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year 2 sem 1 > wk 2 neurology > Flashcards

wk 2 neurology Flashcards

1
Q

CT scan

A 
3D Xray
fast an well-tolerated
goo at detecting blood eg in 
- sub-arachnoid haemorrhage
- intracerebral haemorrhage
- subdural/ extradural haematoma
blood shows up as white
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2
Q

MRI scan

A

most common
looking from feet up for brain usually
diff settings.
- T1 - displays anatomy well - CSF as black
- T2 - good for pathology (path. stands out brighter than other tissue) - CSF is white
- Flair - T2 but computing to suppress CSF (good for seeing pathologies near ventricles)

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3
Q

CSF

A

cerebral spinal fluid
clear and colourless
found in ventricles of CNS and subarachnoid space

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4
Q

where is the CSF made

A

in the choroid plexus

mostly in the lateral ventricles

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5
Q

what is the structure joining the 3rd and the 4th ventricles

A

Cerebral aqueduct

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6
Q

what are the 4 routes for the CSF to get into the sub-arachnoid space from the ventricles

A
  • Central canal of spinal cord
  • Median aperture (foramen of Magendie)
  • 2 x Lateral apertures (foramina of Luschka)
  • Absorbed in cerebral veins (dural venous sinuses) via arachnoid granulations
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7
Q

what are the functions of the CSF

A 
buoyancy
protection from physical injury 
maintenance of brain perfusion
homeostasis
clearing waste
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8
Q

what is the Monro-Kellie Doctrine theory

A

The skull is a “bony box”
There are 3 non-compressible components (brain, blood, CSF)
Increasing volume of one component requires a reduction in one or both others to maintain the same ICP

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9
Q

features of high ICP

A

Headache - worse when lying down, coughing, sneezing, stooping, straining
visual obscurations - grey/ black out

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10
Q

causes of high ICP

A

CSF overproduction - idiopathic intracranial hypertensin
Blocked CSF circulation
Blocked CSF drainage (could be due to high protein in CSF)
Increase in blood or brain tissue in the skull
- intracerebral haemorrhage, cerebral oedema, intracerebral mass

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11
Q

features of low ICP

A

headache - worse when sitting or standing up
blurred vision
dizziness

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12
Q

causes of low ICP

A

underproduction of CSF - dehydration, drugs

CSF leak - Iatrogenic, spontaneous

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13
Q

iontropic neurtransmitter receptors

A
  • ligand gated ion channels
  • FAST
  • Inhibitory – chloride influx – hyperpolarisation – membrane becomes more neg.
  • Excitatory – sodium influx - depolarisation – membrane becomes closer to 0 or pos.
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14
Q

metabotropic receptor

A
  • Induction of second messenger systems
    o Receptor G-couples
    o Activates intracellular enzyme systems to produce an intracellular signal, second messenger
  • SLOW (neuromodulation)
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15
Q

glutamate - general

A

excitatory
involved with grey nuclei of thalamus and basal ganglia
multiple pathways

synthesises from glutamine in astrucytes

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16
Q

subtypes of glutamate receptors

A

o NMDA - ionotropic
o AMPA/ Kainate – “”
o Metabotropic

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17
Q

negative glutamate

A

can be an excito-toxin
sustained activation of NMDA or AMPA receptors kills neurons
glutamate levels rise following strokes - exacerbates injury
glutamate receptor antagonists reduce brain damage following experimental stroke

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18
Q

the importance of glutamate

A

important for learning and memory
high density of NMDA & AMPA receptors in hippocampus
glutamate receptors are activated in long-term potentiation (memory)

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19
Q

GABA general

A

main inhibitory neurotransmitter of CNS (sometimes exc.)
modulate flow of Cl- ions across the membrane
some anti-epileptic drugs mimic effects of GABA or increase its bioavailability

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20
Q

types of GABA receptors

A

iontropic GAGAa

metabotropic GABAb receptors

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21
Q

benzodiazepine

A

enhance effect of GABA
- sedative
- anxiolytic
anti-convulsant

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22
Q

serotonin (5-HT) synthesis

A

tryptophan -> 5-Hydroxytryptophan -> serotonin (5-HT) -(monoamine oxidase)-> 5-Hydroxy indole acetic acid

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23
Q

serotonin receptors

A 
o	5-HT1 receptor family
Metabotropic
o	5-HT2 receptor family
Metabotropic
o	5-HT3 receptor family
Ionotropic
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24
Q

5-HT pathways

A 
Serotonin projections 
o	Originate in raphe nuclei
o	Project throughout cerebral cortex
Sleep-wake cycles
Mood and emotional behaviour
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25
Q

serotonin and depression

A

5-HT compounds are important in treating depression
- tricyclic compounds (imipramine) - block uptake of serotonin - increase bio-availability of serotonin

  • selective uptake inhibitors (Fluoxetine)
  • monoamine oxidase inhibitors (phenelzine) - reduce enzyme degradation of serotonin
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26
Q

acetyl choline synthesis

A

made from choline and acetyl-coA
broken down by acetylcholinesterase in synaptic cleft
re-uptake back into pre-synaptic cleft

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27
Q

acetylcholine pathways in brain

A 
nuclei containing acetylcholine nuclei
- nucleus pyzarus or minartz
- amygdala
- brainstem nuclei
project through thalamus and neocortex
- loss of these pathways in alzheimer's (especially in frontal and temporal lobes)
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28
Q

strategies for increasing cholinergic function

A

acetylcholinesterase inhibitors
- eg tacrine
effective only at mild-mod. AD

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29
Q

what are the main pathologies of AD

A

neurofibrillary tangles and beta-amyloid plaques

30
Q

amyloid pathway in AD

A

Amyloid precursor protein (APP)
APP can be fragmente by enzymes
alpha-secretase = not pathogenic fragements
gamma-secretase = cleaves one of the APP segments into amyloidgenic fragments
- this fragment called beta-amyloid
- accumulates in brain parenchyma in Alzheimer’s

31
Q

therapies to reduce Beta-amyloid

A
  • bapineuzumab
    an antibody targeted against Amyloid-B
    passive immunotherapy that facilitates its clearance
  • immunisation
    reduces amyloid load
    no improvement in CNS function
32
Q

Dopamine synthesis

A

tyrosine -(tyrosine hydroxylase)->L-DOPA -(dopa decarboxylase)-> Dopamine

  • (dopamine beta hydroxylase)-> nor-adrenaline
  • (monoamine oxidase-> DOPAC
33
Q

dopamine neurotransmission

A
  • main pathways are nigrostriatal projections from substantia nigra and basal ganaglia
  • these projections go through frontal lobe (limbic system and cortex)
    > reward and addiction
34
Q

dopamine and Parkinson’s Disease

A
  • degeneration of dopamine pathways in the basal ganglia
  • treatment > L-DOPA
  • adverse effect - psychosis
35
Q

dopamine and schizophrenia

A
  • increased dopamine function in forntal cortex associated with schizophrenia
    treatment
    neuroleptics
  • chlorpromazine and related antipsychotics
  • dopamine receptor antagonists/ blockers
  • adverse effects - parkinsonian syndromes
36
Q

blood Brain Barrier - general info and function

A
  • precise regulation of the ionic microenvironment around axons and synapses is critical for reliable neuronal signalling
  • separates brain from circulatory system
  • protects CNS from potentially harmful chemicals
  • regulates transport of essential molecules and maintains a stable environment
37
Q

BBB - cellular components

A
  • physical barrier tight junctions of endothelial cells
  • pericytes
  • astrocytes end foot processes
38
Q

what can cross the BBB

A
  • lipid soluble agents
  • transport carriers for…
    glucose
    amino acids
  • receptor mediated endocytosis and transcytosis
  • insulin
  • almost all drugs for the brain are lipid soluble small molecules
39
Q

what is the criteria for crossing the BBB

A

(1) MW <400 Da threshold

2) high lipid solubility, ie. low hydrogen bonding (≤7 hydrogen bonds

40
Q

Parkinson’s Disease and the BBB

A
  • dopamine is too large to cross BBB
    alternative. ..
  • L-Dopa (precursor) will cross via transport carrier
  • mono-amine oxidase inhibitors increase bioavailability of D in synaptic cleft
  • inhibitors to prevent peripheral breakdown of L-Dopa before it crosses BBB
41
Q

BBB drug treatment alternatives

A
  • intrathecal pump administers drug directly to the CSF
  • experimental BBB opening
    • uses intracarotid infusion (into the carotid) of hyperosmolar solutions
42
Q

what and where are the 3 neurones that run between the peripheral receptor and the cortex in the spinothalamic pathway

A
  • First order neurone in dorsal root ganglion (spinal nerves)
  • Second order neurone in spinal cord grey matter
  • Third order neurone in contralateral thalamus
43
Q

fibre types in the 2 sensory pathways

A
  • Dorsal column medial meniscus system – large myelinated fibres
  • Spinothalamic tract – small myelinated and unmyelinated fibres
44
Q

propioception

A

where limbs are in position to body and info about movement
mediated by mechanoreceptors in muscle and joint
- muscle spindles
- golgi tendon organs
- joint capsule receptors
fibres run in dorsal columns (position sense and kinaesthesia) , and ventral and dorsal spinal tracts (co-ordination of movements)

45
Q

spinocerebellar tract

A

info from periphery passes into spinal cord
2nd order neurones found at various points in spinal grey matter
axons pass peripherally to form the dorsal and ventral spinocerebellar tracts (also known as direct spinocerebellar tracts)
1st order nuclei found in the dorsal root ganglia

46
Q

what are the 2 main sensory pathways

A

•Dorsal column/ medial lemniscal pathway
– proprioception and fine touch
•Spinothalamic pathway
– pain and temperature sensation

47
Q

what are first order neurones

A
  • convey impulses from the periphery towards the CNS (afferent)
  • cell bodies found in the dorsal root ganglia
48
Q

cutaneous sensory receptors

A

-distribution varies depending on function of that part of the body

49
Q

cutaneous mechanoreceptors

A

In glabrous skin

  • meissner corpuscles at top of dermis
  • pacinian corpuscle
    • free nerve ending responsible for pain sensation
    • scattered throughout the dermis and the epidermis
50
Q

mechanism of fine touch

A

1 neurone is activated
intraneuronal cells switch off adjacent fibres - prohibits them
leads to fine localisation of touch

51
Q

the dorsal column system

A
  • dorsal column fibres pass through dorsal root ganglion
  • then through dorsal spinal nerve roots
  • and into the spinal cord itself
  • fibres don’t synapse with 2nd order neurones
  • travel up in the dorsal columns to the top of the spinal cord to the cervical medullary junction
  • here there are second order neurones in the NUCLEUS CUTANEOUS or nucleus gracillis
52
Q

size of dorsal columns in the spinal cord

A

as fibres travel up the spinal cord the dorsal columns become larger

  • at sacral level vv small
  • lumbar larger as all the sensory info from the legs incorporated
  • thoracic larger
  • cervical largest as convey info from arm, legs and trunk
53
Q

nociceptors

A
  • travel through spinal thalamic pathway
  • often in periphery these are free nerve endings
  • stimulated by…
  • -thermal, mechanical, chemical
  • end point is localised tissue damage which activates nociceptors
54
Q

what can activate/sensitize nociceptors

A
  • substances released by cellular damage
  • Histamine by MastCells
  • -substance P which causes vasodilation
55
Q

spinothalamic pathway

A
  • enter through dorsal spinal nerve roots - through dorsal column ganglion
  • 1st order neurone synapses with 2nd order neurone almost at the point when it enters the spinal cord grey matter
  • fibres then cross over to opposite sides (close to site of entry)
  • travels up spinal cord and brainstem to the THALAMIC NUCLEI
  • then passes to the primary sensory cortex
56
Q

what are the 2nd and 3rd layers of the grey matter of spinal cord

A
  • spinothalamic first order fibres

- substantia gelatinosa

57
Q

what are the 2 parts of the dorsal columns

A

fasciculus cuneatus(upper body) + fasciculus gracillis(lower body)

58
Q

thalamic nucleus

A

where 3rd order neuornes pass to the primary cortex

  • most important is the ventral posterior TN
  • -general sensory afferent
  • -is important in sensory systems
59
Q

primary somatosensory cortex

A
  • in the post-central gyrus of the parietal lobe
  • lies directly behind the central sulcus
  • -primary motor cortex lies in front of this sulcus
  • contralateral half of body represented in a somatotopic pattern
  • -representation based on amount of sensory info coming from these regions eg big for fingers
60
Q

dermatomes

A
  • show pattern of sensory innervation on the peripheral NS
  • when examining patient’s sensory system u should be able to identify areas of sensory loss from knowledge of dermatomes
  • -T4 - nipple level
  • -T10 - level of umbilicus
61
Q

visceral pain

A
  • pain from viscera is commonly referred to surface of the body
  • transmitted through the autonomic NS
  • visceral pain not well localised as peripheral somatic pain
62
Q

headache and facial pain

A
  • generally somatic from the head conveyed by trigeminal nerve (V)
  • -afferent fibres pass to the trigeminal ganglion (first order neurones)
  • -from here axons pass into the pons and terminate in trigeminal sensory nuclei (2nd order neurone)
    • the trigeminothalamic pathway ascends mostly with the medial lemniscal pathway
63
Q

causes of headache

A
  • Direct stimulation of nociceptors via trigeminal nerve – sinuses, toothache, ocular skin
  • Stimulation of – periosteum, arteries, venous sinuses, areas of dura, muscle
  • Unknown causes – migraine
64
Q

disorders of the general sensation

A 
-Spinal cord 
o	Dorsal columns – tabes dorsalis, SCDC
o	Spinothalamic tracts – syringomyelia
-Thalamus 
o	Thalamic pain
-Cerebral cortex
o	Sensory seizures
o	Agnosia/ dyspraxia
65
Q

subacute combines degeneration

A

-Vit D deficiency
-Chronic alcoholics
-Low copper levels
-Degeneration of dorsal columns
o Reduced proprioception passing back to NS
o Wide gait – put down feet with lots of pressure when they walk
 Trying to increase the proprioceptor reflexes returning to CNS

66
Q

tabes dorsalis

A
  • Chronic cephlitic infection

- Degeneration of dorsal columns

67
Q

syringomyelia

A

-Large black space in spinal cord
o Fluid filled cavity
-Causes central enlargement of the spinal cord
-Spinothalamic fibres synapse 2nd order neurones then cross over
o Syringomyelia can cause damage to these fibres as they cross
o Leading to reduced pain perception

68
Q

pain

A

-Pain isn’t felt in the periphery
o This is only localised tissue damage
-Perceived nociceptive input to the CNS – created by CNS
-A sensory and emotional subjective experience of discomfort

69
Q

modulation of pain

A

-Descending pathways can influence how pain is received
-At point of synapse from 1st to 2nd order neurones (point of crossover to spinothalamic pathway)
o Descending pathways can modulate the transmission of the nociceptive signals
o These desc. Path. arise in the periaqueductal grey matter of midbrain, pass down brainstem, synapse in dorsal grey matter of the spinal cord

70
Q

innocous stimulus

A

switches on inhibitory neurones to inhibit pain

eg rubbing arm after you hit it

71
Q

the analgesia pathway from least used to most used

A

paracetamol, codeine containing drugs, morphine

year 2 sem 1 (13 decks)

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