Radiosurgery in Brain mets is evolving paradigm in the brain mets mannagement

1. Brain Metastases
Changing Landscape in 21st Century
Dr.Shankar, MD,DNB
Director, Radiosurgery
HCG cancer center, Mumbai

2. • Metastases are the most common intracranial tumors in adults
(50%)
• Brain metastases develop in approximately
• 10% to 30% - Adult cancers
• 6-10% Ped. Cancers
• Among those with metastatic brain tumors, 70% have multiple
lesions
Brain Metastases: Incidence
• MRI &
• better control of
extracerebral disease.

3. Brain Metastases: Primary Tumors
• In adults, mc carcinoma include
 lung,
 breast,
 kidney,
 colorectal cancers &
 melanoma.
• In children, the most common sources of brain metastases are
 sarcomas,
 neuroblastoma, and
 germ cell tumors
Ca.prostate, esophagus, and
oropharynx and non-melanoma
skin cancers rarely metastasize

4. Increasing incid. with advances in systemic therapy
Breast cancer
o particularly high in those with lung metastases and those with
highly-proliferative, HR - +ve or –ve but HER-2 +ve tumors
o Incidence – 30% ( tumor biology + herception inability to
penetrate BBB)
Colorectal cancer
• Increase attributed to the longer survival seen with newer
systemic therapies
 5-fluorouracil era for metastatic CRC  MS 7mon.
 Introduction of oxaliplatin, irino & biologics  24 months.
Non-Small cell carcinoma:
• Improved diagnosis with newer modalities

5. Oncologic Emergency - Primarily via art.circ. & less via the Batson venous plexus (pelvic and GI Prim.)
Emboli – Escape
lung filter
Deposited in G-W junc.
Or watershed areas – BV
diam. decreased )
0.1% of deposited cells
dev  Metastases
>1mm size – Tumor angio
bgins BBB disrupted
Cerebral (80%) Cerebellar (15%) Brainstem – 2%
Intratumoral Haemorrhage : melanoma, choriocarcinoma , RCC
Brain Metastases – Pathogenesis
Posterior fossa  pelvic (prostatic and uterine), gastrointestinal, and breast tumors
Equal Distribution  Lung

6. Brain Metastases – Clinical Features !
Head ache Siezures Stroke
• Multiple lesions / Post fossa mets
• Bifrontal, Worse ipsilaterally
• Early morning HA - classic /Uncommon
• Worse with bending / coughing/ valsalva
• Exclusively asst. with
supra-tentorial disease
• 10-20% pts
• 20-40% pts
• Depends on the location

7. • Usually Solitary Metastases from
breast,
colon, and
RCC
• Greater tendency for Multiple :
lung cancer and
malignant melanoma
Brain Metastases – Number Tendency

8. Brain Metastases – Imaging
CT ScanMR – T1 MR – T1 POST
Classic Features
 multiple lesions
 Location  at GW jn
 Circumscribed margins
 Disproportionate
vasogenicedema
compared with the size
of the lesion
MRI is more sensitive than CT imaging to detect metastatic lesions &
detects a lesion as small as a dot (2mm).

9. Brain Metastases – Disproportionate Vasogenic Edema
• Contributes significantly to morbidity  disrupt synaptic transmission, alter
neuronal excitability  Headche, siezures, focal deficits, encephalopathy
• BBB Disruption Accumulate protien rich fluid in the extracellular space
 local production of factors VEGF , glutamate, leukotrienes  increase
the permeability of tumor vessels
 Absence of tight endothelial cell junctions in tumor blood vessels
• Vasogenic edema  Spreads in white matter EC Space than gray matter
possibly because of lower resistance to flow within the white matter
DEXONA – preferred choice
• No mineralocorticoid activity ( no fluid retention)
• Lower risk of infection and cognitive impairment than other GC.
upregulates ANG-1 , Strong BBB stabilizing factor
 Downregulates VEGF
• Effects seen within 48hrs – 72 hrs
• Biologic Half life  36 hrs-54hrs – Load at 16mg – severe // 8mg moderate 
taper out stabilisation kicks in.
• Try Beva  Refractory Peritumoral edema

10. Brain Metastases – Imaging
Hemorrhagic Metastases: Renal // Breast // Melanoma //Choriocracinoma
MRI is more sensitive than CT imaging to detect metastatic lesions &
detects a lesion as small as a dot (2mm).
Intra
parenchymal
Leptomeningeal / Sub
Arachnoid spread
Dural
Spread
Epidural
Intraventricular

11. Response Evaluation Brain Mets
• Contrast enhancing lesion 
• minimum size of 10 mm in one dimension,
• visible on two or more axial slices that are at most 5
mm apart with 0-mm skip
• Non-measurable lesions
 Cavities & Cyst  unless there is a nodular
component measuring > 10 mm in longest diameter
and > 5 mm in the perpendicular plane
 All lesions Longest diameter <10mm.
 Dural Mets / Leptomeningal mets / bony skull mets.
Response Criteria
Complete
Response
• Complete disappearence
• No new lesions
• No steroids
• Stable / improved clinically
Partial
response
• > 50% decrease
• No new lesions
• Stable or red. Steroid depend
• Improved clincally
Stable
disease
• Does not qualify for CR/ PR /
PD
• Stable clincally
Progressive
disease
• 25% increase ( sum of
products of enhancing
lesions)
• Any new lesion
• Clinical detarioration
Macdonald Criteria RANO Criteria

12. Response Eval - RANO – Brain Mets
CNS RANO-BM // NON-CNS - RECISTCNS RANO-BM

13. Brain Mets – Pseudo progression
Pre-Treatment 3 mo. Post 6 mo. Post
T2 FLAIR
T1 Post

14. Brain Mets – True progression
Pre-Treatment 3 mo. Post 6 mo. Post
T2 FLAIR
T1 Post

15. Advanced MR Imaging
CE-T1 POST Diffusion DCE-Perf. DCS-Perf. Adv. Processing
“DANGERS ‘’Advanced MR Imaging
Do not loose sight of the clinical relevance in MR Imaging

16. 1month 3 month 6 month 9 monthPre-Rx
PerfusionMRT1-PCMR
Solitary Brain Mets – Pseudoprogression

17. 1month 6mo 1 year 2 yearPre-Rx
Development of a cystic lesion  compatible with late radiation necrosis of brain tissue
Solitary Brain Mets Post SRS – Cystic Lesion
How to differentiate Between necrosis & recurrence ????

18. 3mo.PostSRS
Surgical resection
• because of clinical
deterioration
associated with
progressive lesion
enlargement and
• mass effect
unresponsive to
corticosteroids.
When the contrast-enhanced rim on T1-weighted image was associated with a distinct border on T2,
the pathology was usually recurrent tumor.
Solitary Brain Mets – T1 /T2 Match - Recurrence

19. T1 / T2 Mismatch
T1 / T2 Match & Mismatch
Necrosis
Necrosis + Residual
Necrosis Necrosis
3mo.PostSRS
When the contrast-enhanced rim on T1-weighted image was associated
with a distinct border on T2, the pathology was usually Radtn Necrosis.
Solitary Brain Mets – T1 /T2 mismatch – Radiation Effects

20. 12mo. Post SRS 24mo. Post SRS 30mo. Post SRS
Wanted Dead or Alive – Necrosis vs Recurrence

21. Wanted Dead or Alive – Necrosis vs Recurrence

22. The optimum rCBV threshold was determined to be 2.1 and using this threshold results in
a sensitivity of 100% and specificity of 95.2%
R CBV– Necrosis vs Recurrence

23. Prognostic Indexes to evaluate metastases
• Recursive Partitioning Analysis (RPA)
Gasper L, et al. Int J Radiat Oncol Biol Phys 1997; 73: 745-751
• Score Index for Radiosurgery (SIR)
Weltman E, et al. Int J Radiat Oncol Biol Phys 2000; 46: 1155-1161
• Basic Score for Brain Metastasis (BSBM)
Lorenzoni J, et al. Int J Radiat Oncol Biol Phys 2004; 60: 218-224
• Graded Prognostic Assessment (GPA)
Sperduto PW, et al. Int J Radiat Oncol Biol Phys 2008; 70: 510-514
• Modified RPA
Yamamoto M, et al. Int J Radiat Oncol Biol Phys 2012; 84: 1110-1115

24. Class 1
(Favourable
Prognosis)
Class 2 Class 3
(UnFavourable
Prognosis)
• KPS >70 • KPS > 70 • KPS <70
• Age <65 • Age >65
• Controlled
primary tumor
• Uncontrolled
primary tumor
• Without
extracranial
mets
• Other extra
metastases
Median survival –
7.1 mon
Median survival –
4.2mo
• Median Survival
– 2.3mo
Prognostic Assessment Instruments – brain mets
There is little value of RPA class III (most unfavorable group) for the
same results of 6-month and 1-year survival rate.

25. The sum of scores ranged from 0~10 and score index for radiosurgery was divided into three groups
according to their marks (0 to 3, 4 to 6, and 7 to 10). †The sum of scores was divided into four classes: I
(3.5~4 points, most favorable group), II (3 points), III (1.5~2.5 points), and IV (0~1 points, most
unfavorable group). ‡except for metastatic brain lesions
Prognostic Assessment – brain mets

26. A) SIR provided the most
accurate prediction on
survival after GKRS.
B) There was little value of
RPA class III on survival
model for the same
results from 6 month
survival rate and 1 year
survival rate.
Tuberc Respir Dis. 2012 Jan;72(1):15-2

27. Disease specific Instruments – DS-GPA
Survival results following treatment for brain metastases are highly heterogeneous &
depend in part upon the primary tumor.
Sperduto, DS-GPA ; J Clin Oncol. 2012;30(4):419
●Lung cancer: Age, KPS, extracranial mets +ve, and BM number
●Melanoma: KPS and number of brain metastases
●Renal cell carcinoma: KPS and number of brain metastases
●Breast cancer: KPS , subtype (based upon ER/PR/HER-2 neu) and age
●Gastrointestinal cancers: KPS
Used in clinical trials
statistically significant
survival gradient with
improvement in overall
survival with a better
DS-GPA score

28. • Treatment for patients with brain metastases has been whole-
brain radiation therapy (WBRT) for decades
• The current treatment paradigm for brain metastasis depends
on the
 patient’s overall health status,
 the primary tumor pathology, and
 the number and location of brain lesions
Brain Metastases Management

29. • The main goal of treatment is
 palliation of symptoms and
 maintenance of neurological function
• When selecting the treatment it is very important to
determine what is the best approach
Goal of the Treatment

30.  Corticosteroids
 Whole Brain Radiation Therapy (WBRT)
 Surgery +/- WBRT
 Surgery +/- SRS
 RT+ immunotherapy
 Stereotactic radiosurgery (SRS) +/- WBRT
BM Rx  Individualized
• as surgical and radio-surgical techniques have evolved greatly over last decade.
• as improved systemic therapies have evolved with greater potential for both systemic and
intracranial disease control for certain cancer types and genotypes.
Brain Metastases Management

31. Control vs Congnition
• Choosing an appropriate personalized treatment plan
for patients with brain metastasis maximizes survival
and minimizes morbidity from unnecessary or futile
treatments
• It is important also to use techniques that preserve
neurocognitive functions

33. SINGLE BRAIN METASTASIS – Surgery
STUDY TREATMENT n MOS P - value Functional
Independence
Patchell etal Surgery + WBRT (36gy) vs
WBRT
25
23
40wks
15wks
<0.1 38 wks
8 wks
Noordijk etal Surgery + WBRT (40gy)
WBRT
32
31
10 mo
6 mo
<0.04 33wks
15 wks
Mintz etal Surgery + WBRT (30gy)
WBRT
41
43
5.6 mo
6.3mo
0.24 9
8
Deciding Factors : tumor size and location // degree of mass effect and edema // presence or
absence of symptoms // functional status and extent of systemic disease // patient preferences
with regard to invasive therapy.
Lower KPS and higher proportion of extracranial disease were included
The location and accessibility of the tumor is a crucial factor in surgical decision making.

34. • Leukoencephalopathy and brain atrophy, leading to neurocognitive deterioration
and dementia
• Normal pressure hydrocephalus, causing cognitive, gait and bladder dysfunction
• Neuroendocrine dysfunction, most commonly hypothyroidism
• Cerebrovascular disease
• Radiation necrosis (albiet low) with symptoms related to the site of necrosis
Concerns of WBRT in 21st century

35. Leukencephalopathy & Radiation – FLAIR Seqs.
Grade 1 - Mild
Periventricular white matter changes
Grade 2 - Moderate Grade 3 – Severe /
Diffuse

36. Concerns of WBRT in 21st century
Modest Cognitive effects of WBRT

37. Leukencephalopathy
after WBRT
No Leukencephalopathy
after SRS

38. Brain metastasis are ideal targets for SRS or frac.SRS
• Typically well circumscribed
• Typically displace and are Non-infiltrative
• Can be well demarcated from the normal brain
parenchyma
• Behave like early responding tissue (high α/β)

39. Single endothelial cell subtends a segment of the tumour containing 2000 tumour cells
J. Denekamp, Acta Radiologica Oncol, 1984
Blood vessels are serial architecture
structure
 injury to single focal point in the
vessel may obstruct or completely
halt the downstream blood flow
 results in avalanche of tumour cell
death residing along the defunct
vessel
SRS – Tumor cell & Endothelial cell

40. Why is SRS Treatment of Surgical Bed Challenging
• Intact metastasis:
 Rounded geometry
 No margin for microscopic extn
 Higher conformality
• Surgical bed:
 Irregular geometry
 Microscopic/iatrogenic residual
 Better LC with lower conformality (1) (2mm
CTV)
(1)Soltys SG et al. IJROBP 2008;

41. Solitary Brain Mets – Cavity Radiosurgery
Co-register T1 Post Contrast
Excludes surgical track from TV

42. Cavity radiosurgery – Understanding Margins
Tumor–brain interface showing sharp
circumscription between metas. Adeno. and
surrounding tissue
Metastases Glioma
Proximal end of one biopsy specimen showing
individual malignant astrocytes (arrows)
infiltrating the brain surrounding a glioblastoma.
Lack of evidence of metastatic tumor cell infiltration into surrounding brain suggests the
need to target only a narrow depth of the resection cavity margin to minimize normal
tissue injury and prevent treatment size–dependent stereotactic radiosurgery
complications.  Margins – 1-2mm
IJROBP, Vol. 81, No. 4, pp. 1075–1080, 2011

43. Large Cavity volume dynamics – Timing for adjuvant SRS
Pre-Op T1PC 1wk postop T1 2wk postop T1PC
3wk postop T1PC – cavity
constriction 60%

44. Cavity radiosurgery – Understanding Indications
• Tumors 3 cm with superficial dural/pial involvement demonstrate the highest risk of LF
• Try Frac.SRT in larger tumors
3 mo. Post SRS

45. Cavity radiosurgery – Timing for adjuvant SRS
1 wk Post-Op T1 3 wks Post-Op T1PC 
Tumor progression / Post
surgical injury
1 wk Post-Op T2 1 wk Post-Op T1

46. Eight retrospective cohort
studies with 646 patients (238
with SRS versus 408 with WBRT)
Local Recurrence Distant Progression LMD
SRS of the resection
cavity may offer
comparable survival and
similar local and distant
control as adjuvant WBRT
post-operative
development of physical
and cognitive symptoms
Level 2

47. Multi-institutional trial finds comparable survival, less cognitive decline and
better quality of life following SRS versus whole brain radiotherapy after
resection
LEVEL 2

48. Leptomeningeal Dissemination after Resection + SRS
LMD after Resection + SRS:
• Risk1-3: 8.3-16.9% at 1 yr
• Risk factors:
 Infratentorial location
 Breast cancer histology
 Piecemeal resection
• Pre-op SRS reduces risk of LMD vs.
post-op SRS3
1Atalar B et al. IJROBP 2013
2Johnson MD et al. IJROBP 2016
3Patel KR et al. Neurosurg 2016

49. Developing NRG Oncology Trial
Basic Eligibility: Resected metastasis must be surface lesion, posterior fossa, melanoma/breast cancer, size 2.5-5.0
cm, KPS≥70
PI: Stuart Burri, MD (Levine Cancer Institute)
Co-Chairs: Anthony Asher, MD (Carolina Neurosurgery), and Scott Soltys, MD (Stanford)
Primary endpt: Time to development of leptomeningeal dissemination
Pts with 1-4 brain
mets , one of which
requires resection
S
T
R
A
T
I
F
I
E
D
R
A
N
D
O
M
I
S
E
Lesion number
Lesion size
Pre-operative radiosurgery
Post-operative radiosurgery

51. SINGLE BRAIN METASTASIS – SRS
SRS is a reasonable alternative to surgery or WBRT for small tumors that are not surgically accessible
Consideration of SRS rather than surgery should generally be limited to lesions with a diameter <3 cm
> 3cms size  Increased neurotoxicty and local failure rate
No randomized trials have been
conducted comparing SRS alone to
surgery plus PORT

52. Nomogram - Recurrence Rates SRS Alone
Neuro Onco 2014 Sep;16(9):1283-8.
N = 464 ( Largest study)
• 27% of patients received salvage
WBRT at a median of 5.6 months
from initial therapy
• Time to salvage WBRT was
 longest for patients with HER-2
+ve Breast
 shortest for those with poorly
differentiated lung cancer (3
months) and melanoma (3.3
months).

53. Complications of SRS
Acute  Transient swelling that begins 12 to 48 hours after therapy
Delayed  Radiation necrosis
• Incidence – 10%
• Risk Factors:
• prior radiation (either SRS or WBRT) to the same lesion and
• lesion size (with larger tumor volumes associated with higher
risk)  Hypofractionated SRS decreases
• Prior Targeted therapy and immunotherapy
Asymptomatic – 50% pts.
Focal neurologic signs – 50%

54. • Corticosteroids (limit use)
• Vitamin E 400 u bid – 3 mo
• Trental 400 mg bid- 3 mo
• Celebrex 200 mg qd
• Resection ( if feasible)
• Bevacizumab
• Hyperbaric oxygen
• Focussed Interstitial laser therapy
Mgmt. of Adverse Radiation Effect (ARE)- Radionecrosis

55. Bevacicimab Doses:
• 5 mg/kg every 6 wks.
• 7.5 mg/kg i.v. every 4 wks
Establish Diagnosis
Perfusion & Spectroscopy
Radionecrosis
Pretreatment 30 days 12 mo.

56. 27gy/3frcs
Lesion 3cms (+) or
10 cc Vol
Minniti et al., IJROBP,
95,4,2016
SRS – 138 //FSRT – 151 pts
• Max - Brainstem dose
22gy/3 frcs
• Max optic struc dose –
16.2gy/3frcs
MSKCC Protocol
No more than 3 courses of Rx
to the same site inside the
brain – Atleast 2 need to be
conformal one WBRT allowed
T1 Post – 6mo.
How Big is TOO BIG
FSRT / SRS
T1 Post – PreRx

57. Overview Recent f-SRT (no WBRT)

58. Bleeding Metastases
After 2 wks - Hypofractionation – 25gy in 5 frcs to solid and 20gy in 5 frs for clot which we are unsure

60. 6 month 9 month 12 month 15 month 40 monthAt Diagnosis
Solitary Brain Mets – SRS
A 62-old man with a Solitary Brain Mets from RCC

61. 2 Months FUP
A 63-year-old man with a 40-year history of smoking developed confusion, while at work. Lung biopsy showed NSCLC
14 Months FUP 24 Months FUP
Solitary Brain Mets – SRS

62. Solitary Brain Mets – Regression Velocity
at radiosurgery 2 weeks 4 weeks 6 weeks
 Significant volume reductions of brain metastases measured at either 6 or 12 weeks post-SRS were
strongly associated with prolonged local control.
 Early volume reduction asst. with less corticosteroid use and stable neurological symptoms.

63. Mets Post-Radiosurgery LC – Enhancement Pattern
Homogenous Heterogenous Rim-Enhancing
Enhancemnet pattern is a significant prognostic factor of brain
metastases treated with RS, independent of dose and volume.
Radioresistance of hypoxic tumor cells associated with necrotic regions,.
Day of treatment Imaging

64. Intraventricular brain metastases - SRS
Primary Secondary
Intraventricular metastases were classified as
• primary if they arose within the ventricles or
choroid plexus and
• secondary if they arose within the surrounding
parenchyma but extended into the ventricular
space
MCC  RCC, Melanoma, Breast
• SRS excellent local control with acceptable treatment related toxicity.
• Disease dissemination – 28% , 2nd intraventricular metastatic lesion 12%, leptomeningeal disease 12%
• The propensity for intraventricular dissemination seems to be histologically dependent. ( RCC better)

65. Sellar & Suprasellar Metastases – Lung ca.
Post Radiosurgery
Pre-Treatment

66. Pretreatment 3Mo. Post SRS 6 Mo. Post SRS
Brain Metastases: Lung with Dural based mets

67. Intradural Intrameduallry Mets ( IDIM) – Breast ca.

68. Optimize Control & Cognition
A new era of trials is emerging for investigating the impact of targeted
therapies concurrent with SRS
• Hippocampal-Avoidance WBRT
• Neuroprotection ( Memantine –NMDA Antagonist)
RTOG 06141: Memantine RTOG 0933: Hippocampal avoidance
Brown P et al. Neuro-Oncology 2013 Gondi V et al. J Clin Oncol 2014

69. Radiation Dose Dependent Hippocampal Atrophy
 Mean hippocampal dose was significantly correlated
with hippocampal volume loss
 Mean hippocampal volume was significantly reduced 1
year after high-dose RT (mean 6%, PZ.009) but not after
low-dose RT.
 In multivariate analysis, both RT dose and patient
age were significant predictors of hippocampal
atrophy

70. Hippocampal Avoidance – Expansion Envelope
• 5-mm expnasion envelope around the
hippocampus for conformal avoidance
WBRT represents an acceptable risk,
especially because these patients in
the absence of any other intracranial
disease could be salvaged using
stereotactic radiosurgery

71. Hippocampal Vascular Injury – Temporal Changes Post WBRT
• The mean Ktrans Increased significantly from pre-RT to 1-
month post-RT
• The early hippocampal vascular dose response could be a
predictor of late neurocognitive dysfunction
• DCE MRI scans were performed from pre-RT to 18-
month post-RT
• Temporal Changes - Quantified for
• vascular parameters related to blood-brain
barrier permeability, Ktrans, and the
• fraction of blood plasma volume, Vp.
• Modeled by integrating the dose effects with age,
sex, hippocampal laterality, and presence of tumor
or edema near a hippocampus.
• Early vascular dose response in hippocampi was
correlated with neurocognitive dysfunction at 6 and
18 months post-RT.
Yue cao, Rdtn induced Hippocampal injury, IJROBP, 93,4, 2015

73. What is the issue with treating more than 4 tumors
• Although current Level I evidence supports the use of SRS in patients with
more than 4 metastases
• Many recent studies suggest that the number of brain mets (1- 4 vs more than
5) does not affect the outcome
• It is the total tumor burden that impact tumor control and patient survival !
Grandhi, Kondziolka , et al SRS using GK Perfexion in pts with 10 or more Brain Mets J Neurosurg 2012: 117:5

74. AIM: examine whether SRS without WBRT as the initial treatment for patients with five to ten brain
metastases is non-inferior to that for patients with two to four brain metastases in terms of OS.
Yamamoto et al., IJROBP, 99,1,2017
Interpretation: Our results suggest that stereotactic radiosurgery without WBRT in patients with five to ten brain
metastases is non-inferior to that in patients with two to four brain metastases.
Considering the minimal invasiveness of stereotactic radiosurgery and the fewer side-effects than with WBRT,
stereotactic radiosurgery might be a suitable alternative for patients with up to ten brain metastases.

75. Multiple Brain Mets ( 7 brain mets)
Doses delivered varied as per size of the lesion
 18 Gy for lesions ≤20 mm,
 15 Gy for lesions measuring 21-30 mm, and
 12 Gy for lesions measuring 31-40 mm

76. Multiple Brain Mets 10 Brain Mets

77. Conclusions
• The clinical management of brain metastases has changed
dramatically in the past 5 years
• The most recent guidelines reflect the use of new
technologies in the management of BM
• There is a need of the medical community to be aware of the fact that personalized and individualized
care are key in patient with advanced cancer

78. Brain Metastases – Thin Slice MR Confirmation
Solitary Metastasis
Mass Effect
Gen.Cdtn
Resection
No ME
KPS 2/3
T.B SRS
ME ++
KPS 0/1
SRS
Recurrence
Limited (2–10) Metastases
Assess systemic disease
control & functional status
PoorGood
SRS alone Hippo WBRT
Recurrence
SRS alone
>10 Metastases
Lesion located around
hippocampus
> 5mm
Hippo WBRT
< 5 mm
WBRT
Progression
SRS Boost

79. A personalized plan for each patient, based on
molecular characterizations of the tumor to
better target radiotherapy and chemotherapy, is
the future of brain metastasis treatment
Future and impediments of best RT options

80. Brain & Spine
Cranial – Mets - 220
Cranial SRS ~ 150 cases
 Functional SRS ~ 55 cases
Spine - 240
Stereotactic Program started in 2007 – Gained Momentum since 2013
Sterotactic Journey so far …….. !!!
AND CONITNUING STILL ……