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Neurology > Neuropatholgy III > Flashcards

Neuropatholgy III Flashcards

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1
Q

What is the normal volume of CSF?

A

120-150ml

500ml produced per day with turnover 3-5 times a day

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2
Q

Where is CSF produced?

A

The choroid plexus in the lateral and fourth ventricles

Absorbed by arachnoid granulations

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3
Q

Where is the lumbar cistern located?

A

Between L2 and S2

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4
Q

What is the cytology of normal CSF?

A 
Lymphocytes <4 cells/ml
Neutrophils = 0 cells/ml
No RBCs
Protein <0.4 g/l
Glucose > 2.2mmol/l
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5
Q

What is hydrocephalus?

A

Accumulation of excessive CSF within the ventricular system of the brain

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6
Q

What are the mechanisms that can cause hydrocephalus to occur?

A

Obstruction to CSF flow
Decrease CSF resorption
Overproduction of CSF

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7
Q

What is the classification of hydrocephalus?

A 
Non-communicating = obstruction occurs within ventricular system
Communicating = obstruction occurs outside of ventricular system
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8
Q

What happens if hydrocephalus develops before closure of the cranial sutures?

A

Cranial enlargement occurs

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9
Q

What happens if hydrocephalus develops after closure of the cranial sutures?

A

There is expansion of the ventricles and increase in intracranial pressure

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10
Q

What is hydrocephalus ex vacuo?

A

Dilation of ventricular system and a compensatory increase in CSF volume secondary to loss of brain parenchyma

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11
Q

What happens if the brain enlarges?

A

Some blood +/- CSF must escape from the cranial vault to avoid rise in pressure

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12
Q

What happens once ICP begins to rise?

A

Venous sinuses are flattened and there is little remaining CSF = there will be rapid rise in ICP

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13
Q

What are some causes of raised ICP?

A

Increased CSF, space occupying lesions, oedema, increased venous volume, physiological (hypoxia, hypercapnia, pain)

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14
Q

What effect can have raised ICP have on the brain?

A

Intracranial shifts and herniations, midline shift, distortion and pressure on cranial nerves/neurological centres, impaired blood flow, reduced level of consciousness

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15
Q

What are the types of shift that can occur in the brain?

A

Subfalcine, tentorial (and central), cerebellar, transcavarial

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16
Q

What are the clinical signs of raised ICP?

A

Papilloedema, headache, nausea and vomiting, neck stiffness, reduced consciousness

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17
Q

What are some examples of space occupying lesions?

A

Tumours (primary/metastases), abscess, haematoma, localised brain swelling

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18
Q

What are some symptoms of tumours?

A

Focal symptoms, headache, seizures, vomiting, visual disturbances, focal deficit, papilloedema

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19
Q

How common are tumours of the central nervous system?

A

Primary = 3% of all cancers, 20% of all childhood cancers

Metastases are more common than primary tumours

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20
Q

What is the difference between where tumours arise in adults and children?

A

70% of tumours in children arise below tentorium cerebelli, but 70% of adult tumours arise above tentorium cerebelli

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21
Q

What are some cancers that cause brain metastases?

A

Breast, bronchus, kidney, thyroid, colon carcinoma and malignant melanoma

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22
Q

Where are brain metastases often seen?

A

At the boundary between the grey and white matter

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23
Q

What are grade I-III astrocytomas?

A

Grade I = pilocytic
Grade II = well differentiated
Grade III = anaplastic

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24
Q

What are some features of grade I astrocytomas?

A

Occur in childhood, benign behaving, long hair-like processes, cystic areas

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25
What are some features of grade II astrocytomas?
Display nuclear atypia, mean survival is 5 years
26
What are some features of grade III astrocytomas?
Display greater nuclear atypia and mitotic activity
27
What are the two kinds of grade IV astrocytomas?
Primary and secondary glioblastomas
28
What are some features of primary glioblastomas?
Extreme atypia, mitotic activity, necrosis or neovascularisation, survival is about 10 months
29
What are some features of secondary glioblastomas?
Extreme atypia, mitotic activity, necrosis and/or neovascularisation, survival is >10-12 months
30
What genes are implicated in grade I-III astrocytomas and secondary glioblastomas?
IDHi, P53, PDGFRA, RB and PI3KCA
31
What mutations are associated with primary glioblastomas?
EGFR amplification, PTEN loss, P53 mutation
32
What is the most common tumour of the CNS in children?
Medulloblastoma = 25% of all paediatric CNS neoplasms
33
What are some features of medulloblastomas?
Poorly differentiated = look like primitive undifferentiated embryonal cells Poor prognosis if untreated, but very radiosensitive 75% 5 year survival with resection and radiotherapy
34
What are the most common malignant CNS tumours?
Astrocytoma (all types), oligodendroglioma, medulloblastoma
35
What is the most common benign CNS tumour?
Meningioma
36
What are some sources of infection that may cause a single abscess?
May form from local extension or direct implantation = tend to occur adjacent to source
37
What tends to cause multiple abscesses?
Haematogenous spread = occur at grey and white matter boundary
38
What are some features of abscesses?
Central necrosis with oedema fibrous capsule May cause midline shift Symptoms = fever, raised ICP, underlying cause
39
How are abscesses diagnosed?
CT or MRI, plus do aspiration for culture
40
What organisms may cause abscesses?
Often polymicrobial = staph aureus and strep, fungi and protozoa in immunocompromised
41
What is meningitis?
Inflammation of leptomeninges and CSF within the subarachnoid space
42
What are some features of bacterial meningitis?
Causes severe oedema and raised ICP Abundant polymorphs on CSF and decreased glucose Arachnoiditis can cause lack of CSF absorption = hydrocephalus and raised ICP
43
What are some organisms that cause bacterial meningitis?
Ecoli = neonates H. infulenzae = infants and children N. meningitidis = adolescents and young adults S. pneumoniae = older adults and children L. monocytogenes = older adults (>65)
44
What can head injuries cause?
Skull fractures, parenchymal injury and vascular injury
45
What damage can a penetrating injuries cause?
Focal injury, lacerations, haemorrhage
46
How can blunt trauma cause head injury?
Sudden acceleration/deceleration of head = brain moves within the cranial cavity and makes contact with inner table of cranium and bony protrusions
47
What effect does contact time have on force in blunt trauma?
The smaller the contact time of the object, the greater the force generated
48
What are some causes of blunt trauma?
RTCs, falls, assaults, alcohol
49
What are primary and secondary head injuries?
``` Primary = damage to neurons, irreversible Secondary = haemorrhage and oedema, potentially treatable ```
50
What are some examples of primary head injuries?
Scalp lesions, skull fracture, surface contusions or lacerations, diffuse axonal and vascular injuries, petechial haemorrhages
51
What are some examples of scalp lesions?
Bruising, laceration, bleeding = route for infection
52
What are the types of skull fractures?
Linear = straight and sharp, may cross sutures | Compound and depressed
53
What are compound fractures associated with?
Full thickness scalp lacerations | Base of skull fractures
54
What are skull fractures associated with a higher incidence of?
Intracranial bleeding and haematomas
55
Where do surface head injuries tend to occur?
Lateral surface of hemispheres | Under surface of temporal and frontal lobes
56
What is one cause of surface head injuries?
Coup and contracoup injuries
57
What are contracoup injuries?
Injury to non-impact side = may occur at same time as coup, may occur due to rebound, tend to be worse
58
What are coup injuries?
Injury to brain on the side of impact
59
When do diffuse axonal injuries occur?
At the moment of the insult to the head = occurs due to shearing forces
60
What areas are affected by diffuse axonal injury?
Central areas = brainstem (immediate death occurs), corpus callosum, parasagittal areas, interventricular septum, hippocampal formation
61
What symptoms do patients with diffuse axonal injuries tend to have?
Reduced consciousness and coma = may lead to vegetative state
62
What are some examples of secondary brain injuries?
Intracranial haematoma, reduced cerebral blood flow, hypoxia, excitotoxicity, oedema, raised ICP, infection
63
What are the types of traumatic intracranial haematoma?
20% are extradural/epidural | 80% are intradural = subdural, intracerebral, subarachnoid
64
What are some features of a "burst lobe" traumatic intracranial haematoma?
Subdural in continuity with the intracerebral haematoma particularly in the frontal and temporal lobes
65
What is a common cause of traumatic extradural haematomas?
Usually a complication of a fracture in the tempero-parietal region involving the middle meningeal artery
66
What are some features of traumatic extradural haematomas?
Immediate brain damage often minimal = may cause midline shift if untreated (compression and herniation) Mortality of 10-20%
67
What is a subdural haemorrhage?
Collection of blood between the internal surface of the dura mater and arachnoid mater
68
What causes subdural haemorrhage?
Disruption to bridging veins that extend from the surface of the brain into the subdural space
69
What are some features of acute subdural haemorrhages?
Clear history of trauma = more common in head injury of elderly Mortality of >60%
70
What effect do acute subdural haemorrhages have on the brain?
May be unilateral or bilateral = sulci preserved, swelling of cerebrum on the affected side
71
What happens to untreated non-fatal acute subdural haematomas?
Become liquefied = form yellowish neomembrane
72
What are some features of chronic subdural haematomas?
Less frequently associated with a well-defined traumatic insult Often associated with brain atrophy
73
What are chronic subdural haemorrhages composed of?
Liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by neomembrane

Neurology (48 decks)

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