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PHM BSc - Applied Science > Skull And Head Injury > Flashcards

Skull And Head Injury Flashcards

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1
Q

What GCS corresponds to what head injury severity

A

Mild 14-15
Moderate 9-13
Severe 8 and lower

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2
Q

What skull fracture pattern would you expect in a motor vehicle incident involving a helmet wearer

A

Multiple linear fractures due to forces being spread out across the skull

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3
Q

What are the categories of traumatic head injury

A

Focal - haematoma and contusion

Diffuse - concussion and DAI

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4
Q

What is the most common base of skull fracture

A

Longitudinal fracture of the petrous part of the temporal bone

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5
Q

Describe the signs seen in base of skull fractures and relate them to the location

A

Anterior cranial fossa - racoon eyes, CSF rhinorrhoea, optic nerve damage
Middle cranial fossa - CSF ottorhoea, haemotympanum, Battles sign

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6
Q

Describe that pathophysiology of racoon eyes

A

Bleeding from venous sinuses tracks down but is stopped by the orbital septum leading to tarsal sparing

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7
Q

What is the pathway of CSF to leak out of the nose?

A

Leaks into the paranasal sinuses (particularly ethmoid) and from here to the nasal cavity
OR
Could be coming from the middle ear via the Eustachian tube

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8
Q

How do we test that “CSF” is in fact CSF

A

Look for Halo sign
Bedside test is glucose
Can also test for B2 transferin

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9
Q

What vessel damage leads to Battles sign?

A

Posterior auricular (branch of external carotid)

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10
Q

What is often the first base of skull fracture sign?

A

Haemotympanum

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11
Q

What other structures are you also worried about due to their association with base of skull fractures

A

C-spine

Vertebral arteries

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12
Q

How would you investigate a base of skull fracture

A

Non-contrast CT which will show a fracture and also pneumocephalus
CTA to assess for vascular injury

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13
Q

Compare a longitudinal vs transverse petrous temporal bone fracture in terms of incidence, nerve damage and hearing loss

A

Longitudinal occurs 80% of the time and is associate with conductive hearing loss (TM perforation)
Transverse occurs 20% of the time and can leads to facial nerve injury and sensorineural hearing loss (vestibulocochlear nerve injury)

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14
Q

What bones form the jugular foramen

A

Petrous part of the temporal bone

Occipital

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15
Q

What causes a jugular foramen fracture

A

Axial compression

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16
Q

What is the contents of the jugular foramen

A

Internal jugular vein

CN 9,10,11

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17
Q

How does a jugular foramen fracture present

A

Vernets syndrome which essentially describes damage to CN 9,10,11 so loss of gag reflex, hoarse voice, SCM and trapezius paralysis

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18
Q

What are the complications of a jugular foramen fracture

A

Internal jugular or dural venous sinus thrombosis

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19
Q

Compare the MOI, bleeding source, presentation and CT signs of extradural vs subdural haematoma s

A

Extradural: acceleration/deceleration or blow to pterion leads to an arterial bleed often from middle meningeal but can be DVS. Patient often has a lucid interval. CT shows a hyperdense bioconvex area (due to limitation of suture lines)
Subdural: acceleration/deceleration or blunt trauma leads to bleeding from cortical bridging veins which are more taught in the elderly and alcoholics so more prone to stretching and tearing. Presentation is often slower and can look like an evolving stroke. CT shows a hyperdense cresent

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20
Q

Describe the course of the middle meningeal artery

A

Arises from the first part of the maxillary artery (branch of external carotid) and travels through foramen spinosum.
The anterior division runs anterio-superiorly on the greater wing of sphenoid and under the pterion making a groove in the bone
The posterior division runs horizontally posterior

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21
Q

What do the cortical bridging veins connect?

A

Drain neural tissue into the dural venous sinuses therefore crossing the subdural space

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22
Q

What are the most common berry aneurysm locations

A

Junction of anterior cerebral and anterior communicating
Bifurcation of middle cerebral artery
Junction of internal carotid and posterior communicating

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23
Q

What are risk factors for berry aneurysm rupture

A

Cocaine, PKD, Ehlers-Danlos, HTN, hypercholestrolaemia

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24
Q

Describe the bleeding source, presentation and CT results for a SAH

A

Berry aneurysm rupture, AV malformation, direct traumatic damage to small arteries and veins
Thunderclap headache often occipital in location, meningism, Terson’s syndrome (vitreous haemorrhage)
CT shows hyperdense sulci and basal cisterns

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25
Q

State the cause of a posterior fossa bleed

A

Occipital fracture leading to dural venous sinus bleed

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26
Q

Describe the time frame of a posterior fossa bleed

A

Presentation can be delayed (normally a venous bleed)
But once it presents, patients often deteriorate quickly as the posterior fossa is enclosed and crowded so susceptible to RICP

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27
Q

How would a posterior fossa bleed present

A

Pons and medulla compressed = reduced GCS and ventilatory failure
4th ventricle compressed = hydrocephalus
Lower CN’s compressed = loss of gag reflex
Cerebellum compressed = DANISH

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28
Q

What is a cerebral contusion

A

Small vessel leakage and microhaemorrhages leading to oedema and RICP
The pia-arachnoid membranes are not torn
You get a coup (directly under the site of impact) and contrecoup (impact from the opposing surface as the brain bounces off) injury

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29
Q

What is the most common location of a cerebral contusion and why

A

Inferior surface of the frontal and temporal lobes as they sit on bony and ridgy surfaces

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30
Q

What is a cerebral laceration

A

Similar to a contusion other than that the pia-arachnoid membranes are torn

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31
Q

What is diffuse axonal injury

A

Shearing of the grey-white matter interface leading to Wallarian-degeneration distal to the axonal tear as well as a cascade of events including protein accumulation, transport interruption and the spread of cell death

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32
Q

What is the MOI causing DAI

A

Acceleration-deceleration leading to shearing forces

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33
Q

How does DAI present

A

Patients will initially appear fine before deteriorating later
Doesn’t show up on imaging
It is impossible to tell the difference between DAI and hypoxic damage

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34
Q

What is a concussion

A

Transient change to mental status and consciousness without structural damage following a closed head injury

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35
Q

In rotational forces on the brain, which areas are subjected to high strain

A

Due to the brains fixed attachments (neck, falx etc) this means that the corpus colosum, internal capsule and fornix are most at risk

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36
Q

What are some signs and symptoms of a concussion

A

Headache, memory loss, foggy head, cognitive slowing lasting for weeks to a month

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37
Q

What are the 2 types of posturing and the respective lesion location that causes them

A

Decorticate - lesion above the red nucleus
Decerebrate - lesion below the red nucleus

Red nucleus is located in the midbrain

38
Q

Describe the pathophysiology behind the signs of decorticate posturing

A

Disinhibition of the rubrospinal tracts gives upper limb flexion with hands forming a fist
Disruption of lateral corticospinal tracts (supplying lower limb flexors) leads to unopposed extension of legs (done by vestibulospinal tracts)

39
Q

Describe the pathophysiology leading to the signs of decerebrate posturing

A

Disruption of rubrospinal tracts leads to unopposed upper limb extension (reticulospinal tracts)
Disruption of corticospinal tracts (lower limb flexion) leads to unopposed lower limb extension (vestibulospinal tracts)

40
Q

What would progression from decorticate to decerebrate posturing indicate

A

Uncal or tonsilar herniation

41
Q

What would you include in a focussed neurological examination

A 
GCS
Pupils and extra-ocular movements 
Gross limb movements 
Breathing patterns 
Auscultation of carotids 
C-spine assessment
42
Q

Describe the parts of GCS

A 
Eyes 
1) no eye opening
2) eye opening to pain
3) eye opening to voice
4) spontaneous eye opening 
Voice
1) non verbal
2)incomprehensible sounds
3) inappropriate words 
4) confused 
5) orientated 
Motor
1) no movement
2) extension to pain 
3) flexion to pain 
4) withdraws from pain
5) localising pain 
6) obey commands
43
Q

What are the indications for an adult head CT

A

GCS less than 13 on arrival
GCS less than 15 2 hours after the injury
Vomiting more than once
Seizure
Focal neurological deficit
Suspected base of, open or depressed skull fracture

44
Q

What is a secondary brain injury and some examples

A

Evolving pathophysiological consequences of the primary injury due to a number of neurobiological cascades
Eg RICP, hypoxia, seizures, infection, hydrocephalus, hypercapnia

45
Q

Why do seizures worsen RICP

A

High metabolic demand so increased blood flow so further RICP

46
Q

Describe the Monro-Kellie hypothesis

A

Volume (x axis) vs pressure (y-axis)
The skull is a fixed space. As volume begins to rise, compensatory mechanisms can kick in such as compression of ventricles. However when volume reaches a certain point, these mechanisms are no longer enough and pressure begins to rise. This reduces cerebral perfusion pressure and causes ischaemia

47
Q

How is cerebral perfusion pressure calculated

A

Mean arterial pressure - intracranial pressure

48
Q

Briefly describe the 2 types of cerebral oedema

A

Cytotoxic (cellular) - movement is extracellular to intracellular
Vasogenic - movement is intravascular to interstitial

49
Q

What is malignant MCA

A

Neurological deterioration due to cerebral oedema following a MCA territory stroke

50
Q

How does malignant MCA present differently to the effects of normal cerebral oedema and why

A

Cerebral oedema consequences normally present on day 2-4

Malignant MCA presents within 24 hours (younger patients with less brain atrophy so less compensatory space)

51
Q

Briefly describe the types of brain herniation syndromes

A

Subfalcine - cingulate gyrus pushed under the free edge of falx
Uncal - uncus of the temporal lobe pushed under the free edge of tentorium cerebelli
Tonsilar - cerebellar tonsils pushed through foramen magnum

52
Q

How does a subfalcine herniation present

A

Contralateral leg weakness due to compression of the anterior cerebral artery

53
Q

How does an uncal herniation present

A

Ipsilateral pupil dilated and eye in down and out position due to CN3 compression
Ipsilateral diplopia on horizontal gaze due to CN compression
Reduced GCS due to reticular formation compression
Contralateral homonomous hemianopia with macula sparing due to posterior cerebral artery compression
Ipsilateral hemiparesis due to compression of contralateral descending motor tracts

54
Q

How does a tonsilar herniation present

A

Respiratory and cardiac depression due to compression of cardio-resp centres in the brainstem
Ataxia
Occipital headache

55
Q

Why do you get vomiting in RICP

A

Compression of the chemoreceptor trigger zone in the medulla

56
Q

Why do you get papilloedema in RICP

A

The optic nerve is covered in dura which is continuous with that of the brain so RICP communicates
Compression of veins in the sheath leads to reduced venous return and therefore oedema

57
Q

What is cushings reflex and its pathophysiology

A

Pressure on the brainstem stimulates the sympathetics causing raised BP
Carotid sinus detects this and increases the vagal tone leading to reduced HR
Ischaemia of respiratory centres leads to bradypnoea

58
Q

What are duret haemorrhages

A

Due to stretching of the pontine arteries following herniation syndromes

59
Q

How is RICP managed

A

Raise the head of the bed to 30
Hyperventilate to blow off CO2 leading to vasoconstriction
Mannitol
Manage pain, glucose, sodium and temperature

60
Q

Why don’t Burr holes tend to work

A

Consistency of blood is clotted so won’t come out via the small hole

61
Q

What causes venous sinus thrombosis in trauma

A

Skull fracture that extends to the DVS
Haemoatoma or oedema compressing the sinus
Endothelial injury activating the clotting cascade
Extension of a thrombus from injured emissary veins

62
Q

How does cavernous sinus thrombosis present

A 
Ophthalmoplegia (6 first then 3 ad 4)
Proptosis
Chemosis 
Sensory loss in V1/2 distribution 
Horners syndrome - sympathetics hitchhike of ICA and abducens
63
Q

What is commotio medularis

A

Sudden death of an intoxicated patient following a mild-moderate blunt force head injury due to ethanol’s effects on the cardioresp centres

64
Q

What 2 mechanisms can leads to a carotid artery dissection and what are the 2 possible outcomes

A

Direct trauma to the neck or neck hyperextension (deceleration incident) leading to a stretching of the ICA over vertebrae
Leads to an intimal tear with blood entering the space
The haematoma narrows the actual lumen leading to occlusion and ischaemia or there is clot formation with an emboli breaking free and causing an infarct

65
Q

How does a carotid artery dissection present

A

Often asymptomatic until the cerebrovacsular ischaemia but can have
Neck pain
Ipsilateral horners syndrome (sympathetics hitchike)
Pulsatile tinnitus
Syncope

66
Q

What are the causes of pupil dilation in trauma

A

Herniation leading to CN3 compression
Brainstem ischaemia due to reduced blood flow
Anoxia

67
Q

Describe the types of skull fracture

A

Linear
Depressed
Ping pong - no fracture just a depression
Diastatic - along the suture lines
Growing - non healing fracture widens and brain herniates

68
Q

Why is paediatric head injury more serious

A

Lack of fully developed paranasal sinuses so less buffering
Thinner bones
Larger head to torso ratio
Inability to maintain body temperature

69
Q

Why are extradural haematomas rare in children

A

Dura is tightly attached to periosteum

70
Q

Describe the location of the fluid in caput secundum, subgaleal haemorrhage and cephalhaematoma

A

Caput - soft puffy swelling between skin and aponeurosis
Subgaleal - blood between aponeurosis and periosteum
Cephalhaematoma - blood between periosteum and boney skull

71
Q

Describe the features of an anterior cerebral artery stroke

A

Hemiparesis affecting the leg more
Incontinence
Split brain
Memory, motivation and empathy affected due to cingulate cortex

72
Q

Describe the features of a middle cerebral artery stroke

A

Hemiparesis affecting the arm more
Aphasia (broca or wernike depending if frontal or temporal lobe)
Contralateral homonomous hemianopia
Hemispatial neglect

73
Q

Describe the features of a posterior cerebral artery stroke

A

CN3 affected due to oedema post stroke! (WB)
Contralateral homonomous hemianopia with macula sparing
Hemisensory loss due to thalamus involvement
Brainstem or cerebellar syndrome

74
Q

Describe the features of a vertebral artery stroke

A

DANISH

75
Q

Which side does a stroke commonly cause aphasia

A

Left sided stroke

76
Q

Damage to where causes a conductive aphasia

A

Arcuate fasiculus

77
Q

Gold standard imaging for a stroke

A

Non-contrast CT

78
Q

What is the management of a stroke

A

Thrombolyse with Alteplase within 4.5 hours
Aspirin 300mg for 2 weeks
Clopidogrel 75mg for life

79
Q

What are the layers of the scalp

A

Skin, connective tissue, aponeurosis, loose areolar connective tissue, periosteum

80
Q

Which direction of scalp laceration is more severe and why?

A

Coronal - the two bellies of the occipitofrontalis muscle contract and full apart the aponeurosis

81
Q

Why do scalp lacerations bleed profusely?

A

Many anastamoses
Vessels tightly adhered to dense CT so can’t vasoconstrict
Opposing pull of occipitalis and frontalis
Rich blood supply in order to nourish hair follicles

82
Q

What is a complication of a scalp laceration and how does this occur?

A

Cavernous sinus thrombosis due to infection spreading from the angular vein via valveless ophthalmic veins to the sinus

83
Q

What is the blood supply to the scalp

A

From external carotid: occipital, posterior auricular and superficial temporal
From internal carotid: supratrochlea and supraorbital branch of ophthalmic

84
Q

Where does the anterior meningeal artery originate

A

Internal carotid - ophthalmic - ethmoid

85
Q

Where does the middle meningeal artery originate

A

External carotid - maxillary

+ accessory meningeal artery also branches off maxillary but travels through foramen ovale not spinosum

86
Q

Where does the posterior meningeal artery originate

A

External carotid - ascending pharyngeal (through jugular foramen)
+ 3 branches from ascending pharyngeal (through hypoglossal canal), occipital (through jugular foramen) and vertebral (through foramen magnum)

87
Q

Describe the passage of CSF though the ventricles

A

Lateral - interventricular foramen - 3rd - cerebral aqueduct - 4th

88
Q

What is an arachnoid villi/granulation

A

Protrusion of arachnoid mater into the DVS allowing CSF to exit the subarachnoid space and drain into the DVS

89
Q

What are the funtions of the ventricular system and CSF

A

Shock absorber
Decrease the weight of the brain
Waste removal, nourishment and chemical signalling

90
Q

How much CSF is produced per day

A

450ml

PHM BSc - Applied Science (12 decks)

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