Applied Neurosciences Flashcards

1
Q

What tests may be used to assess the Frontal lobe?

A

Similarities:
- Assesses correct categorisation not just similarities between parts

Lexical fluency:
- Category fluency i.e. items bought in a store or animals
- Alphabet fluency i.e. starting with certain letter
- Speed and switching between object set

Cognitive estimates test:
- Uses abstract knowledge

Trial making test:
- Simple type A i.e. 1 - 2 - 3 - 4
- Complex type B i.e. 1 - A
- Good frontal lobe test but as executive however not specific also attention, visuospatial

Luria sequence test:
- Fist - edge - palm
- Requires motor planning, execution and error correction

Others include:
- Alternate pyramids, squares drawing and proverb interpretation
- Frontal release sign and digit span affect too

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2
Q

What are the tests of parietal function?

A

Copying shapes
- Ability to draw or copy a shape (esp. non-dominant parietal)

Identifying fingers:
- Dominant parietal function - Gerstmann syndrome
- May identify finger with eyes closed or copy examiners hand shape i.e. interlocking fingers

Calculation ability:
- Dominant parietal lobe dysfunction included in Gerstmann syndrome
- Ability to use numbers or copy is inact however arithmetic ability is only dominant parietal lobe

Graphesia:
- Ability to recognise what number is scratched onto someones skin without seeing
- Bilateral parietal lobe funciton

Right left disorientation:
- Dominant parietal lobe dysfunction

Stereognosis:
- Ability to recognise an object without seeing
- Bilateral function due to somatosensory cortices

Two point discrimination:
- Bilateral parietal lobe function due to somatosensory cortices

Visual inattention:
- Hemineglect - feature of parietal lesions
- Letter or star cancellation task, bisection line task or draw a tree/person

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3
Q

How may frontal lobe lesions present?

A

Unilateral:
- Contralateral spastic hemiplegia
- Slight elevation of mood, increased talkativeness, tendency to joke inappropriately
- Primitive reflexes e.g. suck and grasp
- Anosmia
- Motor speech disorder with agraphia with or without oro-buccal apraxia

Bilateral:
- Bilateral hemiplegia
- Abulia (loss of drive)
- Spastic bulbar palsy
- Decomposition of gait and sphincter incompetence
- Varying combinations of grasping, sucking, utlisation movements

There are specific frontal syndromes too: pseudo depressive illness, dysexecutive and pseudeopsychopathic

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4
Q

What is a gelastic seizure?

A

Epileptic seizure of left prefrontal cortex that results in uncontrollable laughing

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5
Q

Describe some presentations linked to unilateral and bilateral parietal lobe lesions?

A

Unilateral:
- Contralateral mild hemiparesis
- Gerstmann’s syndrome (dominant): finger agnosia, right-left disorientation, dyscalculia, dysgraphia)
- Neglect of other side
- Homonomous hemianopia or inferior quadrantopia
- Corticosensory syndrome or sensory extinction

Bilateral:
- Spatial disorientation
- Ideomotor and ideational apraxia (more common with left)
- Anosognosia, dressing and contructional apraxia (more frequent and severe with non-dominant right)
- Tactile agnosia (more common with left)
- Balint syndrome (optic ataxia, oculomotor apraxia, and simultagnosia)

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6
Q

Temporal lobe lesions can present with…

A

Unilateral:
- Homonymous upper quandrantopia
- Some degree of amusia and/or visual agnosia
- Dysnomia
- Reduced verbal memory
- Wernicke’s aphasia

Bilateral:
- Auditory, visual, olfactory hallucinations
- Disturbances of time perception
- Dreamy states with uncinate seizures
- Korsakoff amesiac defect
- Apathy and
- Hypermetamorphosia (compulsion to attend to all visual stimuli), also hyperorality, hypersexuality and blunted emotional reactivity (Kluver Bucy syndrome)

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7
Q

What is Geschwind syndrome?

A

Personality change sometimes observed in TLE - may arise from altered white matter tracts

Signs include hypergraphia, hyperreligosity, hyposexuality, circumstantiality and interpersonal viscosity

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8
Q

Name some auras associated with TLE:

A

Autonomic sensations
- Hypersalivation, gustaroy sensations

Evocation of thought:
- Intrusion of stereotypes words or thoughts

Forced thinking:
- Individual thinking to a certain topic

Psychic seizures

Disturbed perception of time:
- Deja Vu

Panoramic memory:
- Recall of expansive memories in detail +++

Uncinate crisis:
- Taste and smell hallucinations with a lot of detail and reminiscent of the past with altered consciousness

Transient dysphasia:
- L hemisphere in origin

Strong affective experiences:
- Fear or anxiety

Dostoveksys epilepsy:
- Ecastatic sensations in epilepsy

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9
Q

What may unilateral occipital lesions present with?

A

Contralateral homonomyous hemianopia (central or peripheral)

Homonomymous hemiachromatopsia

Elementary hallucinations (lights colours and indiscrete objects)

Visual object agnosia

Visual hallucinations

If corpus callosum or splenum affected - alexia and a colour naming defect

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10
Q

How may bilateral occipital lobe lesions present?

A

Cortical blindness (reactive pupil)

Anton syndrome (visual anosognosia and denial of cortical blindness)

Loss of colour perception achromatopsia

Prosopagnosia

Simultanagnosia

Balint syndrome

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11
Q

In Vascular dementia if there is loss of cognitive functioning does a patient retain insight?

A

Usually

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12
Q

Which orientation is first to go in Delirium?

A

Time

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13
Q

Poor performance in the Hayling tests indicates?

A

Inhibition defects

The hayling test an examiner reads out a sentance leaving the last word blank:
- In part 1 subjects finish the sentance
- In part 2 subjects have to say a word unrelated to the sentance

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14
Q

What is alexia without agrahpia?

A

Impaired ability to read however can still write their own thoughts, understand other speech and speak clearly

Normally affects dominant occipital lobe (left) and posterior corpus callousum (splenium) - subjects may also have right homonymous hemianopia

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15
Q

Name some findings associated with lesions in the following areas:

a) Medial frontal circuit and ACC

b) Dorsolateral prefrontal circuit

c) Orbitofrontal and ventromedial circuit

A

a) Disruptions in motivation and willful behaviour
Apathy
Abulia
Akinetic mutism

b) Disturbed executive planning (planning, goal directed behaviour and attention)
Perseverative behaviour
Deficits in academic and general intellectual functioning

c) Acquired psychopathy and deficits in social intelligence
Frustration and anger
Disturbances in social functioning, behavioural regulation

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16
Q

What visual symptom is seen in conversion disorder?

A

Tunnel vision

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17
Q

What is a semantic paraphrasia?

A

A paraphasia is a substitution

  • Semantic means category/meaning therefore may use a different type of fruit
  • Phonetic will be the sound “fort” rather than “fork”
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18
Q

What is Ribots law?

A

That in retrograde amnesia newest memories are first to go, remote memories are the most resistant

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19
Q

What test may be used to differentiate organic coma from a psychogenic one?

A

Caloric testing - injection of cold water into the external auditory canal

Here normal response is for quick phase nystagmus away from injected site - present in psychogenic coma

In organic coma may get tonic deviation of eyes towards the site injected OR no movement at al

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20
Q

What is a vegetative state?

A

Unconscious dissociative state of wakefulness without awareness

Eyes open spontaneously
EEG shows sleep-wake cycles
May have stereotyped gestures independent of normal context (yawn, smiling etc.)
If wakefulness this indicates brainstem is working
If lack of awareness indicates cortical dysfunction

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21
Q

What is Broca’s aphasia?

A

Non-fluent speech and poor repetition but good comprehension (damage to frontal area BA 44 - left inferior frontal convolution)

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22
Q

Where in the brain does the defect for Gerstmann’s syndrome arise from?

A

Dominant (left) angular gyrus

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23
Q

What is an Argyll-Robertson pupil?

A

Defect of pupil such that it does not react to light but constricts when looking at closely held objects (accomodation)

Irregular, small and asymmetric in size

Historically from syphillis but also diabetic neuropathy and cataracts surgery

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24
Q

What are neglect syndromes?

A

Failure to detect visual or tactile stimuli or move limb in contralateral side of body:
- most commonly result from right sided parietal lesions

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25
Q

What is Wallenberg syndrome and its underlying pathology?

A

Occlusion of posterior inferior cerebellar artery (a branch of the vertebral artery) - causes infarction in the lateral portion of the medulla:

  • Dysarthria - damage of ipsilateral palate (CN nerve IX to XI damage)
  • Contralateral anaesthesia of body from ascending spinothalamic tract
  • Ipsilateral facial numbness (damage of CN V nucleus)
  • Horners syndrome (ptosis, meiosis, anhidrosis)
  • Ataxia (inferior cerebellar peduncle damage)
  • Vestibulocochlear nerve damage - ipsilateral ataxia and nystagmus
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26
Q

Poor score in the seashore musical test could indicate damage to which area of the brain?

A

Right temporal lobe

Seashore musical test is where individuals have to say if non-verbal sounds are the same (S) or different (D)

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27
Q

Which domain of the WAIS test is used to cognitive design with aging?

A

Block design

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28
Q

The most common IQ test used in clinical practice is the Wechsler Adult Intelligence scale - what two categories of tests exist and given examples of each?

A

Verbal:
- Similarities NH
- Arithmetic
- Digit span NH
- Vocabulary H
- Information H
- Comprehension

Performance:
- Picture arrangement
- Block design NH
- Picture completion H
- Digit symbol NH
- Matric reasoning

H - held i.e. should not decline with age - these tests may detect organic illness i.e. dementia
NH - non-held tests i.e these tests decline with age

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29
Q

Outline some tests of set-shifting ability (part of executive functioning)?

A

Trail making test B

Wisconsin Card Sorting Test

Hayling test - sentence completion

Brixton Task

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30
Q

What does the stroop test assess and which part of the brain is associated with this neuropsychological function?

A

Response inhibition - frontal lobe

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31
Q

What is the Raven’s progressive matrix?

A

Test if IQ independent of education and cultural influences - uses visuospatial problem-solving tasks to assess performance IQ

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32
Q

What is the national adult reading test?

A

Tests previous word knowledge before becoming ill (reading ability seems to be resistant to brain damage) therefore NART may be a good measure for premorbid IQ

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33
Q

What is the Weschler Memory Scale-Revised?

A

A memory test battery for adults that produces a memory quotient - this is corrected for age and approximates the WAIS IQ.

For memory decline there may be a low MQ but preserved IQ

WMS-R consists of:
- Verbal paired associated
- Paragraph retention
- Visual memory for designs
- Orientation
- Digit span
- Rote recall of alphabet
- Counting backwards

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34
Q

Name a short term visual memory test?

A

The benton visual retention test:
- A geometric figure is presented for 10 seconds after which the patient attempts to draw the figure from memory

35
Q

What is the bender visual motor gestalt test?

A

A test of visuomotor coordination useful for children and adults

36
Q

What two domains make up consciousness and describe the brain regions responsible for each?

A

Wakefulness (arousal) - achieved via Ascending Reticular Activating System (network that connects brainstem, thalamic nuclei, basal forebrain, hypothalamus and areas of the cortex). Here thalamocortical connections produce rhythmical neuronal activity. ARAS via thalami nuclei synchronises the oscillation. How in synch they are correlates to degree of wakefulness

Attention - maintenance of which is achieved by right frontal love

37
Q

What is stupor?

A

State of decreased consciousness - appears asleep but when vigorously stimulated may become alert with eye opening and ocular movement

Caloric testing is used to distinguish between coma stupor and psychiatric. In psychiatric horizontal nystagmus but tonic deviation/no eye movement in true coma

38
Q

What condition may present with akinetic mutism pre death?

A

CJD

Akinetic mutism - sleep/wake cycle with eye opening but patient immobile, reduced vocalisation and generally eye closure. No spasticity or rigidity.

39
Q

How does akinetic mutism differ from vegetative state?

A

Akinetic mutism:
- No spasticity or rigidity
- Damage to anterior cingulate

Vegetative state:
- Spasticity or rigidity
- Occurs from only ARAS and thalamus acting without higher cortex due to severe damage

At the start the two are in distinguishable

40
Q

What is locked in syndrome?

A

There is total paralysis below CN III but intact consciouness,
Patients can only open eyes, elevate and depress.

Caused by :
- Vental pons
- Pontine tumour
- Pontine haemorrhage
- Central pontine myelinolysis
- Head injury
- Brain stem encephalitis

41
Q

Outline some tests of attention

A

Serial 7s - often incorrectly performed. by elderly

Reverse-order month of the year - good measure of sustained attention

Spell WORLD backwards

Digit span - generally 7 (+/- 2 with age or intellectual ability), 5 may be normal for old people. Reverse digit span generally 1 less than forward.

42
Q

What tests may there be reduced digit span?

A

Delirium, focal left frontal damage, aphasia, moderate-severe dementia

Preseved in MTL damage or amnesiac syndromes e.g. Korsakoff’s syndrome

43
Q

What would disorientation to one’s own name indicate?

A

Psychogenic amnesia

44
Q

What is reduplicative paramnesia?

A

Belief that ones surroundings have been duplicated - they have been moved

Commonly seen in delirium

45
Q

What brain region is responsible for executive control?

A

DLPFC using frontal-subcortical connections

46
Q

How does impulsivity arise

A

Impulsivity is a failure of response inhibition - often associated with inferior frontal lobe pathology

47
Q

What is executive functioning and name some associated cognitive tasks?

A

Initiation, sequencing, coordination, error detection error correction, set shifting and termination

Associated with other frontal lobe functions e.g. abstract reasoning, problem solving, impulse control and judgement

48
Q

What are the “where” and “what” streams of visual information?

A

“where” stream - dorsal - links visual information with spatial info and orientation through the parietal lobe

“what” stream - ventral - links visual information with semantic information through the temporal lobe

49
Q

Where in the brain does a lesion affect to cause neglect of left side personal or extrapersonal space?

A

Right parietal or prefrontal areas
- Left sided visuospatial function comes from right hemiphere
- Right sided visuospatial function has bilateral neural correlates

50
Q

Name some tests of dressing apraxia or constructional ataxias?

A

Dressing - put on a piece of clothing that is turned inside out

Constructional - copy a wire cube, interlocking pentagon or clock fae

51
Q

Classify different types of memory:

A

Explicit (declarative):
- Episodic - time-locked personal (hippocampus-diencephalic) memory loss can be anterograde or retrograde
- Semantic - general knowledge of words

Implicit:
- Procedural skills

Working memory - function of few seconds of memory depends upon andexecutive system (attention, DLPFC), visuospatial sketchpad (R hemisphere) and phonological loop (L hemisphere)

Memory can be immediate (seconds), recent (minutes - days), remote (months years)

52
Q

What parts of the brain are associated with the following memory functions

a) Verbal declarative (episodic memory)
b) Non-verbal declarative memory
c) Navigational memory
d) Semantic memory
e) Procedural memory
f) New learning generally
g) Emotional aspects to memory

A

a) Left hippocampus - verbal episodic

b) Right hippocampus - non-verbal episodic

c) Navigational - orientation and animal place code maps are both hippocampus

d) Semantic memory - anterior temporal lobe

e) Procedural memory - striatum, cerebellum, amygdala and neocortex (motor cortex) associated with procedural memory. In Parkinson’s there may in tact declarative but poor procedural due to nigrostrial degeneration

f) Diencephalic structures - dorsal medial nucleus of thalamus and mamillary bodies

g) Amygdala

53
Q

In transient global amnesia how do patients present?

A

Pronounced anterograde amnesia
Variable retrograde amnesia

54
Q

How does semantic dementia present?

A

Loss of vocabulary - use of “thing” etc when speaking
Loss of comprehension

  • The anomia in semantic dementia is progressive
  • Associated with atrophy of the left temporal lobe
55
Q

Dissociative amnesia presents as?

A

Retrograde episodic amnesia of minutes to years that presents from minutes to years

Memories were fully formed but now unavailable

Memories are usually stressful or traumatic

56
Q

What is the function of Broca’s and Wernicke’s area

A

Wernicke’s area (temporal lobe) is responsible for comprehension (together with higher association cortices) - sound is transmitted from the ears

Broca’s area is the higher motor area of language production (signals are transmitted from here to the lips and teeth)

Arcuate fasciculus connects both

57
Q

What areas of the brain are responsible for fluency?

A

Fluency - Broca’s area
Comprehension - Wernicke’s
Repetition - Broca’s, Wernicke’s and Arcuate Fasciculus but not higher association areas

58
Q

How does fluency, repetition, comprehension and naming alter with

a) Broca’s motor aphasia
b) Wernicke’s aphasia (also termed Jargon Aphasia)
c) Conduction aphasia
d) Transcortical sensory aphasia
e) Transcortical motor aphasia

A

a) Broca’s - not fluent, can’t repeat, can comprehend, can’t name. Speech is telegraphic and agrammatical function words (conjunctions, propositions are lost)

b) Wernicke’s - fluent, can’t repeat, cannot comprehend, can’t name. Speech is fluent but highly paraphasia, circumlocutions and neologisms.

c) Transcortical sensory aphasia - fluency and repetition intact, but comprehension and naming lost

d) Transcortical motor aphasia - fluency lost, repetition and comprehension intact, naming lost

59
Q

What is pure word deafness?

A

Can speak, write and read fluently but comprehension is impaired for spoken language only - bilateral damage to superior temporal pole (or left sided with damage to non-dominant circuit impaired)

60
Q

What is pure word blindness?

A

Alexia with no agraphia:
- Speak normally and write on own or to dictation but unable to read (can’t comprehend when reading)
- Damage to Left Posterior Cerebral Artery with damage to poster corpus callosum (splenium) and left visual cortex

61
Q

What is pure word dumbness?

A

Can’t speak but can understand language, read & write

62
Q

What is isolated limb apraxia indicative of?

A

Corticobasal degeneration

63
Q

Outline the brain regions affected in the following different types of apraxia’s

a) Constructional

b) Ideational

c) Ideomotor

d) Limb kinetic

e) Buccofacial

A

a) Constructional - R cerebral hemisphere often parietal lobe (non-dominant)

b) Ideational (unable to follow a correct sequence of actions) - L parietoccipital or L parietotemporal regions

c) Ideomotor - inability to do goal-directed behaviour that have previously been learned e.g. using a hairbrush - they don’t know what to do with it - usually L hemisphere (frontal/parietal and association areas). Unilateral lesions in R handed patients produce bilateral deficits R>L

d) Limb kinetic - dominant frontoparietal or primary motor cortex. Inability to make fine motor actions

e) Buccofacial - inability to carry out mouth or lip movements normally accompanies broca’s aphasia. Lesions of left inferior frontal lobe and the insula.

64
Q

Where is the fusiform gyrus located?

A

Bilateral or right sided lesions of the occipital-temporal junction

Occassionally can happen in L sided lesions in L handed subjects

65
Q

What is

a) Visual object agnosia
b) Apperceptive visual agnosia
c) Associative visual agnosia

A

a) Unable to identify the object despite in tact perception

b) Unable to identify the object by looking but can do if description read aloud or by touch (in tact semantic knowledge) - bilateral occipoto-temporal lesions

c) The semantic knowledge of the lesion is affected due to anterior temporal lobe lesions

66
Q

What is…

a) Achromatopsia

b) Colour agnosia

c) Colour anomia

A

a) Inability to discriminate between colours and is commonly associated with pure alexia - medial occipotemporal dysfunction (left PCA lesion)

b) Inability to retrieve colour information from semantic memory –> left occipito-temporal damage

c) Can’t name a colour –> disconnection between language structures of temporal lobe and visual cortex

67
Q

What is acalculia?

A

Inability to read, write and comprehend numbers. Acalculia differs from anarithmetrica which is the inability to perform simple equations.

Can test acalculia but given numbers via dictation to be copy, read aloud do calculation and explain answer

68
Q

If I say to you

Simultagnosia
Optic ataxia
Oculumotor apraxia

What is the disease and where in the brain is it affected?

A

Balint syndrome
Bilateral pariteooccipital dysfunction - damage to “where” stream linking spacial and visual cortices
Caused by infarction, carbon monoxide poisoning or dementia

69
Q

Cortically blind but deny a problem (anosognosia) what is the disease?

A

Anton’s syndrome - bilateral occipital damage

70
Q

Name some causes of impaired sense of smell?

A

Early stage Parkinson’s or Alzheimer’s
If unilateral suspect meningioma
Head injury

Olfactory fibres are the only not to have thalamic relay

71
Q

Where in the optic pathway is the defect causing:

a) Unilateral one eye blindness
b) Bitemporal hemianopia
c) Homonomous hemianopia
d) Superior quadrantopia
e) Inferior quadrantopia
f) Cortical blindness

A

a) Eye itself - retina or macula
b) Optic chiasma
c) Any retrochiasmatic structure (optic tract, lateral geniculate body or optic radiation)
d) Temporal lobe - Meyer’s loop
e) Parietal lobe
f) Occipital lobe

72
Q

Which nerve is responsible for the pupillary light reflex?

A

CN III

Afferent fibres from optic nerve to Edinger Westphal nuclei (via pretectal nuclei) then efferent fibres to ciliary muscles

73
Q

Name two important pupils that show near-light dissociation (i.e. the converge but pupil does not constrict)

A

Argyll robertson pupil
Holmes Adie pupil (peripheral pupillary defect producing a tonic pupil)

74
Q

How do the cranial nerves exit the skull?

A

I - Cribiform plate
II - Orbital Canal
III - Superior Orbital Fissure
IV - Superior Orbital Fissure
V - V1 SOF
V - V2 Foramen Rotundum
V - V3 - Foramen Ovale
VI - SOF
VII - Internal auditory meatus
VIII - Internal auditory meatus
IX - Jugular foramen
X - Jugular foramen
XI - Jugular foramen
XII - Hypoglossal canal

75
Q

Outline the function of the cranial nerves

A

I - smell

II - sight

III - innervation to medial recti, inferior recti and inferior oblique
- pupil constriction
- eye lid opening
- accommodation

IV - innervation to superior oblique

V - sensation to face
- mastication
- corneal reflex (afferent)
- jaw jerk (afferent and efferent)

VI - innervation of lateral rectus

VII - taste to anterior 2/3 tongue
- muscles of facial expression
- lacrimation
- salivation
- corneal reflex (efferent)

VIII - balance
hearing

IX - salivation
- swallowing (pharyngeal musculture)
- mediates input to carotid and sinus - passes through CN IX to nucleus solitarus an area important for neural control of BP
- gag reflex (afferent)
- taste to posterior 1/3 tongue

X - phonation
- innervation to viscera (smooth muscles of GI tract (upper and tracheobronchal tree)
- gag reflex (efferent)
- swallowing

XI - innervation to accessory muscles

XII - tongue movements

76
Q

What does a lesion of each cranial nerve result in?

A

III - ptosis, down and out pupil, fixed and dilated

IV - vertical diplopia - due to defective downward gaze

V - trigeminal neuralgia, paralysis of muscles of mastication, loss of sensation to face (ipsilateral), deviation of jaw to weak side

VI - horizontal diplopia

VII - loss taste, flaccid paralysis of muscle of face, hyperacusis, loss of corneal reflex

VIII - Hearing loss, nystagmus, vertigo

IX - hypersensitive carotid sinus or loss of gag reflex

X - loss of gag reflex, deviation of uvula away from affected side

XI - weakness of shoulders and neck

XII - tongue deviates towards side of lesion

77
Q

Where do the cranial nerves originate from?

A

CN I Telencephalon

CN II - Diencephalon

CN III - IV: Midbrain

CN V - VIII: Pons

CN IX - XII: Medulla

78
Q

What are some other causes of horizontal homonymous diplopia other than CN VI lesion?

A

Raised ICP

79
Q

What does bell’s palsy result from?

A

A lower motor neurone lesion to CN VII (ipsilateral facial paralysis and inability to close eye)

A UMN lesion to CN VII only sensation to the bottom half of the face is lost and patient can close eye

80
Q

What is the nucleus ambiguous?

A

The cranial nerve nucleus of CN IX and X often indistinguishable in anatomical position

81
Q

What pathophysiological action leads to coma?

A

Brain contusion

Can occur beneath injury (coup) or contralateral (contrecoup)

Contrecoup is most common in orbitofrontal and temporal regions - bilateral temporal injury may cause behaviour dyscontrol syndrome from contrecoup

82
Q

What is DAI

A

Diffuse axonal injury - can happen to neurons after trauma

83
Q

Where may a head injury occur to cause personality changes?

A

Orbitofrontal cortex or temporal lobes

84
Q

What is post concussion syndrome?

A

headache; dizziness; insomnia; irritability; emotional lability; increased sensitivity to noise, light, etc.; fatigue; poor concentration; anxiety;
and depression.