CNS Tumours Flashcards
What is the Monro-Kellie hypothesis?
The sum of volunes of CSF, intracranial blood and brain remains constant. An increase in one should result in a decrease in the other two.
However, blood, brain and CSF are largely incompressible, thus CSF containing spaces and skull foramina are the only places where volumes can accomodate chage.
Thus, compensation by reducing cerebral CSF and blood volume are the only ways the body can regulate ICP.
What is the Monro-Kellie hypothesis?
The sum of volunes of CSF, intracranial blood and brain remains constant. An increase in one should result in a decrease in the other two.
However, blood, brain and CSF are largely incompressible, thus CSF containing spaces and skull foramina are the only places where volumes can accomodate chage.
Thus, compensation by reducing cerebral CSF and blood volume are the only ways the body can regulate ICP.
How can herniation occur?
Increased ICP can lead to displacement of soft tissue through whatever anatomical openings are available
WHat are the three levels of herniation?
- Subfalcine - Herniation of cingulate gyrus
- Transforaminal - Cerebellar tonsils herniate
- Transtentorial - Brain stem herniation (central transtentorial) and temporal lobe herniation (uncus transtentorial)
How can we measure ICP?
Difficult to do, but can measure CSF pressure as a proxy.
- Normal = 7-15mmHg in SUPINE adult
- >15mmHg = abnormal
- >20mmHg = pathological
Causes of raised ICP?
- Space occupying lesion e.g. tumour, haemorrhage
- CSF flow obstruction
- Cerebral oedema e.g. stroke, traumatic injury
Symptosm and signs of iCP
- Headache
- Seizures
- Vomiting
- Hypertension and bradycardia
- Focal neurological signs
What can occur in compensation of raised ICP?
- Decreased CSF and blood volume
- Parenchymal displcement - midline shift, compressed gyri, effacement of ventricles
- Herniation of brain
What is the most important first step for classifying CNS tumours?
Determining if primary or metastatic.
What are the most commonly identified neoplastic lesions of the brain?
Common sites from which they came?
Metastases from other sites.
Can be any tumour that spread haematogenously, but most common primary sites are the most common cancers:
- Lung
- Breast
- Renal
- Colorectal + GIT carcinomas
- Melanoma
Three common radiographic features of metastatic brain lesions
- Multiple well encapsulated mass lesions
- Mass effect
- Surrounding vasogenic oedema
What does multiple metastases indicate in teh brain?
Multiple sites = very likely to be metastatic, but a single site may also be metastatic.
Describe the incidence of primary brain tumours in teh adult and paediatric population?
Priamry CNS neoplasms are very rare in adults - 2 in 1 million. Most are sporadic mutations.
However, brain tumours account for 20% of paediatric malignancies.
(astrocytic and embryonal tumours)
What is the role of staging in primary brain tumours?
Not so important, as primary brain tumours tend not to spread. More important to type based on pathological features.
What is the difficulty in grading brain tumours as benign or malignant?
Usually, malignant = metastatic spread and ability to cause death.
However, in the brain, even benign tumours in the wrong place can have lethal effects.
What 4 factors are taken into account in management of CNS tumours?
- Tumour type and grade
- Location
- Patient age
- Performance status - co-morbidities.
What is involved in the WHO CNS tumour classification? (3)
Based on combined phenotypic and genotypic features:
- Histology
- Molecular classification (tumours with different biological behaviour can look the same histologically)
- Radiology
What is WHO grading from 1-4?
Grade 1: Low proliferative potential, potential for cure if resection is possible
Grade 2: Generally infiltrative, tendency to progress with recurrence. Survival <5 years
Grade 3: Histological features of malignancy. Require post-op adjuvants
Grade 4: Histological features of high grade malignancy. Usually fatal
Four main categories of primary CNS tumours
Gliomas (diffuse gliomas)
Embryonal (medulloblastoma)
Meningiomas
Cranial and Paraspinal (Schwannoma)
From which cells do gliomas arise?
Pluripotent stem cells
Subtypes of diffuse gliomas by adult/paediatric?
Adult type:
- Astrocytoma
- Oligodendroglioma
- Glioblastoma
Paediatric type:
- Low grade
- High grade
How does IDH gene relate to diffuse gliomas?
Adult type diffuse gliomas arise from mutations in isocitrate dehydrogenase (IDH)
IDH mutant:
- Secondary mutations in TP53 and ATRX cause astrocytoma
- Translocation between chromosomes 1 and 19 become oligodendroglioma
IDH wild type:
- Mutants in EGFR and TERT = rapid progression to high grade tumour glioblastoma (Grade IV)
Prognostic difference between IDH mutant types: Astrocytoma and oligodendroglioma?
Oligodendroglioma has better prognosis.
Prevalence of IDH wild type vs IDH mutant
IDH wild type (EGFR and TERT mutations) = >90%
IDH mutant (ATRX and TP53) = <10%
Most common location for astrocytomas and oligodendrogliomas?
Supratentorial - fronto-temporal lobe regions.
Presentation of astrocytome/oligodendroglioma
- Progressive headache
- Progressive neurological abnormalities
- Seizures, impingement of blood vessels causing collapse
Which type of glioma has the worst prognosis?
What would you expect in radiological findings?
High grade astrocytoma / glioblastoma
Radiology - central necrosis and peripheral vascularity - shows a bright ring around the brain.
Grade and describe the infiltrative properties of meningioma
Grade 1-3
Does not invade the parenchyme
