Neuro Flashcards

(305 cards)

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
What are the functions of the primary somatosensory cortex?
process somatic sensations from body receptors | eg. touch, vibration, pain, temp, etc.
26
What are the functions of the somatosensory association?
interpret significance of sensory information | self awareness and of personal space
27
two areas of the occipital lobe and their functions?
primary visual cortex - process visual stimuli | visual association - interpretation and meaning of visual input
28
two areas of the temporal lobe and their functions?
primary auditory cortex - process auditory stimuli | auditory association - interpretation and meaning of auditory input
29
functions of the prefrontal cortex?
``` attention social behaviour planning personality decision making ```
30
functions of Brocas area?
production of language
31
function of wernickes area?
understanding language
32
what would you observe in a frontal lobe lesion?
personality change | inappropriate behaviour
33
what would you observe in a parietal lobe lesion?
contralateral neglect i.e. lack of awareness of self and extraperosnal space on opposite side
34
what would you observe in a temporal lobe lesion?
agnosia | anterograde amnesia
35
what is agnosia?
inability to recognise objects
36
what is anterograde amnesia?
cannot form new memories
37
what would you observe in a lesion to broca's area?
expressive aphasia - slurred speech but able to understand speech
38
what would you observe in a lesion to wernicke's area?
receptive aphasia - can speak but cannot comprehend speech
39
what would you observe in a primary visual cortex lesion?
blindness in corresponding visual field
40
what would you observe in a visual association lesion?
prosopagnosia (face blindness) | unable to interpret visual information
41
two types of imaging to assess cortical function?
PET - positron emission tomography | fMRI - functional magnetic resonance imaging
42
what does PET look at?
Blood flow directly to brain region (take up of glucose using radioactive isotope) More glucose uptake = more brain activity
43
what does fMRI look at?
the amount of blood oxygen in a brain region
44
What can you use to measure evoked/event-related potentials?
EEG | MEG
45
two methods of brain stimulation?
transcranial magnetic stimulation (TMS) | transcranial direct current stimulation (tDCS) to increase or decrease neuronal firing rates
46
two types of imaging to assess cortical structure?
diffusion tensor imaging (DTI) based on diffusion of water molecules DTI with tractography to assess neuronal tracts
47
Where in the skull is the ear found? How is this beneficial?
The petrous part of the temporal bone. It's v hard so provides the necessary protection
48
name 3 functions of the outer ear?
to capture sound and direct it to the tympanic membrane to amplify sound via resonance protection via hairs and wax
49
How does the middle ear amplify sound?
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
50
name the 3 ossicles?
malleus stapes incus
51
why does sound need to be amplified in the middle ear?
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
52
what is the function of the cochlea?
to transduce sound waves to electrical impulses that can be interpreted by the brain allows pitch and volume to be analysed
53
describe the structural components of the cochlea
``` scala vestibuli (contains perilymph) scala media (contains endolymph) basilar membrane organ of cortisol scala tympani ```
54
how is the basilar membrane arranged? what does this mean?
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
55
what cells does the organ of corti contain and how are they arranged? functions?
Inner hair cells - one column (fewer), sound transduction | outer hair cells - three columns, modulate sensitivity, amplify sound
56
what are the hair cells connected to?
tectorial membrane (only OHC in constant contact)
57
what are the hairs on hair cells called?
sterocillia
58
how do the Scala vestibuli and the Scala tympani communicate?
helicotrema
59
explain how sound is transduced?
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
60
what happens in transduction of louder sounds?
theres more deflection of steroecilia and more potassium channels open leading to greater depolarisation
61
describe the auditory neural pathway
nerves from hair cells → spiral ganglia → vestibulocochlear nerve → ipsilateral cochlear nuclei → superior olive in brainstem (bilateral) → inferior colliculus → medial geniculate body → auditory cortex
62
human range of hearing?
20 - 20000 Hz | 0 - 120 dB
63
Which frequencies are affected first
higher frequencies
64
what is a tuning fork used for?
to establish the probable presence or absence of hearing loss with a significant conductive component
65
what are the two tuning forks tests?
``` weber test (over the head) rinne test (next to ear) ```
66
what is pure tone audiometry?
science of measuring acuity for variations in sound intensity and frequency
67
what device is used in PTA? how are results measured?
audiometer | audiogram
68
What does the central processing assessment assess?
Hearing abilities other than section | Verbal and non-verbal testing
69
What is tympanometry?
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
70
What are otoacoustic emissions?
low intensity sounds produced by outer hair cells in the cochlea when they expand and contract
71
When are OAEs measured?
Newborn hearing screening | Hearing loss monitoring
72
3 methods of measuring auditory evoked potentials?
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
73
Benefits of auditory brainstem response?
objective patients doesn't need to pay attention most commonly used in clinics
74
when are cortical potentials useful?
In neurological conditions or processing problems
75
name and describe the 3 types of hearing loss
conductive - outer or middle ear problem sensorineural - inner ear or auditory nerve mixed - conduction and transduction are affected
76
causes of conductive hearing loss?
outer ear - foreign body or wax buildup (cerumen impaction) | middle ear - otitis or otosclerosis
77
causes of sensioneural hearing loss?
inner ear - presbycusis or ototoxicity | nerve - CN8 tumour
78
what is presybycutis?
loss of outer hair cells, occurs with age
79
4 types of hearing loss treatment?
Underlying cause (eg. remove earwax) Cochlear implant Hearing aids brainstem implant
80
How do hearing aids work?
amplify sound
81
How does the cochlea implant work?
Replaces hair cells → receives and analyses sound → transforms it to electrical signals → auditory nerve (requires functional nerve)
82
When can a brainstem implant be used?
When auditory nerves are damaged electrical signals sent directly to electrodes in brainstem very risky
83
what are the 3 inputs of the vestibular system?
visual proprioceptive vestibular
84
vestibular system outputs?
reflexes to help maintain posture and a stable gaze
85
where is the vestibular system found?
in the posterior region of the inner ear
86
what does the vestibule consist of?
three semicircular canals - anterior , lateral and posterior | all 3 connected (via ampullae) to utricle which is joined to the saccule by a conduit
87
What are the hairs on vestibular hair cells called?
Stereocillia and kinocilium ( the biggest cilia)
88
When are vestibular cells depolarised?
when endolymph is moved via head movement
89
what are the otolith organs? what do they consist of?
utricle and saccule | carbonate crystals that help deflect hairs
90
what are the maculae? how do they differ in the utricle and the saccule?
hair cells → gelatinous metric → otoliths saccule is placed vertically utricule is placed horizontally
91
outline the structure and contents of the semicircular canals
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
92
what is the function of the cupula?
helps movement of hair cells in ampulla of semicircular canals
93
where do primary vestibular afferents end?
vestibular nuclei | cerebellum
94
where do vestibular nuclei project to? (4)
spinal cord extraocular muscle nuclei cerebellum CV and respiratory control centres
95
where is the main vestibular cortex found?
parietal lobe as parieto-insular vestibular cortex
96
3 main functions of the vestibular system?
control posture detect and inform about head movements keep images fixed during movement
97
why do neurons still fire at the resting potential of hair cells? what do you call this discharge?
Because there is the force of gravity and information that you are stationary is still being processes Required to keep you upright Basal discharge
98
what are the three hair cell potentials in the vestibular system and how are they generated?
Resting - always there Excitaion - occurs when sterocilia move towards the kinocilium → depolarisation → ↑ nerve discharge Inhibitoin - stereo cilia move away from kinocilium → hyperpolarization → ↓ nerve discharge
99
What do the otolith organs detect?
Tilt and linear acceleration utricule - horizontal movement saccule - vertical movement
100
What does the semilunar canals detect? And how?
angular acceleration | endolymph flow moves the cupula which then moves hair cells
101
how do opposite semicircular canals work?
lateral work together | anterior of one side works with posterior of opposite side
102
what are the two main vestibular reflexes?
vestibul-ocular reflex | vestibule-spinal reflex
103
Describe the VOR and how it works?
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
104
Describe the VSR and how it works?
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
105
what 7 things are considered in vestibular assessment?
``` anamnesis (history) posture & gait cerebellar function eye movements vestibular tests imaging symptoms & impact assessment ```
106
what are the main symptoms of a balance disorder?
vertigo (objects spinning) | dizziness
107
2 main types of balance disorders?
peripheral & central vestibular disorders
108
give 4 examples of peripheral vestibular disorders
``` vestibular neuritis (acute) benign paroxysmal positional vertigo (intermittent) Meniers disease (recurrent) unilateral and bilateral vestibular hypofunction ```
109
explain bppv
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
110
give 3 examples of what can cause central vestibular disorders
stroke (acute) MS (progresive) tumour eg schwanoma (progressive)
111
differentials for dizziness? (7)
``` heart disorders orthostatic hypotension presyncopal episodes psychological gait problems anaemia hypoglycaemia ```
112
What can have 'modest symptomatic benefit' in the early stages of dementia?
Acetylcholinesterase inhibitors
113
Name 4 common differentials for dementia
Depression alcohol related brain damage vitamin b1/6/12 deficiency endocrine disorders
114
define preclinical dementia?
there is deterioration in neurological cells but no clinical symptoms yet
115
risk factors for dementia? (7)
``` ageing oral health brain trauma genetics mid-life obesity ↓ physical activity infections/ systemic inflammation ```
116
define dementia
severe loss of memory and other cognitive abilities which lead to impaired daily functions
117
what 3 examinations can you carry out if you suspect dementia?
neurological (i.e. testing cranial nerves) mini mental state exam addenbrookes cognitive exam
118
what would you see on an MRI where the patient has dementia?
dilated ventricles atrophied hippocampus wider sulci and narrower gyri
119
what 2 proteins present in the brain are associated with AD?
B amyloid | tau
120
what is the management of dementia? (5)
acetlycholintesterase inhibitors treat behavioural and psychological symptoms eg. w/ antidepressants and antipsychotics monitor progression occupational therapy/social services
121
2 defining features of vascular dementia?
associated w/ cerebrovascular diseases | step wise deterioration
122
3 features of Lewy body dementia?
parkinsonian features fluctuating cognition visual hallucinations
123
2 features of FTD?
behavioural changes | progressive non-fluent aphasia
124
what is the head-turning sign in dementia patients?
they turn to partner/relative because they are unsure/don't know the answer
125
what protein is associated with Lewy body dementia?
a-synuclein
126
outline the production. of tears?
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
what is the function of the tear film?
maintains smooth cornea air surface oxygen supply to cornea removes debris bactericide
128
what's the structure of the tear film?
3 layers superficial lipid layer - reduce tear film evaporation aqueos layer mutinous layer on corneal surface - surface wetting
129
what is the conjunctiva?
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
what are the 3 layers of the eye? (outer to inner)
sclera choroid retina
131
what is the sclera?
outer coat of the eye, protective | high water content
132
what is the cornea? structure and function?
transparent low water content powerful refracting surface - 2/3 eye focusing power ``` 5 layers: epithelium bowman membrane stroma descemets membrane endothelium ```
133
what is the uvea?
vascular coat of eyeball between sclera and retina iris, ciliary body and choroid
134
what is the iris? function?
controls light levels inside eye opening in centre → pupil has tiny muscles which dilate/constrict pupil
135
structure and function of the lens?
outer acellular capsule regular inner elongated fibres - transparency refractive power - 1/3 of eyes focusing power accommodation elasticity
136
what happens when lenses lose transparency?
cataracts form
137
function of the retina?
capturing light rays that enter the eye
138
structure and function of the optic nerve?
electrical impulses from retina to brain connects to eye near macula visible part = optic disc
139
what is the blind spot?
where optic nerve meets retina - no light sensitive cells | optic disc
140
structure and function of the macula?
centre if retina, temporal to optic nerve responsible for detailed central vision eg. reading fovea is the centre of macula
141
what is the proportion of cell types at the fovea?
highest concentration of cones, low of rods
142
how is central vision assessed? what is loss called?
visual acuity assessment | loss of foveal vision = poor visual acuity
143
how is peripheral vision assessed? what does loss lead to?
visual field assessment | loss of visual field = unable to navigate
144
what is the structure of the retina?
outer - photoreceptors detect light middle - bipolar cells, local signal processing inner - retinal ganglion cells , transmit from eye to brain
145
2 types of photoreceptors and differences?
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
different cone cell types and colours?
S - blue M - green L - red
147
what is the commonest form of colour blindness?
deuteranomaly - don't perceive the colour red
148
what is full colour blindness called?
achromatopsia
149
what test can be used for red green colour blindness?
Ishihara test
150
what is emmetropia?
adequate correlation between axial length and refractive power, parallel light rays fall on retina (normal)
151
what is ametropia?
mismatch between axial length and refractive power | parallel rays don't fall in retina
152
types of ametropia?
hyperopia myopia astigmatism presbyopia
153
what is myopia? symptoms? causes?
parallel rays converge anterior to retina (near sightedness) blurred distance vision → squint → headache excessive long globe (axial myopia) excessive refractive power (refractive myopia)
154
treatment for myopia?
diverging lenses contact lenses remove eye lens to reduce refractive power
155
what is hyperopia? symptoms? causes?
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
what can uncorrected hyperopia leas to?
amblyopia (lazy eye)
157
treatment for hyperopia?
converging lenses ± cataract extraction contact lenses intraocular lenses
158
what is astigmatism? cause? symptoms?
paralle rays focus in 2 lines hereditary refractive media is not spherical headache, eyepain, blurred distorted vision, head tilting/turning
159
treatment for astigmatism?
regular : cylinder lenses ± spherical lenses surgery irregular: rigid cylinder lenses surgery
160
what is the near response triad?
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
what is presbyopia?how is it corrected?
naturally occurring loss of accommodation onset ≥40yrs distant vision fine corrected w reading glasses (convex lens) to ↑ refractive power
162
what are the types of optical correction?
contact lenses intraocular lenses surgical - keratorefractive or intraocular
163
what is the visual pathway from the eye to the visual cortex?
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
which fibres cross in the optic chiasma?
those from nasal retina - temporal visual field
165
what visual field defects occur if theres a lesion anterior to the optic chiasm? eg. optic nerve compression
only one eye affected - whole visual field affected
166
what visual field defects occur if theres a lesion at the optic chiasm? eg. pituitary tumour
damages crossed fibres (nasal retinal fibres) | → bitemporal hemianopia
167
what visual field defects occur if theres a lesion posterior to the optic chiasm? eg right sided stroke
affects right temporal fibres and left nasal fibres → left homonymous hemianopia (right temporal and left nasal fields affected)
168
how does homonymous hemianopia with macular sparing occur?
stroke affecting primary visual cortex | maculae receive blood supply from posterior cerebral arteries on both sides
169
what happens to the pupil when exposed to light? how is it mediated?
constriction (miosis) mediated by parasympthateic nerve in CN III → circular muscles contract decreases glare increases depth of field reduces bleaching of photopigments
170
what happens to the pupil when exposed to dark? how is it mediated?
pupillary dilation mediated by sympathetic nerves → radial muscles contract ↑ light sensitivity → more light can enter eye
171
what is the pathway of the pupillary reflex?
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
direct vs consensual reflex?
``` direct = constriction of pupil of the light stimulated eye consensual = constriction of pupil of the other eye ```
173
afferent vs efferent defects and affects in eye?
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
how can a relative afferent pupillary defect be tested for?
swinging torch test
175
2 different types of eye movement?
saccade - short fast burst | smooth pursuit - slow movement
176
different types of saccade?
reflexive scanning predictive memory guided
177
what direction does the superior oblique move the eye?
down and out | trochlear nerve
178
what direction does the inferior oblique move the eye?
up and out
179
what is levoversion and dextroversion?
levo - eyes both move to left, left abduction, right adduction dextro - eyes both move right
180
symptoms of third nerve palsy?
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
symptoms of sixth nerve palsy?
eye cannot abduct (no lateral rectus) → deviates inwards | double vision
182
what is the optokinetic nystagmus reflex?
useful in testing visual acuity in preverbal children | smooth pursuit & fast phase reset saccade
183
what happens when theres damage to the posterior colliery ganglion? what is it known as?
tonically dilated pupil - Adie's pupil | parasympathetic fibres have no effect
184
what is pilocarpine?
muscarinic receptor agonist on M3 receptors in iris sphincter muscle → miosis (independent of parasympathetic nerves)
185
explain Adie's pupil?
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
manoeuvres for BPPV?
epley and semont manouvers
187
3 main blood supply arteries to the brain?
vertebral artery | internal and common carotids
188
circle of willis?
vertebral arteries → basillar artery → posterior cereal → posterior communicating → middle cereal & internal carotid → anterior cerebral →anterior communicating
189
4 types of brain haemorrhage?
extra dural - arterial, trauma esp @ pterion subdural - venous, trauma subarachnoid - circle of willis, ruptured aneurysm intracerebral - spontaneous hypertensive
190
what is a cerebrovascular accident?
rapidly developing focal disturbance of brain function of presumed vascular origin and go ≥24hrs thromboembolic or haemorrhagic
191
how does a TIA differ from a CVA?
it resolves completely within 24 hours
192
infraction vs ischaemia?
degenerative changes in tissue following artery occlusion vs | lack of sufficient blood flow → permanent damage if blood flow not restored
193
5 risk factors for stroke?
``` age smoking hypertension cardiac disease diabetes ```
194
symptoms of an anterior cerebral artery stroke?
paralysis of contralateral structures abulia → disturbance of intellect, judgement loss os appropriate social behaviour
195
symptoms of middle cerebral artery stroke?
contralateral hemiplegia contralateral hemisensory defects hemianopia aphasia if L sided lesion
196
symptoms of posterior cerebral artery stroke?
``` homonymous hemianopia visual agnosia (cannot recognise objects) ```
197
why can you get a headache with a subdural bleed?
build up of intracranial pressure
198
sy,tpoms of a cerebellar lesion?
wobbly eye movements ataxia broad hesitant gait slurred speech
199
what are the major motor descending tracts?
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
function of the primary motor cortex?
precentral gyrus | fine, discrete, precise voluntary movements
201
function of the premotor area?
anterior to primary motor cortex planning movements regulates externally cued movements
202
function of supplementary motor area?
anteriomedial to primary motor cortex planning complex movemnts, internally cued active prior to voluntary movement
203
difference between anterior and lateral corticospinal tracts?
anterior - trunk, decussate in spinal cord | lateral - limbs, decussates at medulla
204
function of the vestibulospinal tract?
stabilise head coordinate head and eye movements postural adjustments
205
function of the reticulospinal tract?
from medulla and pons changes in muscle tone postural stability
206
function of the tectospinal tract?
superior colliculis to midbrain | orientation of head and neck during eye movements
207
function of the rubrospinal tract?
from red nucelus of midbrain | innervate LMNs of flexors of upper limb
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signs of an UMN lesion?
negative : loss of voluntary motor function - paresis or paralysis ``` positive : loss of inhibitory descending inputs spasticity hyperreflexia clonus babinskis sign ```
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what is apraxia? lesion? causes?
disorder of skilled movement lesion in SMA/premotor cortex stroke and dementia
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signs of an LMN lesion?
``` weakness hypotonia hyporeflxia muscle atrophy fasiculations - visible twitches fibrillations - can be seen on EMG ```
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signs of motor neurone disease?
same as UMN and LMN signs dysphagia dysarthria nasal speech
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MND alternative name?
ALS - amyotrophic lateral sclerosis
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what are the basal ganglia?
``` caudate nucleus lentiform nucleus (putamen and external globus pallidus) nucleus accumbens sub thalamic nuclei substantia nigra ```
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what does the striatum consist of?
caudate and putamen
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function of the basal ganglia?
decision to move elaborating associated movements moderating and coordinating movements performing movements in order
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pathophysiology of Parkinson's?
degeneration of the dopaminergic neurons that originate in the substantial nigra and project to the striatum
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signs of parkinsons?
``` bradykinesia hypomimc face akinesia rigidity tremor at rest ```
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pathophysiology of Huntington's disease?
degeneration of GABAergic neurons in striatum | genetic, chromosome 4, autosomal dominant, CAG repeat
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signs of Huntington's?
``` choreic movements rapid jerky involuntary movements speech impairment dysphagia unsteady gait cognitive decline→ dementia ```
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what is ballism?
from stroke affecting sub thalamic nucleus sudden uncontrolled flinging of extremities contralateral symptoms
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what separates cerebrum from cerebellum?
tentorium cerebelli
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vestibulocerebellum function?
regulates gait and posture coordinates head and eye movements damage = gait ataxia
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spinocerbellum function?
coordinate speech and limb movements adjust muscle tone damage = legs , abnormal gait and stance - usually caused by chronic alcoholism
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cerebrocerebellum function?
coordinate skilled movements cognitive function, attention, language processing, emotion control damage = arms, tremor and speech
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signs of cerebellar dysfunction?
``` ataxia dysmetria intention tremor dysdiadokinesia scanning speech ```
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what are the alpha motor neurons?
LMNs of the brainstem and spinal cord innervate extrafusal muscles activation = contraction
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define motor unit
all the muscle fibres innervated by a single motor neon , smallest functional unit able ton produce force
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types of motor unit?
slow (I) fast fatigue resistant (IIA) fast fatiguable (IIB) (cell bodies, dendritic trees, conduction velocity, thickness)
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how are the motor unit types classified?
amount of tension fatiguability speed of contraction
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how is muscle force regulated?
recruitment - size principle, smaller units recruited first, allows fine control rate coding - sloe units with lower frequencies recruited first
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what are neurotrophic factors?
growth factor prevent neuronal death promote neuronal growth after injury
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what do motor unit characteristics depend on? how is it known?
on the nerve fibres that innervate them | cross innervation → muscle fibres changes characteristics
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when do fibres Tina`ge from IIB to IIa?
after training
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when do fibres change from I to II?
severe deconditioning /spinal coed injury | microgravity
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why do contraction times get slower with age?
loss of type I and II fibres but II lost in greater proportion
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what manoeuvre can be used to make reflexes larger?
jendrassik → reduces amount of inhibition CNS exerts on reflexes
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what happens in decerebration? re reflexes
reveals excitatory control from supraspinal areas (loss of inhibitory control) → over active/tonic stretch reflex → rigidity and spasticity
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what is the positive babinski sign?
toes curl upwards (should be downwards) this is normal in babies UMN lesion
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what is MS?
autoimmune disorder → loss of myelin from CNS neurons
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symptoms of MS?
``` blurred vision fatigue difficulty walking paraesthesia muscle stifness/spasms ```
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what is the M wave?
fast response when motor axons are activated → muscle contraction
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what is the h reflex?
stimulus activates sensory neurons | action potentials go nerve → spinal cord → LMN activated → motor neurons → muscle → twitch
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what is the F wave?
large electrical stimulus - APS travel motor neurone → spinal cord (antidromic) → LMN activated → motor neurones → muscle → twitch
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what does antidromic mean?
action potentials travel in the opposite direction to normal | orthodromic is normal
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what is a motor evoked potential?
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)
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how can the motor cortex be stimulated?
transcranial magnetic stimulation
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what is peripheral motor conduction time?
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)
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how is central motor conduction time calculated?
TMCT - PMCT
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effects of MS on TMCT and PMCT?
MEP latency longer than usual = TMCT delayed normal F wave latency = normal PMCT → problem in CNS
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red flags for headaches?
``` thunderclap, acute onset meningism systemic - fever, rash, wt loss visual loss, seizures, confusion, Horner syndrome, 3rd nerve palsy orthostatic strictly unilateral ```
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presentation of a subarachnoid haemorrhage?
sudden headache stiff neck photophobia
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subarachnoid haemorrhage management?
``` nimodipine and BP control neurosurgical assessment CT brain lumbar puncture (RBCs and xanthochromia) MRA angiogram fill aneurysm with platinum coil ```
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what can an acute intracerbeal haemorrhage lead to?
coning due to ↑ ICP
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what is papilloedema?
optic disc swelling due to raised ICP
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treatment for carotid/vertebral artery dissection?
aspirin/anticoag for 6/12
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signs & symptoms of temporal arteritis?
unilateral headache jaw claudication scalp tenderness ↑cRP and ESR
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what will a biopsy show in temporal arteritis?
inflammation | giant cells
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treatment for temporal arteritis?
high dose steroids | aspirin
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what can cause blindness in temporal arteritis?
posterior cilliary artery involvement
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what is affected in temporal arteritis?
internal elastic lamina
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risk factors for cerebral venous thrombosis?
thrombophilia pregnancy Bechets dehydration
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viral causes of meningitis?
coxsackie echovirus mumps EBV
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bacterial causes of meningitis?
meningo/pneumoccoci
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symptoms of meningitis?
``` fever malaise photophobia neck stiffness headache confusion ```
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management of meningitis?
``` treat then diagnose Abx blood and urine cultures CT/MRI lumbar puncture - ↑ WCC, ↓ glucose , antigens, cytology , culture ```
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how will bacterial meningitis present on CT?
cerebral oedema effacement of ventricles & sulci inflamed meninges
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how will sinusitis be seen on xray?
oppacifictaion of sinuses
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symptoms of sinusitis?
malaise fever headache loss of vocal resonance anosmia nasal catarrh
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headache most often seen in obese young women?
idiopathic intracranial hypertension / pseudomotor cerebri
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symptoms of IIH/PC?
``` headache visual obscurations diplopia tinnitus papilloedma visual field loss ```
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causes of IIH/PC?
hormones eg OCP vitamin E Abx steroids
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treatment for IIH/PC?
weight loss diurteics optic nerve sheath decompression lumboperitoneal shunt
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↑ ICP on CT?
effacement of ventricles and sulci with cerebral oedema
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what can cause a low pressure headache?
CSF leak - tear in dura, traumatic, post lumbar puncture, spontaneous
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treatment for a csf leak?
rehydration caffeine blood patch
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how can a low pressure headache present on MRI?
meningeal enhancement
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what is the chiari malformation?
brain that sits very low in skull cerebellar tonsils descend through foramen magnum when coughing they descend further → tug on meninges → headache
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how can OSA lead to a headache?
↑ CO2 retained → vasodilation of blood vessels → accumulation of blood → ↑ICP
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what can trigeminal neuralgia be a symptom of?
MS
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what can cause trigeminal neuralgia pain?
neurovascular conflict at point of entry into pons
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treatment for trigeminal neuralgia?
carbamazepine lamotrigine gabapentin posterior fossa decompression
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management for atypical facial pain?
tricyclics
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risk factors for atypical facial pain?
middle aged women depresed anxious
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management for post traumatic headaches?
explanation prevent analgesic abusee NSAIDs tricyclics eg amitriptyline
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commonest cause of a new onset headache in older patients?
cervical spondylosis, narrowing of joint space
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cervical spondylosis symptoms?
``` bilateral headache occipital pain → frontal steady pain no N&v worsened by moving neck ```
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management for cervical spondylosis?
rest, deep heat, massage | NSAIDs
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5 phases of migraine?
prodrome - mood changes, polyuria, cravings aura - visual, sensory, weakness, speech headache - w nausea and photophobia resolution - rest and sleep recovery - moody, food intolerance, hangover
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what are the symptoms of migraine aura?
+ve - scintilations | -ve - blindpsots
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treatment for an acute migraine attcak?
NSAIDs, paracetamol, metoclopramide Triptans with NSAIDs nap TMS
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migraine prophylaxis?
``` TCAs beta blockers serotonin antagonists CCBs anticonvulsants botox suppress ovulation erenumab - monoclonal antibody ```
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management for a tension type headache?
NSAIDs paracetamol TCAS eg amitriptyline
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symptoms of a cluster headache?
``` severe unilateral pain , 15-180 mins ipsilateral conjunctival redness, lacrimation, nasal congestion, eyelid oedema forehead/facial; sweating miosis/ptosis restelessness ```
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what is a cluster headache classified as?
trigeminal autonomic cephalgia
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treatment for acute cluster headache?
inhaled oxygen - inhibits neuronal activation in the trigeminocervical complex sc or nasal sumatriptan
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prevention for cluster headaches?
predinisolone lithium valproate gabapentin
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differences between migraines and cluster headaches?
``` 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 ```
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structure of the BBB?
capillaries with ++ tight junctions → ↓↓ solute and fluids leakage cross capillary wall
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symptoms of encephalitis?
flu like pyrexia, headache confusion, seizures, personality changes, dysarthria , weakness, loss of consciousness
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commonest causes of encephalitis?
``` viral : HSV measebles varicella rubella ``` (mosquito, trauma, autoimmune, bacterial)
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treatments for encephalitis?
``` anitvirals steorids Abx alagesics anticonvulsants ventilation ```
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commonest causes of meningitis?
``` bacterial: meningococcla pneumococcal HIb streptococcal **neonates ```
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what are MS relapses linked to?
inflammatory activity
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what causes inflammation in MS?
perivascular immune celll infiltration (CD3 T and CD20 B cells)
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what is myelitis?
infection of the spinal cord (encephamyelitis if brain too)