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PPE > Neuro > Flashcards

Neuro Flashcards

1
Q

What are emergent properties of the brain

A

properties of whole system but not individual components e.g. consciousness

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2
Q

what is neocortex and paleocortex involved in

A

neocortex - higher thinking

paleocortex - memory and emotion

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3
Q

what is septum pellucidum

A

separates anterior lateral ventricles

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4
Q

where is limbic system. what it contains. involved in?

A

under cerebrum. contains amygdala, hippocampus, fornix etc.

5 F’s - fighting, fleeing, feeding, feeling, fucking

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5
Q

where is the calcarine sulcus

A

occipital lobe

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6
Q

where is lateral sulcus

A

between temp and parietal lobe

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7
Q

where is insular cortex and what involved in

A

deep folding inside lateral sulcus. consciousness, emotion, homeostasis

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8
Q

what is corona radiata of brain

A

sheet of axons from and to cerebrum

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9
Q

what is caudate nucleus and function

A

part of basal ganglia. voluntary movement

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10
Q

where is basal ganglia and what consist of

A

below cerebrum and surrounds thalamus. corpus striatum + substantia nigra + subthalamic nuclei

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11
Q

what is corpus striatum

A

globus pallidus and (neo)striatum

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12
Q

what separates L and R cerebellum and cerebri

A

falx cerebri, falx cerebelli

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13
Q

what separates cerebrum from cerebellum. What coonects the 2 cerebral hemispheres

A

corpus callosum and anterior and posterior white commussures

tentorium cerebelli

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14
Q

what is striatum

A

caudate nucleus + putamen

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15
Q

what is cerebellum peduncle

A

connecs cerebellum to mid brain. Sup, mid and inf fibres per hemisphere of cerebellum

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16
Q

what is forebrain and brainstem

A

forebrain - cerebrum, thalamus, hypothalamus

brainstem - midbrain, hindbrain (pons, medulla, cerebellum)

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17
Q

give venous sinuses of brain

A

see book

sup and inf sagittal, straight, confluence, transverse, sigmoid, IJ vein

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18
Q

what is conus medullaris

A

Taper end of T12-L1

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19
Q

what is filum terminale

A

strand of fibrous tissue from apex of conus medullaris to end of vertebral foramen

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20
Q

where lumbar puncture and in kids

A

L3/4

kids - L5/S1

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21
Q

where is SG and what is contained

A

lamina 2

contains - C fibres, lissauers fibres synapsing

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22
Q

what is ataxia and apraxia

A

ataxia - loss of full control of body movements

apraxia - unable to perform complex movements

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23
Q

what is aphasia, aphonia, dysarthria

A

aphasia - speech disorder
aphonia - physical inability to produce sound
dysarthria - disruption of articulation of speech

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24
Q

what is chorea

A

involuntary jerks e.g. huntingtons

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25
Q

what is spasticity vs rigidity

A

spasticity is unidirectional, velocity and amplitude dependent
spasticity = corticospinal tract damage
rigidity = extrapyramidal lesion

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26
Q

how detect spina bifida before birth

A

alpha fetoprotein in blood, USS

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27
Q

types of spina bifida

A

occulta - just vertebrae
meningocoele - meningele involvement
myelomeningocoele - neural tissue outside body

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28
Q

symptoms of spina bifida

A

bladder conrol, orthopedic issues, pressure sores, weakness in lower limbs

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29
Q

what is rachischisis

A

posterior neuropore fails to close resulting in motor and sensory deficits

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30
Q

how treat hydrocephalus and symptoms

A

treat with shunt (jugular)

symptoms - tunnel vision, headaches, convulsion, vomiting

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31
Q

parts of neural tube and what they become

A

prosencephalon - telencephalon (cerebrum) and dienceph (thalamus)
mesenceph - mesenceph (midbrain)
rhombenceph - metenceph (pons) and myelenceph (medulla)

Tell Di Mes Met My

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32
Q

label ventricles

A

see book

3rd, 4th, lateral, cerebral aqueduct, IV foramen

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33
Q

what does alcohol effect in neuroembryology

A

neural crest cell migration

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34
Q

what is hirschprungs diseasse

A

lack of ganglions in large intestine, therefore no function

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35
Q

astrocyte functions

A

BBB, removes neurotransmitters, nutrients to neurones

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36
Q

function of microglia

A

phagocytose material and debris. APC

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37
Q

what is BBB made of

A

tight endothelial junction, astrocyte foot process, basement membrane

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38
Q

types of neurotransmitters

A

AAs e.g. GABA, glycine, glutamate
biogenic amines e.g. dopamine, 5-HT, histamine
peptides e.g. dynorphin, CCK

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39
Q

is glutamate excitatory or inhibitory. what receptor types are there

A

excitatory
ionotropic and metabotropic
ionotropic - AMPA, kainate, NMDA

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40
Q

how does LTP occur and what happens in LTP

A

calcium goes through mGluRs or NMDAR.

Upregulation of AMPARs

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41
Q

where is gaba found. what ions does it let in

A

Cl-

found in spinal cord and brainstem

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42
Q

dopamine pathways and function

A

nigrostriatal - motor control (parkinsons)
mesolimbic and mesocortical - mood, arousal and reward (schizophrenia)
tuberoinfundibular - prolactin release and endocrin function

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43
Q

serotonin pathway function

A

sleep, wakefulness, mood, vomiting

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44
Q

label circle of willis

A

see book

ant post comm, ant mid post cerebral, ICA, sup ant inf post inf cerebellar, pontine, basilar, ant spinal, vertebral

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45
Q

what supplies spinal cord blood

A

anterior spinal, paired post spinal, anatastamoses between arteries (arterial vasocorona). Artery of ademkiewicz (thoracolumbar)

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46
Q

what arteries supplies cerebrum

A

outside cerebrum middle cerebral artery does majority of ant cerebrum
sagittal view - anterior cerbral artery does majority of ant cerebrum
posterior cerebral always does posterior section

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47
Q

symptoms of sub acute hemorrhage and cuases

A

thunderclap headache, rapid onset, vomiting, confusion, decrease consc
causes - trauma, cerebral aneurysm rupture in circle of willis

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48
Q

what removes and adds CSF

A

remove - arachnoid granulations at sup saggital sinus

add - ependymal cells of choronoid plexus

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49
Q

how many mls of CSF are there and how much produced per day

A

500 ml per day

125 mls of CSF

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50
Q

what is communicating hydrocephalus? causes

A

impaired csf resborp without csf flow obstruction

caused by scarring of arachnoid granulations

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51
Q

cause of non comm hydrocephalus

A

obstruction

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52
Q

csf composition

A

decrease glucose, ca, protein

increase na, mg, cl than blood

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53
Q

list what CNs go through what foramina

A 
cribiform plate - 1
optic canal - 2
SOF - 3, 4, 5a, 6
foramen rotundum - 5b
foramen ovale - 5c
IAM - 7,8
jugular foramen - 9-11
hypoglossal canal - 12
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54
Q

what does pacinian, merkels, meissners, and riffini sense

A

riffini - temp
pacinian - pressure
merkels - press, vibration, texture
meissners - touch and vibration

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55
Q

what receptors are in muscle. what they sense

A

muscle spindle proprioceptor = length

golgi tendon organs = tension

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56
Q

how is stronger stimuli recognised by receptors

A

increase AP frequence and activation of neighbour cells

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57
Q

difference between tonic and phasic receptors

A

tonic - slow adapting, continual firing

phasic - fast, desensitises

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58
Q

how is acuity achieved in sensation

A

lateral inhibition and divergence

convergence decreases acuity

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59
Q

what factors affect 2 point discrimination

A

size of receptor field and density of sensory receptors

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60
Q

where does sensation go after nerve stimulated

A

to somatosensory cortex on post central gyrus

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61
Q

what is perception

A

sense stimuli and discriminate between different types

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62
Q

what happens in a sensory cortex lesion

A

lose 2 point discrimination, epileptic event

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63
Q

how orientate spinal cord

A

dorsal median sulcus and ventral median fissuer

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64
Q

modality of ascending nerves

A

dorsal column - light touch and conscious proprioception
spinothalamic lateral - pain and temp
spinothalamic ant - crude touch
spinocerebellar ant - golgi tendon (tension), unconscious
spinocerebellar post - muscle spindle (length), unconscious

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65
Q

what 2 fascicles make up dorsal column and where are they positioned. where do they start

A

gracile and cuneate (t6 start)

gracile is medial (sacrolumbar), cuneate lateral (cervicothoracic)

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66
Q

describe route of dorsal column

A

DRG (1) to cuneate and gracile nuclei in medulla (2), then decussates (internal arcuate fibre) and becomes medial lemniscus fibres in pons, then to ventral posterolateral nucleus in thalamus (3), then to post central gyrus

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67
Q

route of spinothalamic

A

ascends 1-2 spinal levels in lissauers fasciculus, then dorsal horn in SG(1) and decussates (via anterior white commissure) to thalamus (2) to sensory cortex (3)

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68
Q

what type of neuron is used in the 1st order for sensory pathways

A

pseudounipolar

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69
Q

route of spinocerebellar ant

A

DRG (1) then decussates in spinal cord (via anterior white commissure) then up to pons and decussates again then to cerebellum.

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70
Q

route of spinocerebellar post

A

DRG (1) then synapse with clarkes nucleus in dorsal horn (2) to cerebellum

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71
Q

modality of descending nerves inc extrapyramidal. damage to vestibular spinal?

A

lateral corticospinal - limb
anterior corticospinal - axial
corticobulbar - face and neck muscles

extrapyramidal:
ruberospinal - voluntary skeletal contraction
reticulospinal - posture and locomotion
tectospinal - automatic reactions to visual and auditory stimuli
vestibularspinal - posture maintenance. damage = loss of righting reflex and posture instability

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72
Q

route of corticospinal

A

lateral - motor cortex to internal capsule to medulla and decussate then to ventral horn
anterior - same but decussates at ventral horn

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73
Q

route of corticobulbar

A

motor cortex to internal capsul to motor nuclei of cranial nerves bilaterally

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74
Q

what is syringomyelia

A

cyst forms in spinal cord causing pain, paralysis, weakness

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75
Q

explain brown sequard syndrome

A

hemilateral lesion of spinal cord - loss of ipsilateral dorsal column therefore ipsilateral proprioception and ifne touch (no decussation). Loss of counterlateral pain and temp due to spinothalamic decussation.

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76
Q

what is friedrichs ataxia

A

sclerosis and degen of DRG, spinocerebellar, corticospinal, and dorsal columns. progressive

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77
Q

what is shingles symptoms

A

increased sensitivity and rash. dormant in DRG. can lead to post herpetic neuralgia and chronic pain.

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78
Q

anatomy of cerebellum

A

see book

vermis, ant lobe, post love, flocculonodular love

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79
Q

give function of cerebellar parts

A

spinocerebellum - vermis - error correction
vestibulocerebellum - follculonodular lobe - balance and ocular reflexes
cerebrocerebellum - lateral parts - movement planning and motor learning

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80
Q

what happens in damage to cerebellum and vermis

A

vermis damage - fall backwards

cerebellum damage - fall and decrease coordination on ipsilateral side

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81
Q

UMN lesion signs

A

increase reflex, tone, spasticity, rigidity, chorea (extrapyramidal), babinski (pyramidal)

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82
Q

LMN lesion signs

A

atrophy, fasciculations, paralysis

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83
Q

where are cell bodies of LMNs found in what lamnia

A

8 and 9

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84
Q

what is a motor unit

A

motoneurone and muscle fibre it supplies

85
Q

define stretch reflex

A

involuntary, unlearned, repeateable, automatic reaction to a specific stimulus which doesnt require brain intact

86
Q

components of stretch reflex

A

strech receptor, affereent fibre, integration centre, efferent fibre, effector

87
Q

muscle tone in newborn

A

suppressed to aid birth

88
Q

extrapyramidal lesion signs

A

akathisia (muscle restlessness), spasm, parkinsonian. Way that movements are carried out

89
Q

parkinsonian symptoms

A

tremor (pill rolling), cog wheel rigidity, postural instability, mask like expression, bradykinesia, shuffling gait

90
Q

decorticate and decerebrate

A

decorticate - mummy. damage to cerebrum, mid brain, thalamus, internal fibres poss
decerebrate - full exntension. brainstem damage

91
Q

why fasciculations occur in LMN lesion

A

hypersensitive ACh receptors

92
Q

what is spinal shock

A

damage to descending tracts leads to areflexia and flaccid which then become UMN signs. Due to release of GABA in damage

93
Q

what symptoms of cerebellar dysfunction

A

DANISH

dysdiadochokinasia, ataxia, nystagmus, intention tremor, scanning dysarthria, hypotonia + heel shin positivity test

94
Q

what romberg test and what positive meants

A

tests proprioception of lower body. suggests cerebellar damage

95
Q

Thalamic nuclei

A

VPL - spinothalamic and dorsal column
VPM - trigeminal - Face sensation and taste - Makeup on Face
LGN - Cn2 - vision - lateral = light
MGN - Hearing - Medial = music
VL - cerebellum and basal ganglia - Motor

96
Q

hypothalamic functions

A

TANHATS
Thirst and water balance, ant pit regulation, neural hormone release, hunger, autonomic regulation, temp regulation, sexual urges

97
Q

what is the cause of parkinsons

A

nigrostriatal and SN degeneration

98
Q

what is nociception

A

percetion of pain

99
Q

how does pain thershold and tolerance vary for people

A

threshold same, tolerance varies

100
Q

stages of nociception

A

transduction - activation of fibres
transmission - to CNS
modulation - CNS or other peripheral nerves can inhibit
perception

101
Q

what type of pain does Adelta and C fibre feel

A

Adelta - mechanical

C - mechanical, thermal, chemical

102
Q

properties of adelta and c fibre

A

a delta - sharp, stabbing, well localised, lower threshold, withdrawal reflex

C - burning, throbbing, poorly localised, higher thershold, tissue damage ongoign

103
Q

how is cerebellum mostly damaged and what is parkinsons damage of

A

parkinsons damage to extrapyramidal

cerebellum - tumours and strokes

104
Q

through what lamina do adelta C and visceral fibres travel

A

adelta - 1, 5
C - 1, 2 and 5
visceral - 5

105
Q

explain process of pain transduction

A

damage to tissue releases K, prostaglandins, serotonin, bradykinin and activates nociceptor. AP occrs and substance P is released. Substance P releases histamine from mast cells

106
Q

how do NSAIDs and steroids act as analgesics

A

NSAIDs inhibit prostaglandins

steroid inhibit IL

107
Q

explain pain modulation

A

gate control theory. Endorphins reduce nociception

Periaqueductal grey matter in midbrain projects to nucleus raphe magnus and both mediate pain.

108
Q

define chronic pain

A

> 3 mths and no ongoing tissue damage.

109
Q

define hyperalgesia and allodynia

A

allodynia - non painful stimulus = pain

hyperalgesia - lowered threshold to pain.

110
Q

explain process of winding up

A

repeated nociceptor stimulation leads to upregulation of neurones (reduced threshold and increased receptive field). Also change in somatosensory mapping

111
Q

chronic pain types

A

nociceptive, neuropathic, visceral, FMS (fibromyalgia)

112
Q

what is neuropathic pan. tgive example

A

sponteanous, shooting, pins and needles. not responsive to opioids.
e.g. phantom limb

113
Q

what is complex regional pain syndrome type 1 and 2

A

type 1 - no identifiable lesion

type 2 - lesion

114
Q

What is complex regional pain syndrome. give stages 1 to 3

A

severe continous burning pain.
1 - acute
2 - thickening skin. muscle atrophy. odema
3 - limited ROM. contractures. waxy skin

115
Q

function of opioid receptor

A

close vocc, open K, inhibit cAMP and neurotransmission

116
Q

give the 3 types of endorphin receptors and the associated endorphin

A

MOP - endomorphin
KOP - dynorphin
DOP - enkephalin

117
Q

give exmaple of strong and weak opioid

A

strong - fentanyl, morphine

weak - codein

118
Q

what is WHO pain ladder

A

1) non opioid e.g. paracetemol or NSAID, adjuvant
2) weak opioid +/- adjuvant
3) strong opioid +/- adjuvant

119
Q

how treat central pain

A

antidepressant, AED, anasthetic, opioid

120
Q

what causes inner ear deafness

A

teratogneic agents and infections e.g. rubella

121
Q

what is coloboma and what causes

A

hole in structyure of eye. caused by fialure of optic stalk to fuse

122
Q

give optic tract anatomy

A

see book

optic nerve to chiasm to tract to LGN to radiation

123
Q

what happens in full lesion of optic radiation, temporal lesion and nasal lesion?

A

full - homonymous hemi
temporal - homonymour superior quadrantanopia
nasal - homonymous inferior quadrantanopia

124
Q

what happens in midline lesion of optic chiasm

A

bitemporal hemianopia

125
Q

what is meyers loop

A

temporal part of optic radiation

126
Q

properties of rods and cones

A

rods - dark, not in fovea, converge on bipolar

127
Q

what are the neurons in the eye

A

photoreceptors, interneurons, ganglion cells

128
Q

give types of interneurons and their function

A

interneurons combine photoreceptor signals

bipolar, horizontal, amacrine

129
Q

what is the magnocellular and parvocellular cells

A

both in LGN. Magno responsible for resolving motion and outlines. Parvo responsible for colour contract

130
Q

give sign of fovea hyperplasia

A

nystagmus

131
Q

what is amblyopia and give causes

A

decreased vision in 1 eye due to disuse in childhood
cause - strabismus (inability to focus both eyes on a object), anisometropia (refractive diff in both eyes), deprivation e.g. ptosis or cataracts

132
Q

give types of strabismus and lesion causing

A

esotropia - inwards. CN 6 palsy
exotropia - outwards
hypertropia - upwards. CN 4 palsy

133
Q

how treat amblyopia

A

glasses or eyepatch

134
Q

waht is glaucoma

A

increased intraocular pressure poss cause opitic nerve damage or peripheral field defect

135
Q

what is function on inner and outer hair cells of ear. where is high and low frequency heard

A

outer - amplification
inner - sense
high frequency at base, low at apex

136
Q

how does AP in hair cells occur

A

bending of stereocilia opens K channels leading to depolarisation and calcium influx and neurotransmitter release to spiral ganglia neurones (afferents axons of CN 8)

137
Q

what is function of olivocochlear system

A

regulates outer hair amplification

138
Q

how is sound localised

A

delays and difference in volume between left and right ear

139
Q

how are loud sounds transmitted

A

increase AP and recruitment of neighbour cells

140
Q

give auditory pathway

A

cochlear nerve to cochlear nucleus to olivary nucleus to colliculus to MGN to auditory cortex

141
Q

give causes of hearing impairment

A

congenital, age, infection, gentamicin, loud noise

142
Q

how treat hearing loss

A

hearing aid or cochlear implant

143
Q

what artery casues most strokes

A

mid cerebral

144
Q

what does the PCA feed

A

occipital, midbrain, thalamus, half temporal

145
Q

define stroke and TIA

A

stroke - poor blood flow to brain over 24 hours symptoms

TIA -

146
Q

symptoms of temporal lobe stroke

A

tsate and smell, memory, superior quadrantanopia, wernickes aphasia

147
Q

what is wernickes and brocas aphasia

A

wenickes - problem comprehending

brocas - problem talking

148
Q

parietal lesion symptoms

A

speech, sensation, inferior quadrantanopia

149
Q

symptoms of lacunar stroke

A

pure motor, sensory, sensorimotor, ataxic, hemiparesis

150
Q

what structures involve din a POCS

A

brainstem, cerebellar, occipital

151
Q

how investigate and treat stroke

A

ct or mri

treat alteplase

152
Q

how can spinal cord blood supply be damaged and symptoms

A

cause - vasculitis, sickle cell, hypotension

symptoms - spinal shock, motorsymptoms

153
Q

what is flaccid and reflex bladder. where is lesion

A

flaccid - lesion below T12. LMN

reflex - T12 or above. UMNL

154
Q

how manage head trauma or loss of conscious

A

ABCD, history, exam

O2, if hypo IV glucose

155
Q

what is function of reticular activating system. affected by?

A

regulates sleep wake cycle

affected by alcohol, senses, drugs, parkinsions, schizo, PTSD, depression, alzheimers

156
Q

what is coup and contrecoup injury

A

coup - front brain

contrecoup - rebound

157
Q

what is contrusion

A

bruise

158
Q

what is primary and secondary insult to brain

A

primary - haematoma, hemorrhage, contusion

secondary - hypoxia, oedema, increased ICP

159
Q

what happens in disruption of BBB?

A

vasogenic oedema due to protein influx, increase ICP

160
Q

what is cytotoxic oedema

A

Na retention in cells leads to swelling and increase ICP

161
Q

how is increase ICP compensated. wjhat is cushings reflex

A

decrease venous blood and CSF

cushings reflex - increase BP, irregular breathing, decrease HR

162
Q

why might use barbiturates or propofol in increase ICp

A

both reduce cerebral metabolic rate of o2

163
Q

symtpoms of opioid

A

antitussive, analgesia, constipation, hypotensive

164
Q

function of mannitol

A

decrease cerebral oedema. osmotic diuretic

165
Q

what are the 4 brain waves and when are they seen

A

alpha - awake and resting
beta - awake and mental activity
theta - sleeping
delta - deep sleep

166
Q

what happens in locked in syndrome

A

loss of RAS descending pathways by lesion below pons

167
Q

what is coma, brain death

A

coma - state of unconsciousness which patient cannot be roused from. no voluntary movement but signs of active brain
brain death - irreversible loss of all features of brain

168
Q

function of sleep

A

allows cns to reset and memories to proces

169
Q

what control sleep wake cycle

A

RF and hypothalamus (by inhibiting RF)

170
Q

what happens in REM and non REM sleep

A

REM - active brain inactive body. increase RR, HR, BMR. Alpha and beta waves

non REM - inactive brain active body. neuroendocrine. decrease RR, HR, BMR. theta and delta waves

171
Q

what happens to wake us up

A

serotonin and ACh release stimulates thalamus

172
Q

what is parasomnia, hypersomnia, narcolepsy

A

parasomnia - sleep paralysis
hypersomnia - day time sleepiness
narcolepsy - constant hypersomnia

173
Q

if loss of consciousness occurs, why?

A

damage to Reticular formation

174
Q

give GCS

A

eye 1-4 - none, pain, speech, spontaneous
verbal 1-5 - none, incomprehensible, inappropriate words, confused, orientated
motor 1-6 - none, extension to pain, flexion, flexion to pain, localise pain, obey commands

175
Q

symptoms of extradural hemorrhage

A

trauma, slow onset, lucidity then decrease consc, increasing severity headache, vomiting and confusion

176
Q

subdural features and subarachnoid hemorrhage

A

subdural - slow onset, atrophy of brain, age, trauma, fluctuating consciousness, insidious physical or intellectual slowing

SAH - thunderclap headache, vomiting, seizures, neck stiffness

177
Q

parietal dominant and non dominant features

A

dom - speech, logic, sensation integration

non dom - emotion, language, music/art, visioaspatial, body awareness

178
Q

anterior frontal lesion

A

apathy, loss of personality, asocial, amoral, loss of social inhibition

179
Q

temporal lesion

A

speech (dominant), memory

180
Q

function of angular gyrus

A

takes written word interpretation from occipital to wernickes area

181
Q

where 2 diffeerent type sof memory stored

A

declarative - hippocampus, cortex

procedural - cerebellum, basal ganglia

182
Q

how is memory consolidated in neurones. techniques to consolidate memory?

A

rehearsal, association, emotion

via LTP

183
Q

causes of amnesia

A

trauma, stroke, infection, dementia

184
Q

hippocompal lesion

A

anterograde amnesia

185
Q

define dementia and symptoms. how does delirium differ

A

acquired loss of brain function significant enough to affect daily function and QOL. decrease intellect, reason, personality without loss of consciousness (delirium is loss of consciousness)

symptoms - progressive loss of memory. intellect, personality, behaviour, spech, movement

186
Q

causes of dementia

A

vascular, alzheimers, lewy bodies, drugs, fronto-temporal dementia

187
Q

describe pathogenesis of AD. RF?

A

aB amyloid deposits, tau neurofibrillary tangles.

RF - age and female

188
Q

lewy body dementia pathogenesis and symptoms

A

alpha synuclein amyloidosis. REM sleep behaviour disturbed, delusions, paranoia, goes on to have AD features

189
Q

AD pre-dementia, early, mid, late symptoms

A

pre - subtle - forgetfullness, planning, apathy
early - anterograde amnesia starts (harder to learn things), loss oral and written fluency
mid - speech problems, aggression, irritability,
late - complete loss language, exhaustion, extreme apathy, poss bedridden

190
Q

fronto-temporal dementia

A

increase tau protein, lack of empathy, disinhibiton, personality loss

191
Q

normal pressure hydrocephalus symptoms

A

dementia, incontinence, gait

192
Q

causes of meningitis

A

neonates - e coli
1-5 - h influenza
5-30 - n meningitidis
>30 - strep pneumoniae

193
Q

what is encephalitis

A

viral infection of brain parenchyma

194
Q

what brain part does herpes infect and symptom

A

infect temporal lobe, lead to seizures

195
Q

what is perviascular cuffing

A

aggregation of lymphocytes around a BV in encephalitis

196
Q

what is normal brain pressure, in coughing, and what can it get up to

A

normal - 0-10
coughing - 20
up to 60mmHG

197
Q

what is subfalcine hernia. ischemia of?

A

cingulate gyrus goes under falx cerebri. ischemia of parietal, frontal, corpus callosum

198
Q

what is tentorial hernia. damage to?

A

uncus and parahippocampus through tentorial notch. damage to CN3 and occlusion of PCA and sup cerebellar arteries

199
Q

what is tonsillar hernia and damage?

A

cerebellar tonsils through foramen magnus, compressing brainstem. apnoea.

200
Q

symptoms of increased ICP

A

headahce, vomiting, papilloedema - leading to pupil dilation, coma

201
Q

types of brain tumours

A

meningioma, astrocytoma (malignant), metastases (Skin, lungs, kidney, breast, GI)

202
Q

difference taste and flavour

A

flavour inc smell

203
Q

what produces and absorbs intraocular fluid

A

produced - ciliary body

absorbed - schlemm (venous sinuses)

204
Q

what is presbyopia

A

long sighted with age

205
Q

what is scotomata

A

pathological blind spot

206
Q

how test colour vision

A

ishihara chart

207
Q

symptoms of TACS and PACS

A

TACS is all of HHHH, PACS is 2 of 4

hemiparesis, higher cerebral dysfunction (dysphagia, hemineglect, agnosia), hemianopia, hemisensory loss

208
Q

POCS symptoms

A

loss of consciousness, visual disturbance, DANISH

PPE (18 decks)

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