Week 4 Flashcards

1
Q

What does the acronym SCALP stand for?

A

Skin
Connective tissue (dense, fibrous and fatty, blood vessels and nerves)
Aponeurosis (galea aponeuortica, from frontalis to occipitalis)
Loose connective tissue (collagen I and II in random layers)
Periosteum/pericranium (nutrients and repair)

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2
Q

Why is the aponeurosis of the skull clinically important?

A

Laceration through the aponeurosis = loss of anchoring of superficial layers, wide gaping wound needing sutures
Laceration not though aponeurosis = glue can be used

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3
Q

What 2 portions can the skull be divided into?

A

Vault and base

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4
Q

How is the skull designed to withstand a blow to the head?

A

Convex shape allows distribution of force to prevent fracture

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5
Q

What type of injury is caused by a hard blow to the skull?

A

Depressed skull fracture

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6
Q

What is a linear fracture?

A

Fracture at site of impact on vault with fracture lines radiating away

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7
Q

What type of fracture may take hours to present?

A

Base of skull fracture

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8
Q

How does a base of skull fracture present?

A

Bruising over mastoid process may be only initial sign; over time panda/raccoon eyes bruising is seen

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9
Q

What is the pterion?

A

The thin bony region where the frontal, parietal and temporal bones meet at the side of the skull

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10
Q

What major blood vessel lies near to the pterion and why is this clinically important?

A

Middle meningeal artery branches

At risk of intracranial bleeding as the bone is thin here

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11
Q

What are the 2 layers of the dura mater?

A

Periosteal layer - adheres to surface of cranium

Internal meningeal layer - continuous except at sinuses and reflections

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12
Q

What are the types of intracranial haematoma?

A

Extra/epidural haematoma
Subdural haematoma
Intracerebral haematoma

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13
Q

Explain the origin and distribution of epidural haematomas

A

Arterial bleeding from middle meningeal artery collects between periosteal layer of dura and skull
Blood strips dura away from periosteum but periosteum is fixed at point of sutures which stops blood spreading around whole skull

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14
Q

Explain the origin and distribution of subdural haematomas

A

Venous blood between dura and arachnoid junction

No limitation of flow so blood spreads more thinly

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15
Q

Why might an extradural haematoma be difficult to image on CT?

A

White blood can turn grey after some time, which makes it more difficult to differentiate from brain matter

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16
Q

What are the CT features of an extradural haematoma?

A

Characteristic lens shape of blood
Midline shifted away from blood
Swelling obstructs ventricles on the same side

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17
Q

What are the CT features of a subdural haematoma?

A

Thinly spread blood around brain circumference in crescent shape
Midline shift and swelling

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18
Q

What does the Monroe-Kellie principle dictate?

A

Intracranial volume is constant

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19
Q

How can volume expansion in the cranial cavity be compensated for?

A

CSF can displace small amount into spinal theca and venous system via arachnoid granules (75ml)
Intracranial blood can redistribute peripherally in a small amount (75ml)

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20
Q

What volume of mass will cause a rapid increase in ICP and what is this called?

A

100-120ml

Critical point

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21
Q

What 2 factors are not involved in compensation as they are fixed?

A
Brain volume (incompressible)
Arterial volume (blood flow to brain is constant)
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22
Q

How does ICP affect cerebral perfusion pressure?

A

Blood moves from high to low pressure

Raised ICP decreases the pressure gradient which normally favours blood flow to the brain

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23
Q

What is cerebral perfusion pressure measurement used for medically?

A

Surrogate marker of blood flow to the brain

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24
Q

What is the formula linking cerebral blood flow, mean arterial pressure and intracranial pressure?

A

CPP = MAP - ICP

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25
Q

How does the brain normally maintain a constant blood flow?

A

Autoregulation of blood flow to brain independent of MAP by altering resistance of cerebral vessels

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26
Q

How is ICP monitored?

A

Neurological observations chart every 15 minutes - GCS, vital signs (pulse, temp), pupil response, motor/sensory response

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27
Q

What are the signs of increasing ICP?

A

Decreasing Glasgow Coma Scale score
Diminished pupil response to light
Lateralising signs

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28
Q

Briefly describe various stages of brain herniation

A
Displacement of cingulate gyrus to opposite side under falx cerebri (asymptomatic/drowsy/confused/weak)
Brain moves downwards; uncus is squashed against midbrain which compresses oculomotor nerve (fixed, dilated pupil and then down and out)
Brainstem compression (coma)
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29
Q

What is the Glasgow coma scale and what are its components?

A

Clinical assessment of consciousness

Check, observe, stimulate and rate the response - eyes, verbal, motor

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30
Q

How are the eyes, verbal and motor components of the GCS scored?

A

Eyes - spontaneous, to sound, to pressure, none
Verbal - orientates, confused, words, sounds, none
Motor - obeys commands, localising, normal flexion, abnormal flexion, extension, none

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31
Q

How is the olfactory nerve tested?

A

With eyes closed and one nostril plugged, ask the patient to identify a familiar smell; test the other nostril with a different smell
Can also just ask the patient if there has been any changes to their sense of smell

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32
Q

How is the optic nerve tested?

A

Visual acuity
Visual fields
Pupil reflexes
Fundoscopy

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33
Q

How are the oculomotor, trochlear and abducens nerves tested?

A

Ask the patient to follow the movement of your finger with their eyes as you trace a letter H in the air in front of them

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34
Q

How is the trigeminal nerve tested?

A

Sensory - ask the patient to close their eyes, touch them lightly in various areas with a cotton wool ball and ask them to let you know when they can feel it
Motor (masseter and temporalis) - place your fingertips on the patient’s temples and then jaw, asking them to clench their teeth each time
Jaw jerk reflex
Corneal reflex

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35
Q

How is the facial nerve tested?

A

Ask the patient to raise their eyebrows, frown, smile and puff out their cheeks as well as asking them to close their eyes tightly and resist your attempts to open them

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36
Q

How is the vestibulocochlear nerve tested?

A

Stand behind the patient and whisper numbers which they should repeat
Hold a ticking watch from a distance and bring it slowly towards the patient until they can hear it
Rinne’s and Weber’s tests for hearing loss

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37
Q

How is Rinne’s test conducted?

A

Place a sounding tuning fork on the patient’s mastoid process and the next to their ear and ask which is louder (ear should be louder)

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38
Q

How is Weber’s test conducted?

A

Place the tuning fork base down on the centre of the patient’s forehead and ask if it is louder in either ear (should be equal)

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39
Q

How is the vestibular portion of the vestibulocochlear nerve tested?

A

Not usually tested in routine cranial nerve exam

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40
Q

How is the glossopharyngeal nerve tested?

A

Gag reflex

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41
Q

How is the vagus nerve tested?

A

Ask the patient to say “aah” and check their uvula for deviation
Normal speech is also indicative of functioning vagus nerve

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42
Q

How is the accessory nerve tested?

A

Ask the patient to turn their head whilst you apply resistance with your hand on their cheek (sternocleidomastoid)
Place your hands on the patient’s shoulders and ask them to shrug while you apply resistance (trapezius)

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43
Q

How is the hypoglossal nerve tested?

A

Ask the patient to stick out their tongue and check for fasiculations, deviation or wasting

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44
Q

What nerve supplies sensory innervation for touch and temperature to the nasal cavity?

A

Trigeminal nerve

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45
Q

What areas of the eye are under parasympathetic control?

A

Constrictor pupillae

Ciliary muscle

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46
Q

What are the afferent and efferent nerves involved in the corneal reflex?

A

Afferent - trigeminal

Efferent - facial

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47
Q

What nerves supply taste innervation to the tongue?

A

Facial nerve anterior 2/3

Glossopharyngeal posterior 1/3

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48
Q

What are the afferent and efferent nerves involved in the gag reflex?

A

Afferent - glossopharyngeal

Efferent - vagus

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49
Q

Where is a berry aneurysm likely to be found?

A

Circle of Willis

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50
Q

What cognitive processes can attention be subdivided into?

A

Arousal
Vigilance
Divided attention
Selective attention

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51
Q

What is an example of a domain-specific cognitive process?

A

Spatial awareness

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52
Q

What is attention?

A

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

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53
Q

What is the result of a breakdown in global attention?

A

Delirium/acute confusional state

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54
Q

What is the result of impaired arousal?

A

Drowsiness

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55
Q

What is the result of impaired vigilance?

A

Impersistence (inability to sustain simple voluntary acts)

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56
Q

What is the result of impaired divided or selective attention?

A

Distractible (easily distracted)

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57
Q

What parts of the brain are involved in inattention/neglect?

A

Prefrontal, parietal and limbic cortex

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58
Q

What part of the brain is involved in drowsiness/delirium/coma?

A

Ascending reticular activating system (ARAS)

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59
Q

What is the ARAS?

A

Ascending reticular activating system - set of connected nuclei in the brain responsible for regulating wakefulness and sleep-wake transitions

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60
Q

What is top-down modulation?

A

Ability to direct attention toward encountered stimuli based on our goals

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61
Q

What is bottom-up modulation?

A

Ability to direct attention based on stimulus characteristics (e.g. novelty or salience)

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62
Q

What cortical areas are involved in top-down modulation?

A

Prefrontal cortex
Parietal cortex
Limbic cortex

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63
Q

What is the limbic system?

A

A complex brain network which controls basic emotions (fear, pleasure, anger) and drives (hunger, sex, dominance, care of offspring)

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64
Q

What are the components of the limbic system?

A

Cingulate gyrus, hippocampus, fornix, amygdala, orbital cortex, prefrontal cortex, mamillary bodies

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65
Q

What brain area is involved in bottom-up regulation?

A

ARAS

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66
Q

What does the ARAS consist of?

A

Brainstem nuclei, thalamic nuclei, cortex

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67
Q

What clinical tests are there for attention?

A

Orientation in time and place
Serial 7s (counting down from 100 in 7s)
Digit span and backwards
Months of the year/days of the week in reverse order
Alternation tasks
Stroop test (saying different coloured words)
Star cancellation test

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68
Q

What are the 2 types of memory?

A

Long-term and immediate/working

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69
Q

What are the 2 types of long-term memory?

A

Explicit/declarative

Implicit/procedural

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70
Q

What are the 2 types of explicit/declarative memory?

A

Episodic and semantic

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71
Q

What are the 2 types of implicit/procedural memory?

A

Motor skills and classical conditioning

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72
Q

What is immediate/working memory?

A

Immediate recall of small amounts of verbal or spatial information

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73
Q

What area of the brain is involved in central executive function of memory?

A

Dorsolateral prefrontal cortex

74
Q

What is episodic memory?

A

A form of explicit/declarative memory

Personally experienced, temporally specific episodes/events

75
Q

What is the circuit of Papez/medial limbic circuit?

A

Neural circuit for the control of emotional expression involving medial temporal lobe (hippocampus, entorhinal cortex) and diencephalon (mamillary bodies, thalamic nuclei)

76
Q

What neural networks/areas are involved in episodic memory?

A

Circuit of Papez

Dorsolateral prefrontal cortex

77
Q

What are acute causes of episodic memory impairment?

A

Pure amnesia - transient global amnesia, transient epileptic amnesia
Mixed deficit - delirium

78
Q

What are the chronic causes of episodic memory impairment?

A

Pure amnesia - hippocampal damage (HSV, Alzheimer’s), diencephalic disease (thalamic stroke, sub-arachnoid haemorrhage)
Mixed deficit - dementia

79
Q

How can episodic memory be tested?

A

Recall of complex verbal information (e.g. recall of stories in the Wechsler Memory scales)
Word-list learning (e.g. California verbal learning test)
Recognition of newly encountered words and faces (Warrington’s recognition memory test)
Recall of geometric figures (e.g. Rey-Osterrieth Figure test)

80
Q

What is semantic memory?

A
A form of explicit/declarative memory
Factual information (general knowledge) and vocabulary
81
Q

What is the proposed anatomy of semantic memory?

A

Information is initially processed via episodic memory systems – after repeated rehearsal gets transferred to semantic storage structures

82
Q

What brain areas are involved in semantic memory?

A

Left hemisphere anterior temporal lobe
Anterior temporal cortex
Angular gyrus

83
Q

What is meant by category-specific semantic memory?

A

Theoretical ‘gradients’ of different semantic processes arranged anatomically
Ventral (visual) to dorsolateral (non-visual)
Posterior (basic objects) to anterior (complex)

84
Q

What can cause semantic memory impairment?

A

Anterior temporal cortical destruction/atrophy - HSV, trauma, tumours

85
Q

What is prosopagnosia and what type of memory is affected?

A

Neurological disorder characterised by the inability to recognise faces
Semantic memory

86
Q

How can semantic memory be tested?

A

Tests of general knowledge and vocabulary (e.g. Wechsler Adult Intelligence Scale)
Fluency (generate exemplars from specific semantic categories e.g. name as many animals as possible in 60 secs)
Object naming to confrontation (e.g. Boston naming test)
Tests of verbal knowledge (e.g. what colour is a banana?)
Person-based tasks (e.g. naming photographs of famous people)

87
Q

What types of memory are available to conscious access and reflection?

A

Episodic and semantic

88
Q

What type of memory is not available to conscious access and reflection?

A

Procedural memory

89
Q

What is procedural memory?

A

Ability to acquire motor skills required to perform certain tasks (e.g. playing a musical instrument)

90
Q

What is Korsakoff’s syndrome?

A

A chronic memory disorder caused by severe deficiency of thiamine

91
Q

What brain areas are involved in procedural memory?

A

Basal ganglia and cerebellum

92
Q

How is procedural memory tested?

A

Cannot be done at bedside

93
Q

What are the components of sensory memory?

A

Iconic (sight)
Echoic (hearing)
Haptic (touching)

94
Q

What are the components of working memory and what are they responsible for?

A

Visual sketchpad - spatial information

Phonological store - words, numbers, melodies

95
Q

What part of the brain is responsible for integrating the visual sketchpad and phonological store information in working memory?

A

Central executive - dorsolateral prefrontal cortex

96
Q

How does the bony palate contribute to the nasal cavity?

A

Floor

97
Q

What is the soft palate made of?

A

Fibrous tissue and skeletal muscle

98
Q

What is the nasal septum made of?

A

Cartilage and bone

99
Q

What type of cartilage is the epiglottis composed of and what colour is it?

A

Elastic

Yellow

100
Q

What are the boundaries of the nasopharynx?

A

From end of nasal septum to end of soft palate

101
Q

What are the divisions of the pharynx in order?

A

Nasopharynx
Oropharynx
Laryngopharynx

102
Q

What are the 2 mucosal folds found in the pharyngeal area and what are they associated with?

A

Palatoglossal and palatopharyngeal folds

Muscles of the same name

103
Q

Where is the palatoglossal fold found?

A

Where the oral cavity becomes the oropharynx

104
Q

Where is the palatopharyngeal fold found?

A

End of soft palate

105
Q

What marks the boundary between the oro and laryngopharynx?

A

Tip of the epiglottis

106
Q

What 2 recesses are found in the pharyngeal area?

A

Piriform fossa and pharyngeal recess

107
Q

What is the clinical importance of the piriform fossa?

A

Shallow area where fish-bones have a propensity to get stuck

108
Q

What is the anatomical position of the piriform fossa?

A

Near inlet to larynx

109
Q

What is the anatomical position of the pharyngeal recess?

A

Passes behind the auditory tube, near the passage of the internal carotid artery

110
Q

What is the pharyngeal recess also known as?

A

Fossa of Rosenmuller

111
Q

Where does the auditory tube open?

A

Side wall of nasopharynx

112
Q

What is the tubal elevation?

A

Raised area around the opening of the auditory tube

113
Q

What is the tubal tonsil?

A

Lymphoid tissue found above and behind the tubal elevation

114
Q

Where is the pharyngeal tonsil and by what name is it commonly referred?

A

Upper back wall of nasopharynx

Adenoid

115
Q

What tonsil is commonly referred to as the adenoid?

A

Pharyngeal tonsil

116
Q

Where is the palatine tonsil?

A

Between palatoglossal and palatopharyngeal folds

117
Q

Which tonsil is visible on opening the mouth and depressing the tongue?

A

Palatine tonsil

118
Q

What is Waldeyer’s ring?

A

Interrupted ring of tonsil tissue near the start of the respiratory tract which provides protection

119
Q

What is glue ear?

A

Chronic otitis media with effusion; result of recurrent throat infection with antibiotic treatment which can lead to hypertrophy of tubal tonsil and subsequent blockage of the auditory tube

120
Q

Which tonsil is implicated in glue ear?

A

Tubal tonsil

121
Q

How do ventilation tubes work in treatment of glue ear?

A

Allows air to enter the inner ear which causes mucus to be resorbed; falls out after a few months

122
Q

What position does the ear need to be in to examine with an auriscope and why?

A

Pinna must be pulled up and back to straighten the external auditory meatus

123
Q

What is the umbo of the tympanic membrane?

A

Concave part

124
Q

What is the cone of light of the tympanic membrane?

A

Light reflection of auriscope

125
Q

What is the pars tensa of the tympanic membrane?

A

Three layered area (skin, fibrous, mucosa) which is most commonly associated with perforations

126
Q

What are the 3 types of fibres in the middle fibrous layer of the pars tensa of the tympanic membrane?

A

Radial
Circular
Parabolic

127
Q

What does the middle fibrous layer of the pars tensa of the tympanic membrane enclose?

A

Handle of malleus

128
Q

What is the pars flaccida of the tympanic membrane?

A

Fragile, two-layered upper region associated with auditory tube dysfunction and cholesteatomas

129
Q

What is a cholesteatoma?

A

An abnormal, non-cancerous skin growth in the middle ear; birth defect or caused by repeated middle ear infections

130
Q

What are ceruminous glands?

A

Specialised apocrine sweat glands located subcutaneously in the external auditory canal, in the outer 1/3; inner secretory cells and outer myoepithelial cells

131
Q

What does the auditory canal connect?

A

Pharynx and middle ear cavity

132
Q

What are the middle ear ossicles?

A

Malleus (hammer)
Incus (anvil)
Stapes (stirrup)

133
Q

Where are the middle ear ossicles located?

A

In the tympanic cavity

134
Q

How is sound amplified in the ear?

A

Tympanic membrane is 20x bigger than the footplate of the stapes bone

135
Q

What holds the footplate of the stapes in place at the fenestra vestibuli?

A

Annular ligament

136
Q

What aspect of the ear can become calcified in old age, leading to hearing loss?

A

Annular ligament

137
Q

In the ear, what is the attic?

A

Area of tympanic cavity above the level of the tympanic membrane

138
Q

What is the mastoid antrum?

A

Air space in the petrous portion of the temporal bone

139
Q

What muscles are present in the ear to stabilise the ossicles and protect the ear?

A

Tensor tympani muscle (supplied by CN 5) and stapedius muscles (CN 7)

140
Q

How are traumatic brain injuries classified?

A

Mild (GCS >12)
Moderate (GCS 9-12)
Severe (GCS <9)

141
Q

What 2 types of head injury are there? Give examples

A

Focal (e.g. scalp, skull, intracranial haemorrhage, brain contusion)
Diffuse - diffuse axonal injury, ischaemia, swelling

142
Q

What blood vessels are most commonly associated with extradural haematomas?

A

Middle meningeal arteries

143
Q

What blood vessels are most commonly associated with subdural haematomas?

A

Bridging veins

144
Q

What brain lobes are most commonly affected by intracranial haematoma?

A

Frontal or temporal

145
Q

Which type of TBI has a lucid interval and rapid deterioration?

A

Extradural haematoma

146
Q

What type of TBI has a gradual deterioration?

A

Subdural haematoma

147
Q

What type of haemorrhage is associated with a contusion?

A

Subarachnoid haemorrhage

148
Q

What is a diffuse axonal injury?

A

Axonal damage due to shear forces on acceleration/deceleration; present in all severities of TBI

149
Q

What brain matter is affected by DAI?

A

White matter of corpus callosum and dorsolateral brainstem

150
Q

How does brain ischaemia occur in TBI?

A

Consequence of raised intracranial pressure, hypoxaemia and reduced cerebral perfusion pressure

151
Q

What is a diffuse vascular injury?

A

Multiple small haemorrhages of the cerebral hemispheres/brain stem resulting in death within minutes of injury

152
Q

What is concussion?

A

Mild traumatic brain injury; a (temporary) disturbance in brain function as a result of trauma

153
Q

What are the symptoms of concussion and when do they appear?

A

Headache, dizziness, memory disturbance, balance problems, ‘seeing stars’
Onset may be delayed

154
Q

What are the risk factors for concussion?

A

History of previous concussion, artificial pitches, gumshield, female sex, helmet/headgear, age <18

155
Q

What is second impact syndrome?

A

Occurs when the brain swells rapidly due to a concussion only minutes/days/weeks after an initial concussion, before symptoms have subsided

156
Q

What is sub-concussion?

A

Hits below the concussion threshold; the brain is shaken, but not so violently that the damage to brain cells is severe enough to see symptoms

157
Q

What is punch-drunk syndrome?

A

Chronic traumatic encephalopathy

A condition seen in boxers and alcoholics, caused by repeated cerebral concussions

158
Q

What are the characteristics of punch-drunk syndrome/chronic traumatic encephalopathy?

A
Weakness in the lower limbs
Unsteadiness of gait
Slowness of muscular movements
Hand tremors
Hesitancy of speech and mental dullness
159
Q

What is the effect of chronic traumatic encephalopathy on the brain?

A

Septal and hypothalamic (cavum septum, fornix and mamillary bodies atrophied)
Cerebellar (tonsillar scarring, reduction in Purkinje cells)
Substantia nigra (loss of pigment)
Neurofibrillary tangles
Amyloid plaques

160
Q

What is declarative memory?

A

Episodic and semantic
Factual information, life events
Available to consciousness, easily formed/forgotten

161
Q

What is non-declarative memory?

A

Procedural
Skills and habits, classical conditioning
Not available to consciousness, less easily formed/forgotten

162
Q

What 2 strategies are involved in the control of voluntary movements?

A

Ballistic/pre-programmed

Pursuit/visual feedback

163
Q

What are ballistic movements? Give an example

A

Movements based largely on a set of pre-programmed instructions
Rapid but at expense of accuracy (little opportunity for compensation for unexpected changes)
E.g. striking a cricket ball, returning a tennis serve

164
Q

What are pursuit movements? Give an example

A

Motor command continually updated according to sensory feedback (e.g. visual)
Highly accurate (can be modified while in progress) but slow
E.g. visual tracking

165
Q

What areas of the cortex are involved in voluntary movement?

A

Area 6 - SMA, PMA
Area 4 - M1
Area 5 and 7 - posterior parietal cortex

166
Q

What types of sensory information are crucial for control of movement?

A

Proprioception - somatic sensory cortex
Vision - eyes, visual system and visual cortex
Vestibular - feedback from organs of balance

167
Q

How does stroke affect movement?

A

Paralysis and loss of sensation on contralateral side to haemorrhage

168
Q

What area of the brain is involved in rehearsal of a movement before it is carried out?

A

Supplementary motor area (SMA)

169
Q

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

A

Basal ganglia and cerebellum

170
Q

What is the function, input and output of the basal ganglia?

A

Function - initiation of movement, planning complex movement
Input - prefrontal cortex
Output - thalamus to premotor area

171
Q

What are the symptoms of Parkinson’s disease?

A

Tremors, hypokinesia, shuffling gate

Progressing to general cognitive decline

172
Q

What are the treatments for Parkinson’s disease?

A

L-DOPA, deep brain stimulation

173
Q

What are the symptoms of Huntington’s disease?

A

Choreas, difficulty speaking and swallowing

Progressing to general cognitive decline

174
Q

What is the function, input and output of the cerebellum (in control of movement)?

A

Function - co-ordination and smooth execution of movements, motor learning, error detection
Input - sensory cortex
Output - thalamus to primary motor cortex

175
Q

What lateral pathways are involved in control of movement?

A

Corticospinal and rubrospinal

Voluntary, distal muscles

176
Q

What ventromedial pathways are involved in control of movement?

A

Tectospinal, vestibulospinal, pontine reticulospinal, medullary reticulospinal
Involuntary, axial muscles, posture

177
Q

What are spinal pattern generators?

A

Intrinsic circuits of the spinal cord which produce rhythmic motorneuron activity for stepping; alternating, co-ordinated activity in flexor and extensor muscles

178
Q

How does the circuit for rhythmic alternating activity work?

A

Two sets of pattern generating neurons project to flexor and extensor motoneurone pools, respectively; reciprocal inhibitory connections between the two sets of pattern generating neurones help to co-ordinate their activity, so that there is alternating excitation of flexors and extensors

179
Q

What comprises a motor unit?

A

A motorneuron and the muscle fibres it innervates

180
Q

What are collections of motoneurons in the ventral horn called?

A

Motonuclei

181
Q

How is strength of muscle contraction graded?

A

By recruitment of motorneurons