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BRS 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

Gyri vs sulci?

A

Gyri are ridges/folds

Sulci are grooves

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2
Q

What is the microscopic organisation of the cerebral cortex?

A

Layers and columns

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3
Q

What is the basis of cytoarchitecture?

A

cell size
spacing/packing density
layers

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4
Q

Functions of the frontal lobe?

A 
Motor function 
Language motor aspects
Cognitive functions eg planning
atttention
memory
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5
Q

Parietal lobe functions?

A

Sensations
Language sensory aspects
Spatial orientation
Self perception

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6
Q

Occipital lobe function?

A

Processing visual info

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7
Q

Temporal lobe function?

A

Auditorty processing
emotions
memories

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8
Q

What structures make up the limbic lobe?

A

Mamillary body
Amygdala
Cingulate gyrus
Hippocampus

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9
Q

What are the functions of the limbic lobe?

A

Learning
memory
emotion
motivation and reward

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10
Q

where is the insular cortex found?

A

deep in lateral fissure

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11
Q

What are the functions of the insular cortex?

A 
Visceral sensations
Autonomic control
Interoception
Auditory processing
Visual-vestibular integration
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12
Q

Describe the internal structure of the cerebral cortex

A

grey matter - neuronal cell bodies and glial cells

white matter - myelinated neuronal axons in tracts

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13
Q

What are the three types of fibres in white matter tracts?

A

Association
Commissural
Projection

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14
Q

What do association fibres connect?

A

connect areas in same hemisphere

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15
Q

What do commissural fibres connect?

A

connect homologous structures in left and right hemispheres

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16
Q

What do projection fibres connect?

A

connect cortex with lower brain strcutures

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17
Q

what are the 4 association fibres? what do they connect?

A

superior longitudinal fasciculus - frontal → occipital
arcuate fasciculus - frontal → temporal
inferior longitudinal fasciculus - temporal → occipital
uncinate fasciculus - anterior frontal → temporal

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18
Q

What are the three types of projection fibres?

A

afferent - towards cortex
efferent - away from crotec
corona radiata - deeper to cortex

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19
Q

Where do projection fibres converge?

A

through internal capsule between thalamus and basal ganglia

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20
Q

What are three differences between primary and secondary/association cortices?

A

Primary : have predictable functions, organised topographically, left and right symmetry

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21
Q

What are the three frontal lobe motor areas?

A

primary
supplementary
premotor

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22
Q

What are the functions of the primary motor cortex?

A

controls fine, discrete, voluntary movements

descending signals

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23
Q

What are the functions of the supplementary and premotor area?

A

Planning complex movements
s - internally cued
pm - externally cued

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24
Q

What are the two parietal lobe areas?

A

primary somatosensory

somatosensory assoication

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25
Q

What are the functions of the primary somatosensory cortex?

A

process somatic sensations from body receptors

eg. touch, vibration, pain, temp, etc.

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26
Q

What are the functions of the somatosensory association?

A

interpret significance of sensory information

self awareness and of personal space

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27
Q

two areas of the occipital lobe and their functions?

A

primary visual cortex - process visual stimuli

visual association - interpretation and meaning of visual input

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28
Q

two areas of the temporal lobe and their functions?

A

primary auditory cortex - process auditory stimuli

auditory association - interpretation and meaning of auditory input

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29
Q

functions of the prefrontal cortex?

A 
attention
social behaviour
planning
personality
decision making
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30
Q

functions of Brocas area?

A

production of language

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31
Q

function of wernickes area?

A

understanding language

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32
Q

what would you observe in a frontal lobe lesion?

A

personality change

inappropriate behaviour

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33
Q

what would you observe in a parietal lobe lesion?

A

contralateral neglect i.e. lack of awareness of self and extraperosnal space on opposite side

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34
Q

what would you observe in a temporal lobe lesion?

A

agnosia

anterograde amnesia

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35
Q

what is agnosia?

A

inability to recognise objects

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36
Q

what is anterograde amnesia?

A

cannot form new memories

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37
Q

what would you observe in a lesion to broca’s area?

A

expressive aphasia - slurred speech but able to understand speech

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38
Q

what would you observe in a lesion to wernicke’s area?

A

receptive aphasia - can speak but cannot comprehend speech

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39
Q

what would you observe in a primary visual cortex lesion?

A

blindness in corresponding visual field

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40
Q

what would you observe in a visual association lesion?

A

prosopagnosia (face blindness)

unable to interpret visual information

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41
Q

two types of imaging to assess cortical function?

A

PET - positron emission tomography

fMRI - functional magnetic resonance imaging

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42
Q

what does PET look at?

A

Blood flow directly to brain region (take up of glucose using radioactive isotope)
More glucose uptake = more brain activity

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43
Q

what does fMRI look at?

A

the amount of blood oxygen in a brain region

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44
Q

What can you use to measure evoked/event-related potentials?

A

EEG

MEG

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45
Q

two methods of brain stimulation?

A

transcranial magnetic stimulation (TMS)

transcranial direct current stimulation (tDCS) to increase or decrease neuronal firing rates

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46
Q

two types of imaging to assess cortical structure?

A

diffusion tensor imaging (DTI) based on diffusion of water molecules
DTI with tractography to assess neuronal tracts

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47
Q

Where in the skull is the ear found? How is this beneficial?

A

The petrous part of the temporal bone. It’s v hard so provides the necessary protection

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48
Q

name 3 functions of the outer ear?

A

to capture sound and direct it to the tympanic membrane
to amplify sound via resonance
protection via hairs and wax

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49
Q

How does the middle ear amplify sound?

A

vibrations move from the tympanic membrane w a large surface area to the oval window (smaller sa) via the ossicles → sound pressure increases and it is amplified

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50
Q

name the 3 ossicles?

A

malleus
stapes
incus

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51
Q

why does sound need to be amplified in the middle ear?

A

bc the sound waves are moving from air in the middle ear to fluid in the inner ear where it is more difficult for sound waves to travel

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52
Q

what is the function of the cochlea?

A

to transduce sound waves to electrical impulses that can be interpreted by the brain
allows pitch and volume to be analysed

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53
Q

describe the structural components of the cochlea

A 
scala vestibuli (contains perilymph)
scala media (contains endolymph)
basilar membrane
organ of cortisol
scala tympani
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54
Q

how is the basilar membrane arranged? what does this mean?

A

Tonotopically (think xylophone)
narrow and thicker at the base compared to the apex
means the base can receive higher frequencies and thE apex lower ones

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55
Q

what cells does the organ of corti contain and how are they arranged? functions?

A

Inner hair cells - one column (fewer), sound transduction

outer hair cells - three columns, modulate sensitivity, amplify sound

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56
Q

what are the hair cells connected to?

A

tectorial membrane (only OHC in constant contact)

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57
Q

what are the hairs on hair cells called?

A

sterocillia

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58
Q

how do the Scala vestibuli and the Scala tympani communicate?

A

helicotrema

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59
Q

explain how sound is transduced?

A

sound travels through perilymph of scala vestibule and scala tympani
causes basilar membrane to vibrate → tectorial membrane is pushed against hair cells → stereo cilia are deflected → potassium channels open → potassium from endolymph enters hair cell → cell depolarises → calcium enters through VGCCs → glutamate vesicle exocytosis → glutamate to afferent nerve → auditory cortex

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60
Q

what happens in transduction of louder sounds?

A

theres more deflection of steroecilia and more potassium channels open leading to greater depolarisation

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61
Q

describe the auditory neural pathway

A

nerves from hair cells → spiral ganglia → vestibulocochlear nerve → ipsilateral cochlear nuclei → superior olive in brainstem (bilateral) → inferior colliculus → medial geniculate body → auditory cortex

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62
Q

human range of hearing?

A

20 - 20000 Hz

0 - 120 dB

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63
Q

Which frequencies are affected first

A

higher frequencies

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64
Q

what is a tuning fork used for?

A

to establish the probable presence or absence of hearing loss with a significant conductive component

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65
Q

what are the two tuning forks tests?

A 
weber test (over the head)
rinne test (next to ear)
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66
Q

what is pure tone audiometry?

A

science of measuring acuity for variations in sound intensity and frequency

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67
Q

what device is used in PTA? how are results measured?

A

audiometer

audiogram

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68
Q

What does the central processing assessment assess?

A

Hearing abilities other than section

Verbal and non-verbal testing

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69
Q

What is tympanometry?

A

testing the condition of the middle ear and the mobility of the tympanic membrane and the ossicles
does this by creating varying pressures in the ear canal

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70
Q

What are otoacoustic emissions?

A

low intensity sounds produced by outer hair cells in the cochlea when they expand and contract

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71
Q

When are OAEs measured?

A

Newborn hearing screening

Hearing loss monitoring

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72
Q

3 methods of measuring auditory evoked potentials?

A

Electrocochleography (cochlea and CN8) 0.2-4.0ms
auditory brainstem response (CN8 and brainstem nuclei and tracts) 1.5.10ms
late responses (primary auditory and association cortex) 80-500ms

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73
Q

Benefits of auditory brainstem response?

A

objective
patients doesn’t need to pay attention
most commonly used in clinics

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74
Q

when are cortical potentials useful?

A

In neurological conditions or processing problems

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75
Q

name and describe the 3 types of hearing loss

A

conductive - outer or middle ear problem
sensorineural - inner ear or auditory nerve
mixed - conduction and transduction are affected

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76
Q

causes of conductive hearing loss?

A

outer ear - foreign body or wax buildup (cerumen impaction)

middle ear - otitis or otosclerosis

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77
Q

causes of sensioneural hearing loss?

A

inner ear - presbycusis or ototoxicity

nerve - CN8 tumour

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78
Q

what is presybycutis?

A

loss of outer hair cells, occurs with age

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79
Q

4 types of hearing loss treatment?

A

Underlying cause (eg. remove earwax)
Cochlear implant
Hearing aids
brainstem implant

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80
Q

How do hearing aids work?

A

amplify sound

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81
Q

How does the cochlea implant work?

A

Replaces hair cells → receives and analyses sound → transforms it to electrical signals → auditory nerve
(requires functional nerve)

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82
Q

When can a brainstem implant be used?

A

When auditory nerves are damaged
electrical signals sent directly to electrodes in brainstem
very risky

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83
Q

what are the 3 inputs of the vestibular system?

A

visual
proprioceptive
vestibular

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84
Q

vestibular system outputs?

A

reflexes to help maintain posture and a stable gaze

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85
Q

where is the vestibular system found?

A

in the posterior region of the inner ear

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86
Q

what does the vestibule consist of?

A

three semicircular canals - anterior , lateral and posterior

all 3 connected (via ampullae) to utricle which is joined to the saccule by a conduit

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87
Q

What are the hairs on vestibular hair cells called?

A

Stereocillia and kinocilium ( the biggest cilia)

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88
Q

When are vestibular cells depolarised?

A

when endolymph is moved via head movement

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89
Q

what are the otolith organs? what do they consist of?

A

utricle and saccule

carbonate crystals that help deflect hairs

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90
Q

what are the maculae? how do they differ in the utricle and the saccule?

A

hair cells → gelatinous metric → otoliths
saccule is placed vertically
utricule is placed horizontally

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91
Q

outline the structure and contents of the semicircular canals

A

canal contains potassium rich endolymph
ends in ampulla which opens into utricle
ampulla has crista where hair cells are found
hair cells are surrounded by the cupula

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92
Q

what is the function of the cupula?

A

helps movement of hair cells in ampulla of semicircular canals

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93
Q

where do primary vestibular afferents end?

A

vestibular nuclei

cerebellum

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94
Q

where do vestibular nuclei project to? (4)

A

spinal cord
extraocular muscle nuclei
cerebellum
CV and respiratory control centres

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95
Q

where is the main vestibular cortex found?

A

parietal lobe as parieto-insular vestibular cortex

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96
Q

3 main functions of the vestibular system?

A

control posture
detect and inform about head movements
keep images fixed during movement

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97
Q

why do neurons still fire at the resting potential of hair cells? what do you call this discharge?

A

Because there is the force of gravity and information that you are stationary is still being processes
Required to keep you upright
Basal discharge

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98
Q

what are the three hair cell potentials in the vestibular system and how are they generated?

A

Resting - always there
Excitaion - occurs when sterocilia move towards the kinocilium → depolarisation → ↑ nerve discharge
Inhibitoin - stereo cilia move away from kinocilium → hyperpolarization → ↓ nerve discharge

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99
Q

What do the otolith organs detect?

A

Tilt and linear acceleration
utricule - horizontal movement
saccule - vertical movement

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100
Q

What does the semilunar canals detect? And how?

A

angular acceleration

endolymph flow moves the cupula which then moves hair cells

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101
Q

how do opposite semicircular canals work?

A

lateral work together

anterior of one side works with posterior of opposite side

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102
Q

what are the two main vestibular reflexes?

A

vestibul-ocular reflex

vestibule-spinal reflex

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103
Q

Describe the VOR and how it works?

A

connects the vestibular and oculomotor nuclei
keeps images fixed in the retina
the eyes move in the opposite direction to the head but at the same velocity and amplitude

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104
Q

Describe the VSR and how it works?

A

from vestibular nuclei:
motor neurones to the limbs via the lateral tract
motor neurons to the neck and back via the medial tract
controls posture and prevents you from falling

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105
Q

what 7 things are considered in vestibular assessment?

A 
anamnesis (history)
posture & gait
cerebellar function
eye movements
vestibular tests
imaging
symptoms & impact assessment
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106
Q

what are the main symptoms of a balance disorder?

A

vertigo (objects spinning)

dizziness

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107
Q

2 main types of balance disorders?

A

peripheral & central vestibular disorders

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108
Q

give 4 examples of peripheral vestibular disorders

A 
vestibular neuritis (acute)
benign paroxysmal positional vertigo (intermittent)  
Meniers disease (recurrent)
unilateral and bilateral vestibular hypofunction
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109
Q

explain bppv

A

benign paroxysmal positional vertigo
crystals detach from gelatinous matrix in the utricle which move to the ampulla of the canals and put extra pressure on the cupula making you feel dizzy

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110
Q

give 3 examples of what can cause central vestibular disorders

A

stroke (acute)
MS (progresive)
tumour eg schwanoma (progressive)

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111
Q

differentials for dizziness? (7)

A 
heart disorders 
orthostatic hypotension
presyncopal episodes
psychological
gait problems
anaemia
hypoglycaemia
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112
Q

What can have ‘modest symptomatic benefit’ in the early stages of dementia?

A

Acetylcholinesterase inhibitors

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113
Q

Name 4 common differentials for dementia

A

Depression
alcohol related brain damage
vitamin b1/6/12 deficiency
endocrine disorders

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114
Q

define preclinical dementia?

A

there is deterioration in neurological cells but no clinical symptoms yet

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115
Q

risk factors for dementia? (7)

A 
ageing
oral health
brain trauma
genetics
mid-life obesity
↓ physical activity
infections/ systemic inflammation
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116
Q

define dementia

A

severe loss of memory and other cognitive abilities which lead to impaired daily functions

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117
Q

what 3 examinations can you carry out if you suspect dementia?

A

neurological (i.e. testing cranial nerves)
mini mental state exam
addenbrookes cognitive exam

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118
Q

what would you see on an MRI where the patient has dementia?

A

dilated ventricles
atrophied hippocampus
wider sulci and narrower gyri

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119
Q

what 2 proteins present in the brain are associated with AD?

A

B amyloid

tau

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120
Q

what is the management of dementia? (5)

A

acetlycholintesterase inhibitors
treat behavioural and psychological symptoms eg. w/ antidepressants and antipsychotics
monitor progression
occupational therapy/social services

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121
Q

2 defining features of vascular dementia?

A

associated w/ cerebrovascular diseases

step wise deterioration

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122
Q

3 features of Lewy body dementia?

A

parkinsonian features
fluctuating cognition
visual hallucinations

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123
Q

2 features of FTD?

A

behavioural changes

progressive non-fluent aphasia

124
Q

what is the head-turning sign in dementia patients?

A

they turn to partner/relative because they are unsure/don’t know the answer

125
Q

what protein is associated with Lewy body dementia?

A

a-synuclein

126
Q

outline the production. of tears?

A

parasympathetic efferent nerves use Ach
tears produced by lacrimal gland, drain through 2 punch into superior and inferior canaliculi into tear sac and exit via tear duct into nasal cavity

127
Q

what is the function of the tear film?

A

maintains smooth cornea air surface
oxygen supply to cornea
removes debris
bactericide

128
Q

what’s the structure of the tear film?

A

3 layers
superficial lipid layer - reduce tear film evaporation
aqueos layer
mutinous layer on corneal surface - surface wetting

129
Q

what is the conjunctiva?

A

thin. transparent tissue that covers outer surface of eye (starts at cornea, covers visible eye and inside of eyelids)
nourished by tiny blood vessels

130
Q

what are the 3 layers of the eye? (outer to inner)

A

sclera
choroid
retina

131
Q

what is the sclera?

A

outer coat of the eye, protective

high water content

132
Q

what is the cornea? structure and function?

A

transparent
low water content
powerful refracting surface - 2/3 eye focusing power

5 layers:
epithelium
bowman membrane
stroma
descemets membrane
endothelium
133
Q

what is the uvea?

A

vascular coat of eyeball
between sclera and retina
iris, ciliary body and choroid

134
Q

what is the iris? function?

A

controls light levels inside eye
opening in centre → pupil
has tiny muscles which dilate/constrict pupil

135
Q

structure and function of the lens?

A

outer acellular capsule
regular inner elongated fibres - transparency
refractive power - 1/3 of eyes focusing power
accommodation
elasticity

136
Q

what happens when lenses lose transparency?

A

cataracts form

137
Q

function of the retina?

A

capturing light rays that enter the eye

138
Q

structure and function of the optic nerve?

A

electrical impulses from retina to brain
connects to eye near macula
visible part = optic disc

139
Q

what is the blind spot?

A

where optic nerve meets retina - no light sensitive cells

optic disc

140
Q

structure and function of the macula?

A

centre if retina, temporal to optic nerve
responsible for detailed central vision eg. reading
fovea is the centre of macula

141
Q

what is the proportion of cell types at the fovea?

A

highest concentration of cones, low of rods

142
Q

how is central vision assessed? what is loss called?

A

visual acuity assessment

loss of foveal vision = poor visual acuity

143
Q

how is peripheral vision assessed? what does loss lead to?

A

visual field assessment

loss of visual field = unable to navigate

144
Q

what is the structure of the retina?

A

outer - photoreceptors detect light
middle - bipolar cells, local signal processing
inner - retinal ganglion cells , transmit from eye to brain

145
Q

2 types of photoreceptors and differences?

A

rod cells - more sensitive to light (more pigment, higher spatial and temporal summation) , slow response, night/scotopic vision, more numerous, peripheral

cone cells - faster response, fine & colour vision (photopic), central

146
Q

different cone cell types and colours?

A

S - blue
M - green
L - red

147
Q

what is the commonest form of colour blindness?

A

deuteranomaly - don’t perceive the colour red

148
Q

what is full colour blindness called?

A

achromatopsia

149
Q

what test can be used for red green colour blindness?

A

Ishihara test

150
Q

what is emmetropia?

A

adequate correlation between axial length and refractive power, parallel light rays fall on retina
(normal)

151
Q

what is ametropia?

A

mismatch between axial length and refractive power

parallel rays don’t fall in retina

152
Q

types of ametropia?

A

hyperopia
myopia
astigmatism
presbyopia

153
Q

what is myopia? symptoms? causes?

A

parallel rays converge anterior to retina (near sightedness)
blurred distance vision → squint → headache
excessive long globe (axial myopia)
excessive refractive power (refractive myopia)

154
Q

treatment for myopia?

A

diverging lenses
contact lenses
remove eye lens to reduce refractive power

155
Q

what is hyperopia? symptoms? causes?

A

parallel rays converge at a point posterior to the retina (far sightedness)
blurred near vision, can be intermittent, worse when tired
eyepian, headache, burning sensation
excessive short globe (axial hyperopia)
insufficient refractive power (refractive hyperopia)

156
Q

what can uncorrected hyperopia leas to?

A

amblyopia (lazy eye)

157
Q

treatment for hyperopia?

A

converging lenses ± cataract extraction
contact lenses
intraocular lenses

158
Q

what is astigmatism? cause? symptoms?

A

paralle rays focus in 2 lines
hereditary
refractive media is not spherical
headache, eyepain, blurred distorted vision, head tilting/turning

159
Q

treatment for astigmatism?

A

regular :
cylinder lenses ± spherical lenses
surgery

irregular:
rigid cylinder lenses
surgery

160
Q

what is the near response triad?

A

adaptation for near vision
pupillary miosis (constriction) with sphincter pupillae to increase depth of field
convergence with medial recti
accommodation with circular cillary muscles contracting → ↑ refractive power (lens thickens)

161
Q

what is presbyopia?how is it corrected?

A

naturally occurring loss of accommodation
onset ≥40yrs
distant vision fine
corrected w reading glasses (convex lens) to ↑ refractive power

162
Q

what are the types of optical correction?

A

contact lenses
intraocular lenses
surgical - keratorefractive or intraocular

163
Q

what is the visual pathway from the eye to the visual cortex?

A

eye (1st&2nd order) → optic nerve (3rd order) → optic chiasm (half fibres cross) → optic tract → lateral geniculate nucleus (fibres synapse) → optic radiation (4th order) → primary visual cortex in occipital lobe

164
Q

which fibres cross in the optic chiasma?

A

those from nasal retina - temporal visual field

165
Q

what visual field defects occur if theres a lesion anterior to the optic chiasm? eg. optic nerve compression

A

only one eye affected - whole visual field affected

166
Q

what visual field defects occur if theres a lesion at the optic chiasm? eg. pituitary tumour

A

damages crossed fibres (nasal retinal fibres)

→ bitemporal hemianopia

167
Q

what visual field defects occur if theres a lesion posterior to the optic chiasm? eg right sided stroke

A

affects right temporal fibres and left nasal fibres → left homonymous hemianopia (right temporal and left nasal fields affected)

168
Q

how does homonymous hemianopia with macular sparing occur?

A

stroke affecting primary visual cortex

maculae receive blood supply from posterior cerebral arteries on both sides

169
Q

what happens to the pupil when exposed to light? how is it mediated?

A

constriction (miosis) mediated by parasympthateic nerve in CN III → circular muscles contract
decreases glare
increases depth of field
reduces bleaching of photopigments

170
Q

what happens to the pupil when exposed to dark? how is it mediated?

A

pupillary dilation mediated by sympathetic nerves → radial muscles contract
↑ light sensitivity → more light can enter eye

171
Q

what is the pathway of the pupillary reflex?

A

rod& cone photoreceptors → bipolar cells → retinal ganglion cells → optic tract → lateral geniculate nucleus → edinger-westphal nuclei → occulmotor nerve efferent → ciliary ganglion → short posterior cilliary nerve → pupillary sphincter

172
Q

direct vs consensual reflex?

A 
direct = constriction of pupil of the light stimulated eye
consensual = constriction  of pupil of the other eye
173
Q

afferent vs efferent defects and affects in eye?

A

afferent defect eg damage to optic nerve → no constrcition of either pupil when damaged side is stimulated with light, normal contraction in both eyes when other side is stimulated

efferent defect eg. CNIII lesion, no constriction on affected side no matter which side is stimulated. unaffected side will constrict regardless

174
Q

how can a relative afferent pupillary defect be tested for?

A

swinging torch test

175
Q

2 different types of eye movement?

A

saccade - short fast burst

smooth pursuit - slow movement

176
Q

different types of saccade?

A

reflexive
scanning
predictive
memory guided

177
Q

what direction does the superior oblique move the eye?

A

down and out

trochlear nerve

178
Q

what direction does the inferior oblique move the eye?

A

up and out

179
Q

what is levoversion and dextroversion?

A

levo - eyes both move to left, left abduction, right adduction
dextro - eyes both move right

180
Q

symptoms of third nerve palsy?

A

occulmotor affcvetd → superior, inferior, medial rect & inferior oblique
eye is down and out (unopposed superior oblique and lateral rectus)
droopy eye lid (levator palpabrae superioris)

181
Q

symptoms of sixth nerve palsy?

A

eye cannot abduct (no lateral rectus) → deviates inwards

double vision

182
Q

what is the optokinetic nystagmus reflex?

A

useful in testing visual acuity in preverbal children

smooth pursuit & fast phase reset saccade

183
Q

what happens when theres damage to the posterior colliery ganglion? what is it known as?

A

tonically dilated pupil - Adie’s pupil

parasympathetic fibres have no effect

184
Q

what is pilocarpine?

A

muscarinic receptor agonist on M3 receptors in iris sphincter muscle → miosis
(independent of parasympathetic nerves)

185
Q

explain Adie’s pupil?

A

light-near dissociation
damage to posterior cilliary ganglion → ↑ regulation of postsynaptic receptors in iris instead of ciliary body → more meiosis with accommodation than with light

186
Q

manoeuvres for BPPV?

A

epley and semont manouvers

187
Q

3 main blood supply arteries to the brain?

A

vertebral artery

internal and common carotids

188
Q

circle of willis?

A

vertebral arteries → basillar artery → posterior cereal → posterior communicating → middle cereal & internal carotid → anterior cerebral →anterior communicating

189
Q

4 types of brain haemorrhage?

A

extra dural - arterial, trauma esp @ pterion
subdural - venous, trauma
subarachnoid - circle of willis, ruptured aneurysm
intracerebral - spontaneous hypertensive

190
Q

what is a cerebrovascular accident?

A

rapidly developing focal disturbance of brain function of presumed vascular origin and go ≥24hrs

thromboembolic or haemorrhagic

191
Q

how does a TIA differ from a CVA?

A

it resolves completely within 24 hours

192
Q

infraction vs ischaemia?

A

degenerative changes in tissue following artery occlusion vs

lack of sufficient blood flow → permanent damage if blood flow not restored

193
Q

5 risk factors for stroke?

A 
age
smoking
hypertension
cardiac disease
diabetes
194
Q

symptoms of an anterior cerebral artery stroke?

A

paralysis of contralateral structures
abulia → disturbance of intellect, judgement
loss os appropriate social behaviour

195
Q

symptoms of middle cerebral artery stroke?

A

contralateral hemiplegia
contralateral hemisensory defects
hemianopia
aphasia if L sided lesion

196
Q

symptoms of posterior cerebral artery stroke?

A 
homonymous hemianopia
visual agnosia (cannot recognise objects)
197
Q

why can you get a headache with a subdural bleed?

A

build up of intracranial pressure

198
Q

sy,tpoms of a cerebellar lesion?

A

wobbly eye movements
ataxia
broad hesitant gait
slurred speech

199
Q

what are the major motor descending tracts?

A

pyramidal : (pass though medulla pyramids), voluntary, motor cortex to spinal cord
corticospinal
corticobulvar

extrapyramidal: involuntary, brainstem nuclei to spinal cod
vestibulospinal
reticulspinal
tectospinal
rubrospinal
200
Q

function of the primary motor cortex?

A

precentral gyrus

fine, discrete, precise voluntary movements

201
Q

function of the premotor area?

A

anterior to primary motor cortex
planning movements
regulates externally cued movements

202
Q

function of supplementary motor area?

A

anteriomedial to primary motor cortex
planning complex movemnts, internally cued
active prior to voluntary movement

203
Q

difference between anterior and lateral corticospinal tracts?

A

anterior - trunk, decussate in spinal cord

lateral - limbs, decussates at medulla

204
Q

function of the vestibulospinal tract?

A

stabilise head
coordinate head and eye movements
postural adjustments

205
Q

function of the reticulospinal tract?

A

from medulla and pons
changes in muscle tone
postural stability

206
Q

function of the tectospinal tract?

A

superior colliculis to midbrain

orientation of head and neck during eye movements

207
Q

function of the rubrospinal tract?

A

from red nucelus of midbrain

innervate LMNs of flexors of upper limb

208
Q

signs of an UMN lesion?

A

negative :
loss of voluntary motor function - paresis or paralysis

positive :
loss of inhibitory descending inputs
spasticity
hyperreflexia 
clonus
babinskis sign
209
Q

what is apraxia? lesion? causes?

A

disorder of skilled movement
lesion in SMA/premotor cortex
stroke and dementia

210
Q

signs of an LMN lesion?

A 
weakness
hypotonia
hyporeflxia
muscle atrophy 
fasiculations - visible twitches 
fibrillations - can be seen on EMG
211
Q

signs of motor neurone disease?

A

same as UMN and LMN signs
dysphagia
dysarthria
nasal speech

212
Q

MND alternative name?

A

ALS - amyotrophic lateral sclerosis

213
Q

what are the basal ganglia?

A 
caudate nucleus 
lentiform nucleus (putamen and external globus pallidus)
nucleus accumbens
sub thalamic nuclei
substantia nigra
214
Q

what does the striatum consist of?

A

caudate and putamen

215
Q

function of the basal ganglia?

A

decision to move
elaborating associated movements
moderating and coordinating movements
performing movements in order

216
Q

pathophysiology of Parkinson’s?

A

degeneration of the dopaminergic neurons that originate in the substantial nigra and project to the striatum

217
Q

signs of parkinsons?

A 
bradykinesia
hypomimc face
akinesia
rigidity 
tremor at rest
218
Q

pathophysiology of Huntington’s disease?

A

degeneration of GABAergic neurons in striatum

genetic, chromosome 4, autosomal dominant, CAG repeat

219
Q

signs of Huntington’s?

A 
choreic movements
rapid jerky involuntary movements 
speech impairment
dysphagia
unsteady gait
cognitive decline→ dementia
220
Q

what is ballism?

A

from stroke affecting sub thalamic nucleus
sudden uncontrolled flinging of extremities
contralateral symptoms

221
Q

what separates cerebrum from cerebellum?

A

tentorium cerebelli

222
Q

vestibulocerebellum function?

A

regulates gait and posture
coordinates head and eye movements

damage = gait ataxia

223
Q

spinocerbellum function?

A

coordinate speech and limb movements
adjust muscle tone

damage = legs , abnormal gait and stance - usually caused by chronic alcoholism

224
Q

cerebrocerebellum function?

A

coordinate skilled movements
cognitive function, attention, language processing, emotion control

damage = arms, tremor and speech

225
Q

signs of cerebellar dysfunction?

A 
ataxia
dysmetria
intention tremor
dysdiadokinesia
scanning speech
226
Q

what are the alpha motor neurons?

A

LMNs of the brainstem and spinal cord
innervate extrafusal muscles
activation = contraction

227
Q

define motor unit

A

all the muscle fibres innervated by a single motor neon , smallest functional unit able ton produce force

228
Q

types of motor unit?

A

slow (I)
fast fatigue resistant (IIA)
fast fatiguable (IIB)

(cell bodies, dendritic trees, conduction velocity, thickness)

229
Q

how are the motor unit types classified?

A

amount of tension
fatiguability
speed of contraction

230
Q

how is muscle force regulated?

A

recruitment - size principle, smaller units recruited first, allows fine control
rate coding - sloe units with lower frequencies recruited first

231
Q

what are neurotrophic factors?

A

growth factor
prevent neuronal death
promote neuronal growth after injury

232
Q

what do motor unit characteristics depend on? how is it known?

A

on the nerve fibres that innervate them

cross innervation → muscle fibres changes characteristics

233
Q

when do fibres Tina`ge from IIB to IIa?

A

after training

234
Q

when do fibres change from I to II?

A

severe deconditioning /spinal coed injury

microgravity

235
Q

why do contraction times get slower with age?

A

loss of type I and II fibres but II lost in greater proportion

236
Q

what manoeuvre can be used to make reflexes larger?

A

jendrassik → reduces amount of inhibition CNS exerts on reflexes

237
Q

what happens in decerebration? re reflexes

A

reveals excitatory control from supraspinal areas (loss of inhibitory control) → over active/tonic stretch reflex → rigidity and spasticity

238
Q

what is the positive babinski sign?

A

toes curl upwards (should be downwards)
this is normal in babies
UMN lesion

239
Q

what is MS?

A

autoimmune disorder → loss of myelin from CNS neurons

240
Q

symptoms of MS?

A 
blurred vision
fatigue
difficulty walking 
paraesthesia
muscle stifness/spasms
241
Q

what is the M wave?

A

fast response when motor axons are activated → muscle contraction

242
Q

what is the h reflex?

A

stimulus activates sensory neurons

action potentials go nerve → spinal cord → LMN activated → motor neurons → muscle → twitch

243
Q

what is the F wave?

A

large electrical stimulus - APS travel motor neurone → spinal cord (antidromic) → LMN activated → motor neurones → muscle → twitch

244
Q

what does antidromic mean?

A

action potentials travel in the opposite direction to normal

orthodromic is normal

245
Q

what is a motor evoked potential?

A

seen on EMG when UMN. are activated so that action potentials travel along upper and lower motor neurons to cause muscle contraction
gives total motor conduction time (TMCT)

246
Q

how can the motor cortex be stimulated?

A

transcranial magnetic stimulation

247
Q

what is peripheral motor conduction time?

A

time from spinal cord to muscle along motor axon
PMCT = (M wave + F wave - 1) /2

(-1 is for time estimated for action potentials at LMN to turn around)

248
Q

how is central motor conduction time calculated?

A

TMCT - PMCT

249
Q

effects of MS on TMCT and PMCT?

A

MEP latency longer than usual = TMCT delayed
normal F wave latency = normal PMCT
→ problem in CNS

250
Q

red flags for headaches?

A 
thunderclap, acute onset
meningism
systemic - fever, rash, wt loss
visual loss, seizures, confusion, Horner syndrome, 3rd nerve palsy 
orthostatic 
strictly unilateral
251
Q

presentation of a subarachnoid haemorrhage?

A

sudden headache
stiff neck
photophobia

252
Q

subarachnoid haemorrhage management?

A 
nimodipine and BP control
neurosurgical assessment
CT brain 
lumbar puncture (RBCs and xanthochromia)
MRA
angiogram 
fill aneurysm with platinum coil
253
Q

what can an acute intracerbeal haemorrhage lead to?

A

coning due to ↑ ICP

254
Q

what is papilloedema?

A

optic disc swelling due to raised ICP

255
Q

treatment for carotid/vertebral artery dissection?

A

aspirin/anticoag for 6/12

256
Q

signs & symptoms of temporal arteritis?

A

unilateral headache
jaw claudication
scalp tenderness
↑cRP and ESR

257
Q

what will a biopsy show in temporal arteritis?

A

inflammation

giant cells

258
Q

treatment for temporal arteritis?

A

high dose steroids

aspirin

259
Q

what can cause blindness in temporal arteritis?

A

posterior cilliary artery involvement

260
Q

what is affected in temporal arteritis?

A

internal elastic lamina

261
Q

risk factors for cerebral venous thrombosis?

A

thrombophilia
pregnancy
Bechets
dehydration

262
Q

viral causes of meningitis?

A

coxsackie
echovirus
mumps
EBV

263
Q

bacterial causes of meningitis?

A

meningo/pneumoccoci

264
Q

symptoms of meningitis?

A 
fever
malaise
photophobia
neck stiffness 
headache 
confusion
265
Q

management of meningitis?

A 
treat then diagnose
Abx
blood and urine cultures
CT/MRI
lumbar puncture - ↑ WCC, ↓ glucose , antigens, cytology , culture
266
Q

how will bacterial meningitis present on CT?

A

cerebral oedema
effacement of ventricles & sulci
inflamed meninges

267
Q

how will sinusitis be seen on xray?

A

oppacifictaion of sinuses

268
Q

symptoms of sinusitis?

A

malaise fever headache
loss of vocal resonance
anosmia
nasal catarrh

269
Q

headache most often seen in obese young women?

A

idiopathic intracranial hypertension / pseudomotor cerebri

270
Q

symptoms of IIH/PC?

A 
headache
visual obscurations
diplopia
tinnitus
papilloedma 
visual field loss
271
Q

causes of IIH/PC?

A

hormones eg OCP
vitamin E
Abx
steroids

272
Q

treatment for IIH/PC?

A

weight loss
diurteics
optic nerve sheath decompression
lumboperitoneal shunt

273
Q

↑ ICP on CT?

A

effacement of ventricles and sulci with cerebral oedema

274
Q

what can cause a low pressure headache?

A

CSF leak - tear in dura, traumatic, post lumbar puncture, spontaneous

275
Q

treatment for a csf leak?

A

rehydration
caffeine
blood patch

276
Q

how can a low pressure headache present on MRI?

A

meningeal enhancement

277
Q

what is the chiari malformation?

A

brain that sits very low in skull
cerebellar tonsils descend through foramen magnum
when coughing they descend further → tug on meninges → headache

278
Q

how can OSA lead to a headache?

A

↑ CO2 retained → vasodilation of blood vessels → accumulation of blood → ↑ICP

279
Q

what can trigeminal neuralgia be a symptom of?

A

MS

280
Q

what can cause trigeminal neuralgia pain?

A

neurovascular conflict at point of entry into pons

281
Q

treatment for trigeminal neuralgia?

A

carbamazepine
lamotrigine
gabapentin
posterior fossa decompression

282
Q

management for atypical facial pain?

A

tricyclics

283
Q

risk factors for atypical facial pain?

A

middle aged women
depresed
anxious

284
Q

management for post traumatic headaches?

A

explanation
prevent analgesic abusee
NSAIDs
tricyclics eg amitriptyline

285
Q

commonest cause of a new onset headache in older patients?

A

cervical spondylosis, narrowing of joint space

286
Q

cervical spondylosis symptoms?

A 
bilateral headache
occipital pain → frontal
steady pain 
no N&v
worsened by moving neck
287
Q

management for cervical spondylosis?

A

rest, deep heat, massage

NSAIDs

288
Q

5 phases of migraine?

A

prodrome - mood changes, polyuria, cravings
aura - visual, sensory, weakness, speech
headache - w nausea and photophobia
resolution - rest and sleep
recovery - moody, food intolerance, hangover

289
Q

what are the symptoms of migraine aura?

A

+ve - scintilations

-ve - blindpsots

290
Q

treatment for an acute migraine attcak?

A

NSAIDs, paracetamol, metoclopramide
Triptans with NSAIDs
nap
TMS

291
Q

migraine prophylaxis?

A 
TCAs
beta blockers
serotonin antagonists
CCBs
anticonvulsants 
botox
suppress ovulation
erenumab - monoclonal antibody
292
Q

management for a tension type headache?

A

NSAIDs
paracetamol
TCAS eg amitriptyline

293
Q

symptoms of a cluster headache?

A 
severe unilateral pain , 15-180 mins 
ipsilateral conjunctival redness, lacrimation, nasal congestion, eyelid oedema 
forehead/facial; sweating 
miosis/ptosis
restelessness
294
Q

what is a cluster headache classified as?

A

trigeminal autonomic cephalgia

295
Q

treatment for acute cluster headache?

A

inhaled oxygen - inhibits neuronal activation in the trigeminocervical complex
sc or nasal sumatriptan

296
Q

prevention for cluster headaches?

A

predinisolone
lithium
valproate
gabapentin

297
Q

differences between migraines and cluster headaches?

A 
women vs men 
3-12hrs vs 45mins-3hrs
monthly vs daily
                   long remissions
N&V
pulsating hemicranial pain vs severe well localised unilateral pain
auras vs autonomic symptoms 
lie in dark vs pacing about
298
Q

structure of the BBB?

A

capillaries with ++ tight junctions → ↓↓ solute and fluids leakage cross capillary wall

299
Q

symptoms of encephalitis?

A

flu like
pyrexia, headache

confusion, seizures, personality changes, dysarthria , weakness, loss of consciousness

300
Q

commonest causes of encephalitis?

A 
viral :
HSV
measebles
varicella
rubella

(mosquito, trauma, autoimmune, bacterial)

301
Q

treatments for encephalitis?

A 
anitvirals
steorids
Abx
alagesics
anticonvulsants 
ventilation
302
Q

commonest causes of meningitis?

A 
bacterial:
meningococcla
pneumococcal
HIb
streptococcal **neonates
303
Q

what are MS relapses linked to?

A

inflammatory activity

304
Q

what causes inflammation in MS?

A

perivascular immune celll infiltration (CD3 T and CD20 B cells)

305
Q

what is myelitis?

A

infection of the spinal cord (encephamyelitis if brain too)

BRS 2 (12 decks)

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