Presentation and Management of Intracranial - PowerPoint Presentation

1. Presentation and Management of Intracranial Space Occupying lesions (ICSOL)

2. Types of ICSOL’sNeoplasms: Primary, secondaryInflammatory: Abscess, Tuberculoma, Syphilitic gumma, Fungal granulomas.Parasitic: Cysticercosis, Hydratid cyst, Amebic abscess, Schistosoma japonicum.Traumatic: Chronic subdural haematomaCongenital: Arachnoid and other benign cysts

3. 3Mass effectCSF obstructionIrritation of cortexCompressionInvasionImpairment of regional circulationIncreased ICPSeizuresFocal neurological deficitMechanisms leading to symptoms

4. Presenting Symptoms & SignsThe main groups: Symptoms of raised ICPSeizuresNeurological deficit (focal signs)Endocrine dysfunctionPersonality changes & impaired higher functionsVery important

5. I. Symptoms & Signs of Raised ICP Headache: Worsens inEarly morningFlat positionNausea and/or vomiting (projectile in the morning)Visual disturbances:PapilledemaAbducent nerve palsy (False localizing)Impaired consciousness

6. II. Seizures:Benign lesions tend to present more with seizuresGeneralized:Partial:SimpleComplex

7. III. Neurological deficit (Localizing signs)Depends on the location of the lesionIncludes:Cranial nerve deficits: mainly in skull base tumors Motor weaknessSensory deficit

8. IV. Endocrine dysfunctionMainly caused by pituitary lesionsHyperscretion:ProlactinomaAcromegalyCushing diseaseHyposecretion:Non-secreting pituitary adenomaCraniopharyngioma

9. V. Personality Changes & Impaired Higher FunctionsPersonality alterationChanges in moodInability to concentrateMemory disturbance

10. ManagementFull medical historyComplete general & neurol. ExaminationInvestigationsTreatment

11. 11Neurological ExaminationDo not forget: PAPILLEDEMANormalPapilledema

12. InvestigationsLab work up: CBC, U&E, PT, PTT, blood group, etcRadiological imaging: CT-scan: Method of choice for emergencyMRI: shows more anatomical details of the lesion Cerebral angiography: Mainly for vascular lesions Others: plain skull x-rays, isotope scanNeurophysiological tests: EEG, EVOP’s

13. TreatmentInitial treatment (Emergency)Definitive treatment

14. Initial treatmentOften started in the ERGoals:Control of raised ICPControl of seizuresPrepare patient for definitive treatmentVery important

15. Management of raised ICPElevate the head to about 30°Adequate oxygenationAvoid fluid overloadDexamethasone HyperventilationMannitolICP monitoringOnly in patients with decreased LOC

16. Control of SeizuresInterruption of a seizure or status epilepticus: BenzodiazepinesPerioperative prophylaxis: Phenytoin

17. Definitive treatmentDepends on the type and location of the lesion.Most intracranial tumors need surgical excision.Radiotherapy for:Inoperable tumorsPostoperative for malignanciesChemotherapy: adjuvant in malignancies.

18. Intracranial tumorsResponsible for 2% of all cancer death.Overall incidence: 8-10 cases per 100.000 population per yearTwo peaks: Early childhood5th-7th decades of lifeBenign or malignant.

19. EtiologyUnknown for most of brain tumors in humans.Chromosomal abnormalities have been noted in various benign & malignant brain tumors. Clear genetic factors play a minor role: 5% of patients have family H/o brain tumorsNeurofibromatosis: autosomal dominant NF I: causative gene on the long arm of chromosome 17NF2: causative gene on the long arm of chromosome 22Increased incidence of brain tumors following cranial irridiation

20. ClassificationsBased on the cell of origin glial(gliomas)and non-glial In relation to brain tissue: Extrinsic vs. intrinsic In relation to their site: Supratentorial vs. infratentorial (posterior fossa) Age of presentation: Pediatric vs. adult.

21. WHO ClassificationBased on the cell of originNeuroepithelial tumors: e.g. gliomas Primitive neuro-ectodermal tumors: e.g. medulloblastoma Nerve sheath tumors (neuroma): e.g. vestibular schwannoma Meningeal tumors: e.g. Meningiomas Pituitary tumorsGerm cell tumors: e.g. germinomaLymphomasMalformative tumors: e.g. craniopharyngeomaVascular tumors Metastatic tumorsLocal extensions from regional tumors: e.g. Glomus jugulare

22. GliomaMost common primary brain tumor (50%)Arise from the supporting cells of the brain.Neuroectodermal in origin.Usually supratentorial.Rarely metastasize.Tumor in single lobe may be treated by lobectomy.Recurrence is common despite postoperative radiotherapy.

23. AstrocytomaArise from the astrocyte cellsComprise 80% of all glioma and 40% of all brain tumorsPeak incidence: 35 - 45 yrs (early middle age)Males > females All are inflitrative.

24. Histopathological GradingBenign (Low grade) Grade 1Grade 2Malignant (High grade)Grade 3Grade 4

25. Clinical presentation :Duration of symptoms: Benign : Often long (years) Malignant : Often short (wks.)Symptoms of SOLHeadache (70%) Papilledema (60%)Seizures (40 - 75%)Focal neurological deficit (20 - 40% ).Mental changes (30%)

26. Investigations Low grade astrocytoma:CT: Hypodense non-enhancing area.MRI: Hyperintense T2 + non-enhancing hypointense T1High grade astrocytoma:CT: Mixed density area with strong, irregular contrast enhancementMRI: Hyperintense T2 + enhancing hypointense T1

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28. TreatmentBenign A. (grade 1 & 2): Surgical Excision (+/- Radiotherapy)Malignant A. (grade 3 & 4): Surgical Excision + Radiotherapy (+/- Chemotherapy)

29. Prognosis :Benign A. (grade 1 & 2):VariableCure possible after complete excision in grade I A.Malignant A. (grade 3 & 4):Generally POOR!Mean survival: about 2 years 

30. MeningiomaArises from the arachnoid villi & granulationsComprises 15-20% of all intracranial tumorsIt is the most benign intracranial tumor Peak incidence: 35 – 70 yrs (Rare in children)Female preponderance (f:m ratio = 2:1)

31. Clinical presentationOften long history (for many years)Symptoms of SOL:Focal neurological deficit depending on the site of meningiomaEpilepsy: mainly in frontal & temporal convexity meningiomaCranial nerve deficits: common in basal M.Mental changes: in large anterior & middle fossa M.

32. InvestigationsPlain skull X-rays: Positive findings in up to 70% of casesDirect signs: Hyperostosis, calcification, bone erosionIndirect signs: Shifted pineal gland, sella changesCT scan MRI (Investigation of choice )Angiography: Indicated in M. neighboring major vessels & sinusesShows:Tumor relationship to major cerebral vesselsBlood supply of tumorWhether pre-operative embolization is needed  

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34. Treatment & PrognosisTreatment of choice:TOTAL EXCISIONHigh recurrence rates occur in cases of:Incomplete excisionMalignant M.Radiotherapy plays a very limited role 

35. Pituitary TumorsPituitary tumors represent between 10% and 15% of all intracranial tumors.Slightly more frequent in womenMost pituitary tumors occur in young adults

36. Pituitary tumors:Classification & PresentationSecretary : ~70-80%Prolactinoma:In women → amenorrhea-galactorrhea syndrome.In men → impotence.GH secreting: cause gigantism, acromegalyACTH secreting: cause Cushing’s diseaseNon-secretary: Produce compressive symptoms:On optic chiasm → bitemporal hemianopiaOn secretory cells → hypopituitarism

37. Investigation:MRI: Method of choice.CT : is contraindicated if MRI available because of radiation of optic chiasm.Ophthalmological assessment.Endocrinological assessment.

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39. TreatmentProlactinomas: Medical treatmentDopamin agonistsOther pituitary adenomas:Surgical excision: TranssphenoidalTranscranial Radiotherapy: as adjunct to surgery for large or recurrent tumors Hormonal substitution

40. Vestibular Schwannoma(Acoustic Neuroma)Arise in the internal auditory meatus from the nerve sheath (Schwann) cells of the vestibular branch of the 8th cranial nerveEarly symptoms:Unilateral sensori-neural deafness, tinnitus & vertigoLate symptoms Loss of corneal reflexes Facial weakness and unilateral taste loss. Dysphagia, dysarthria and hoarseness.Ataxia and nystagmus.

41. InvestigationsENT assessment:AudiometryRadiological imaging:MRICT-scanAre helpful in determining the location and size of a tumor and also in planning its removal.Neurophysiological testing:Brainstem auditory evoked response (BAER)

42. 42Preop.Postop.Vestibular Schwannoma: MRI

43. Treatment Standard treatment: Surgical excisionMain surgical risk in large tumors: Facial paralysisAlternative options:Observation for patients with small lesion and little symptomsRadiosurgery: Can be used to reduce the size or limit the growth of tumors up to 25 mm in diameter

44. MedulloblastomaA highly cellular, malignant tumorOriginates from the external granular layer of the fetal cerebellum (Obersteiner’s layer)Comprises ~3% of all brain tumors2/3 of patients are childrenHigher involvement of males

45. Clinical Presentation Relatively short history (1-4 months)Symptoms & signs of raised ICP mainly due to obstructive hydrocephalus→ 80%Focal neurological signs → 60% Cerebellar: Truncal & gait ataxiaFalse localizing : 6th nerve palsyBrain stem: Nystagmus

46. InvestigationsCT scan MRI: Brain & spine (Diagnostic test of choice)

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48. Treatment Surgical excision + Radiotherapy (+Chemotherapy)Ventriculoperitoneal shunt often neededPrognosis:5-year survival = 70%

49. Brain Metastasis It account almost 50% of brain tumors.Lung (most common)BreastKidneyMelanomaColon (the least)

50. Surgical Intracranial infectionsA large spectrum of microorganisms can give rise to infectious intracranial mass lesions Causative organisms include:Bacteria ParasitesFungiMost common:Brain abscessIntracranial tuberculoma

51. Brain abscessBrain abscess is a focal infection, which begins when organisms are inoculated into the brain parenchyma, usually from a site distant from the central nervous system (CNS).Male > femalePeak incidence in the 3rd to 5th decades of lifeUp to 25% of abscesses are cryptogenic and have no clear primary source.

52. There are 3 mechanisms of entry of organisms to the brain:1- Direct extension: Infections stemming from the sinuses, teeth, middle ear, or mastoid 2- Hematogenous: Seeding of the brain occurs from distant infection sites and often results in multiple brain abscesses.3- Following penetrating head injury or neurosurgeryPathogenesis

53. Clinical PresentationThere are no specific symptoms for brain abscess.Mainly present with symptoms of ICSOL, including:HeadacheVomitingLethargyNeurological deficitAlso can present with symptoms of toxicity include:FeverIrritabilityNeck stiffnessSymptoms from the primary site of infection e.g. middle ear infection

54. InvestigationsImaging:CT-scanMRILab work-up:Lumbar puncture:Should be avoidedThere is a high risk of transtentorial herniation

55. 55Right frontal brain abscess Before contrastAfter contrast

56. TreatmentThe main treatment of brain abscess is the antimicrobial therapy.Surgery is necessary for 2 reasons:Gain samples of the infectuous material to identify the causative organism and the suitable antibiotic(s) Decrease the mass effect & ICPSurgery consists typically of:Burr hole &Aspiration of abscess

57. Intracranial TuberculomaTuberculosis may affect the central nervous system in which case it is called TB meningitis, TB cerebritis, and TB myelitis ,respectively.Granulomas from CSF extension or blood spreadWidely distributedUsually multiple and less than 1cm diameterCentral zone of caseatin

58. Clinical presentation:The patient may be asymptomatic , have pulmonary symptoms or have Symptoms and signs of raised intracranial pressure ( the usual presenting feature).

59. 59Incidence:In western countries: <1% of all ICSOLIn Saudi Arabia: ~5% of all ICSOLIn last 2 decades there was a worldwide rise in association with AIDSOften affects children & young adults

60. Intracranial TuberculomaIncidence:In western countries: <1% of all ICSOLIn Saudi Arabia: ~5% of all ICSOLIn last 2 decades there was a worldwide rise in incidence secondary to AIDS.

61. 61Intracranial TuberculomaETIOLOGY & PATHOGENSISCaused by human type of Mucobacterium tuberculosis, but rarely by atypical strainsSecondary hematogenous spread from another lesion elsewhere in the body, usually lungsMost patients have no history of T.B. meningitis50% of patients have a +ve history of T.B. or contact with T.B. patientConcomitant extracranial T.B. lesions detected:In 10% of patients in clinical series, and In >70% of autopsied patients

62. 62Intracranial TuberculomaCLINICAL PRESENTATIONSymptoms & signs of progressive ICSOL:Raised ICP: in nearly all infratentorial and most (80%) of supratentorial tuberculomasEpileptic seizures: in 70 – 85% of patients with supratentorial tuberculomasFocal neurological deficit: ~50% of patientsGeneral symptoms (malaise, anorexia, perspiration, fever): ~50% of cases

63. 63Intracranial TuberculomaINVESTIGATIONSLab work-up:Increased WBC: 60% of casesESR: elevated or normalMantoux test: Often positiveCXR: +ve findings for T.B. in ~50% of casesMethods of choice: CT- scan MRI

64. 64Multiple intracranial tuberculomas

65. Treatment & PrognosisThe main treatment is a combined anti-TB drug therapy for at least one year or even longer.Surgery is often required for histopathological confirmation of diagnosisPrognosis is generally good

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