRS treatment, at six month intervals for following two years and annually thereafter for detailed neurological examination to demonstrate the improvement or worsening of preexisting signs and symptoms, development of any new sign and symptom, and any change in images. The mean and median follow-up time for each lesion was as follows. Meningioma: mean and median follow-up time was 63.71 and 61 months (range, 6-158). Schwannoma: mean and median follow-up time was 59.53 and 49 months (range, 6-149). MBTs: mean and median follow-up time was 18 and 9 months (range, 3-137). Astrocytomas: mean and median follow-up time was 9.2 and 7.2 months (range, 3-32). Pituitary adenomas: mean and median follow-up time was 45 and 30.48 months (range, 2.5-157). AVM: mean and median follow-up time was 32.65 and 35.23 months (range, 3-134).TGN: mean and median follow-up time was 38.73 and 33.16 months (range, 2-151).
Commercially available software, SPSS version 21.0 (SPSS, Inc., Chicago, Illinois), was used for statistical analysis. Overall survival and progression free survival were analyzed using the Kaplan Meier test. The log-rank (Mantel-Cox) test was used to analyze the survival difference in the cases. Cox regression model was used to demonstrate the predictive factors of the outcome Univariate analysis was performed to indentify the predictive factors for obliteration of AVM and pain relief in TGN. A Chi square test was also used when applicable. A p value <0.05 was considered as significant.
Benign and malignant intracranial tumors and vascular malformations can cause disability with neurological deficits and death in the patients who harbor them. This kind of damage provokes a significant cost to society. (17) In the past decades, patients with intracranial tumors, vascular malformation and functional disorders were managed primarily with microsurgical resection or radiation therapy. (18,24) Even after recurrence of the tumors following primary therapies, repeat resection was considered. However, GKRS became a popular therapeutic option for the many patients with intracranial tumors, vascular malformations and functional neurological disorders. (1,9,24,25) In our case series, we planned to demonstrate the clinical outcome, radioimaging changes in the lesions, complications and predictive factors of improvement in the patients after GKRS. Each lesion in the brain posed unique clinical challenges with the varieties of the issues including volume and location of the tumors or AVM nidus, radiation dosing etc. Therefore, we have kept the track of the radiological and clinical outcomes of each lesion separately which is described below.
The radiological and clinical outcome of GKRS in the patients with VS is described in Table 2. In this retrospective study, the overall control of VS growth was 90% after GKRS which was consistent with previous studies. (26,27) The progression free survival rate was 90% 10 years after GKRS, which was consistent with an earlier report. (27) In our case series, the preservation of hearing after GKRS was 80% which was supported by previous studies (range, 38%-94%). (28-29) Likewise, consistent with an earlier report, (27) this study revealed the significant lower rate of facial nerve affection (6%) after GKRS in the overall number of patients. Four percent of patients experienced trigeminal neuropathy which was comparable with a previous report 30. Moreover, the present study also determined that overall quality of life was improved after GKRS which could be due to improvement in signs and symptoms of the disease including ataxia, hearing loss and impairment facial nerve function. (31) The present study did not reveal any major complications such as hydrocephalus and edema after GKRS in new patients. Thus, GKRS is beneficial for VS either as a primary or adjuvant therapy.
The radiological and clinical outcome of GKRS in the patients with meningiomas is reported in the Table 3. In the present study, the average tumor control was 86% after GKRS in new (91%) and recurrent (81%) patients, which was comparable with other previous reports (range, 75-100% of tumor growth control). (32-33) The less favorable results of GKRS on recurrent meningiomas usually depend on the characteristics and Simpson grades of tumor resection. (34) Consistent with an earlier report, this study showed that the progression free survival rate was 98%, 95% and 85% at 3, 5 and 10 years respectively after GKRS. (35) The improvement of neurological deficits and other systemic symptoms in affected patients are very important to verify the patient's response to therapy. Findings of this study demonstrated that GKRS therapy improved 30% of total signs and symptoms including visual impairment, facial nerve and trigeminal nerve dysfunctions, which was comparable with a previous report. (36) This study also noted that overall quality of life in the patients was significantly improved after GKRS which could be due to improvement of visual impairment and facial nerve dysfunction. (37) The present study showed complications including hydrocephalus, seizure, preexisting visual problem, ataxia, etc. after GKRS; comparable with a previous study. (37) Therefore, GKRS is an important treatment option for meningioma either as a primary or adjuvant therapy. (38)
Metastatic Brain Tumors:
The radiological and clinical outcome of GKRS in the patients with MBTs is represented in the Table 4. In the present case series, the median overall survival after GKRS in MBTs was 17 months which was comparable with earlier reports (range 9-18 months). (39-41) The Cox regression analysis identified hydrocephalus (p < 0.0001, RPA class (p < 0.0001), recurrent MBTs (p = 0.01) and KPS (p = 0.007) as the predictors of survival, which was consistent with previous studies. (5,42-43) This study demonstrated that the tumor growth control occurred in 76% patients, which is fairly comparable with the range of 70-100% as reported by a previous study. (40) Forty (13.4%) patients required GKRS, 15 (5.0%) patients required resection and 2 (0.6%) patients required well-being therapy (WBT) after initial GKRS due to newly developed lesions and complications (e.g. hydrocephalus, hemorrhage) which was consistent with the earlier report. (45) Lastly, GKRS is an important treatment option for MBTs but the timing of treatment for recurrent cases needs to be further investigated.
The outcome of GKRS on astrocytomas is noted in Table 5. The average tumor size was 11.1 cm3 in the entire cohort. There are conflicting results regarding the overall survival benefits following GKRS therapy for astrocytomas. (46-48) Results of GKRS on astrocytomas depend on tumor size. The median overall survival in our series was 18.2 months from diagnosis and 7.25 from recurrence, which is lower than another previous report (49) on MBTs with GKRS (18.2 vs. 26 months). Our finding is consistent with previous reports. (47,50) Our series showed that overall survival rate at 1 year, 2 years and 3 years from diagnosis of the disease was 75%, 35% and 20% respectively, which is consistent with a previous report p=examining GKRS at time of recurrence. (46) Cox regression analysis also identified age Y 50yr (p = 0.008), KPS > 70 (p = 0.034), prior external beam radiation therapy (p = 0.042), absence of neurodeficits (p=0.013) and GKRS at recurrence of tumor (p = 0.023) as the positive predictors of the survival which is consistent with earlier reports. (46-51) Unfortunately, data in our case series confirms that the overall prognosis of GBM remains dismal. Despite attempting to attain local tumor growth control with GKRS, 75% patients in our series had tumor progression during the follow-up period. Comparable to our study, previous studies have demonstrated that the failure rate of local tumor growth control was 78% to 90%. (48-51) Although our morbidity and mortality is high for a GKRS series, this reflects our practice pattern of referring high-risk patients with recurrence for GKRS treatment prior to considering more invasive treatments like repeat microsurgical resection. Therefore, GKRS is an important treatment option for astrocytoma as an adjunct therapy during progression time of the tumors.
The clinical and radiological outcome of GKRS on pituitary adenoma is described in Table 6. Recent large GKRS series for pituitary adenomas showed 87-97% local tumor growth control and 42-78% tumor regression. Our study demonstrated that the overall tumor growth control rate was 93%, and that the progression free survival rate at 3, 7 and 10 years was 100%, 95% and 90% respectively, which are very consistent with previous studies. (52-54) Although 95% of patients demonstrated preservation of visual functions, 5% of patients showed some degree of preexisting or newly developed visual impairment which is consistent with previous reports. (55,56) New cranial nerve III palsy was observed in 2 (2.1%) patients in this case series, which is also consistent with earlier study. (53) The present study revealed that 12% of the patients developed hypopituitarism after GKRS therapy which is comparable with a previous report. (56) The present study also showed that overall quality of life was improved (KPS, pre-GKRS, 87 vs. post-GKRS, 94) after GKRS which could be due to improvement in signs and symptoms of the disease including visual impairment and neurodeficits. Although complications including radionecrosis, CVA and neoplasia were not found in our series, hydrocephalus was observed in one patient, and that is comparable to an earlier study. (56) Thus, GKRS is a good option to treat pituitary adenomas.
The outcome of GKRS on AVM is reported in Table 7. Obliteration of nidus volume is important after GKRS on AVM. This case series demonstrated that the obliteration of the nidus was 79%, which is very consistent with earlier studies with 65-95% of nidus obliteration. (57-58) The usual period of nidus obliteration is 2-3 years and our series showed that the median time of nidus obliteration was 31 months which is also comparable with the earlier studies. (59) In univariate analysis, although Spetzler-Martin grade I-III (p = 0.002), female gender (p = 0.02) and absence of neurodeficit (p = 0.01) were significant for nidus obliteration in our case series, prior hemorrhage (p = 0.27) and embolization (p = 0.24) did not show any significant relation with nidus obliteration. These are consistent with previous series. (60,61) There are few complications in our series including hemorrhage, hydrocephalus, neurodeficits, seizure and cystic degeneration after GKRS which are comparable with previous series. (61-63) Therefore, GKRS is a good therapeutic option to treat AVM.
The clinical outcome and predictive factors of GKRS in the patients with TGN is described in Table 8. The present study showed that TGN pain was completely relieved in 94 (55.6%) patients, partially relived in 38 (22.4%) patients and aggravated in 37 (22%) patients which was very consistent with our earlier report and other published studies. (64-66) In univariate analysis, age <70 years was significant for pain relief in our case series, and gender, ethnicity and pain distribution had no significant relation with resolution of pain which is also consistent with earlier report. (65) Thus, GKRS is a good therapeutic option to treat TGN.
The strengths of this study include using of the Leksell Gamma Plan software version 5.34 for determination of radiation dose-volume, and single fraction GKRS technique for entire cohort. Despite having a large number of patients with long term follow-up, this study also has a few limitations that could influence the external validity of the study. First, this study was single-center, retrospective design. Second, there was lack of a true control group in this study. Third, slightly variability in the standard treatment offered to patients. Fourth, the median follow-up time for several disorders including NFPAs, AVM and TGN was less than 36 months which is inadequate to exclude the late complications of GKRS. Lastly, although majority of the patients were observed by other subspecialists including neuro-ophthalmologists or oncologists after GKRS, we did not comply their strict protocols before and after GKRS. However, this study allows clinicians a guide for the treatment strategies of GKRS for the treatment of various intracranial lesions.
Taken together, given the good control of different tumor growth, obliteration of AVM nidus and trigeminal neuralgia pain, good overall and progression free survival rate, possible preservation of neurological functions, lesser number of complications, and improvement of quality of life, GKRS is an important treatment option for patients with different benign tumors, AVM and trigeminal neuralgia. In addition, GKRS can also be a good treatment option for patients with recurrent benign tumors, AVM and trigeminal neuralgia to avoid repeated microsurgical resections along with craniotomy related complications. However, as of now, GKRS is not so effective for recurrent malignant tumors. Further randomized controlled studies with a large volume of patients with various tumors, AVM and trigeminal neuralgia are required to accomplish a good comparison of treatment modalities.
Shyamal C. Bir MD, PhD; Tabitha Ward MS; Papireddy Bollam MD; Anil Nanda MD, MPH
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Drs. Nanda, Bir, Bollam and Ms. Ward are all associated with the Department of Neurosurgery, LSU Health Sciences Center, Shreveport, LA.
Table 1: Basal characteristics of the patients and number of different disorders Variables Value Total no. of surgeries 1,017 Total no. cases 911 Age Median 55 Range 14-101 Gender Male 394 (43.2%) Female 517 (56.8%) Ethnicity Caucasians 687 (75.4%) African Americans 221 (24.2%) Asian 3 (0.3%) Intracranial lesions treated by GKRS Vestibular Schwanomma 82 (9%) Meningioma 136 (14.9%) Metastatic brain tumors 298 (32.7%) Astrocytoma 49 (5.3%) Pituitary adenoma 92 (10%) AVM 85 (9.3%) TGN 169 (18.5%) Table 2: Outcomes of GKRS on vestibular schwannoma Postop Parameter Preop Decreased Unchanged Radiological Changes Number of patients 82 44 30 Tumor size 3.24 1.72 2.93 Time required (mo) 40 34 KPS Scale 79 90 Changes in Neurological Symptoms and Symptoms Hearing loss 80 (98%) 16 (20%) Facial nerve affection 16 (20%) 5 (6%) Ataxia 22 (27%) 6 (7%) Complications Hydrocephalus 0 1 Left hemiparesis 0 2 Trigeminal nerve affection 0 3 Parameter Progressed p Value Radiological Changes Number of patients 8 Tumor size 4.2 Time required (mo) 29 KPS Scale Changes in Neurological Symptoms and Symptoms Hearing loss <0.0001 Facial nerve affection 0.001 Ataxia <0.001 Complications Hydrocephalus Left hemiparesis Trigeminal nerve affection Table 3: Outcomes of GKRS on meningioma Postop Parameter Preop Decreased Unchanged Radiological Changes Number of patients 136 69 47 Tumor size 5.40 2.05 5.73 Time required (mo) 38 34 KPS Scale 80 92 Changes in Neurological Sysmptoms and Symptoms Imbalance 6 (4%) 5 (3%) Visual imparement 25 (18%) 7 (5%) Trigeminal nerve 4 (3%) 3 (2%) dysfunction Facial nerve dysfunction 8 (6%) 4 (3%) Hearing deficit 9 (7%) 7 (5%) Complications Hydrocephalus 0 2 Seizure 0 5 Parameter Progressed p Value Radiological Changes Number of patients 20 Tumor size 11.80 Time required (mo) 22 KPS Scale Changes in Neurological Sysmptoms and Symptoms Imbalance NS Visual imparement 0.009 Trigeminal nerve NS dysfunction Facial nerve dysfunction NS Hearing deficit NS Complications Hydrocephalus Seizure Table 4: Outcomes of GKRS on metastatic brain tumors Parameter Preop Postop Postop Decreased Unchanged Radiological Changes Number of patients 298 135 91 Brain edema response 63 18 Parameter Postop p Value Progressed Radiological Changes Number of patients 72 304 Brain edema response 40 Prognosis Factors for Improved Survival 95% CI HR (lower) Upper p Value RPA classification 0.28 0.14 0.57 <0.0001 Hydrocephalus (yes) 4.48 2.17 9.27 <0.0001 Number of MBTs 1.29 0.92 1.83 0.14 Extra-cranial metastasis 0.98 0.61 1.57 0.93 Recurrent tumor 1.53 1.07 2.18 0.01 Gender 1.14 0.83 1.57 0.40 Ethnicity 0.75 0.53 1.06 0.10 Age >65yr 1.26 0.87 1.82 0.21 KPS 1.60 1.14 2.25 0.007 Table 5: Outcomes of GKRS in a strocytomas Postop Parameter Preop Decreased Unchanged Progressed p Value Radiological Changes Number of patients 49 2 10 37 Prognosis Factors for Improved Survival HR 95% CI Upper p Value (lower) Age >50yr 0.38 0.19 0.78 0.008 Gender 1.24 0.62 2.50 0.54 KPS 2.17 1.06 4.44 0.03 GKRS at 0.36 0.15 0.87 0.02 recurrence vs. upfront Neurodeficit 2.56 1.22 5.33 0.01 Marginal dose 0.58 0.28 1.20 0.14 Chemotherapy 1.23 0.57 2.65 0.59 Table 6: Outcomes of GKRS in pituitary adenomas Postop Parameter Preop Decreased Unchanged Radiological Changes Number of patients 92 54 32 Tumor size 5.2 2.93 5.7 Time required (mo) 45 KPS scale 87 94 Changes in neurological symptoms and symptoms Visual impairment 46 (64.7%) 5 (7%) Neurodeficits 20 (28.1%) 3 (4.2%) Complications Hypopituitarism 11 (15.5%) Panhypopituitarism 3 (4.2%) Diabetes insipidus 1 (1.4%) Visual deterioration 6 (2.8%) New CN III palsy 2. (2.8%) Hydrocephalus 1 (1.4%) Parameter Progressed p Value Radiological Changes Number of patients 6 Tumor size 6.60 Time required (mo) 43 KPS scale Changes in neurological symptoms and symptoms Visual impairment Neurodeficits Complications Hypopituitarism Panhypopituitarism Diabetes insipidus Visual deterioration New CN III palsy Hydrocephalus Table 7: Outcomes of GKRS in AVM Postop Parameter Preop Obliterated Expanded p Value Radiological Changes Number of patients 85 67 18 Time Required (mo) 35 23 Prognosis Factors for Improved Survival Gender (male vs. female) 0.04 H/O of hemorrhage 0.24 H/O embolization 0.27 Spetzler-Martin grade 0.002 (grade I-III) Presence/absence of 0.01 neurodeficits Table 8: Outcomes of GKRS in trigeminal neuralgia Parameter Preop Complete Postop Relief Partial Relief Radiological Changes Number of patients 169 94 38 Predictors of Pain Relief Age [greater than or equal to] 70yr Gender Pain distribution (V2, 3) Ethnicity (Caucasian) Parameter No Relief p Value Radiological Changes Number of patients 37 Predictors of Pain Relief Age [greater than or equal to] 70yr 0.02 Gender 0.94 Pain distribution (V2, 3) 0.31 Ethnicity (Caucasian) .01 Table 9: Summary of overall control of intracranial lesions by GKRS Parameter Preop Postop Postop p Value Controlled Uncontrolled Intracranial Tumors Benign 310 276 (89%) 34 (11%) <0.0001 Malignant 347 244 (70%) 103 (30%) <0.0001 AVM 85 67 (79%) 18 (21%) <0.0001 TGN 169 132 (78%) 37 (22%) <0.0001
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|Author:||Bir, Shyamal C.; Ward, Tabitha; Bollam, Papireddy; Nanda, Anil|
|Publication:||The Journal of the Louisiana State Medical Society|
|Date:||Mar 1, 2015|
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