2. STROKE –MALIGNANCY Leading causes of death. Age related. Common risk factor-smoking. Asymptomatic-1/2 pt’s. May be presenting feature.
3. INTRODUCTION Cerebrovascular complications including hmge and infarction are 2nd only to mets in frequency of CNS lesions in autopsy series of pts with cancer. Graus et al. found in 15% of cancer pts pathological evidence of cerebrovascular disease. Half of them had clinical symptoms of stroke. Graus F, Rogers LR, Posner JB. Cerebrovascular complications in patients with cancer. Medicine 1985;64:16–35.
4. INCIDENCE Chaturvedi et al-only 3.5% cancer population experienced strokes. Arteriosclerosis and coagulation disorders were the most relevant patho physiology. Risk of recurrent ischaemic events was also similar to that of the non-cancer population. Chaturvedi S, Ansell J, Recht L. Should cerebral ischaemic events in cancer patients be considered a manifestation of hypercoagulability? Stroke 1994;25:1215–8.
5. No significant differences in vascular risk profile for cancer pts compared with a large series of stroke pts. Inc. risk for hmgic strokes in the cancer Pt’s. Chemotherapy-induced thrombocytopenia, DIC. Haematologicalmalig.- higher risk for ICH compared with the non-cancer population. Prognosis worse with cancer pt’s –poor GC. Zhang YY, Chan DKY, Cordato D, Sheng AZ. Stroke risk factor, pattern and outcome in patients with cancer. ActaNeurol Scand 2006;114:378–83.
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7. VASCULARAL EVENTS IN CANCER PTS Ischaemic. Haemorrhagic. Cerebral venous thrombosis (CVT).
8. VASCULARAL EVENTS IN CANCER PTS Tumour-related. Coagulation abnormalities. Infections. Therapy-related . Para neoplastic ?.
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10. W. Grisold; Stroke and cancer: a review; Acta NeurolScand 2009: 119: 1–16
12. CANCER-IS Mucinouscystadenocarcinomas. Lung cancer ,primary brain tumour ,prostate , GI tumours , genitourinary , lymphoma. Brest cancer –infrequently leads to stroke unless in late and given CT. Head &neck cancers . RT – IS <6 months of RT.
17. Lab. parameters in cancer pts asso. with stroke. D-dimer elevation. Acquired protein S def. Protein C def. Activated protein C resistance . Antiphospholipid antibodies. Hyperfibrinogenaemia . CA 125 tumour marker evaluation . Thrombocytosis.
18. Infection Pts with haematologicalmalig. are often immunocompromised. RT and treatment with anti-cancer drugs results in addl. immunosuppression. JC 40 virus-PML. Cerebral aspergillus infections from lungs. Candidal infections from GIT. Reactivation of Varicella-Zoster infection. Sepsis and bacterial endocarditis-septic cerebral infarction.
19. Therapy-related Surgery-embolic. RT- Vasculopathy Stroke like migraine attacks after radiation therapy (SMART) Pseudo-aneurysms and ruptures of the carotid artery - carotid blow out syndrome. CT- Cisplatin, MTX l-asparaginase. Ia CT – In primary brain tumours(nitrosureas, cisplatin and carboplatin, etoposide and MTX).
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21. Management Blood and heart investigations, u/s of the extracranial arteries and CT , MRI. MRI techniques are superior. DWI including ADC -acute vascular lesions. Treatment based on anticoagulation, but no established treatment is available.
23. Intracranial haemorrhage More common with Leukaemia, lymphoma and multiple myeloma. Intraparenchymal bleeding (e.g. hyperleucocytosis, coagulation disorders). Secondary to venous occlusion. Hmge into a primary -astrocytomas, Meningioma. brain metastases from Lung cancer, melanoma, renal,thyroid,choriocarcinoma & pancreas . Ruptured neoplastic aneurysm . Subdural haematoma-Leukaemia, lymphoma and cancer (e.g. prostate and breast cancer).
24. Types of intraparenchymatosehaemorrhagein leukaemia: (A) large intracranial haemorrhage into the cerebellum in a fairly classic shape.(B) Large, terminal polygonal haemorrhage into the brainstem. Diffuse and irregular haemorrhagic invasion of adjacent brain parenchyma. (C) Diffuse and spot-like haemorrhages resulting from coagulopathy in leukaemia.
25. Aetiologicalsubclassification of ICH Direct tumour involvement-Neoplastic infiltration of arteries-Cardiac myxomas, choriocarcinoma and lung cancer. Coagulation disorder-DIC, hyperleucocytic syndrome,thrombocytopenia, vit K deficiency (poor diet or antibiotic treatment with iatrogenic sterilization of the gut), protein synthesis deficiency (liver damage). Infection and hmge-fungal (e.g. aspergillus, candida)vasculitis or mycotic aneurysms. Therapy-related hmge.
26. Metastasis Oedema surrounding the hmge at the presentation. Perihematomal enhancement. Presence of other enhancing lesions. Multiple hmges into brain parenchyma. Atypical location of the hmge(grey white junction). Non-haemorrhagic tissue within the hmge. Uneven distribution of density within the hmge. Delayed hematoma evolution. Diminished or absent hemosiderin deposition. Ratio of vasogenic edema to mean hematoma diameter >100%.(Tung etal ,neuroradiology,2003.)
27. Dural metastasis in prostate cancer causing subdural haematoma (A, B). Nodular lumps (*)
28. (C) Dural biopsy with HE staining. (D) PSA staining. (E) Racemase staining.
29. Cerebral venous thrombosis Cancer and tumours accounted for 7.4% of all CVT. 2.2% were associated with CNS malignancy. 3.2% with solid tumours outside the CNS . 2.9% with haematological disorders.
30. Direct tumour effect Coagulation disorder Infection Therapy-related Paraneoplastic
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34. D. M. Cestari ETAL ;Stroke in patients with cancer: Incidence and etiology;Neurology 2004;62;2025-2030
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40. Stroke 1994;25;1215-1218 Should cerebral ischemic events in cancer patients be considered a manifestation of hypercoagulability? S Chaturvedi, J Ansell and L Recht
41. 33 pts representing 3.5% of all stroke consultations and admissions seen at the University of Massachusetts Medical Center were identified during the period 1988 through 1992. Large-vessel atherosclerosis was the most frequent cause of stroke. 30% were determined to have hypercoagulability as a cause , in only 1 of 9 pts in whom tests were done was sufficient evidence present to make a presumptive diagnosis of DIC.
42. Irrespective of therapy, recurrent cerebral ischemic events were noted in only 6% of pts during a follow-up period averaging greater than 9 months, similar to that for the risk of repeated events in the noncancer population.
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46. Ischemic Stroke in Cancer Patients With and Without Conventional Mechanisms A Multicenter Study in Korea SeonGyeong Kim, MD; Stroke. 2010;41:798-801
47. Results 161 pts. 97 (60.2%) pts in the CSM group . 64 (39.8%) inthe cryptogenic group. Pts in the CSM group were olderand vascular risk factors were more prevalent than in the cryptogenicgroup. DWI patterns of multiple lesionsinvolving multiple arterial territories were observed more frequentlyin the cryptogenic group than in the CSM group.
48. Levels of the D-dimer -cryptogenic group > CSM group (11.5±14.6 versus 3.6±10.3 µg/dL). In multivariate analysis, the DWI lesionpattern of multiple vascular territories (odds ratio, 11.2;95% CI, 3.74 to 33.3), and D-dimer levels of >1.11 µg/dL(odds ratio, 10.6; 95% CI, 3.29 to 33.8) were associated independentlywith the cryptogenic group.
49. Conclusions Stroke outside of CSM occurred in a largenumber in cancer patients. In stroke patients with cancer, D-dimerlevels and diffusion-weighted imaging lesion patterns may behelpful in early identification of non-CSMs (especially coagulopathyassociated with cancer) and possibly in guiding preventive strategiesfor stroke.
