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Neurology > Raised intracranial pressure, SOL and trauma > Flashcards

Raised intracranial pressure, SOL and trauma Flashcards

1
Q

The brain behaves mechanically like a ____ filled _____ solid; ______. It lies within the skull (_____/_____ volume). Suspended in ________ ____ which supports the brain (_____ buoyancy). It is supported by the ____.

A

The brain behaves mechanically like a fluid filled porous solid; viscoelastic. It lies within the skull (rigid/fixed volume). Suspended in cerebrospinal fluid which supports the brain (neutral buoyancy). It is supported by the dura.

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2
Q

What happens when the process of CSF escaping from cranial vault to avoid rise in pressure is exhausted?

A

Venous sinuses are flattened and there is little or no CSF. Any further increase results in rapid increase in ICP.

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3
Q

What are the causes of raised ICP?

A
  • Increased CSF
  • Focal lesion in brain
  • Diffuse lesion in brain
  • Increased venous volume
  • Physiological (hypoxia, hypercapnia, pain)
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4
Q

Define hydrocephalus

A

Accumulation of excessive CSF within the ventricular system of the brain

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5
Q

What is the normal volume of CSF

A

120-150ml

500ml (turnover of 3-5 times per day)

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6
Q

Where is CSF produced?

A

By the chorioid plexus in the lateral and fourth ventricles of the brain

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7
Q

Where is CSF absorbed?

A

Absorbed by arachnoid granulations

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8
Q

CSF is a clear fluid containing;

________ <4 cells/ml

Neutrophils _ cells/ml

Protein <___g/l

_______ >2.2mmol/l

No ___.

A

CSF is a clear fluid containing;

lymphocytes <4 cells/ml

Neutrophils 0 cells/ml

Protein <0.4g/l

Glucose >2.2mmol/l

No RBCs

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9
Q

What are the causes of hydrocephalus?

A

Obstruction to flow of CSF (e.g. inflammation, pus and tumours)

Decreased resorption of CSF (post SAH, or meningitis)

Overproduction of CSF (v. rare: tumours of choroid plexus)

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10
Q

What are the two main types of hydrocephalus?

A

Non-communicating

Commiunicating

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11
Q

What is non-communicating hydrocephalus?

A

Obstruction to flow of CSF occurs within ventricular system

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12
Q

What is communicating hydrocephalus?

A

Obstruction to flow of CSF outside of the ventricualr system e.g. in subarachnoid space or at the arachnoid granulations

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13
Q

Why is the timing of hydrocephalus important?

A

If hydrocephalus occurs before closure of cranial sutures then cranial enlargement occurs

If hydrocephalus develops after the closure of the cranial sutues, then there is expansion of ventricles and increase in intracranial pressure

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14
Q

What is hydrocephalus ex vacuo

A

Dilatation of the ventricular system and a compensatory increase in CSF volume secondary to a loss of brain parenchyma (e.g. in alzheimers disease)

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15
Q

What are the effects of raised intracranial pressure?

A
  • intracranial shifts and herniations- coning
  • midline shift
  • distortion and pressure on cranial nerves and vital neurological centres
  • impaired blood floow
  • reduced level of consciousness
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16
Q

What are the types of herniations?

A
  1. subfalcine
  2. tentorial
  3. cerebellar
  4. transcalvarial
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17
Q

What are the clinical signs of raised ICP?

A

Papilloedema

Headache

Nausea and vomiting

Neck stiffness

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18
Q

What are SOL?

A
  • tumours- primary brain tumours, metastases
  • abscess- single/multiple
  • haematomas
  • localised brain swelling- e.g. swelling and oedema around cerebral infarct
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19
Q

70% of brain cancers in children occur where?

A

Below the tentorium cerebelli

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20
Q

70% of brain cancers in adults occur where?

A

Above the tentorium cerebelli

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21
Q

What are the commonest metastasic brain cancers?

A
  • breast
  • bronchus
  • kidney
  • thyroid
  • colon carcinomas
  • malignant melanomas
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22
Q

Where are brain mets usually seen?

A

Boundaries between grey and white matter

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23
Q

How are brain tumours graded?

A
  • mitoses
  • neovascularisation
  • necrosis
  • also atypia, cellularity etc
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24
Q

What are the commonest malignant brain tumours in adults

A
  1. Astrocytoma 45%
  2. oligodendroglioma 6%
  3. ependymoma 5%
  4. medulloblasotma 2%
  5. haemangioblastoma 2%
  6. lymphoma 1%
  7. pineal (germ cell) <1%
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25
Q

What ar the commonest malignant brain tumours in children?

A
  1. Astrocytoma 50%
  2. Medulloblastoma 25%
  3. Ependymoma 6%
  4. Oligogendroglioma 1%
  5. haemangioblastoma <1%
  6. lymphoma <1%
  7. pineal (germ cell) <1%
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26
Q

What are the commonest benign brain tumours in adults?

A

Meningioma 18%

Pituitary adenoma 10%

Schannoma 8%

Craniopharyngioma 2%

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27
Q

What are the commonest benign brain tumours in adults?

A

Craniopharyngioma 9%

Meninigoma 3%

Schwannoma 1%

Pituitary adenoma <1%

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28
Q

What are the WHO astrocytoma gradings

A

Grade I: Pilocytic

Grade II: well differentiated

Grade III: Anaplastic

Grade IV: Glioblastoma

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29
Q

Describe grade I pilocytic astrocytoma

A
  • childhood
  • benign behaving
  • long, hair like processes
  • cystic areas
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30
Q

What is seen in Grade II Astrocytoma?

A

Nuclear atypia

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31
Q

What is seen in Grade III Astrocytoma?

A

Greater nuclear atypic

Mitotic activity

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32
Q

What is seen in Grade IV Astrocytoma?

A

Extreme nuclear atypia

Mitotic activity

Necrosis and/or neovascularisation

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33
Q

Medulloblastomas are poorly _________/______ (look like primitive undifferentiated embryonal cells)

A

Medulloblastomas are poorly differentiated/embryonal (look like primitive undifferentiated embryonal cells)

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34
Q

Where do medullloblastomas occur?

A

Midline of cerebellum

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35
Q

What is the prognosis for medulloblastoma?

A

Untreated has dismal prognosis, but is exquisitely radiosensitive

75% 5 year survival with resection and radiotherapy

36
Q

how do single abscesses occur?

A

Through local extension e.g. mastoiditis

Direct implantation e.g. skull fracture

37
Q

Where do single abscesses tend to occur?

A

Adjacent to source

38
Q

How to multiple abscesses occur?

A

Via haematogenous spread e.g. bronchipneumonia, bacterial endocarditis

Tend to occur at grey and white matter boundary

39
Q

Describe the appearance of an abscess

A

Central necrosis, oedema and fibrous capsule

40
Q

How may an abscess present?

A

Fever, raised ICP

41
Q

How are abscesses diagnosed?

A

CT or MRI

42
Q

What happens after an abscess has been diagnosed?

A

Aspiration for culture and treatment

43
Q

What is the definition of bacterial meningitis?

A

Inflammation of the leptomeninges and CSF within the subarachnoid space

44
Q

What does bacterial meningitis cause?

A

Severe oedema and raised ICP

45
Q

What is seen on CSF in bacterial meningitis?

A

Abundant polymorphs on CSF, decreased glucose

46
Q

Arachnoiditis can later cause lack of CSF ______, ______ and raised ___

A

Arachnoiditis can later cause lack of CSF absorption, hydrocephalus and raised ICP

47
Q

In bacterial meningitis

_____ is at peak incidence in neonates; it is a gram ___ rod

A

In bacterial meningitis

E.coli is at peak incidence in neonates; it is a gram -ve rod

48
Q

In bacterial meningitis

_____ is at peak incidence in infants and adolescents ; it is a gram ___ ____ ______

A

In bacterial meningitis

H. influenzae is at peak incidence in infants and adolescents ; it is a gram -ve cocco bacilli

49
Q

In bacterial meningitis

N. meningitidis is at peak incidence in ________ and ____ _____ ; it is a gram ___ ________

A

In bacterial meningitis

N. meningitidis is at peak incidence in adolescents and young adults ; it is a gram -ve diplococci

50
Q

In bacterial meningitis

_. _______ is at peak incidence in older adults and children ; it is a gram ___ ______ in _____

A

In bacterial meningitis

S. pneumoniae is at peak incidence in older adults and children ; it is a gram +ve cocci in chains

51
Q

In bacterial meningitis

_. _______ is at peak incidence in older adults ; it is a gram ___ ____

A

In bacterial meningitis

L. Monocytogenes is at peak incidence in older adults ; it is a gram +ve rod

52
Q

What are the different types of head injury?

A

Missile or Non-missile

Penetrating or blunt

53
Q

What is a missile injury?

A

Penetrating injury

54
Q

What does a missile injury result in?

A

Lacerations in region of brain damage

Haemorrhage

55
Q

What is non-missile (blunt injury) caused by?

A

Sudden acceleration/decelleration of head

56
Q

Describe blunt injury to the head

A

Brain moves within cranial cavity and makes contact with the inner table of the cranium and bony protrusions

57
Q

What causes blunt injury?

A

RTCs

Falls

Assaults

Alcohol

58
Q

The ______ the contact time the ______ the force

F= mv-mu

t

A

The smaller the contact time the larger the force

F= mv-mu

t

59
Q

Describe the primary injury of trauma to head?

A

Injury to neurones

Irreversible

Preventative measures

60
Q

Describe the secondary injury of trauma to head?

A

Haemorrhage

Oedema

Potentially treatable

61
Q

Give examples of primary injuries

A

Scalp lesions

Skull fractures

Surface contusions

Surface lacerations

DIffuse axonal injury

Diffuse vascular injury

Petechial haemorrhages

62
Q

Why are scalp lesions so dangerous

A

Bleed profusely

Route for infection

63
Q

What are the different types of skull fracture?

A

Linear

Compound

Depressed

64
Q

Describe linear skull fracture

A

straight sharp fracture line, that may cross sutures (diastatic fracture)

65
Q

Describe compound skull fracture

A

Associated with full thickness scalp lacerations

66
Q

Where are contusions and lacerations common?

A

Lateral surface of hemispheres

Under surface of temporal and frontal lobes

67
Q

What are coup and contra-coup injuries?

A

Coup: primary impact of the skull

Contra-coup: rebound against cranium

68
Q

Why are contra-coup injuries worse than coup injuries?

A

theory 1; Denser CSF moves to impact (coup) side first, forcing brain to contra-coup side 1st.

theory 2; Cavitation- low pressure in brain moving away from zone opposite the impact side. low pressure created cavitation bubbles, which damages brain parenchyma

69
Q

When does DAI occur?

A

At moment of injury

70
Q

Where does DAI affect?

A

Central areas

71
Q

What does DAI cause?

A

Reduced consciousness and coma

Can lead to vegetative state

Grades of increasing severity- correlate with patients clinical state

72
Q

Describe the pathophysiology of secondary brain injury?

A
  • Intracranial haematoma
  • Reduced cerebral blood flow
  • Hypoxic brain damage
  • Excitotoxicity
  • Oedema
  • Raised ICP
  • Infection
73
Q

What does calcium influx result in?

A

Protease activation

Mitochondrial dysfunction

Oxidative stress

74
Q

What causes cytotoxic oedema?

A

Intoxication, reye’s and severe hypothermia

75
Q

What causes ionic oedema?

A

Also called osmotic oedema, occurs in hyponatraemia and excess water intake e.g. in SIADH

76
Q

What causes vasogenic oedema?

A

Most important occuring in:

trauma, tumours, inflammation and infection and hypertensive encephalopathy

77
Q

What is haemorrhagic conversion?

A

conversion of a bland infarction into an area of hemorrhage

78
Q

__% of traumatic intracranial haematomas are extra dural

A

20% of traumatic intracranial haematomas are extra dural

79
Q

80% of traumatic intracranial haematomas are intradural;

__% are subdural

__% are intracerebral haematomas

_% are subarachnoid

A

80% of traumatic intracranial haematomas are intradural;

13% are subdural

15% are intracerebral haematomas

3% are subarachnoid

80
Q

What is a burst lobe?

A

Subdural in continuity with intracerebral haematoma particularly in frontal and temporal lobe

81
Q

What are traumatic extradural haematomas usually a result of?

A

Complication of fracture in tempero-parietal region that involves middle meningeal artery

82
Q

Describe the pathophysiology of extradural haematomas?

A

Immediate brain damage is often minimal but if left untreated- midline shift, compression and herniation

83
Q

What are subdural haematomas?

A

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

84
Q

Why are gyral contours preserved in subdural haemorrhages?

A

pressure is evenly distrubuted

85
Q

Non-treated, non fatal haematomas become _______ and form a _______ neomembrane

A

Non-treated, non fatal haematomas become liquiefied and form a yellowish neomembrane

86
Q

What are chronic subdural haemorrhages associated with?

A

Brain atrophy

Neurology (41 decks)

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