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Neurology > Raised intracranial pressure, SOL and trauma > Flashcards

Raised intracranial pressure, SOL and trauma Flashcards

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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
What ar the commonest malignant brain tumours in children?
1. Astrocytoma 50% 2. Medulloblastoma 25% 3. Ependymoma 6% 4. Oligogendroglioma 1% 5. haemangioblastoma \<1% 6. lymphoma \<1% 7. pineal (germ cell) \<1%
26
What are the commonest benign brain tumours in adults?
Meningioma 18% Pituitary adenoma 10% Schannoma 8% Craniopharyngioma 2%
27
What are the commonest benign brain tumours in adults?
Craniopharyngioma 9% Meninigoma 3% Schwannoma 1% Pituitary adenoma \<1%
28
What are the WHO astrocytoma gradings
Grade I: Pilocytic Grade II: well differentiated Grade III: Anaplastic Grade IV: Glioblastoma
29
Describe grade I pilocytic astrocytoma
* childhood * benign behaving * long, hair like processes * cystic areas
30
What is seen in Grade II Astrocytoma?
Nuclear atypia
31
What is seen in Grade III Astrocytoma?
Greater nuclear atypic Mitotic activity
32
What is seen in Grade IV Astrocytoma?
Extreme nuclear atypia Mitotic activity Necrosis and/or neovascularisation
33
Medulloblastomas are poorly \_\_\_\_\_\_\_\_\_/\_\_\_\_\_\_ (look like primitive undifferentiated embryonal cells)
Medulloblastomas are poorly differentiated/embryonal (look like primitive undifferentiated embryonal cells)
34
Where do medullloblastomas occur?
Midline of cerebellum
35
What is the prognosis for medulloblastoma?
Untreated has dismal prognosis, but is exquisitely radiosensitive 75% 5 year survival with resection and radiotherapy
36
how do single abscesses occur?
Through local extension e.g. mastoiditis Direct implantation e.g. skull fracture
37
Where do single abscesses tend to occur?
Adjacent to source
38
How to multiple abscesses occur?
Via haematogenous spread e.g. bronchipneumonia, bacterial endocarditis Tend to occur at grey and white matter boundary
39
Describe the appearance of an abscess
Central necrosis, oedema and fibrous capsule
40
How may an abscess present?
Fever, raised ICP
41
How are abscesses diagnosed?
CT or MRI
42
What happens after an abscess has been diagnosed?
Aspiration for culture and treatment
43
What is the definition of bacterial meningitis?
Inflammation of the leptomeninges and CSF within the subarachnoid space
44
What does bacterial meningitis cause?
Severe oedema and raised ICP
45
What is seen on CSF in bacterial meningitis?
Abundant polymorphs on CSF, decreased glucose
46
Arachnoiditis can later cause lack of CSF \_\_\_\_\_\_, ______ and raised \_\_\_
Arachnoiditis can later cause lack of CSF absorption, hydrocephalus and raised ICP
47
In bacterial meningitis \_\_\_\_\_ is at peak incidence in neonates; it is a gram ___ rod
In bacterial meningitis E.coli is at peak incidence in neonates; it is a gram -ve rod
48
In bacterial meningitis \_\_\_\_\_ is at peak incidence in infants and adolescents ; it is a gram ___ \_\_\_\_ \_\_\_\_\_\_
In bacterial meningitis H. influenzae is at peak incidence in infants and adolescents ; it is a gram -ve cocco bacilli
49
In bacterial meningitis N. meningitidis is at peak incidence in ________ and ____ \_\_\_\_\_ ; it is a gram ___ \_\_\_\_\_\_\_\_
In bacterial meningitis N. meningitidis is at peak incidence in adolescents and young adults ; it is a gram -ve diplococci
50
In bacterial meningitis \_. _______ is at peak incidence in older adults and children ; it is a gram ___ \_\_\_\_\_\_ in \_\_\_\_\_
In bacterial meningitis S. pneumoniae is at peak incidence in older adults and children ; it is a gram +ve cocci in chains
51
In bacterial meningitis \_. _______ is at peak incidence in older adults ; it is a gram ___ \_\_\_\_
In bacterial meningitis L. Monocytogenes is at peak incidence in older adults ; it is a gram +ve rod
52
What are the different types of head injury?
Missile or Non-missile Penetrating or blunt
53
What is a missile injury?
Penetrating injury
54
What does a missile injury result in?
Lacerations in region of brain damage Haemorrhage
55
What is non-missile (blunt injury) caused by?
Sudden acceleration/decelleration of head
56
Describe blunt injury to the head
Brain moves within cranial cavity and makes contact with the inner table of the cranium and bony protrusions
57
What causes blunt injury?
RTCs Falls Assaults Alcohol
58
The ______ the contact time the ______ the force F= _mv-mu_ t
The smaller the contact time the larger the force F= _mv-mu_ t
59
Describe the primary injury of trauma to head?
Injury to neurones Irreversible Preventative measures
60
Describe the secondary injury of trauma to head?
Haemorrhage Oedema Potentially treatable
61
Give examples of primary injuries
Scalp lesions Skull fractures Surface contusions Surface lacerations DIffuse axonal injury Diffuse vascular injury Petechial haemorrhages
62
Why are scalp lesions so dangerous
Bleed profusely Route for infection
63
What are the different types of skull fracture?
Linear Compound Depressed
64
Describe linear skull fracture
straight sharp fracture line, that may cross sutures (diastatic fracture)
65
Describe compound skull fracture
Associated with full thickness scalp lacerations
66
Where are contusions and lacerations common?
Lateral surface of hemispheres Under surface of temporal and frontal lobes
67
What are coup and contra-coup injuries?
Coup: primary impact of the skull Contra-coup: rebound against cranium
68
Why are contra-coup injuries worse than coup injuries?
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
When does DAI occur?
At moment of injury
70
Where does DAI affect?
Central areas
71
What does DAI cause?
Reduced consciousness and coma Can lead to vegetative state Grades of increasing severity- correlate with patients clinical state
72
Describe the pathophysiology of secondary brain injury?
* Intracranial haematoma * Reduced cerebral blood flow * Hypoxic brain damage * Excitotoxicity * Oedema * Raised ICP * Infection
73
What does calcium influx result in?
Protease activation Mitochondrial dysfunction Oxidative stress
74
What causes cytotoxic oedema?
Intoxication, reye's and severe hypothermia
75
What causes ionic oedema?
Also called osmotic oedema, occurs in hyponatraemia and excess water intake e.g. in SIADH
76
What causes vasogenic oedema?
Most important occuring in: trauma, tumours, inflammation and infection and hypertensive encephalopathy
77
What is haemorrhagic conversion?
conversion of a bland infarction into an area of hemorrhage
78
\_\_% of traumatic intracranial haematomas are extra dural
20% of traumatic intracranial haematomas are extra dural
79
80% of traumatic intracranial haematomas are intradural; \_\_% are subdural \_\_% are intracerebral haematomas \_% are subarachnoid
80% of traumatic intracranial haematomas are intradural; 13% are subdural 15% are intracerebral haematomas 3% are subarachnoid
80
What is a burst lobe?
Subdural in continuity with intracerebral haematoma particularly in frontal and temporal lobe
81
What are traumatic extradural haematomas usually a result of?
Complication of fracture in tempero-parietal region that involves middle meningeal artery
82
Describe the pathophysiology of extradural haematomas?
Immediate brain damage is often minimal but if left untreated- midline shift, compression and herniation
83
What are subdural haematomas?
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
Why are gyral contours preserved in subdural haemorrhages?
pressure is evenly distrubuted
85
Non-treated, non fatal haematomas become _______ and form a _______ neomembrane
Non-treated, non fatal haematomas become liquiefied and form a yellowish neomembrane
86
What are chronic subdural haemorrhages associated with?
Brain atrophy

Neurology (41 decks)

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