Space Occupying Lesions Flashcards

(67 cards)

1
Q

what happens when the brain enlarges

A
some blood +/‐
CSF must escape from cranial vault
to avoid rise in pressure.
• Once this process is exhausted,
venous sinuses are flattened and
there is little or no CSF.
• Any further increase in brain volume
results in rapid increase in ICP
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2
Q

what can cause raised ICP

A
increased CSF (hydrocephalus)
focal lesion in brain (SOL)
diffuse lesion in brain (oedema)
increased venous volume 
physiological (hypoxia, hypercapnia, pain)
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3
Q

what is hydrocephalus

A

accumulation of excessive CSF within the ventricular system of the brain

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4
Q

what is the normal volume of CSF

A

120-150 mls

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5
Q

how much CSF is made per day

A

500ml

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6
Q

where is CSF produced

A

by the choroid plexus in the lateral and fourth ventricles of the brain

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7
Q

what absorbs CSF

A

arachnoid granulations

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8
Q

what does the CSF usually contain

A
lymphocytes <4 cells 
neutrophils 0
protein < 0.4 g/l
glucose >2.2 mmol/l
no RBCs
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9
Q

what does increased lymphocytes in CSF mean

A

inflammation/ infection

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10
Q

what does increased polymorphs in CSF mean

A

bacterial meningitis

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11
Q

what can cause hydrocephalus

A

obstruction to CSF flow (inflammation, pus and tumours)
decreased resorption of CSF (post SAH, meningitis)
overproduction of CSF (v. rare: tumours of choroid plexus)

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12
Q

what is non communicating hydrocephalus

A

obstruction of flow of CSF occurs within ventricular system

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13
Q

what is communicating hydrocephalus

A

obstruction to flow of CSF outside of the ventricular system (e.g. in subarachnoid space or at the arachnoid granulations)

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14
Q

what happens if hydrocephalus occurs before/ after the closure of cranial sutures

A

before- cranial enlargement

after- expansion of ventricles and increased in ICP

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15
Q

what is hydrocephalus ex vacuo

A

dilatation of the ventricular system and a compensatory increase in CSF volume secondaryto loss of brain parenchyma (e.g. in alzheimers)

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16
Q

what are the physical effects of raised ICP

A
• Intracranial shifts and
herniations – “Coning”
•Midline shift
•Distortion and pressure on cranial nerves and vital
neurological centres
• Impaired blood flow
• Cerebral Perfusion Pressure =
MAP – ICP
•Reduced level of consciousness
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17
Q

what are the causes of raised ICP

A
infections
tumours
stroke
aneurysm
epilepsy
seizures
hydrocephalus
hypoxemia
meningitis
haemorrhage
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18
Q

describe a tentorial herniation

A

when medial aspect of temporal lobe herniates over the tentorial cerebellum

=compression of CN 3 (pupillary dilatation and impaired eye movements on side of lesion)

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19
Q

describe a subfalcine herniation

A

unilateral expansion of cerebral hemisphere which displaces the singular gyrus underneath the falx cerebri= weakness and sensory loss on opposite side

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20
Q

describe a cerebellar herniation (uncal)

A

inferior descent of cerebellar tonsils below the foramen magnum (aka coning)
=puts pressure on brain stem

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21
Q

describe a central herniation

A

the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli

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22
Q

describe a transcalvarial herniations

A

herniation through any defect in the skull (e.g. following fracture)

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23
Q

what are the clinical signs of raised ICP

A

papilloedema
headache
neck stiffness
N&V

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24
Q

what are the most common space occupying lesions

A

tumours
abscess
haematomas
localised swelling (swelling and oedema around cerebral infarct)

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25
what are the most common clinical presentations of tumours
``` focal symptoms headache (worse in morning) vomiting seizures visual disturbances papilloedema ```
26
where do most brain tumours in children occur
below the tentorium cerebelli
27
where do most brain tumours in adults occur
above the tentorium cerebelli
28
what are the commonest cancers to mets to brain
breast, bronchus, kidney, thyroid, colon, malignant
29
how are brain tumours graded
``` mitosis neovascularisation necrosis atypia cellularity ```
30
what are the most common types of malignant primary brain tumour
astrocytomas oligodendrogliomas medulloblastoma (most common in children)
31
what is the most common type of benign primary brain tumour
meningioma schwannoma craniopharyngioma pituitary adenoma
32
why are astrocytomas hard to resect
insidious brain infiltration
33
what is a glioblastoma
grade 4 astrocytoma
34
do grade 1 astrocytomas become malignant
no
35
what are the features of a astrocytoma (grades 2+)
``` nuclear atypia mitosis necrosis (4) neovascularisation (4) proliferation anaplasia palisading ```
36
what is the most common tumour in children
medulloblastoma
37
what are the features of a medulloblastoma
poorly differentiated embryonal occurs in midline of cerebellum very radiosensitive- good prognosis
38
what are the causes of single brain abscesses
``` local extension (e.g. mastoditis) direct implantation (e.g. skull fracture) ``` (tend to occur adjacent to the source)
39
what are the causes of multiple abscesses
haemotogenous spread (bronchopneumonia, bacterial endocarditis, congenital heart disease, IV drug use) (tend to occur at grey and white matter boundary)
40
what are the symptoms of an abscess
fever raised ICP + symptoms of underlying cause
41
what investigations and Tx for brain abscess
CT/ MRI to diagnose apsirate for culture and Tx weeks of antibiotics (hard to get into CNS)
42
what is bacterial meningitis
inflammation of the leptomeninges | and CSF within the subarachnoid space
43
how does bacterial meningitis cause raised ICP
severe oedema
44
what is seen in CSF in bacterial meningitis
polymorphs | low glucose
45
what can arachnoiditis cause
lack of CSF absorption = hydrocephalus = raised ICP
46
e coli: | what type of bacterial is it and who does it cause bacterial meningitis
gram -ve rod | neonates
47
H influenza: | what type of bacterial is it and who does it cause bacterial meningitis
gram -ve cocco-bacilli | infants and children
48
n meningitidis: | what type of bacterial is it and who does it cause bacterial meningitis
gram -ve diplococci | adolescents and young adults
49
s pneumoniae: | what type of bacterial is it and who does it cause bacterial meningitis
gram +ve cocci in chains | older adults or children
50
L monocytogenes: | what type of bacterial is it and who does it cause bacterial meningitis
gram +ve rods | older adults
51
what are missile and non missile injuries
missile= penetrating | non missile- blunt
52
what can penetrating brain injuries cause
focal damage lacerations in region of brain damage haemorrhage
53
does a high or low velocity penetrating brain injury cause more damage
high
54
what is a non missile injury and what determines the extend of its damage
sudden acceleration/ deceleration of head smaller the contact time the larger the force
55
what is a primary brain injury
* Injury to neurones * Irreversible * Preventative measures (hallmark is change in consciousness immediately)
56
what is a secondary brain injury
* Haemorrhage * Oedema etc * Potentially treatable
57
what are the types of scalp lesions
bruising (contusions) lacerations bleeding (route for infection)
58
what are the types of skull fracture
• Linear ‐ straight sharp fracture line, that may cross sutures (diastatic fracture) •Compound ‐ associated with full thickness scalp lacerations •Depressed if base of skull fracture then compound or open as damage to paranasal sinus
59
what is coup and contra coup
in the context of brain surface contusions and lacerations: - Coup- brain hits side of injury - Contra coup- hits opposite side, tend to be worse than coup
60
what is a diffuse axonal injury
Occurs at moment of injury a blunt trauma puts a shearing strain on axons which tear affects central areas causes reduced consciousness and coma can lead to vegetative state
61
what can cause secondary injury to the brain
``` -Intracranial haematoma • Reduced cerebral blood flow • Hypoxic brain damage • Excitotoxicity • Oedema • Raised ICP • Infection ```
62
what does Ca2+ influc do to protease and phospholipase
activates them- causing lipid membrane disruption
63
where are most traumatic intracranial haematomas
intradural (sub dural, intracerebral, subarachnoid)
64
what are traumatic extradural haematomas like
``` •Usually a complication of fracture in tempero‐parietal region that involves middle meningeal artery • Immediate brain damage often minimal •But untreated, midline shift – compression and herniation ```
65
what is a subdural haemorrhage and what causes it
• Collections of blood between the internal surface of dura mater and arachnoid mater • Caused by disruption of bridging veins that extend from the surface of the brain into subdural space
66
what is the pressure put on the brain by a subdural haemorrhage like
Gyral contours preserved – | pressure evenly distributed
67
what are chronic subdural haemorrhages associated with
brain atrophy less associated with trauma will present subtly