Brain metastasis

1. BRAIN METASTASIS

2. INTRODUCTION
 Most common intracranial tumors in adults.
 Accounting for more than one-half of brain tumors
 15 -30% of the patients with cancer develop brain metastases.
 The route of metastatic spread to the brain is usually hematogenous, although
local extension can occur.

3.  SOLITARY METASTASIS:
 CT: At the time of neurological diagnosis, 50% are solitary on CT.
 MRI: If the same patients have an MRI, <30% will be solitary
 Autopsy: Solitary in one- third of patients with brain mets.

4.  Incidence of brain metastases increasing due to:
 Increasing length of survival of cancer patients as a result of improvement of
systemic cancers
 Enhanced ability to diagnose CNS tumors due to availability of CT or MRI
 Inabilty of most chemotherapeutic agents to cross BBB
 Some chemotherapeutic agents may transiently weaken the BBB and allow CNS
seeding.

5. LOCATION OF CEREBRAL METS
 Parenchymal in approximately 75%
 May involve the leptomeninges in a carcinomatous meningitis
 80% of the solitary mets are located in the cerebral hemispheres
 Highest incidence:
 Posterior to the sylvian fissure near the junction of the temporal, parietal and
occipital lobes.

6.  The cerebellum is a common site of brain mets and 16% of solitary brain mets
occur here
 Brain metastases is the most common posterior fossa tumor in adults
 “A solitary lesion in the p- fossa of an adult is considered a metastases until
proven otherwise”

7.  Sources of cerebral mets in adults (autopsy data):

8.  Sources of cerebral mets in peadiatrics:
 Neuroblastoma
 Rhabdomyosarcoma
 Wilm’s tumor

10. SYMPTOMS
Symptom Patients %
 Headache 50
 Cognitive dysfunction 31
 Focal weakness 27
 Seizure 20
 Gait ataxia 17
 Sensory disturbance 6
 Speech problems 10

11. IMAGING STUDIES
 Metastasis usually appear as “non-complicated” masses, often arising at the
grey white junction.
 Contrast-enhanced MRI is preferred imaging study
 Radiographic features that can help differentiate brain metastases
from other CNS lesions include:
I. Presence of multiple lesions
II. Localization at the junction of the grey and white matter
III. Round, well- circumscribed.
IV. Large amounts of vasogenic edema compared to the size of the lesion (“fingers
of edema”)

16.  MRI
 T1
 typically iso to hypointense
 if haemorrhagic may have intrinsic high signal
 non-haemorrhagic melanoma metastases can also have intrinsic high signal
due to the paramagnetic properties of melanin
 T2
 typically hyperintense (cysts,edema)
 FLAIR: typically hyperintense with hyperintense peri-tumoural
oedema

17.  MR spectroscopy
 Intra tumoral choline peak with no choline elevation in the peritumoraloedema
 Any tumor necrosis results in a lipid peak.
 NAA depleted.
 DWI: oedema is out of proportion with tumour size and appears dark on trace-
weighted DWI

18. Nuclear medicine
PET
 Considered the best imaging tool for metastases.
 Only detect mets up to 1.5 cm in size, therefore contrast MRI
remains the gold standard to rule out small mets(1 to 2mm).

24. DIFFERANTIALS
Mets GBM Abscess
Multiplicity Multiple lesions completly
seperated on FLAIR
Multiple lesions linked by
abnormal FLAIR signals
Does not attanuate to FLAIR
Location Commonly found at grey-white
matter deferentiation
centered on subcortical
white matter
Can occur anywhere
Morphology More well circumscribed Mostly asymmetrical Mostly well circumscribed,
smoother inner wall
MR contrast Equally enhancing peritumoral
component
Non enhancing peritumoral
component
Ring enhancement
MR spectroscopy High Lipid/Cr ratio High Cho/Cr and NAA/Cr
ratio
High Lipid/Lactate,
succinate, acetate

25. METASTATIC WORKUP
 Chest CT, Abdomen and Pelvis
 Mammogram in women
 Radionuclide Bone scan
 PSA in men
 PET scan
 Urine Analysis
 CBC, UCE, LFTs and LDH
 Skin survey for suspicious lesions

26.  If the metastatic workup is negative, then pathology of a metastatic brain lesion as
determined by biopsy may implicate specific primary sites
 Small cell carcinoma metastatic to the brain is mostly from the lung
 Adenocarcinoma: Lung is the most common primary

27. OVERVIEW OF MANAGEMENT
 With optimal treatment, median survival of patients with brain mets is only 26 -32
weeks.
 Specific treatments directed against the brain metastases
 Management or prevention of complications (eg, seizures, cerebral edema,
prevention of deep venous thrombosis)
 Treatment of systemic malignancy if appropriate

28. PROGNOSTIC CLASSIFICATION
RECURSIVE PARTITIONINGANALYSIS (RPA)
 Parameters that determine survival are:
i. Performance status
ii. The extent of extracranial disease
iii. Age
iv. Primary diagnosis

29. RECURSIVE PARTITIONING ANALYSIS (RPA)

31. MANAGEMENT OF BRAIN METS BASED ON RPA
 Patients having a favorable prognosis - treatment focuses on the eradication or
control of the brain metastases. Includes surgical resection and various forms of
radiation therapy (eg, whole brain, stereotactic radiosurgery).
 Patients having a poor prognosis- treatment focuses on control of symptoms
caused by the brain metastases, as well as maintenance of neurologic function to
as great an extent as possible.

33. • Various modalities :
1.WBRT
2.SRS (STEREOTACTIC RADIOSURGERY)
3.SURGERY
4. SUPPORTIVE CARE WITH DEXAMETHASONE

37. SURGERY
 En bloc resection method should be choose (disection around or inside the
pseudocapsule)
 This method is superior to piecemeal method because it prevents spilage of
tumor cells and symetrically devascularise the tumor
 Margin of 5 mm is ideal
 CUSA is very helpful

38. WBRT AFTER SURGERY
 Decreases local recurrence.
 Eliminates micrometastasis.
 DOSE: 30Gy in 10 fractions.
 INDICATION:
 Multiple tumors
 Small tumors <2cm.
 Radiosensitive tumors.

39. RADIOSURGERY
 Tumor less then 3cm
 Unfit for surgery.
 Deep seated tumors.
 Increased age.
RADIORESISTANTTUMORS (Melanoma,renal cell ca, soft tissue sarcoma) .
RECURRENCE 15%.

40. RADIOSURGERY
 ADVANTAGES:
 No incision.
 Treats surgically inaccessible lesions.
 More easily tolerated .
 Short hospital stay.
DISADVANTAGES:
 Poor targeting for >3cm tumors.
 Tumors persists on scan.
 No tissue diagnosis.
 Persistant edema or radionecrosis.
 Cannot be used within 5mm of optic nerve or chiasm.

41. RECURRENTTUMORS
 10 to 20%.
 More in multiple metastasis then single.
 Poor outcome if occurs in less then 4 months.
 Supportive treatment (progressive, extracranial with recurrence).
 Healthy patients (radiosurgery,reoperation,radiotherapy)
 Reoperation 9 to 11 m survival and neurological improvement 62% to 75%

42. CHEMOTHERAPY
 Last resort if other therapies fail.
 Able to cross BBB.(TEMOZOLOMIDE)
 Considered breast ca,small cell ca of lung, non seminomatous germ cell tumor of
testis.

43. SYMPTOM MANAGEMENT
 Control of peritumral edema and increased intracranial pressure with
corticosteroids
 Treatment and prevention of seizures
 Management and prevention of venous thromboembolic disease

44. CONTROL OFVASOGENIC EDEMA
 Dexamethasone is the standard agent:
 relative lack of mineralocorticoid activity reduces the potential for
fluid retention.
 dexamethasone associated with a lower risk of infection and
cognitive impairment compared to other glucocorticoids
 Dose and schedule —
 Dexamethasone regimen consists of a 10 mg loading dose, followed
by 4 mg four times per day or 8 mg twice daily.

45. TREATMENT AND PREVENTION OF
SEIZURES
 Patients who have one or more seizures associated with a primary or metastatic
brain tumor, initial treatment with a single agent antiepileptic drug (AED) (Grade
1A)(PHENYTOIN)
 Patients without a history of seizures and who have not undergone a
neurosurgical procedure, recommend NOT using prophylactic AEDs (Grade 1B)

46. MANAGEMENTAND PREVENTION OFVENOUS
THROMBOEMBOLIC DISEASE
Treatment of venous thromboembolism
 Anticoagulation in all patients with brain tumors and venous thromboembolism (VTE) except those
that have a high rate of intracranial hemorrhage (ie, metastases from melanoma, choriocarcinoma,
thyroid carcinoma, and renal cell carcinoma)
 VTE in low-grade glioma and benign tumors should be treated for three to six months.
 Long-term anticoagulation is recommended for malignant gliomas.

47.  LMW heparin rather than warfarin for anticoagulation Prophylaxis ofVTE
 Patients undergoing surgery, use pneumatic compression stockings combined with
postoperative LMW heparin or unfractioned heparin beginning 12 to 24 hours after
surgery and continuing until ambulation is resumed.

48. SURVIVAL
 RADIOTHERAPY + STERIODS 3-6 MONTHS
 FOCAL RESECTION 9-12 MONTHS
 SINGLE BRAIN METASTASIS 1-2YEAR