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Phase 2- HNN > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is attention?

A

A global cognitive process encompassing multiple sensory modalities, operating across sensory domains

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2
Q

What various component cognitive processes can attention be subdivided into?

A

Arousal: a general state of wakefulness and responsivity
Vigilance: capacity to maintain attention over prolonged periods of time
Divided attention: ability to respond to more than one task at once
Selective attention: ability to focus on one stimulus while suppressing competing stimuli

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3
Q

What is the clinical importance of attention?

A

Breakdown of global attention: delirium/acute confusional state
- impaired arousal: ‘drowsiness’
- impaired vigilance: ‘impersistence’
- impaired divided and selective attention: ‘distractible’
Breakdown of domain-specific attention e.g. following non-dominant hemisphere stroke
- visual inattention
- sensory inattention
- neglect

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4
Q

What are the two main groups of structures involved in attention?

A

Top-down regulation (prefrontal, parietal and limbic cortex) and bottom-up regulation (ascending reticular activating system)

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5
Q

What are the important structures of attention in the parietal cortex?

A

Postcentral gyrus and

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6
Q

What are the important structures of attention in the limbic cortex?

A

Cingulate gyrus, hippocampus, fornix, amygdala, orbital and prefrontal cortex, maxillary bodies

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7
Q

What is the ARAS composed of?

A

Brainstem nuclei, thalamic nuclei and cortex

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8
Q

How is attention tested in clinical practice?

A

Ask about orientation in time and place, serial 7s, digit span and digits backwards, months of the year or days of the week in reverse order

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9
Q

How is memory classified?

A

Long-term memory and immediate (working) memory

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10
Q

What is immediate memory?

A

Immediate recall of small amounts of verbal or spatial information, which appears to function independently of (but in parallel with) long-term memory

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11
Q

What are the subcomponents of working memory?

A

‘Visual sketchpad’, dorsolateral prefrontal cortex , and ‘phonological store’

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12
Q

How is long-term memory subdivided?

A

Explicit (declarative), divided into episodic and semantic, and implicit (procedural), divided into motor skills and classical conditioning

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13
Q

What is episodic memory?

A

A form of explicit, declarative memory- available to conscious access and reflection
Personally experienced, temporally specific episodes/events
Extended limbic system: medial temporal lobe (particularly hippocampus and entorhinal cortex), diencephalon (particularly maxillary bodies and thalamic nuclei)
Dorsolateral prefrontal cortex: temporal organisation of episodic memory, interacts with structures within the extended limbic system

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14
Q

How is episodic memory tested?

A

Recall of complex verbal information, word-list learning, recognition of newly encounters words and faces, recall of geometric figures

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15
Q

What is semantic memory?

A

A form of explicit memory: available to conscious access and reflection
- factual information (general knowledge) and vocabulary
- independent of context, time and personal relevance
Anatomical basis- storage, maintenance and retrieval not dependent on limbic system- perhaps information is initially processed via episodic memory systems- after repeated rehearsal gets transferred to semantic storage structures
Semantic memory network:
- left hemisphere anterior temporal lobe is a key integrative region
- anterior temporal cortex and angular gyrus integrate incoming information
Category-specific semantic memory:
- theoretical ‘gradients’ of different semantic processes arranged anatomically
- ventral (visual) to dorsolateral (basic objects) to anterior (complex)

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16
Q

What clinical problems affect semantic memory?

A

Herpes simplex encephalitis, trauma, tumours, Alzheimer’s dementia, semantic dementia (a form of frontotemporal dementia)

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17
Q

What are key features of semantic dementia?

A

Progressive right temporal lobe atrophy (a variant of frontotemoral dementia)
‘Prosopagnosia’- behavioural disturbance (social disinhibition, hyper-religiosity, aggression)

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18
Q

Describe implicit (procedural memory)

A

No conscious access to implicit memory stores
We progressively acquire motor skills to perform tasks (but we cannot easily explain the procedure)
e.g Learning to play a musical instrument, learning to ride a bike
Profound amnesia can occur in context of normal implicit memory (e.g. Korsakoff’s syndrome)
Dependent on networks involving basal ganglia and cerebellum
Cannot be tested at the bedside

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19
Q

How are traumatic brain injuries (TBI) classified with GCS?

A

Severe <9
Moderate 9-12
Mild >12

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20
Q

Disruption of what artery and vein, often by fracture of the squamous temporal bone, can cause extradural haematoma?

A

Middle meningeal artery (or vein)

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21
Q

What can happen (in 1/3rd) in extradural haematoma?

A

Lucid interval with deterioration (may be rapid)

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22
Q

Injury to what veins is responsible for subdural haematoma?

A

Bridging veins

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23
Q

What is a ballistic movement?

A

Movement based largely on a set of pre-programmed instructions, rapid but at the expense of accuracy- little opportunity for compensation for unexpected changes

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24
Q

What is a visual pursuit or feedback movement?

A

Motor command that is continually updates to sensory feedback. Highly accurate (can be modified while in progress) but slow

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25
Q

What is area 6 (SMA and PMA) of the neocortex involved in?

A

Planning and decision making for movement

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26
Q

What are the main non-cortical structures involved in control of movement?

A

Basal ganglia and cerebellum

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27
Q

What is the function of the basal ganglia?

A

Initiation of movement and planning of complex voluntary movement

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28
Q

Where are the inputs and outputs for the basal ganglia?

A

Input mainy from the prefrontal cortex

Output to the pre-motor area (via thalamus )

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29
Q

What disorders can affect the basal ganglia?

A

Parkinson’s disease (loss of dopaminergic neurones leading to difficulty in initiating movement) and Huntington’s disease (random involuntary movements)

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30
Q

What are some of the symptoms of Huntington’s disease?

A

Choreas, difficulty speaking and swallowing, progressing to general cognitive decline

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31
Q

What is the function of the cerebellum in motor control?

A

Co-ordination and smooth execution of movements- motor learning and error detection

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32
Q

Where are the inputs and outputs for the cerebellum?

A

Input: mainly from sensory cortex
Output: to primary motor cortex (via thalamus)

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33
Q

How is the forebrain divided?

A

Into the cerebral hemispheres and diencephalon

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34
Q

How are the cerebral hemispheres divided?

A
  • Cerebral cortex
  • Frontal lobes
  • Temporal lobes
  • Parietal lobes
  • Occipital lobes
  • Corpus callosum
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35
Q

What are some important structures in the cerebral hemispheres?

A
  • Amygdala
  • Basal ganglia
    • caudate nucleus
    • putamen
    • globus pallidus
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36
Q

What are the functions of the cerebral cortex?

A

Sensory areas interpret sensory muscles, motor areas control muscle movement and association areas function in emotional and intellectual processes

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37
Q

What are the functions of the different lobes?

A
  • Frontal: reasoning, behaviour, mood and movement
  • Temporal: hearing, memory and semantics
  • Parietal: sensory (pain, pressure and temperature)
  • Occipital: sight
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38
Q

Which area of the brain is predominantly involved in memory?

A

Hippocampus (located in the medial temporal lobe)

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39
Q

What is the corpus callosum?

A

White matter structure connecting the cerebral hemispheres, allowing communication between them

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40
Q

What is the amygdala and what is its function?

A
  • Almond shaped group of neurons located deep within the medial temporal lobes that perform a primary role in the processing and memory of emotional reactions
  • Part of the limbic system that supports a variety of functions including emotion, behaviour and long-term memory
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41
Q

What is the function of the basal ganglia?

A

Coordinate gross, automatic muscle movements and regulate muscle tone

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42
Q

What structures make up the diencephalon?

A
  • Epithalamus
  • Thalamus
  • Subthalamus
  • Hypothalamus
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43
Q

What is the function of the epithalamus?

A

Consists of the pineal gland that secretes melatonin (biological clock and sleepiness) and the habenular nuclei (emotional response to olfaction)

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44
Q

What are the functions of the thalamus?

A
  • Relays all sensory input to the cerebral cortex (provides crude perception of touch, pressure, pain and temperature)
  • Includes nuclei involved in voluntary motor actions and arousal
  • Anterior nucleus functions in emotions, memory, cognition and awareness
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45
Q

What are the functions of the subthalamus?

A
  • Contains the subthalamic nuclei and portions of the red nucleus and substantial migration, which are positioned mostly lateral to the midline
  • Communicates with the basal ganglia, cerebellum and cerebrum to control body movements
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46
Q

What are the functions of the hypothalamus?

A
  • Controls and integrates activities of the ANS and pituitary gland
  • Regulates emotional and behavioural patters and circadian rhythms
  • Controls body temperature and regulates eating and drinking behaviour
  • Helps maintain the waking state and establishes patterns of sleep
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47
Q

What are the important structures of the midbrain?

A

Midbrain, superior and inferior colliculus

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48
Q

What are important functions of the midbrain?

A

Relays motor impulses from the cerebral cortex to the pons and sensory impulses from the spinal cord to the thalamus

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49
Q

What are the important functions of the superior and inferior colliculi?

A
  • Superior colliculi coordinate movements of the eyeballs in response to visual and other stimuli
  • Inferior colliculi coordinate movements of the head and trunk in response to auditory stimuli
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50
Q

What are the functions of the substantial migration and red nucleus?

A

Most of substantial migration and red nucleus contribute to control of movement

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51
Q

What origins of CNs does the midbrain contain?

A

CN II and IV

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52
Q

What structures make up the hindbrain?

A

Cerebellum, pons and medulla oblongata

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53
Q

What are the important functions of the cerebellum?

A
  • Compares intended movements with what is actually happening to smooth and coordinate complex, skilled movements
  • Regulates posture and balance
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54
Q

What are the important functions of the pons?

A
  • Relays impulses from one side of the cerebellum to the other and between the medulla and midbrain
  • Contains nuclei of origin for CN V, VI, VII and VIII
  • Pneumotaxic area and apneustic area, together with medulla, help control breathing
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55
Q

What are the important functions of the medulla oblongata?

A
  • Relays motor and sensory impulses between other parts of the brain and spinal cord
  • Reticula formation (also in pons, midbrain and diencephalon) functions in consciousness and arousal
  • Vital centres regulate heartbeat, breathing (together with pons) and blood vessel diameter
  • Other centres coordinate swallowing, vomiting, coughing, sneezing and hiccupping
  • Contains nuclei of origin for CN IX, X XI and XII
56
Q

What foramen does CN I travel through the skull in?

A

Cribiform plate

57
Q

What foramen does CN II travel through the skull in?

A

Optic canal

58
Q

What foramen do CNs III and IV travel through the skull in?

A

Superior orbital fissure

59
Q

What foramen does CN V travel through the skull in?

A
  • V1: superior orbital fissure
  • V2: foramen rotundum
  • V3: foramen ovale
60
Q

What foramen does CN VII travel through the skull in?

A

Superior orbital fissure

61
Q

What foramen do CNs VII and VIII travel through the skull in?

A

Internal auditory canal

62
Q

What foramen do CNs IX, X and XI travel through the skull in?

A

Jugular foramen

63
Q

What foramen does CN XII travel through the skull in?

A

Hypoglossal canal

64
Q

What is the function of CNs I and II?

A
  • Olfactory: smell

- Optic: vision

65
Q

What is the function of CN III?

A
  • Movement of the eyelid (levator palpabrae superiors) and eyeball (medial superior and inferior rectus, inferior oblique)
  • Pupillary constriction and accommodation of lens for near vision (sphincter pupillae)
66
Q

What is the function of CN IV?

A

Movement of the eyeball (superior oblique)

67
Q

What is the function of CN V?

A
  • Sensory to face (ophthalmic, maxillary and mandibular)

- Motor to muscles of mastication (masseter, temporalis and pterygoid)

68
Q

What is the function of CN VI?

A

Movement of the eyeball (lateral rectus)

69
Q

What is the function of CN VII?

A
  • Sensory to skin of external ear
  • Taste (anterior 2/3rds of tongue)
  • Motor to muscles of facial expression
  • Secretion of saliva and tears
70
Q

What is the function of CN VIII?

A

Hearing and equilibrium

71
Q

What is the function of CN IX?

A
  • Taste (posterior 1/3rd of tongue)
  • Sensory to carotid body and sinus
  • Swallowing and speech
  • Secretion of saliva
72
Q

What is the function of CN X?

A
  • Swallowing and speech

- Parasympathetic innervation

73
Q

What is the function of CN XI?

A
  • Movement of head and shoulders (SCM and trapezius)
74
Q

What is the function of CN XII?

A

Movement of tongue

75
Q

What is the test for the olfactory nerve?

A
  • With eyes closed, the subject is asked to sniff substances through each nostril ion turn and to name the odours
  • Non-irritant substances such as coffee or vanilla or toothpaste are used
  • Irritating odours stimulate ending of the ophthalmic division of the trigeminal nerve
  • Anosmia (loss of smell) is due to a neurological lesion and is most commonly the effect of trauma
  • Fracture passing through a cribriform plate of the ethmoid bone readily traumatises the fascicles of the olfactory nerve
76
Q

How are the optic and oculomotor nerves tested?

A
  • Test for visual acuity, check visual fields and inspect optic discs
  • Inspect the size and shape of the pupils and compare one side with the other
  • Test pupillary reactions to light
  • If they are abnormal, test reaction to near effort
77
Q

How are the oculomotor, trochlear and abducens nerves tested?

A
  • Subject should be sitting upright with head held still by the examiner
  • Subject is asked to follow the examiner’s finger, or a thin pencil, with eyes
  • Movement of eyes along horizontal plane -> medial and lateral rectus muscles
  • Movement of eyes along vertical plane (looking outwards) -> superior and inferior rectus muscles
  • Movement of eyes along vertical plane (looking inwards) -> superior and inferior oblique muscles
  • Note for any strabismus (squint), ptosis, nystagmus, deviation of the eye and ask the patient if they have diplopia (double vision)
78
Q

How is the function of the trigeminal nerve tested?

A
  • Cutaneous sensation can be tested in appropriate areas of face
  • Jaw muscles can be tested by asking the subject to clench their teeth and palpating the contracting masseter and temporalis muscles
  • Jaw jerk reflex
  • Pterygoids -> if subject opens their mouth against a resistance and there is a unilateral weakness, the jaw will deviate to one side
79
Q

How is the function of the trigeminal and facial nerve tested?

A
  • Wisp of cotton wool is carefully applied to cornea -> resulting in blinking of both eyes
  • Sensory limb is the ophthalmic division of CN V
  • Motor response, a contraction of orbicularis oculi, receives its motor innervation from CN VIII
80
Q

How is the hearing function of the vestibulocochlear nerve tested?

A
  • Each ear is tested separately
  • Vibrating tuning fork is held close to the external auditory meatus and its base is then pressed gently against the mastoid bone -> subject is asked which of these two stimuli is loudest
  • Fork is left applied to mastoid bone until the vibrations are no longer heard and the fork is held against the ear -> subject is asked if note can still be heard
  • For a normal subject, air conduction > bone conduction
  • If this is not the case may be due to middle ear infection
  • Weber’s test -> tuning fork is placed in centre of forehead and subject is asked which side is louder
  • Both equally (normal), left (R sensorineural impairment) and right (L sensorineural impairment)
81
Q

How are the vestibulo-occular reflexes tested?

A
  • Reflex movements of the eyes consequent upon rotation of a subject in a rotating chair
  • Horizontal nystagmus (rotate as per normal) -> eyes move horizontally
  • Vertical nystagmus (head bend and tilt to one side) -> eyes move vertically
  • Rotational nystagmus (head bent) -> eyes swing upwards from left to right
  • Ask subject to observe the pictures on the slowly rotating drum and observe eye movements -> optokinetic nystagmus (normally observed by looking at objects moving across field of vision)
82
Q

How is the function of the glossopharyngeal and vagus nerves tested?

A
  • Test are not very impressive especially in normal subject

- Subject has no huskiness, dysphonia, dysphagia and palate moves symmetrically when the subject says “AH”

83
Q

How is the function of the accessory nerve tested?

A

Subject should be able to lift shoulders against resistance -> testing strength of trapezius muscle

84
Q

How is the function of the hypoglossal nerve tested?

A

When the subject is asked to protrude the tongue it will deviate to the weak side (lick own wounds)

85
Q

What accompanies two thirds of skull fractures?

A

Intracranial lesions

86
Q

What do skull fractures provide pathways for?

A

Entry of bacteria (meningitis) or air (pneumocephalus) to the CSF and for leakage of CSF out of the dura

87
Q

What cranial nerves are likely to be injured in a skull fracture?

A
  • Olfactory
  • Optic
  • Oculomotor
  • Trochlear
  • Trigeminal (V1 and 2)
  • Facial
  • Auditory (CN 8)
88
Q

What are the different types of brain injury?

A

Primary and secondary

89
Q

What causes primary brain injury and what is classified as primary brain injury?

A

Primary injuries are caused by impact and include

  • diffuse axonal injury
  • focal lesions of;
    • lacerations
    • contusions
    • haemorrhage
90
Q

What causes secondary brain injury and what is classified as secondary brain injury?

A

Secondary injuries are often diffuse or multifocal and include;

  • concussion
  • infection
  • hypoxic brain injury
91
Q

How do cerebral contusions cause primary brain damage?

A
  • Focal brain damage resulting from contact between bony protuberances of the skull base
  • Characteristic distribution
    • orbital surface of the frontal lobes
    • frontal poles
    • around Sylvian fissure (lateral sulcus)
    • temporal poles
    • undersurface of the temporal lobes
  • Occurs at crests of gyri but also commonly extend into subcortical white matter
92
Q

How does traumatic axonal injury occur/cause primary brain damage?

A
  • Most common cause of coma in the absence of intracranial haematoma and may result in disability -> detected in majority of fatal head injury
  • Widespread axonal injury occurs as a consequence of shear and tensile strains occurring immediately after impact
  • If patient survives 5 weeks or more after injury, there is Wallerian degeneration of the long tracts and white matter of the cerebral hemisphere
  • Even minor injury causing transient loss of consciousness produces some neuronal damage -> neuronal regeneration is limited so the effects of repeated minor injuries are cumulative
  • Spectrum of traumatic axon injury exists
93
Q

How do lesions occur/cause primary brain damage?

A
  • Occur in the scalp and skull
  • Skull fractures are indicative forces of the injury but many are sustained without associate brain damage and conversely many fatal head injuries have no skull fracture
94
Q

How do haematomas occur/cause secondary brain damage?

A
  • Result from vascular injury and bleeding
  • Depending on the anatomical position of the ruptures vessels, bleed can occur in any of several compartments including;
    • epidural space
    • subdural space
    • subarachnoid space
    • intracerebral haematoma
95
Q

How does epidural haematoma occur/cause secondary brain damage?

A
  • Develops between the inner bones of the skull and dura
  • Usually results from a tear in an artery -> most often middle meningeal artery
  • Usually in association with head injury in which the skull is fractured
  • Rapid expansion of the haematoma compresses the brain
  • More common in a young person because the dura is less firmly attached to the skull surface than in an old person -> dura can easily be separated from the inner surface allowing expansion of haematoma
96
Q

How does epidural haematoma present?

A
  • Presents with a history of head injury and a brief period of unconsciousness follows by a lucid period in which consciousness is regained
  • This is followed by a rapid progression to unconsciousness
  • Lucid interval does not always occur, but when it does it is of great diagnostic value
  • With rapidly developing unconsciousness, there are focal symptoms related to the area of brain involved
97
Q

What symptoms does epidural haematoma present with?

A

Ipsilateral -pupil dilation

Contralateral - hemiparesis from uncal herniation

98
Q

What happens with progression of epidural haemorrhage?

A
  • If haematoma is not removed, the condition progresses, with increased ICP, tectorial herniation and death
  • Prognosis is excellent if the haematoma is removed before loss of consciousness occurs
99
Q

How does subdural haematoma occur/cause secondary brain damage?

A
  • Develops in the area between the dura and arachnoid -> subdural space
  • Usually a result of a tear in the small bridge veins that connect veins on the surface of the cortex to the dural sinuses
  • Bridging veins pass from the pial vessels through the subarachnoid space, penetrate the arachnoid and the dura and empty into the intramural sinuses
  • Veins are readily snapped in head injury when the brain moves suddenly in relation to the cranium
  • Bleeding can occur between the dura and arachnoid -> subdural haematoma
  • Can also occur in the subarachnoid space -> subarachnoid haematoma
  • Venous source of bleed in a subdural haematoma develops more slowly than the arterial bleeding a epidural haematoma
100
Q

How is subdural haematoma classified?

A
  • As acute, subacute or chronic
  • Based on the approximate time between then appearance of symptoms
  • Symptoms of acute haematoma are seen within 24 hours of injury
  • Subacute -> 2-10 days after injury
  • Chronic haematoma -> several weeks after injury
101
Q

How do subdural haematomas progress?

A
  • Acute subdural haematomas progress rapidly and have a high mortality rate because of the sever secondary injuries related to oedema and increased ICP
  • High mortality rate has been associated with uncontrolled ICP increase, loss of consciousness, decerebrate posturing and delay in surgical removal
  • By contrast, in subacute subdural haematoma, there may be a period of improvement in level of consciousness and the neurological symptoms, only to be followed by deterioration if the haematoma is not removed
  • Symptoms of chronic subdural haematoma develop weeks after a head injury
102
Q

How do subdural haematomas occur in older people?

A
  • More common in older people because brain atrophy causes the brain to shrink away from the dura and stretch fragile bridging veins
  • These veins rupture, causing slow seepage of blood into the subdural space
  • Fibroblastic activity causes the haematoma to become capsulated
  • Sanguineous fluid in this encapsulated area has high osmotic pressure and draws in fluid from the surrounding subarachnoid space
  • Mass expands -> exerts pressure on cranial contents
103
Q

How does cerebral oedema and swelling occur/cause secondary brain injury?

A
  • Vasogenic cerebral oedema (defective BBB allows extravasation of water, sodium and protein molecules) occurs around contusions and haematomas
  • Congestive oedema (diffuse swelling of one or both hemispheres) may also occur
  • Pathogenesis is not well understood
104
Q

How does ischaemic brain damage occur/cause secondary brain injury?

A
  • Common and occurs in 60-70% of fatal head injuries
  • Often adjacent to contusions and haematomas or secondary to ICP, but ischaemia may also occur in arterial boundary zones or as diffuse hypoxic damage
  • Occurs soon after injury and there is a relation with episodes of systemic hypotension and hypoxia
  • Caused by raised ICP, hypoxaemia or reduced CPP -> lack of O2 and nutrients for cellular metabolism
  • Initiates the ischaemic cascade that leads to further neuronal damage
105
Q

How does infection occur/cause secondary brain injury?

A
  • Spread of micro-organisms may occur via open-skull fractures or base of skull fractures -> increased risk of meningitis
  • Brain abscess is more commonly a complication of missile head injury
106
Q

What are the cellular and biochemical mechanisms of brain damage?

A
  • Cerebral hypo perfusion and hypoxaemia result in lack of O2 and nutrients essential for cellular functioning and survival
  • Resultant energy failure leads to a failure in membrane homeostasis and a cascade of further events contributing to cell damage and dysfunction
  • Ischaemic cascade
  • Mechanically injured neurons have a heightened susceptibility to these effects and there is a complex interaction between events at a cellular and a systemic level
  • Different mechanisms give rise to neuronal damage and cell death -> not fully established in man
    • raised intracellular Ca2+
    • increased release of neurotoxic transmitters such as glutamate
    • production of free radicals
    • receptor dysfunction
    • inflammation
107
Q

What responses does the Glasgow Coma Scale (GCS) asses?

A
  • Best motor response
  • Best verbal response
  • Eye opening
    (minumum score 3)
108
Q

What is the significance of consciousness level?

A
  • State of awareness of self and the environment and of being able to become orientated to new stimuli
  • Has traditionally been divided into two compartments;
    • arousal and wakefulness -> require concurrent functioning of both cerebral hemispheres and an intact reticular activating system in the brainstem
    • content and cognition -> determined by a functioning cerebral cortex
109
Q

What determines intracranial pressure?

A
  • Pressure-volume relationships among the brain tissue, CSF and blood in the intracranial cavity
  • Mono-Kellie hypothesis, which relates to reciprocal changes among the intracranial volumes
  • Compliance of the brain and its ability to buffer changes in intracranial volume
110
Q

What is the relationship between intracranial volumes and pressure?

A
  • ICP represents the pressure exerted by the essentially incompressible tissue and fluid volumes of the three compartments contained within the skull
  • Brain tissue and interstitial fluid -> 80%
  • Blood -> 10%
  • CSF -> 10%
111
Q

What is the Monro-Kellie hypothesis?

A
  • Normally, a reciprocal relationship exists among the three intracranial volumes such that the ICP is maintained within normal limits
  • Because these volumes are practically incompressible, a change in one component must be balanced by an almost equal and opposite effect in one or both of the remaining components
  • CSF compartment is the most easily displaced
  • CSF can be displaced from the ventricles and cerebral subarachnoid space into the spinal subarachnoid space
  • It can also undergo increased absorption or decreased production
  • Because most of the blood in the cranial cavity is contained in the low pressure venous system, venous compression serves as a means of displacing blood volume
112
Q

What is compliance and how does it relate to ICP?

A
  • Compliance is the ease with which a substance can be compressed or deformed
  • Measure of the brain’s ability to maintain its ICP during changes in intracranial volume
  • Compliance (C) represents the ratio of change in volume (V) to change in pressure (P)
  • C = deltaV/deltaP
113
Q

What is the relevance of cerebral perfusion pressure ?

A
  • Survival of nervous tissue is dependent on adequate blood supply
  • Cerebral blood flow is normally held constant in the face of changing CPP within certain limits by a variety of local mechanisms by;
    • autoregulation
    • chemoregulation
  • High perfusion pressure may increase the cerebral blood flow, break down the BBB and produce cerebral oedema as in hypertensive encephalopathy
  • CPP is related to ICP as -> CPP =MAP-ICP
  • Minimum CPP of 70 mmHg is necessary for adequate cerebral function
  • Rise in ICP and resultant fall in CPP will eventually reach a critical level -> significant reduction in cerebral blood flow occurs
  • If autoregulation is impaired, these effects develop even earlier
  • When ICP reaches the MAP, blood flow ceases
114
Q

What is autoregulation of CPP?

A
  • Autoregulation may be impaired after a head injury and cerebral blood flow then becomes “pressure passive” _> drop in CPP is more likely to reduce cerebral blood flow and cause ischaemia
115
Q

What are the clinical effects of raised ICP?

A
  • Headache -> worse in morning and aggravated by stopping or bending
  • Vomiting -> occurs with acute rise in ICP
  • Papilloedema -> swelling of the optic disc and retina that may result in disc haemorrhages
116
Q

Describe brain herniation:

A
  • Consequence of increased ICP
  • Brain is protected by the skull and two supporting septa (falx cerebri and the tentorium cerebelli)
  • Brain herniation represents a displacement of brain tissue under the falx cerebri or through the tentorial notch or incisura of the tentorium cerebelli
  • Occurs when an elevated ICP in one brain compartment causes displacement of the cerebral tissue towards an area of lower pressure
  • Different types of herniation syndromes are based on the area of brain that has herniated and the structure under which it has been pushed
117
Q

What is the falx cerebri?

A

CT separating the two cerebral hemispheres

118
Q

What is the tentorium cerebelli?

A

CT dividing the cranial cavity into anterior and posterior fossae

119
Q

What two categories are brain herniations divided into?

A

Supra and infra tentorial

120
Q

What clinical signs indicate supra-tentorial herniations?

A
  • Ocular, motor and respiratory functions become impaired

- This pattern follows the predictable continuum of rostral-to-caudal failure

121
Q

What are the two major types of supra-tentorial hernia?

A

Cingulate and transtentorial

122
Q

Describe cingulate herniation:

A
  • Displacement of the cingulate gyrus and hemisphere beneath the sharp edges of the falx cerebri to the opposite side of the brain
  • Can compress local blood supply and cerebral tissue -> oedema and ischaemia which further increase the degree of ICP elevation
  • May be compression of branches of the anterior cerebral artery with unilateral or bilateral leg weakness
123
Q

What does transtentorial herniation result in?

A
  • Central and uncal syndrome
  • Clinically they display distinct patterns in their early course but merge into similar pattern once they begin to involve the midbrain level and below
124
Q

Describe central transtentorial herniation:

A
  • Involve downward displacement of the cerebral hemispheres, basal ganglia, diencephalon and midbrain through the tentorial incisors
  • Bilateral small, reactive pupils and drowsiness are heralding signs
125
Q

Describe uncal herniation syndrome:

A
  • Pushes the medial aspect of the temporal lobe, which contains the uncus and hippocampal gyrus, through the incisura of the tentorium
  • As a result, the diencephalon and midbrain are compressed and displaced laterally to the opposite side of the tentorium
  • CN III and the posterior cerebral artery frequently are caught between the uncus and tentorium
  • CN III controls pupillary muscle constriction so entrapment causes ipsilateral pupillary dilation and is usually an early sign of uncal herniation
  • Consciousness may be unimpaired because the reticular activating system (RAS), which is responsible for wakefulness, has not yet been affected
126
Q

How does uncal herniation progress?

A
  • As uncal herniation progresses, there are changes in motor strength and coordination of voluntary movements because of compression of the descending motor pathways
  • Not unusual for initial changes in motor function to occur ipsilateral to the side of the brain damage because of compression of the contralateral cerebral peduncles
  • Changes in consciousness and coma may follow due to compression of the midbrain against the opposite tentorial edge
  • Decerebrate posting may develop, follows by dilated fixed pupils, flaccidity and respiratory arrest
127
Q

Describe infratentorial herniation:

A
  • Results from increased pressure in the infratentorial compartment
  • Herniation may occur superiorly or inferiorly
  • Upward displacement of brain tissue can cause blockage of the aqueduct of Sylvius and lead to hydrocephalus and coma
  • Downward herniation involves displacement of the midbrain through the tentorial notch or the cerebellar tonsils through the foramen magnum
  • Often progresses rapidly and can cause death because it is likely to involve lower brainstem centres that control vital cardiopulmonary functions
128
Q

What are the effects of local ischaemia and hypoxia on the brain?

A
  • Brain requires continuous perfusion with well-oxygenated blood
  • If supply is interrupted for more than a few minutes, permanent ischaemic neuronal damage results
  • Normally, a fall in BP does not produce a drop in cerebral perfusion because cerebrovascular autoregulation results in cerebral vasodilation
  • Following head injury, cerebrovascular autoregulation is often impaired and the brain therefore becomes even more susceptible to hypotension and hypoxia
  • Presence of systemic hypotension results in a doubling of mortality after severe head injury
129
Q

What are the causes of hypoxic brain damage?

A
  • Extracranial blood loss -> common in association with severe head injury
  • Uncontrolled seizures -> further source of secondary insults following head injury due to increased metabolic rate associated with the seizures and the respiratory impairment which often accompanies them
130
Q

How is acute head injury managed?

A

Assessment, resuscitation, investigation and referral

  • main principle in the acute management of head injury is the prevention of secondary insults
  • Most head trauma occurs in the context of multiple trauma -> principles of acute management are the same as in other types of trauma
  • CT scans are the investigation of choice in acute management of head injury -> provide all the necessary information for initial management
131
Q

What are the principles of acute management in trauma?

A
  • Airways and cervical spine control
  • Breathing and ventilation
  • Circulation and haemorrhage control
  • Disability and neurological status
  • Exposure and environment
132
Q

How is head injury surgically managed?

A

No hard and fast rule concerning surgical intervention for intracranial mass lesions

  • mass lesions (>5mm midline shift) may require surgical intervention but small haematomas (<5mm midline shift) in patients who are alert and neurologically intact may be managed conservatively
  • Intraparenchymal contusions associated with raised (> 30 mmHg) or rising ICP require surgery
  • Large temporal lobe haematomas are more at risk than similar sized frontal or parieto-occipital lesions
  • Mannitol and mild hyperventilation (pCO2 25-30 mmHg) are commonly used intra-operatively to reduce intracranial hypertension
133
Q

What does non-surgical management of raised or rising ICP include?

A
  • No obstruction to venous drainage
  • Adequate systolic BP
  • Compliance with artificial ventilation
  • More active means of lowering ICP include ventricular drainage, use of mannitol and hyperventilation
134
Q

What are medical treatments of head injury?

A
  • Mannitol: directive widely used to relieve ICP but long-term use may worsen brain oedema
  • Furosemide: diuretic used synergistically with mannitol to relieve ICP
  • Anti-convulsants: used to prevent or reduce the severity of post-traumatic seizures that develop in 15% of patients with severe head injury
  • Antibiotics: large doses used to treat bacterial meningitis
  • Barbituates: CNS depressants effective in reducing ICP and may have a protective effect in brain anoxia and ischaemia
135
Q

Discuss regeneration of neurons in CNS?

A
  • Adult CNS neurons have a milted capacity to regenerate compared to PNS neurons
  • Due to lack of factors which facilitate growth or presence of factors which actively inhibit growth
  • Oligodendrocytes synthesise glycoproteins which inhibit axon outgrowth
  • This is not present in myelinating processes of Schwann cells of PNS neurons
  • Some evidence of axonal sprouting and re-innervation in diffuse axonal injury
  • Despite limited regeneration with the adult CNS, there is substantial recovery of function after traumatic brain injury
  • Presumably reflects neural plasticity: recovery of tissue which had been partially but not irreversibly damaged by the injury and adaptation of uninjured tissue to undertake some of the functions previously subserved by tissue which has been irreparably damaged
  • Behavioural adaptation also plays a large part in compensating for and minimising residual disability
136
Q

What is sequelae?

A

Pathological condition resulting from a prior disease, injury or trauma, major causes of morbidity and can have serious social and medico-legal consequences

137
Q

What are long term sequelae of head injury?

A
  • Incomplete recovery -> cognitive impairment, hemiparesis
  • Post-traumatic epilepsy
  • Post-traumatic (post-concussional) syndrome
    • describes age complaints of headache, dizziness and malaise that follow even minor head injuries
    • litigation is frequently an issue
    • depression is prominent
    • symptoms may be prolonged
  • Benign paroxysmal positional vertigo
  • Chronic subdural haematoma
  • Hydrocephalus
  • Chronic traumatic encephalopathy
  • Follow repeated and often minor injuries
    • punch-drunk syndrome
    • consists of cognitive impairment, extrapyramidal and pyramidal signs

Phase 2- HNN (6 decks)

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