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Head, Neck And Neuro > PBL - Expanding Mass Lesion > Flashcards

PBL - Expanding Mass Lesion Flashcards

1
Q

How do you test the olfactory nerve function?

A

Ask subject to sniff substances through each nostril in turn and name the substance
- e.g. Non irritants such as vanilla, toothpaste and coffee

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2
Q

What can cause olfactory nerve dysfunction?

A

Neurological lesion

  • commonly trauma
  • fracture passing through ethmoid bone
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3
Q

How do you test the optic nerve function?

A

Test for visual acuity, check visual fields and inspect optic disks
Inspect size and shape of pupils
- compare both sides
- test reactions to light

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4
Q

How do you test the trochlear, occulomotor and abducens nerve function?

A

Subjects head is held still by an examiner
Subject is asked to follow the examiner’s finger with eyes
- horizontal plane - medial and lateral rectus
- vertical plane (outwards) - superior and inferior rectus muscles
- vertical plane (inwards) - superior and inferior oblique

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5
Q

What problems would you also look for when testing the trochlear, occulomotor and abducens nerve function?

A 
Squint 
Ptosis
Nystagmus 
Derivation of eye
Diploplia
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6
Q

How do you test the trigeminal nerve function?

A

Cutaneous sensation in appropriate areas of the face
Ask to clench jaw muscles (clenching teeth)
- palate the masseter and temporalis muscles
Jaw jerk reflex
Ask subject to keep mouth open against resistance
- pterygoids

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7
Q

How do you test the facial nerve function?

A

Puff out cheeks against resistance - buccinator
Keep eyes closed against resistance
Raise eyebrows

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8
Q

How do you test the vestibulocochealr nerve function? - hearing aspect

A

Rinne’s tests - press tuning fork against mastoid and then held next to pinna - sound should be heard longer through the air conduction
Weber’s test - press tuning fork against middle of the forehead

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9
Q

What are the different results you can get in a Weber’s test - and what do they mean.

A

Equal sound in both ears - normal hearing
Sound louder in right - left sensorineural problem
Sound louder in left - right sensorineural problem

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10
Q

How do you test the vagus and glossopharyngeal nerve function?

A

Subject has no huskiness, days phonic, dysphasia and palate moves symmetrically when subject says AHHHHHHHHHHHHH

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11
Q

How do you test the accessory nerve function?

A

Subject should be able to lift shoulders against resistance

- testing trapezium muscle

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12
Q

How do you test the hypoglossal nerve function?

A

Subject can hold tongue out of their mouth out of their mouth - equally on both sides

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13
Q

What are the main causes of head injury?

A 
Motor and bicycle crashes
Pedestrian impacts
Sports
Falls
Assaults
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14
Q

What kind of problems can a head injury cause?

A

Skull fractures
Brain injury
Vascular damage

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15
Q

What other problems are heavily associated with a skull fractures?

A

Underlying sub/epidural heamorrhage
Entrance of bacteria (meningitis) or air (pneumocephalus)
CSF leaking
Cranial nerve damage

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16
Q

Which cranial nerve are most likely to be damaged in a skull fracture?

A

Olfactory, optic, oculomotor, trochlear, trigeminal, facial and auditory

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17
Q

What is the difference between a primary and secondary head injury? - list types of each

A

Primary - caused by the impact
- diffuse atonal injury
- focal lesions like lacerations, contusions and heamorrhage
Secondary - an injury resulting from a process started by impact
- concussion
- infection
- hypoxia brain injury

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18
Q

What is a cerebral contusion?

A

Focal brain damage resulting from contact between bony protuberances of the skull base

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19
Q

What are the characteristic distributions for cerebral contusions?

A 
Orbital surface of the frontal lobes 
Frontal poles
Around the lateral sulcus
Temporal poles
Under surfaces of the temporal lobes
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20
Q

What is a traumatic atonal injury?

A

Widespread axonal injury - as a result of shear and tensile forces acting on the brain when the head is accelerated or decelerated suddenly

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21
Q

What happens to the brain 5 weeks after getting a diffuse axonal injury?

A

Degeneration of the long tracts and white matter of the cerebral hemisphere

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22
Q

Describe the spectrum of traumatic axon injury.

A

Graded I-III with the most severe occurring without a lucid interval

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23
Q

Which compartments can a heamatoma arise in?

A

Epidural space
Subdural space
Subarachnoid space
Intracerebral heamatoma

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24
Q

Which artery tear is most common in causing an epidural heamatoma?

A

Middle meningeal - crosses the pterion of the skull

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25
Q

Why are epidural haemorrhages more common in young people?

A

Because the dura mater is less firmly attached to the skull - so is more easily separated from the inner surface, allowing expansion of the heamatoma

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26
Q

Does someone with an epidural heamatoma have a lucid period?

A

After the initial unconsciousness from the injury, they have a lucid period in which consciousness is regained.

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27
Q

What happens after the lucid interval in an epidural heamatoma?

A

Rapidly developing unconsciousness and focal symptoms related to the area of brain involved

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28
Q

What are the symptoms of an epidural heamatoma?

A 
Ipsilateral symptoms 
- pupil dilation
- eyes point down and out
Contralateral symptoms 
- hemiparesis (from uncal herniation)
- loss of visual field
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29
Q

What is the pathophysiology of a subdural heamatoma?

A

A tear in the small bridge veins that connect veins on the surface of the cortex to the venous sinuses
- readily snapped in head injury when brain moves suddenly in relation to the cranium

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30
Q

What is the largest danger with a subdural (venous) heamatoma?

A

Venous blood collects more slowly - and may not be recognised and the patient is sent home

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31
Q

Name the time frames of acute, subacute and chronic subdural heamatomas.

A

Acute - symptoms witching 24 hours
Subacute - symptoms seen from 2-10 days after injury
Chronic -symptoms seen several weeks after injury

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32
Q

What’s the main clinical difference between a subdural and an epidural heamatoma.

A

No lucid interval

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33
Q

Which factors often lead to a high mortality rate for a heamatoma?

A 
Increased ICP
Loss of consciousness 
Delay in surgical removal 
Oedema
Ischaemia
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34
Q

Why are subdural heamatomas more common in old people?

A

The brains in older people begin to atrophy causing the brain to shrink away from the dura and stretch the fragile bridge veins

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35
Q

What causes the subdural heamatoma to become capsulated?

A

Fibroblastic activity

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36
Q

What is vasogenic cerebral oedema?

A

Defective blood brain barrier around contusions or heamatomas allows extravasion of water, sodium and protein molecules to enter the brain

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37
Q

What is congestive heamatoma?

A

Diffuse swelling of one or both hemispheres

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38
Q

What causes ischaemic brain damage?

A

Raised ICP
Hypoxaemia
Reduced cerebral perfusion pressure
- these all cause lack of oxygen and nutrients
- ischaemic cascade is initiated and leads to further neuronal damage

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39
Q

What is the difference between a missile and non-missile head injury?

A

Missile - open skull fracture

Non-missile - base of skull fracture

40
Q

Which neurons are more susceptible to the effects of the ischaemic cascade?

A

Mechanically injured neurons

41
Q

What are the main mechanisms involved in neuronal damage and cell death (ischaemic cascade)?

A 
Raised intracellular calcium
Increased neurotoxic (glutamate) release 
Increased free radical production 
Receptor dysfunction 
Inflammation
42
Q

What are the three types of response that are assessed in the Glasgow coma scale?

A

Best motor response
Best verbal response
Eye opening

43
Q

What are the max and min scores on the GCS?

A

15

3

44
Q

What are the two compartments of state of awareness of self and the environment.

A

Arousal and wakefulness
- concurrent functioning of both hemispheres and intact reticular activating system in the brainstem
Content and cognition
- determined by function cerebral cortex

45
Q

What three things determine intracranial pressure?

A

Pressure-volume relationships with brain tissues, CSF and blood in intracranial cavity
Monro-Kellie hypothesis, relates to reciprocal changes among the intracranial volumes
Compliance of the brain

46
Q

What are the percentages of brain tissue, blood and CSF within the skull?

A

Brain - 80%
CSF- 10%
Blood - 10%

47
Q

Which compartment is the most easily displaced in the skull?

A

CSF - can be displaced form the ventricles and cerebral subarachnoid space into the spinal subarachnoid space
- can also undergo increased absorption or decreased production

48
Q

How is blood volume from the skull displaced?

A

Most of the blood in the skull is in venous sinuses - these are easily compressible, forcing blood out of the cranial cavity

49
Q

Define compliance

A

Ease at which as substance can be compressed or deformed

- so a measure of the brain’s ability to maintain ICP during changes in intracranial volume

50
Q

What is the compliance formula?

A

Compliance = change in volume/change in pressure

51
Q

What mechanisms maintain cerebral perfusion pressure?

A

Auto regulation

Chemoregulation

52
Q

What happens if auto regulation is damaged (e.g. After a head injury)?

A

Cerebral blood becomes pressure passive

  • drop is CPP
  • cerebral blood flow is reduced, causing ischaemia
53
Q

How is CPP related to ICP?

A

CPP=MAP-ICP

  • as ICP rises, the CPP will continually drop until it reaches a critical level
  • blood flow ceases when ICP reaches MAP
54
Q

What is the minimum CPP required for adequate cerebral function?

A

70mmHg

55
Q

What are the clinical effects of raised ICP?

A

Headache - worse in morning or when stopping and bending
Vomiting - occurs with acute rise in ICP
Papilloedema- swelling of the optic disk and retina that can cause a disk heamorrhage

56
Q

Which three ways can a brain herniate?

A

Under falx cerebri
Through tentorial notch
Incisura of tentorium cerebelli

57
Q

All brain herniations fit into one of two categories, what are they?

A

Supratentorial

Infratentorial

58
Q

What are the two main types of supratentorial herniation?

A

Cingulate

Transtentorial

59
Q

Describe a cingulate herniation.

A

Displacement of the cingulate gurus and hemisphere beneath sharp edges of the flax cerebri to opposite side of the brain

60
Q

What does a cingulate herniation commonly compress?

A

Branches of the anterior cerebral artery

- causes oedema and ischaemia, further increasing ICP

61
Q

What are the two syndromes associated with a transtenorial herniation?

A

Central

Uncal

62
Q

What happens during a central transtenorial herniation?

A

Downward displacement of the cerebral hemispheres, basal ganglia, diencephalon and midbrain through tentorial incisors

63
Q

What clinical signs does a central transtenorial herniation cause?

A

Bilateral small, reactive pupils

Drowsiness

64
Q

What pathology is happening during an uncal herniation syndrome?

A

The medial aspect of the temporal lobe is pushed through the incisura of the tentorium

65
Q

Which cranial nerve is commonly affected in uncal herniation syndrome?

A

Oculomotor - causes ipsilateral pupillary constriction

66
Q

What other structures are compressed during an uncal herniation?

A

Posterior cerebral artery

The contralateral cerebral peduncle

67
Q

Increased pressure in which compartment causes an infratentorial herniation?

A

The infratentorial compartment

68
Q

What problems does an upward herniation from the infratentorial compartment cause?

A

Blocks the aqueduct of Sylvius

- causes hydrocephalus and coma

69
Q

What problems does a downward herniation from the infratentorial compartment cause?

A

Displacement of the midbrain through the tentorial notch
or
the cerebellar tonsils through the foramen magnum

70
Q

Out of supratentorial and infratentorial herniation - which is more serious?

A

Infratentorial

- involves lower brainstem centres that control cardiopulmonary functions

71
Q

How does the brain normally compensate for a drop in BP, to keep CPP up?

A

Cerebrovascular autoregulation causes cerebral vasodilation

72
Q

Name two causes of hypoxic brain damage.

A

Extracranial blood loss
Uncontrolled seizures
- source of secondary insults due to increased metabolic rate and respiratory impairment

73
Q

Name the four main stages of acute management of head injury

A

Assessment
Resuscitation
Investigation
Referral

74
Q

What is the investigation most used when checking head injuries.

A

CT scan

75
Q

What is the aim of the initial head injury assessment?

A

Prevent secondary trauma

Identify patients who require specialist neurosurgical care

76
Q

When should surgery be used to manage a haematoma?

A

Mass lesions with a greater than 5mm midline shift

Intraparenchymal contusions with raised ICP

77
Q

What is the management plan for those with a small haematoma?

A

if the patient is alert and neurologically intact - they can be managed conservatively

78
Q

What can be used during surgery to reduce intracranial hypertension?

A

Mannitol

Mild hyperventilation

79
Q

Describe the non-surgical management of rising ICP.

A 
No obstruction to venous drainage
Adequate systolic BP
Compliance with artificial ventilation
Ventricular drainage 
Mannitol
Hyperventilation
80
Q

List the medical treatments for head injuries

A

Mannitol
Furosemide - used with mannitol
Anticonvulsants - reduces severity of post-traumatic seizures (occur in 15% of patients)
Antibiotics - for bacterial meningitis
Barbituates - CNS depressors help reduce ICP

81
Q

Can adult neurons regenerate?

A

Yes - but CNS neurons have a limited capacity compared to PNS neurons

82
Q

Why is neuron regeneration poor?

A

Lack of factors which facilitate growth

Presence of factors which actively inhibit growth

83
Q

Why is neuronal regeneration worse in the CNS neurons?

A

Because oligodendrocytes synthesis glycoproteins which inhibit axon outgrowth

84
Q

Describe certain nerve grafts attempted in people with damaged nerves

A

Peripheral nerve grafts to promote growth to central axons

Transplantation of embryonic neurons into the adult brain can promote recovery of function

85
Q

If neurons don’t regenerate easily - how does almost complete recovery occur in most brain injury patients?

A

Neuronal plasticity

  • recovery of tissue that has only been partially damaged
  • adaptation of uninjured tissue to undertake some of the function of the damaged tissue
86
Q

List the main causes of morbidity after brain injury, one the person has been treated.

A 
Incomplete recovery - cognitive impairment, hemiparesis 
Post-traumatic epilepsy 
Post-traumatic syndrome
Benign paraoxysmal position vertigo
Chronic subdural haematoma
Hydrocephalus 
Chronic traumatic encephalopathy
87
Q

Describe post-traumatic syndrome.

A

Describes vague complications of headache, dizziness and malaise
Depression is prominent
Prolonged symptoms

88
Q

What is punch drunk syndrome?

A

Consists of cognitive impairment
Pyramidal and extrapyramidal signs
Little and often head injuries can eventually lead to one giant fuck up

89
Q

What are the signs and symptoms of concussion?

A 
Headache
Dizziness
Memory disturbances 
Balance problems
Loss of consciousness
Seizure
Irritable
Performance
90
Q

Where is an intra-cerebral haemorrhage most likely to be found?

A

Frontal and temporal lobes

91
Q

What kind of haemorrhage is associated with cerebral contusions?

A

Sub-arachnoid haemorrhage

92
Q

How does diffuse axonal injury damage axons?

A

Sudden, shear, twisting force of the brain compared to the skull causes the axons to turn from being rubbery, to being brittle and then snapping

93
Q

Describe the pathophysiology of diffuse axonal injury.

A

Initial glutamate bombardment of the axon

  • excitatory neurotransmitters are released that excite the brain (reason for seizure)
  • calcium enters
  • neuronal death
  • axonal degeneration (stretch)
94
Q

Describe diffuse vascular injury

A

Multiple small haemorrhages
Cerebral hemispheres, brain stem
Death within minutes due to massive amount of force required to tear vessels in the first place

95
Q

What is second impact syndrome?

A

Common in adolescents and young people

Even a mild injury (first or second) causes uncontrollable brain swelling

96
Q

What is the pathology of punch drunk syndrome?

A

Loss of pigment in Substantia Nigra
Neurofibrillary tangles
Amyloid plaques
Cavum septum split

Head, Neck And Neuro (19 decks)

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