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Neuro Flashcards

1
Q

where does pain sensation travel?

A

anterolateral tract

crosses over + make connections immediately

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2
Q

ependymal cells of CNS

  • what are they
  • what do they look like
A

cells that line central canal of spinal cord + ventricle in brain

low columnar/cuboidal cells
may have cilia (aid CSF flow)
non basal laminar - diff from epithelial
=> have processes that extend below where BM would be

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3
Q

what is the choroid plexus

  • where is it found
  • what does it look like
  • what does it do
A

lines ventricles

vascular structure arising from wall of each ventricle

produces CSF

look like specialised epithelium

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4
Q

neurons
- morphology
-

A

morph:
have soma (body) = metabolic centre
dendrite = receive info
axons - main conducting unit

various morphologies

most of the cell is dendrites + axons => damage often involves axon

cytoskeleton regulates morphology (actin, intermediate processes, mucrotubules)

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5
Q

astrocytes

- functions (passive, active)

A

passive support functions

  • when a neuron fires
  • nt uptake from synaptic cleft
  • K+ homeostasis (clean in released K+)
  • neuronal energy supply (shunt glucose from blood -> neuron)
  • maintenance of BBB
  • injury response, recovery

active functions

  • modulate neuronal function
  • modulate blood floow
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6
Q

how do astrocites modulate neuronal function

how do they modulate blood flow

A

(1) modulate intracellular calcium -> communicate with each other with a wave of Ca2+ through neural tissue

this can be initiated by nt’s, trauma, inflammation

(2) have synaptic vessels; small number released comp to neurons

(3) can directly regulate neuronal function
- inhibits neurons through release of ATP (stim by Ca2+ wave)

(4) modulation of blood flow
- surround blood vessels, and regulate vascular tone
- Ca3+ wave causes changes in constriction/dilation

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7
Q

oligodendrocytes + Scwann cells

  • function
  • how do they differ
A

function: myelin sheath

oligodend

  • CNS
  • each one has processes that wrap around parts of several axons

scwann

  • PNS
  • wrap only around one axon
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8
Q

microglia

  • function
  • morphology
A

immune cells of CNS - CNS is immune privileged

also regulate synapses

look like macrophages - phagocytic

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9
Q

which motor units are recruited first?

A

smaller motor units

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10
Q

what happens if muscle stays unactivated? (3)

A

hypersensitivity + ↑AchR expression on muscle cells - want to increase their capacity to get excited

(1) fibrillation - 1 mucle cell activity
(2) fasciculation - groups of fibres contracting involuntarily (motor unit)
(3) atrophy if LR = irreversible

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11
Q

which category of nerves is involved in reflexes?

A

LMN

golgi + muscle spindle

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12
Q

Which category of nerves is responsible for voluntary muscle activation

A

UMN

  • spinal interneurons
  • muscle spinkdles
  • UMN from brain
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13
Q

what is normal UMN activity (onto LMN)

A

= inhibitory

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14
Q

what are the UMN tracts in the spinal cor? where do they run

A

lateral (from cortex)
- corticospinal
- rubriospinal
= distal muscles

ventromedial (from brainstem)
- medial MN = proximal muscles (posture)

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15
Q

what is the rubriospinal tract

  • origin
  • pathway
  • function
A

mediates voluntary movement

origin: red nucleus (midbrain)
- crosses in midbrain, descends in lateral spinal cord

function: flexors, upper limb

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16
Q

UMN vs LMN sins

A

UMN lesion

  • weakness
  • spasticity - ↑tone, reflexes
  • clonus
  • babinsky sign
  • ↓fine motor movement

LMN lesion

  • weak
  • ↓reflexes, tone
  • fasciculation, fibrillation
  • atrophy
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17
Q

Lateral motor tracts

  • what do they do
  • where do they descend
  • what are the tracts involved
A

control movements of extremities (cf postural)

descend in contralateral spinal cord

tracts: lateral corticospinal, rubriospinal

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18
Q

Lateral corticospinal tract
- what kind of movements are involved

origin
decussation
termination
function

A

controls movements of extremities (cf postural) wiht rubriospinal

origin - primary motor cortex

decussation - pyramidal (lower medulla)

terminates - whole cord

function: moving contralateral limbs; rapid, dextrous movements

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19
Q

rubriospinal tract

origin
decussation
termination
function

A

red nucleus

decussate - midbrain

terminate - cervical cord (upper limb flexors)

function: move contralateral upperlimbs

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20
Q

describe pathway of lateral corticospinal tract

A

start in primary cortex (50%) or premotor, supplementary parietal lobe

move through internal capsule
- somatotopic (face–>arm -> trunk -> leg)

move through middle 1/3 of basis pedunculi (anterior cerebral peduncles)

at medullary pyramids

  • 80% of fibres decussate
  • other 15% of fibres continue ipsilaterally as anterior corticospinal tract

at the spinal cord, synapse onto LMN in ventral horn

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21
Q

what are the parts of the internal capsule?

A

genu in middle

anterior limb - separates head of caudate from globus pallidus + putamen

posterior limb - separates thalamus from globus pallidus + putamen

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22
Q

Medial motor systems

  • what movements do they control
  • where do they descend
  • how do lesions present?
  • what tracts make it up

which one decussates

A

proximal axial/girdle muscles => posture, balance, orienting head/neck movement, autonomic gait

descend either ipsilaterally or bilaterally

lesions tend to produce no obvious deficits as they tend to terminate on interneurons that project to both sides of the cord

tracts: 
anterior corticospinal
vestibulospinal
reticulospinal 
tectospinal

tectospinal decussates in midbrain

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23
Q

anterior corticospinal tract

  • what does it do
  • what is its origin, path, level of termination
A

controls bilateral axial + girdle muscles

from primary motor cortex -> no decussation -> terminates at cervical + upper thoracic levels

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24
Q

vestibulospinal tract

  • what does it do
  • what is its origin, path, level of termination
A

balance + postural control

vestibular nuclei, runs ipsilaterally

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25
Q

reticulospinal tract- what does it do

- what is its origin, path, level of termination

A

maintain muscles of midline

pontine + medullary reticular formation, runs ipsilaterally

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26
Q

how can you localise damage in spinal cord with postural signs?

A

postural signs

decorticate rigidity - upper flex, lower extend

decerebrate ridigity - upper extend, lower extend

=> use reticulospinal + rubriospinal tracts

reticulospinal tract - starts in the pontomedullary reticular formation; results in extension > flexion

rubriospinal tract starts in red nucleus (midbrain); main role is flexors of upper limb

UMN inhibit both of these

=> if the lesion is above the red nucleus - the person will be decorticate => remove inhibition on both -> upper flex, lower extend

=> if the lesion is below the red nucleus - the person will be decerebrate => red nucleus is compromised, and will have no flexion of upper limbs => extension of both

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27
Q

define

decorticate rigidity -

decerebrate ridigity -

A

decorticate rigidity - upper flex, lower extend

decerebrate ridigity - upper extend, lower extend

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28
Q

what is the corticobulbar tract?

is innervation bilateral or unilateral

A

UMN for cranial nerves

get bilateral innervation of nuclei from cortex EXCEPT

NVII (facial)
NXII (tongue)

=> only get contralateral innervation

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29
Q

what is involved in reflexes + postural control?

A

anticipation - tense muscles when know a force is coming, prepare for postural disturbance
=> occurs through corticospinal tracts running ventrally/ipsilaterally

reflex control of muscle

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30
Q

what controls locomotion?

what stimuli are involved

A

lumbar-sacral spinal cord = pattern generating circuilts
- alternating patterns of MN activity to R&L flexors/extensors

limb alternates betweeen swing (flex) and stance (extend) phases

cortex inputs on top of this to change pattern

stretch of muscle signals full extension, and signals to start flexion phase

golgi tell you if you’re bearing weight on a limb -> flex once the force drops

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31
Q

how do decerebrate cats locomote?

how do they respond to changing speeds on a treadmill?

A

pattern generation from lumbar-sacral spinal cord

can increase gait when treadmill speed increases

  • stretch on muscle signals end of extension phase
  • golgi tells you if limb is weight-bearing - only flex once weight is lifted
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32
Q

where is the abnormality in..

ataxic gait
hemiparetic gait
circumducting gait
parkinsonian gait

A

ataxic gait - cerebellum

hemiparetic gait - cerebrum
- loss of desc. motor tracts -> stiff leg, no bending of knee/ankle, swing leg out while rotating/tilting hip

circumducting gait - cerebrum - stroke
- weaken one leg - swing leg around

parkinsonian gait- basal ganglia

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33
Q

how is the primary cortex organised?

A

neurons represent functionally relevant movements (not just bits of body) => bc same muscle can do different types of movements

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34
Q

what is the function of each of these in movement:

  • premotor areas
  • supplementary motor areas
  • primary motor
  • basal ganglia
  • cerebellum
A
  • premotor areas - motor activation
  • supplementary motor areas - sequence learning
  • primary motor
  • basal ganglia - learning + selection of motor programs/strategies
  • cerebellum - coordination, optimise sensory motor integration
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35
Q

what are the premotor areas? what do they do?

A

rostral to lateral part of primary motor cortex

involved in motor activation

+ higher level sensory association
+ integrate value, salience, consequences of movement

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36
Q

what are the supplementary motor areas? what do they do?

A

rostral to medial part of motor cortex

  • involved in more complex movements - sequences etc
  • involved in mental rehearsal of movements
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37
Q

functions of basal ganglia (3)

A

sequence of muscle activation, complex skills

(1) allow selection of complex patterns of voluntary movement
(2) evaluate success of actions in achieving goals
(3) intitiating movements

Parkinson’s - know goal, but can’t get out of chair

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38
Q

how does the basal ganglia impact movement?

A

loops with thalamus and cortex (motor, limbic, oclulomotor, prefrontal regions)

there are 2 parallel streams of info - is basically the cortex talking to itself

(1) direct - stimulates movement
(2) indirect - excitatory, stimulates movements, leaves you with a program

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39
Q

functions of cerebellum

A

(1) coordinate timing, sequence of muscle actions + movements
(2) maintain muscle tone

(motor learning

(3) plannign sequences of muscle activation for complex movement

=> optomises patterns of movements, and the precise onset/offset of muscle for smooth movements

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40
Q

anatomy of the cerebellum

A

3 lobes

  • anterior
  • flocculonodular
  • posterior

has fragmented somatotopy - middle represents midline; lateral = lateral etc.

cerebellar pedunces connect it to the pons

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41
Q

cerebellar influence on the body - contralatera, ipsilateral?

A

cerebellum -> motor cortex = decussation
motor cortex -> body = decussation

=> ispilateral control of body

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42
Q

how do the basal ganglia + cortex + cerebellum talk to each other

A

Cerebral cortex -> basal ganglia -> thalamus -> cortex
- basal ganglia -> brainstem -> body

cerebral cortex -> pons -> cerebellum -> thalanus -> cortex
- cerebellum -> brainstem -> body

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43
Q

what is the function of the substantia nigra?

A

produces melanin (part of dopamine synthesis pathway)\

signals with dopamine to corpus striatum to produce tonic inhibition

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44
Q

pathophys of parkinson’s

A

degeneration of dopaminergic nerves in substantia nigra -> ↓DA

involves alpha-synuclein
(found in Lewy bodies - round inclusions in cytoplasm of cells in the substantia nigra in Parkinson’s)

alpha synuclein - normally sits unfolded on outer surface of synaptic vesicle, is soluble

in metal env: dopamine becomes redox active => abnormal folding
=> disrupt DA vesicle function

  • alpha -synuclei -> misfolding -> Lewy bodies -> toxicity to neurone
  • alpha synuclein -> DNA mutation -> mitochondrial dysfucntion

mt dysfunction -> ROS -> toxicity
mt dysfucntion -> ROS -> ↑ alpha-synuclein (/misfolding)

an inherited form has mutations in parkin (ubiquinin protease system ) -> parkin normally degrades proteins that are toxic to DA neurons

=> all lead to neuronal cell death

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45
Q

risk factors for parkinson’s

protective factors

A

alpha-synuclein mutation

mitochondria

pesticides - decouple mt - ↑ROS
(rotenone, paraquat)

age

protective factors

  • coffee
  • cigarettes
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46
Q

first signs of parkinson’s

A

↓olfaction

bowel,bladder issues

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47
Q

drugs used in parkinson’s

A

levodopa = LDOPA isomer - try to increase DA formation in sub nigra

dopamina agonists

amantamide - increase release of stored DA

selegilin + entacapone - stop degradation of DA/L-DOPA) - given as adjunct

if give L-DOPA -
carbidopa - peripheral DDC inhibitor (doesn’t cross BBB) -> stops the increase of DA in the rest of the body, only want increase in the sub nigra
(problem - ↓degen of neurons - DA metabolism - ↓ROS?)

(DDC = change L-DOPA -> DA)

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48
Q

where is the auditory cortex?

how is it organised?

A

Brodmann’s 41 in temporal lobe

  • tonotopic
  • alternating regions of each ear

usually
L= speech
R= music

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49
Q

cognition - function of

  • frontal lobe
  • temporal lobe
  • parietal lobe
  • occipital lobe
A

frontal

  • plan
  • execution + regulation of behaviour
  • higher level processing

temporal

  • audition
  • language
  • music
  • memory
  • emotion

parietal
- somatic + visuospatial representation

occipital

  • vision
  • role in visuospatial
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50
Q

emotion - which structures are involved

A

limbic system (hippocampus, amygdala)

orbitofrontal cortex - identifies + expresses

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51
Q

lesion in orbitofrontal cortex

A

report normal emotion but have difficutly expressing

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52
Q

how do cognition and emotion influence each other?

A

internal dialogue required to process emotion

cognitive appraisal directly changes physiological response
=> your perception affects emotion

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53
Q

what is executive function?

function of which part of brain

A

inter-related processes responsible for goal directed, purposeful behaviour

includes emotional + social behaviour + cognition

frontal lobe function

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54
Q

what is the prefrontal cortex?

functions

regions

A

cerebral cortex which covers the front part of the frontal lobe

= coordinator of executive functioning

regions:

  • dorsolateral
  • medial
  • orbitofrontal
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55
Q

function of dorsolateral pre-frontal cortex

arterial supply

A

traditional executive functions

  • working memory
  • respose selection and changing strategy
  • planning + organising
  • hypothesis generation
  • flexibly maintaining or shifting set (between ideas)
  • insight
  • moral judgement

supplied by MCA

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56
Q

function of medial pre-frontal cortex

arterial supply

A

motivation + initiation

self-awareness - understanding own emotions + attributing emotion to others

supply: ACA

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57
Q

function of orbitofrontal prefrontal cortex

arterial supply

A

emotional processing
inhibition
impulsivity

supply: ACA + MCA

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58
Q

development of executive function

A

maturation of frontal lobe = last lobe to develop, first to degenerate

executive function - among last ability to develop
- need good stimuli as kids

progression:

  • lower order functions develop first
  • higher order (Set shifting, reasoning) develop later

is a dynamic process of neuronal proliferation + pruning

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59
Q

what is executive dysfunction?

where is the defect?

A

not a unitary disorder

executive function - mainly thought to be a frontal lobe thing
but executive dysfunction =/= frontal lobe dysfunction

  • highly connected to other parts of brain
  • lesion anywhere in system can cause executive dysfunction

PFC = “coordinator” of executive functioning

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60
Q

symptoms of executive dysfunction

A

positive symptoms

  • distractability
  • social disinhibition
  • emotional instability
  • perseveration (unable to stop when has started something)
  • impulsivity
  • hypergraphia (write lots)

negative symptoms

  • lack of concern
  • restricted emotion
  • deficient empathy
  • failure to complete tasks
  • lack of initiation
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61
Q

tests of the dorsolateral PFC

A

tower of london - planning, impulsivity, learning from mistakes

stoop test (say name of colour, not read word)

key complex figure test - copy the figure

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62
Q

language - where is it located

A

generally hemispheric dominance

L = language

R = visuospatial function, paralinguistic aspects, prosody (rhythm, stress, intonation), non-propositional speech

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63
Q

what change in language might you get if there is a R hemisphere lesion?

A

disorder in social aspects of language

  • picking key messages
  • intonation
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64
Q

Production disorder

  • what kind of aphasia
  • where is the lesion
  • describe syndrome
A

non-fluent language disorder = Broca’s aphasia

Lose ability to produce appropriate output sequences - content is ok, but no grammar

Lesion: anterior (frontal lobe) = Broca’s area (produces speech)

Syndrome

  • effortful language output
  • preserved comprehension
  • right face + arm weakness (frontal lobe)
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65
Q

Selection disorder

  • what kind of aphasia
  • where is the lesion
  • describe syndrome
A

fluent language disorder = Wernicke’s

Lose ability to choose appropriate content (right words for objects etc) but have intact grammatical structure

Lesion: posterior (temporoparietal lobe) = Wernicke’s area (understanding language)

Syndrome

  • fluent - lots of output
  • jargonistic (wrong words) - neologisms (made up words - may be consistent), paraphasic (boap for boat)
  • impaired comprehension
  • right quadrantonopia
  • no motor weakness
66
Q

what is the arcuate fasciculus?

A

hypothetical whtie matter tract that connects Wernicke’s and maybe Broca’s areas

67
Q

what is a conduction aphasia

A

fluent aphasia, but more meaningful than Wernicke’s

relatively intact auditory comprehension

but poor repetition

probably due to arcuate fasciculus damage (connection bw Broca’s and Wernicke’s)

68
Q

what is a transcortical motor aphasia?
where is the lesion
syndrome

A

lesion in cingulate, prefrontal cortex, medial prefrontal lobe

non-fluent aphasia, at most severe: mute

repetition is preserved but no spontaneous language

69
Q

how might one recover from an aphasia?

A

(1) contralateral transfer - some of the function moves to the other hemisphere
- only occurs if timin is right (eg kids)

(2) ipsilateral re-organisation - surrounding tissue reorganises

70
Q

what is declarative memory?
what is non-declarative memory?

where do you see a breakdown clinically

A

declarative = episodic (events) + semantic (facts)

non-declarative = skills, habits, priming
= long term, implicit

usually clinically you see breakdown of declarative memory, rather than non-declarative

71
Q

what is priming (regarding memory)

A

eg give someone a list of words, which includes the word ‘table’
then later ask them for words starting with ‘t’ - they will say ‘table’

72
Q

what is episodic memory

A

autobiographical - events put into personal context

- each person’s memory of this is slightly different

73
Q

what is semantic memory

A

general facts, not specific to the individual

shared knowledge, everyone remembers the same

74
Q

anatomy of memory

A

enterhinal + perhinal - uptake of info

hippocampus - consolidates + stores information
medial temporal lobe

75
Q

patient H.M - where was the lesion?

what did they present with clinicalyl

A

bilateral resection of medial structures of temporal lobe (bc of severe epilepsy)

profound impairment of recent memory

76
Q

mechanism of memory storage

  • SR
  • LR
A

hippocamus grows (eg in london cabbies)

SR - insertion of AMPA receptors, phosphorylation

LR - protein synthesis, structural changes, LR plasticity

molecular pathways:
glutamate receptors in the hippocampus = NDMA receptors
- made up of NR1 + one of NR2A (adults) NR2B (kids)

NR2B - greater plasticity

77
Q

is there lateralisation of the hippocampus regarding memory?

A

L hipp

  • verbal memory
  • lists
  • paired association

R hipp

  • non-verbal
  • visuospatial
  • face recall
78
Q

Temporal lobe epilepsy

  • cause
  • memory disturbance
A

hippocampal sclerosis

= declarative memory disturbance

79
Q

what is mild cognitive impairment?

A

subclinical, precursor to Alzheimer’s

transitional phase bw normal ageing + dementia

  • self-reported memory complaints
  • mild objective memory impairment
  • unaffected general cognitive functioning
  • normal capacity for ADL
80
Q

Cognitive rehab principles

A
  • take place in real world context - actually practice skills the person needs (as opposed to just getting better at worksheets)
  • want to enhance participation, reduce functional limitation (focus away from what can’t do)
  • tailor to the individual (eg use of diary) => pre-injury traits are important
  • collaboration with client/family/treatment team
81
Q

types of cognitive rehab interventions

A

(1) env modification - reduce impact of cognitive/behav difficulties
- heavily used early on
- useful if reduced insight, self-monitoring, regulation

(2) compensatory strategies
- use skills they have to circumvent
- internal strategies (eg menumonics) - if have insight
- external strategies (eg smartphone) - cues + aids

82
Q

raised ICP

  • compensation
  • possible consequences
  • possible causes
A

compensate initially by expelling CSF + blood
- reduce ventricle size
- gyral flatenning
=> then the ICP will reduce

consequences: ↓perfusion, herniation
causes: oedema, obstruction to CSF flow, tumour of choroid plexus (↑CSF production)

83
Q

cerebral oedema - what are the 2 types

  • what brain tissue is affected
  • can it be treated?

possible causes of each

A

vasogenic + cytotoxic

  • vasogenic - disruption of BBB + ↑vasc. permeability => extravasation of fluid into interstital space
  • primarily white matter
  • responsive to steroids + isotonic pressure manipulations
  • causes: tumours, infections etc.

cytotoxic

  • increased intracellular fluid, secondary to neuronal, glial, endothelial cell membrane injury
  • grey + white matter affected
  • not responsive to therapy (steroids etc)
  • eg. stroke
84
Q

herniations due to ↑ICP (3)

  • structure that herniates
  • symptoms
A

(1) subfalcine herniation
- cingulate gyrus pushed under falx
- often asymptomatic
- usually first to occur

(2) transtentorial herniation = uncal
- medial part of temporal lobe pushed through opening formed by tentorium
- brain stem pushed over and compressed
- signs: CNIII paresis - dilated pupil; contralateral hemiparesis, sometimes ipsilateral (compressed cerebral peduncle)

(3) -tonsilar herniation
- cerebellar tonsills herniate into spinal cord
- LOC, death

85
Q

what is a possible complication of transtentorial herniation?

A

occpital infarction - ipsilateral PCA is compressed (sometimes bilat)

86
Q

what are Duret haemorrhages

A

Duret haemorrhages = bleed due to tearing of pontine perforating branches when brainstem is pushed down due to ↑ICP

(secondary to brainstem herniation)

get bleed into brainstem/pons

87
Q

Traumatic head injury - what injury can you get to the scalp?

A

laceration

88
Q

what are some secondary effects of traumatic head injury

- time frame

A

may be delayed, or contribute to immediate clincal income

ischaemia, hypoxia - due to accident itself

↑ICP, infection, epilepsy - delayed

89
Q

what is concussion?

pathogenesis

A

instantaneous loss of consciousness, temporary respiratory arrest, loss of reflexes

follows sudden change in the momentum of the head
uncertain pathogenesis - maybe effect is at brainstem level?

brain moves -> injury at a level we can’t pick up on scan?

90
Q

what are some long term sequalae of brain trauma? (8)

A

infection (if connection with outside)

hydrocephalus (ventricles dilate -> brain tissue compressed; old blood may block off exit foramia)

epilepsy (old or acute injury)

chronic traumatic encephalopathy (punch drunk syndrome)

brain atrophy due to neuronal loss (w recurrent trauma)

abnormal deposition of Tau protein

diffuse deposition of A-beta plaques in cortex

91
Q

subdural haematoma

  • which structure is damaged
  • what kind of bleed
  • what are the consequences
  • risk factors
A

bleed in subdural space

subdural veins damaged
- low P bleed -> can be acute or chronic

consequences: slow ↑ICP, neurological decline

risk factors: age - ↑tension in veins

92
Q

extradural haematoma

  • which structure is damaged
  • what kind of bleed
  • what are the consequences
  • risk factors
A

MMA is damaged

high P bleed -> quick ↑ICP -> rapidly kills

risk factor: usualyl associated with severe injury

93
Q

why do you have ↓risk of extradural haematoma with age?

A

dura - more adherent to skull with age

but ↑risk subdural - + brain atrophy

94
Q

what is a contusion? what are the types in the brain

A

contusion = haemorrhagic necrosis (bruise)
- as brain impacts on skull

coup = at imact site

contrecoup = on geometric opp site (if head not immobilised at time of injury)

stereotypic contusions = on base of brain (inf frontal lobe, inferolateral temporal lobe) - bc brain is knocked on bony bits

95
Q

contusion in brain - what does it look like when healed

A

tissue collapses down

get orange stain (macrophages)

scarring

96
Q

why might you get anosmia in traumatic brian injury?

A

contusions at base of brain -> damage olfactory nerves

97
Q

Diffuse brain injury

  • how does it occur
  • what is a characteristic site

what are some types

A

not macroscopic - injury may damage individual axons

  • corpus callosum vunerable

types:

  • diffuse vascular injury
  • traumatic/diffuse axonal injury (secondary injury)

Diffuse vasc injury

  • tear of small vessels
  • spotty haemorrhages

TAI/DAI

  • brain looks normal
  • spotty haemorrhage in corpus callosum = clue that axons have been damaged => may be torn all over
98
Q

traumatic/diffuse axonal injury

  • what does it look like histologically?
  • long term effects
A

if silver stain to show axons
- get areas of swelling = axon has been transected and there is a buildup of axonal material
= axonal sphenoids

Long term effects
- brain atrophy (dilated ventricle, thin corpus callosum, decreased white matter)
(damage + removal by macrophages)

99
Q

patterns of meningitis CSF

  • virus
  • bacterial
  • tb
=> pressure
=> colour
=> WBC
=> RBC 
=> gram stain
=> protein
=> glucose (blood = >60%)
A

=> pressure

  • virus - normal
  • bact + TB ↑

=> colour

  • virus - clear
  • bact + TB - cloudy

=> WBC

  • virus + TB = 100s L
  • bact = 1000s N

=> RBC = all none

=> gram stain
- virus none, bact yes, tb - ZN

=> protein (normal 1.0
- tb 1-5.0

=> glucose (>60% of blood)

  • virus - >60% of blood
  • bact - <30% of blood
100
Q

treatment of meningitis

A

treat as bacterial always

adults: 3rd gen cephalosporin
kids: IV penicillin, IV gentamicin, + 3rd gen cephalosporin (for E. coli)

101
Q

bacterial meningitis pathogen

  • adults
  • kids
A

adults:

  • N. meningitides
  • S. pneum
  • HiB

neonates (from birth canal)

  • E. coli, GNRs
  • Strep. agalacticae (grp B)
  • Listeria monocytogenes
102
Q

pathogenesis of meningitis

A

nasopharynx colonisation + infection

blood

BBB crossed -> meninges

↑permeability of BBB -> inflam mediators get in -> neuronal injury

103
Q

encephalitis

  • distinguishing from meningitis
  • pathogens
  • consequences
  • treatment
A

encephalitis = changed conscious state

VIRAL - usually HSV 1+2

almost always death

treat with acyclovir (bc of HSV)

104
Q

how do viruses spread into the brain?

- examples of pathogens

A

(1) though peripheral nerves (come in through axon fibres)
- peripheral nerves - no MHV - protected
- eg rabies, HSV

(2) through the blood stream
- go through cerebral/meningeal blood vessels/choroid plexus
- eg polio, mumps, measles, coxsackie

(3) through olfactory bulb
- eg coronavirus, hsv

105
Q

what secondary syndromes can viruses cause in the CNS (without being present in the CNS)

A

post-infectious encephalomyelitis

  • viruses look like myelin - autoimmune (no virus in cns)
  • measles, vzv, rubella, mumps

Guillain-Barre syndrome

  • inflammatory demyelinating disease after infection
  • partial/total paralysis
  • ebv, cmv, hiv

Reye’s

  • cerebral oedema - but no inflammatory cells get in
  • vv, influenza in kids
106
Q

why should you not give aspiring to kids with the flu/chicken pox?

A

reye’s syndrome

- cerebral oedema - but no inflammatory cells gettingin

107
Q

poliovirus

  • neuroinvasive, neurovirulent?
  • virus relationship to nerve cells

pathogenesis

consequences in cns

A

↓neuroinvasiveness, ↑neurovirulence

polio - cytocidal - kills cell to get out, doesn’t hide in nerve cells, doesn’t have to grow in nerve cells

pathogen

  • ingested -> lymphoid tissue -> blood
  • travels free in blood
  • can cross BBB
  • replicates in anterior horn cells -> paralysis

rarely gets into cns, but when it does - paralysis in hours

  • lower limbs > upper limbs
  • death if affects resp muscles, may attack MN of brainstem

50% of cases are <3yo

108
Q

VZV in cns

  • neuroinvasive, neurovirulent?
  • virus relationship to nerve cells

pathogenesis

A

↓neuroinvasiveness, ↑neurovirulence

growth in nerve cells is obligatory

pathogenesis

  • primary replication on mucosal surface
  • latent phase - sit in PNS ganglia
  • may cause serious cns infection if secondary infection disseminates to CNS (or may just be shingles)
109
Q

HSV type 1 in cns

pathogenesis

A

primary infection - mouth, throat = local infection
may enter local nerve endings and migrade to dorsal root ganglion = latent infection
if remerges into CNS = encephalitis

110
Q

rabies in cns

  • neuroinvasive, neurovirulent?
  • virus relationship to nerve cells

pathogenesis

symptoms

A

↑neuroinvasiveness, ↑neurovirulence

growth in nerve cells is obligatory

pathogenesis
- spread in saliva -> bite punctures skin -> replicates in myocytes-> gets to nerve
- travels up spinal cord to brain
from brain travels to salivary gland

(replication in nerve body -> rabies glycoprotein displayed on surface = target for antibody = cell death)

symptoms - aggression, thirst, but muscle spasm if you try (doesnt want to get diluted)

111
Q

stroke - how common are

  • haemorrhage
  • infarction
  • subarachnoid
A

infarct - 75%

haemorrhage - 20%

subarachnoid - 5%

112
Q

cerebral infarct mechanisms (3)

A

(1) hypoperfusion

(2) narrowed vessel lumen
- atheroscl, thrombosis, hypertensive vessel thickening, diabetes, amyloid angiopathy

(3) vessel occlusion - embolus
= most common

113
Q

cerebral infarct definition

A

= necrosis of cerebral tissue in a particular vascular distribution, due to vessel occlusion or severe hypoperfusion

114
Q

sources of embolus causing stroke

A

cardiac

  • AF
  • endocarditis
  • probe patent interatrial septum (venous origin embolus)

large artery occlusion - usually embolic

small vessel occlusion - usually thrombotic

venous occlusion - thrombotic always (embolus would have got stuck elsewhere)

115
Q

what are teh common sites for atherosclerosis in circle of willis? (4)

A

vertebral arteries

basilar artery 

internal carotid termination areas  

proximal medial cerebral artery
116
Q

pathological + histological changes in brain tissue after infarct

  • 36hrs
  • days->weeks
  • months->years
A

36 HOURS
- swelling of brain
= cytotoxic oedema (cell memb breakdown - cell accumulates fluid - tissue swells)
- can lead to herniation
- loss of demarcation between white + grey matter

histo

  • swollen neurons
  • dead neurons (hypereosinophilic, shrunken, pyknotic nucleus)

DAYS -> WEEKS

  • less swelling, tissue breaking down
  • liquefactive necrosis
  • sharp demarcation bw normal and infarct

histo
- necrotic tissue + macrophages (coming in to take away debris)

MONTHS -> YEARS

  • cystic space (CSF)
  • tissue gone
117
Q

how can infarcts develop haemorrhage?

A

Thromboembolus lodges, but as it was not formed at that site, it is likely to break down

Embolus causes infarction at the site -> blood vessels become necrotic and die

Once the area is reperfused -> dead blood vessels can no longer hold blood -> secondary haemorrhagic infarct
=> also - the blood that comes in is at arterial pressure -> even more damage

=> neurological deficit becomes works because of more tissue damage

118
Q

what causes death in people with cerebral infarcts>

A

Possible, but uncommon
=> involvement of vital centres
=> cerebral swelling

Mostly, people die as a consequence of incapacitation, or because they already have the risk factors for other cardiovascular events
=> pneumonia
=> cardiovascular disease
=> pulmonary thromboembolism

119
Q

causes of intracerebral haemorrhage (5)

A
  • hypertensive haemorrhage
  • cerebral amyloid angiopathy
  • multifocal synchronous haemorrhage
  • iatrogenic
  • congenital malformation (AV malformation)
120
Q

hypertensive haemorrhage (stroke)

  • what characterises it
  • which sites does it generally affect
  • pathogenesis
A

characterised by presence of small vessel disease (hyaline arteriolosclerosis)

sites = deep structures

  • basal ganglia/thalamus
  • lobar white matter
  • cerebellum (may cause obstruction of 4th ventricle)
  • pons - quick death

pathogenesis

  • thickened wall
  • weakens
  • balloons
  • haemorrhage

if it gets into ventricular system -> ↑ICP

121
Q

cerebral amyloid angiopathy

  • pathogenesis
  • histology
  • characteristic location
  • what is it associated wtih?
A

deposition of Abeta amyloid in walls of superficial supratentorial blood vessels

  • thickened wall
  • liable to rupture

histo

  • bright pink, dense material
  • thickens walls of small vessels

location: superficial haemorrhages - often multiple and of varying age

associated with alzheimers

122
Q

multifocal synchronous haemorrhage

- causes

A

systemic problem

= coagulopathy (eg leukaemia)
= watershed - hypoperfusion

123
Q

causes of subarachnoid haemorrhage (non-traumatic) (3)

A

rupture berry aneurysm (congenital weakness in wall)

rupture of mycotic/atherosclerotic aneurysm

extension of intracerebral haemorrhage

124
Q

risk factors for development of saccular aneurysm

A 
female
old
hypertension
smoking
PCOS
type 3 collagen defect
125
Q

saccular aneurysm in CNS

  • where do they occur?
  • complications of rupture
A

occur at sites of congenital weakness - arterial bifurcations

  • anterior circulation > posterior
  • bi/trifurcation of MCA
  • anterior communicating
  • junction of internal carotid and posterior communicating

complications

  • subarachnoid haemorrhage
  • cerebral oedema, ↑ICP
  • vasospasm, infarct
  • ventricular obstruction -> hydrocephalus
126
Q

what are the 4 types of alzheimer’s?

A
  • amnesic (temporal)
  • visuospatial (R>L)
  • aphasic (L>R)
  • frontal
127
Q

risk factors for alzheimers

A

age
small effect of demographics, env
genetics

128
Q

genetics of alzheimers

early onset
late onset
other

A

early - chr 21, 14, 1
late - chr 19 (apolip e)

other

  • downs trisomy 21
  • gene dosage - Abeta/APP
129
Q

how long does MCI take to progress to alzheimers

how prevalent is mci

A

mci - >30% of 75yo

takes ~20 years to get from 1.5 load of amyloid -> 2.33 (alzheimers)

(and 12years to get from 0 to 1.5)

130
Q

pathogenesis of alzheimers

A

amyloid plaque formation + tau protein aggregation

APP = amyloid precursor protein (may be mutated)

  • cleavage by secretases is to p3 (normal soluble protein)
  • or Abeta monomer (changes form to insoluble)
  • Abeta monomers polymerise, fibrillise to form plaque - can’t be cleared -> inflammation
  • Abeta monomers also reassemble in synaptic membrane
  • interfere with synapses
  • synaptic toxicity

plaques may also drive tau aggregation

ApoE = RF that may drive polymerisation of Abeta

131
Q

drug targets in alzheimers

A

target amyloid plaque formation

secretase enzymes - to stop cleavage of APP to Abeta monomers (but these are involved in many protein cleavage)

MPAC - competes for metal binding sites on Abeta dimers - dimers fall apart

132
Q

examples of transmissible spongiform encepahalopathies

what change is seen (histo)

give examples

A

spongiform change

  • minute vacuoles in nerve cell cytoplasm
  • classic reaction to toxins

eg.
- kuru
- CJD
- variant CJD (younger onset, circulates in blood - human transmission)

133
Q

Creutzfeldt–Jakob disease pathogenesis

A

prion - Pr(pres)

  • insoluble
  • resistant to proteolytic degradation

can induce normal proteins to take on prion form

134
Q

what is a seizure

what causes them

A

paroxysmal, excessive, synchronous, abnormal firing patterns of neurons

caused by anything that disrupts brain homeostasis

  • tumours
  • vascular lesions
  • sclerosis (eg hippocampus)
135
Q

partial (focal) seizures vs generalised

A

partial - limited number of cortical neurons in one hemisphere affected, may spread
- usually structural/metabolic anomally

generalised - arise simultaneously in both hemispheres
- prob genetic

136
Q

pathogenesis of epilepsy

A
  • disturbance in balance between inhibition + excitation of cortical neurons and networks

= change in neuronal network components (↓inhib, ↑excite)
= change in intrinsic cellular excitabiltiy (ion channels are plastic)
= change synaptic transmission
= change extraneuronal env

also - seizures beget seizures - neurobio change

137
Q

which structure is most commonly sclerosed in epilepsy

A

hippocampus - most pathology is here

unilateral circuit between 4 regions

138
Q

drugs that modulate epilepsy

A

want to decrease excessive discharge

↑inhibition - ↑GABA
- eg benzodiazepenes (↑GABA r activity)

↓excitation - ↓glutamate
- eg phenytoin (inhibits Na+ channel - block action potential)

139
Q

pathological chagnes seen in schizophrenia

A

change in brain connectivity

  • ↓neuron size, ↓connections (less synapses, dendrites)
  • change in cell skeleton - prob through Wnt pathway

↓glia density in DLPFC

↑microglia - maybe role of inflammation in schizophrenia?q

140
Q

autism

  • which cell change is seen
  • genetics
A

see ↑microglia activated, but no proinflammatory cytokines
- maybe reacting to seizures?

genetics -

  • some protective SNPs, some risky SNPs
  • seem to be able to diagnose autism with 237 snps (87%)
141
Q

contributing factors to frailty (3)

A

(1) low grade chronic activation of immune system
(2) abnormal endocrine/coag system

(3) similar biomarkers to chronic disease
- ↑cytokines - catabolic effect on muscles?
- ↑CRP
- ↑IL6
TNFa mixed

142
Q

frailty - what is it

A

high vulnerability for adverse health outcomes

143
Q

geriatric syndromes - how do they differ from medical syndromes/

A

medical syndrome - aggregate of symptoms that have one pathogenesis pathway

geriatric - one symptom/complex with and increased prevalence in geriatrics
- results form multiple diseases

eg falls - meds, vision, arthritis, dementia

144
Q

anxiolytic classes

A

benzodiazepines

non-benzodiazepines

  • beta blockers (block physical signs)
  • busiprone (5HT1A receptor agonist)
  • zopiclone (binds gaba a r)
  • zolpidem (gaba agonist)

barbiturates (obsolete)

145
Q

which neutrotransmitters are targets for sedation/anxiety/both

A

anxiety

  • noradrenaline (peripheral tachy)
  • neuropeptide y

sedation
- histamine (h1r antagonists are sedative)

sedation + anxiety

  • gaba
  • serotonin
146
Q

benzodiazepine mechanism of action

A

interfere with GABA A receptor

  • let cl- into cell
  • allosteric (bind regulatory site)
  • increase receptor affinity for GABA (inc freq of channel opening)
147
Q

what is the difference between the mechanism of action of benzos and barbiturates

which one is safer

A

both interact with GABA receptors to increase Cl- entry into cell (hyperpolarise)

benzos

  • specific to GABA A R
  • bind regulatory site - inc frequency of receptor opening
  • has ceiling effect on cl (there is a point at which no more can get in)

barbiturates

  • prolong opening of channel
  • unlimited cl- can get in
  • increases max response of gaba
  • can overdose
148
Q

what is the effect of drugs of dependence in the cns

A

↑dopamine in nucleus accumbens (reward centre)

= reinforce need to keep using drug

149
Q

amphetamines

  • mechanism of action
  • effects
  • overdose
  • dependence
  • withdrawal
A

moa
- releases DA, 5-HT, NA

effects - vary with mood, personality, env, dose

  • mood elevation
  • ↑locomotor activity
  • improved physical/mental performance

overdose

  • anxiety, nervous, tremors, dizziness etc.
  • death with hyperthermia, tachycardia, hypertension, vascular collapse

dependence
- dopaminergic actions in nucleus accumbens

withdrawal
- lethargy, sleep, depression, desire for food

150
Q

MDMA (ecstasy)

  • moa
  • effects
  • dependence
  • overdose
A

moa - release DA and serotonin (>NA)

effects - stimulant + hallucinogenic, feeling of closeness, love, empathy

dependence
- psychological (just like feeling)

overdose

  • ↑hr, bp
  • disrupted thermoregulation
151
Q

LSD

  • moa
  • effect
  • dependence
  • tolerance
A

agonist at 5-HT2 receptors

effect

  • visual, auditory, tactile hallucinations
  • aware is drug-induced

dependence - prob none

tolerance to dose

152
Q

caffeine

  • moa
  • effects
  • overdose
  • dependence
A

moa
- adenosine antagonist, phosphodiesterase inhibitor => ↓breakdown of cAMP - ↑cAMP

effects

  • incrased alertness, well being, delayed onset of sleep
  • stimulate mental activity

overdose - anxiety, tension, tremors

dependence

  • in animals - not addictive physiology
  • humans - social aspect
153
Q

THC

  • moa
  • effects
  • dependence
A

moa - canabinoid recepors
= GPCRs - inhibition of adenylate cyclase - inhibit transmission
- decrease activity within neurons - tend to decrease inhibition -> excitation of pathways

central receptors
- increased appetite, anti-emetic

peripheral
- tachycardia, vasodilation, bronchodilation

effects - subjective

  • relaxation
  • sharpened sensory awareness

dependence - some evidence in heavy users

154
Q

ethanol

  • moa
  • effects
  • tolerance
  • dependence
A

moa

  • inhibits ca2+ channel opening - stop neurotransmission
  • enhance GABA action
  • inhibit glutamate receptors

effects

  • behavoural (subjective) - loud, outgoing or depressive
  • motor - loss of coord, slurred speect

marked tolerance - switch on liver enzymes

dependence - physical, behavioural, neurological,

155
Q

glutamate receptors

A

NDMA

156
Q

classes of antidepressants

A

1st gen - tricyclic, monoamine oxidase inhibitors

2nd gen - ssris, snris

3rd gen - novel

157
Q

tricyclic antidepresants

  • moa
  • selectivity
  • use
A

Inhibit neuronal uptake of noradrenaline + serotonin
=> Antagonise a-adrenoceptors, Muscarinic receptors, Histamine receptors, Serotonin receptors

selectivity - poor

use

  • take weeks to develop
  • narrow therap window (side effects)
158
Q

monoamine oxidase inhibitors as antidepressants

  • moa
  • use
A

↑levels of 5-ht, na, da

use
- some are irreversible - get ‘cheese reaction’ - hypertensive crisis if eat foods with tyramine

159
Q

Selective serotonin reuptake inhibitors

  • moa
  • use
A

selective for 5-ht uptake

use

  • high therapeutic index (min toxicity unless combine with other drugs)
  • caution in adolescents - suicide, anxiety when start
160
Q

Selective serotonin and noradrenaline uptake inhibitor

A

moa

- change balance of neurotransmitters

Neuro (2 decks)

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