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Neurology > Neuropatholgy III > Flashcards

Neuropatholgy III Flashcards

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
Q

What are some features of grade II astrocytomas?

A

Display nuclear atypia, mean survival is 5 years

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26
Q

What are some features of grade III astrocytomas?

A

Display greater nuclear atypia and mitotic activity

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27
Q

What are the two kinds of grade IV astrocytomas?

A

Primary and secondary glioblastomas

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28
Q

What are some features of primary glioblastomas?

A

Extreme atypia, mitotic activity, necrosis or neovascularisation, survival is about 10 months

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29
Q

What are some features of secondary glioblastomas?

A

Extreme atypia, mitotic activity, necrosis and/or neovascularisation, survival is >10-12 months

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30
Q

What genes are implicated in grade I-III astrocytomas and secondary glioblastomas?

A

IDHi, P53, PDGFRA, RB and PI3KCA

31
Q

What mutations are associated with primary glioblastomas?

A

EGFR amplification, PTEN loss, P53 mutation

32
Q

What is the most common tumour of the CNS in children?

A

Medulloblastoma = 25% of all paediatric CNS neoplasms

33
Q

What are some features of medulloblastomas?

A

Poorly differentiated = look like primitive undifferentiated embryonal cells
Poor prognosis if untreated, but very radiosensitive
75% 5 year survival with resection and radiotherapy

34
Q

What are the most common malignant CNS tumours?

A

Astrocytoma (all types), oligodendroglioma, medulloblastoma

35
Q

What is the most common benign CNS tumour?

A

Meningioma

36
Q

What are some sources of infection that may cause a single abscess?

A

May form from local extension or direct implantation = tend to occur adjacent to source

37
Q

What tends to cause multiple abscesses?

A

Haematogenous spread = occur at grey and white matter boundary

38
Q

What are some features of abscesses?

A

Central necrosis with oedema fibrous capsule
May cause midline shift
Symptoms = fever, raised ICP, underlying cause

39
Q

How are abscesses diagnosed?

A

CT or MRI, plus do aspiration for culture

40
Q

What organisms may cause abscesses?

A

Often polymicrobial = staph aureus and strep, fungi and protozoa in immunocompromised

41
Q

What is meningitis?

A

Inflammation of leptomeninges and CSF within the subarachnoid space

42
Q

What are some features of bacterial meningitis?

A

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
Q

What are some organisms that cause bacterial meningitis?

A

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
Q

What can head injuries cause?

A

Skull fractures, parenchymal injury and vascular injury

45
Q

What damage can a penetrating injuries cause?

A

Focal injury, lacerations, haemorrhage

46
Q

How can blunt trauma cause head injury?

A

Sudden acceleration/deceleration of head = brain moves within the cranial cavity and makes contact with inner table of cranium and bony protrusions

47
Q

What effect does contact time have on force in blunt trauma?

A

The smaller the contact time of the object, the greater the force generated

48
Q

What are some causes of blunt trauma?

A

RTCs, falls, assaults, alcohol

49
Q

What are primary and secondary head injuries?

A 
Primary = damage to neurons, irreversible
Secondary = haemorrhage and oedema, potentially treatable
50
Q

What are some examples of primary head injuries?

A

Scalp lesions, skull fracture, surface contusions or lacerations, diffuse axonal and vascular injuries, petechial haemorrhages

51
Q

What are some examples of scalp lesions?

A

Bruising, laceration, bleeding = route for infection

52
Q

What are the types of skull fractures?

A

Linear = straight and sharp, may cross sutures

Compound and depressed

53
Q

What are compound fractures associated with?

A

Full thickness scalp lacerations

Base of skull fractures

54
Q

What are skull fractures associated with a higher incidence of?

A

Intracranial bleeding and haematomas

55
Q

Where do surface head injuries tend to occur?

A

Lateral surface of hemispheres

Under surface of temporal and frontal lobes

56
Q

What is one cause of surface head injuries?

A

Coup and contracoup injuries

57
Q

What are contracoup injuries?

A

Injury to non-impact side = may occur at same time as coup, may occur due to rebound, tend to be worse

58
Q

What are coup injuries?

A

Injury to brain on the side of impact

59
Q

When do diffuse axonal injuries occur?

A

At the moment of the insult to the head = occurs due to shearing forces

60
Q

What areas are affected by diffuse axonal injury?

A

Central areas = brainstem (immediate death occurs), corpus callosum, parasagittal areas, interventricular septum, hippocampal formation

61
Q

What symptoms do patients with diffuse axonal injuries tend to have?

A

Reduced consciousness and coma = may lead to vegetative state

62
Q

What are some examples of secondary brain injuries?

A

Intracranial haematoma, reduced cerebral blood flow, hypoxia, excitotoxicity, oedema, raised ICP, infection

63
Q

What are the types of traumatic intracranial haematoma?

A

20% are extradural/epidural

80% are intradural = subdural, intracerebral, subarachnoid

64
Q

What are some features of a “burst lobe” traumatic intracranial haematoma?

A

Subdural in continuity with the intracerebral haematoma particularly in the frontal and temporal lobes

65
Q

What is a common cause of traumatic extradural haematomas?

A

Usually a complication of a fracture in the tempero-parietal region involving the middle meningeal artery

66
Q

What are some features of traumatic extradural haematomas?

A

Immediate brain damage often minimal = may cause midline shift if untreated (compression and herniation)
Mortality of 10-20%

67
Q

What is a subdural haemorrhage?

A

Collection of blood between the internal surface of the dura mater and arachnoid mater

68
Q

What causes subdural haemorrhage?

A

Disruption to bridging veins that extend from the surface of the brain into the subdural space

69
Q

What are some features of acute subdural haemorrhages?

A

Clear history of trauma = more common in head injury of elderly
Mortality of >60%

70
Q

What effect do acute subdural haemorrhages have on the brain?

A

May be unilateral or bilateral = sulci preserved, swelling of cerebrum on the affected side

71
Q

What happens to untreated non-fatal acute subdural haematomas?

A

Become liquefied = form yellowish neomembrane

72
Q

What are some features of chronic subdural haematomas?

A

Less frequently associated with a well-defined traumatic insult
Often associated with brain atrophy

73
Q

What are chronic subdural haemorrhages composed of?

A

Liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by neomembrane

Neurology (48 decks)

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