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Medicine - Phase 1 > Neuro > Flashcards

Neuro Flashcards

1
Q

when does neurulation beging?

A

week 3

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2
Q

the neural tube arises from which embryological layer?

A

ectoderm

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3
Q

First step of neurulation:
Starts around?
The [a] induces differentiation of the [b] along the midline.
This thickening forms the [c]

A

Day 17
[a] notochord
[b] ectoderm
[c] neural plate

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4
Q

Step 2 of neurulation:
when does it start?
the process of [a] causes a depression to form along the centre - the [b]

A

day 18
[a] differential mitosis
[b] neural groove

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5
Q

step three of neurulation:
the upper most cells of the neural groove (called what?) differentiate into what?

A

Neural crest cells:

form: PNS-DRG, Schwann cells, adrenal medulla, meninges, skull, dermis, V/VII/IX/X

NOT ASTROCYTES

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6
Q

when does the nueral tube form?
how?

A

the neural groove completeley closes around week 4 to form the neural tube.

otherwise neural tube defects
Requires FOLATE

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7
Q

failure of the spinal chord to close in the cephalic region =?

A

anencephaly

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8
Q

Failure of neural tube to close spinal region?

A

spina bifida

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9
Q

what are these three types of neural tube defects?

A
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10
Q

Monogenic causes of neural tube defects have a higher recurrance risk the polygenic.

a sibling of affected child has what chance of being affected?

A

1/4

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11
Q

when would the brain look like this?

A

week 4

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12
Q

when would the brain look like this?

A

week 6

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13
Q

when does eye formation begin?
when do basic brain structures aris?
when does myelination occur?

A

eye formation = week 3
basic brain structures = 3 months
myelination = 5 months

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14
Q

what are the red cells in this diagram?
what is their role?

A

Glia Cells

During development, stem cells divide and migrate outwards to various layers of the cortex
Stopped by the red cell – glia – at different levels

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15
Q

what develops into the forebrain?

A

prosencephalon

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16
Q

what does the diencephalon form?

A

3rd venrricle, thalamus, hypothalamus

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17
Q

what does the telencephalon form?

A

cerebral cortex, basal ganglia, lateral ventricles

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18
Q

[?] –> midbrain
[?] —> hindbrain?

A

mesencephalon –> midbrain
rhomencephalon —> hindbrain

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19
Q

myelencephalon —> [?] + [?]

A

myelencephalon —> medulla + 4th venrticle

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20
Q

metecephalon —> ?

A

pons + cerebellum

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21
Q

is micocephaly or macrocephaly more likely to be indicitive of underlying neurological disorder?

A

microcephaly

- stem cells have not sufficiently divided.

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22
Q

what does this V1 (black water) show?

A

Periventricular nodular heterotopia

bumpy ventricles

can be associated with epilepsy

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23
Q

how many ml of CSF is there?

A

around 120ml

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24
Q

what kind of hydocephalus would a tumour or haemorrhage be?

A

Obstructive (non communicating)

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25
Q

what kind of hydocephalus would increased CSF production be

A

non-obstructive (communicating)

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26
Q

function of CSF?

A

cushions brain, helps circulate metabolites (waste products)

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27
Q

what makes up the outer ear?

A

pinna
external acoustic meatus
tympanic membrane

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28
Q

what makes up the middle ear?

A

muscles
eustachian tube
ossicles

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29
Q

what makes up the inner ear?

A

Cochlear
Labyrthinth
Vestibular cochlear nerve

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30
Q

what is the function of the pinna?

A

Channel sound towards the meautus
Filters out lower frequencies

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31
Q

what is the external acoustic meautus made of?

A

1/3 cartilage, 2/3 bone

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32
Q

what does the tympanic membrane do?

A

vibrates in response to sound?

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33
Q

how does the middle ear amplify airborne sound vibrations?

A

Ratios - force amplifies the sound by amplifying the movement.

TM:Stapes = 14:1
malleolus handle: incus process (lever action) = 1.3:1

total amplification 200x amplification!

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34
Q

What are the muscles of the inner ear?

A

stapedius
tensor tympani.

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35
Q

what is the function of the muscles of the inner ear?

A

protect inner ear from acoustic trauma by dampening = involuntary contraction to prevent excess vibration

strapedieus stiffens ossicular chain.

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36
Q

what is the function of the eustachian tube?

A

equalises pressure.

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37
Q

why does the eustachean tube clog up when ill?

A

its is formed from respiratory epithelieum which is mucus secreting.

drains into nasopharynx

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38
Q

what are the ossicles?
coonnected by?

A

malleus
incus
stapes

connected by synovial joints

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39
Q

what is the function of the labrynth?

A

balance

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40
Q

Innervation of inner ear?

A

verstibularcochlear nerve.

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41
Q

what, in the ear, detects dynamic changes and what detect static changes?

A

semi-circular canals detect dynamic changes (affects eyes)
vestibule (utricleand saccule) detect static changes (endolymph and stereocilia)

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42
Q

explain the oculocephalic reflex

A

head rotates –> endolymph movement bends cupula + ampulla hair cell stereocillia in opposite direction –(CN8)–>medulla nuclei –> both eyes move in opp direction to head

=fixed gaze

cupula + ampula = semicircular canals

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43
Q

how many turns does the cochlea have?

A

2.5

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44
Q

how many compartments does the cochlea have?

A

3 compartments: scala vestibuli, scala media, and scala tympani

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45
Q

how many openings does the cochlea have?

A

2 openings: round window and oval window (andhelicotrema?)

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46
Q

what are the two ionic fluids of the cochlea?

A

endolymph (K+) and perilymph (Na+)

ionic gradients maintained by pumps

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47
Q

explain how pressure moves along the cochlea

A

scala vestibulli —> heliocotrema —> scala tympani —> round window

this moves the BASILAR MEMBRANE

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48
Q

how does the basilar membrane respond to different frequencies?

A

the outer end / base is stiff and narrow = high frequencies

inner end / apex is broad and floppy = low frequencies

tonotopt

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49
Q

what allows the cochlea to detect intensity/loudness of sound?

A

number of nerves responding and firing in cochlear

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50
Q

what is the organ of corti?

A

3 rows of outer hair cells
1 row of inner hair cells

movement of basilar membrane —> inner hair cells —[transducing cells]–>auditory nerve activation

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51
Q

what is responsible for fine tuning of sound?

A

the outer hair cells

  • pull the tympanic membran down either side of the best nerve for that frequence/pitch
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52
Q

how does the brian localise sound?

A

the brainstem and coincidence detectors
-intraneural time difference

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53
Q

what are the steps of the auditory pathway?

A

ECOLIMA

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54
Q

what can cause hearing loss in the outer/middle ear?

A

conductive issues - no mechanical transmission to oval window

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55
Q

what can cause hearing loss in the inner ear?

A

sensorineural issues - cochlear not working

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56
Q

Neurons are specialised for [a]
Inputs via [b]
Action potentials propogate along the [c]

A

electrical signalling
dendrites
axons

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57
Q

there are two types of neuronal communications. explain how both work.

A

Chemical = majority; via neuro transmitters
Electrical = via direct flow of ions = breathing, hormone secretion

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58
Q

how can you tell which neuron is post synaptic and which is pre synaptic?

A

This is a chemical synapse.
* vesicles in the presynaptic axon
* mitochondira in presynaptic axon
* electron dense material in post synaptic dentrite (proteins)

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59
Q

outline how chemical synaptic transmission happens

A
  • axon potential depolarises synaptic terminal membrane
  • opening of voltage-gated calcium channels leads to calcium influx
  • clacium influx triggers neurotransmitters
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60
Q

what kind of synapse is this? How can you tell?

A

this is an electrical synapse.

differs from structure of chemical synapse in that there are no synapse vesicles, and electron dense material can be seen on both sides.

NO SYNAPTIC CLEFT (ONLY CHEMICAL) - INSTEAD IT HAS GAP JUNCTIONS

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61
Q

what is neural plasticity and what does it allow for?

A
  • changes in neuroal/synaptic structure and function in response to neural activity.
  • allows for learning/memory

relevent to diseases like alzheimers - decreased spine density postmortem

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62
Q

neurons can differ from eacchother in 4 ways:

A
  1. size
  2. morpology
  3. neurotransmitter content
  4. electrical properties
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63
Q

what are Betz cells - describe their morphology

A

betz cells = upper motor neuron cells

large, long, pyramidal, excitory,

vulnerable in MND

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64
Q

describe the morphology of medium spiny neurons

A

striated, small, inhiibitory

vulnerable in huntingtons

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65
Q

what are glia cells?

A

non-neuronal cells (i.e. not nerves) of the brain and nervous system.

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66
Q

what are oligodendrocytes?

A

myelinating cells of CNS

unique to vertebrates

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67
Q

what does myelin do?

A

insulate axon segments, enabling rapid nerve conduction
metabolic support for axons

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68
Q

difference in myelination in CNS and PNS?

A

In the central nervous system (CNS), oligodendrocytes myelinate multiple axons; in the peripheral nervous system (PNS), Schwann cells (SCs) myelinate a single axon.

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69
Q

why does the myelin sheath appear white?

A

70% lipids

30% protein

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70
Q

what are the immune cells of the CNS?

A

Microglia

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71
Q

when would the microglia look like these different forms?

A

Ramified when body is “helathy” - exploring environment
Unramified when encounters pathogen - mobile and phagocytic

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72
Q

what cells in the CNS are responsible for pruning of spines, phagocytosis and immune surveillance?

A

microglia

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73
Q

x6 purposes

what type of cell is this? what is its purpose?

A

Astrocyte
- blood-brain barrier contribution
- structural: brain’s micro architecture
- envelop synampses = buffer excess K+, glutamate etc = homeostasis @ synapse
- metabolic support = glutamate-glutamine shuttle
- neurvasuclar coupling = changes in blood flow in repsonse to neural activity
- proliferate in disease = glyosis/astrocytosis

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74
Q

which cell in the CNS maintains homeostasis at the synapse?

A

astrocytes
- buffer excess K+/glutamate

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75
Q

what are the most numerous cells in the CNS?

A

astrocytes

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76
Q

which cells are the neural stem cells?

A

radial glia (specialised astrocyte)

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77
Q

which cells are iimportant for cerebellum structure?

A

bergmann glia

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78
Q

what do müller cells do?

A

scaffold for other cells in retina

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79
Q

MND spinal cord shows pathological changes in which cells?

A

Motor Neurons
Mircoglia
Astrocytes

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80
Q

MND sypotoms are su

MND symptoms are due to a loss of what cells?

A

Motor Neurons

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81
Q

Acute symptoms in MS refelct dysfunction of what cells?

A

Neurons

primary pathology due to oligodendrocytes

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82
Q

pathology of CNS lesions in MS involve what cells?

A

neurons, oligodendrocytes, T cells

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83
Q

what feauturs of the blood brain barrier make it more difficult to penetrate (4)?

why can this be an issue?

A
  1. endothelial tight junctions
  2. unfenestrated basement membrane
  3. astrocyte feet envelop
  4. pericytes = contractile

can be an issue for drug delivery - neuro drugs therefore need to me small and hydrophobic

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84
Q

how is CSF resorbed?

A

by the arachnoid granulations

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85
Q

what cells produce CSF?

A

ependymal cells:
- epethelial like
- ciliate = flow of CNS
- allows solute exchange between nervous tissue and CFS

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86
Q

what is the main site of CSF production?

A

Choroid plexus
-formed from modifies ependymal cells
- projections in ventricles
- highly vasuclarised
- gap junction for blood-CSF barrier

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87
Q

what are the three connective tissues of the skeletal muscle?

A

epimysium
perimusium
endomysium

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88
Q

what is the function of the basement membrane?

A

tensile strength, regeneration, development

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89
Q

How many nerves is each skeletal muscle fibre innervated by?

A

Each individual muscle fiber in a muscle is innervated by one, and only one, motor neuron (make sure you understand the difference between a muscle and a muscle fiber). A single motor neuron, however, can innervate many muscle fibers.

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90
Q

At the synapse, rapid transmissions of depolarises impulses is facilitated by what neurotransmitter?

A

Acetyl Choline - binds post synaptic AChR(eceptor)

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91
Q

what do muscle spindles do?

A

important to mediate stretch reflections and propioception (muscle position)

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92
Q

what do Golgi tendon organs measure?

A

tension

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93
Q

what are type 1 muscle fibres?

A

slow twitch - oxidative , fatigue resistant

long distance running muscles

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94
Q
A
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95
Q

what are type 2a muscle fibres?

A

Fast Twitch : intermediate types - glycolytic AND oxidative

power, lactic

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96
Q

what are type 2B muscle fibres?

A

fast twitch - glycolytic (white)

power, lactic

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97
Q

Do neurons innervate different types of fibres, or the same type of fibres?

A

same type.

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98
Q

what has happened here?

A
  • Loss of innervation has caused a cell to atrophy
  • Adjacent motor units are induced to sprout in order to re-innervate that muscle
  • Motor unit therefore larger
  • Fibres will shift its type to fit the adjacent neurons type
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99
Q

What is a sarcomere?

A

basic unit of contraction
-repeating arrangement of thick (myosin) and thin (actin) filaments

or intermediate filaments = cell type specific

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100
Q

what is linked to the actin that is important for calcium regulation?

A

troponin/tropomyosin complex

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101
Q

what is required for the myosin and actin to slide over eachother?

A

ATP

binding of ATP allows release and hydolysis of ADP which allows movement of myosin head (rowing) ADP released during power stroke

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102
Q

what initiates the sliding of the actin and myosin?

A

increase in intracellular caclium

calcium increase mediated by troponin and tropomyosin

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103
Q

ATP is the immediate source of energy for muscle fibres.

what can be used as a short term energy store?

A

Creatine Phosphate

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104
Q

what is creatine phosphare replenished by?

A

CK Creatine Kinase

CK is released on muscle fibre damage - clinical meausre

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105
Q

mitochondrial cytopathies general affect the [?] but not always

A

muscle - (some tissue affected some not - heteroplasmy)

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106
Q

which protein is essential for muscle cell membrane stability during contraction?

A

Dystrophin - inside the sarcolemma

if pathology = distrophy = many types, progressive

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107
Q

what are the two types of dystophin related dystrophy?

A
  1. Duchenne
    - deletion: disruption in reading frame (almost no normal dystrophin produced)
    - more severe
  2. Becker’s
    - in frame deletion (some normal dystrophin produced)
    - less severe
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108
Q

Outline the steps of axonal neurotransmission

A

1.Neurotransmitters activate receptors on dendrites / soma
2. Receptors open ion channels
3. Ions cross plasma membrane, changing the membrane potential
4. The potential changes spread through the cell
5. If the potential changes felt at the axon hillock are positive (+mV), and large enough, an action potential is triggered (ie action potential must meet threshold to be “felt” at axon hillock)

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109
Q

What is the resting voltage inside a neuron?
What keeps it this way?

A

-70mV
maintined by semipermiable membrane: diffusion, electrostatic pressure and sodium-potassium pump

Large A-‘s stay inside - can’t leave
K+ want into the negative inside
Na+ also wants in (ellectrostatic and diffusion), but harder to cross membrane, and pump pushes back out
Cl- wants out the negative area, can move readily

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110
Q

What do excitory neurotransmitters do to the cell membrane?

A

Depolarise the cell membrane.
↳causes Excitory Post Synaptic Response
↳increases probibility of reaching action potential threshold

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111
Q

what two factors can work together to generate an action potential?

A

temporal and spatial summation

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112
Q

What do inhibitory neurtransmitters do to the cell membrane?

A

hyperpolarise the cell membrane
↳ Inhibitory Post Synaptic Potential (IPSP)
↳ decreases probablity of action potential being elicited

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113
Q

Label the steps of the Action Potential generation

A
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114
Q

Explain how the action potential is self perpetuating in axonal neurotransmission

A

voltage changes control ion channels
ion channels control voltage changes

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115
Q

how does myelin speed up propogation of action potentials?

A

Saltatory Conduction
- decremental (jumping)conduction between nodes of ranvier - boosted each time
- most CNS neurons

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116
Q

during which period can another cation potential not be generated?

A

during the Absolute refratory period

prvevent backwards flow of action potential

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117
Q

during which period can an action potential be generated if there is a stronger than normal stimulus?

A

relative refractory period

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118
Q

Outline Neuromuscular Transmission (Synaptic Neurotransmission, no axonal)

A
  1. Acetylcholine release
  2. Acetylcholine’s action
  3. Increasing endplate potential
  4. Reaching the threshold for endplate action potential
  5. Acetylcholine is destroyed

Nerve impulse or action potential

￬

Opening of voltage-gated calcium channels

￬

Influx of calcium ions inside the cell increases

￬

Opening/rupture of vesicle and release of acetylcholine

￬

Acetylcholine comes to the synaptic cleft

￬

Acetylcholine binds with nicotinic receptors to form the acetylcholine-receptor complex

￬

Opening of ligand-gated sodium channels

￬

Influx of sodium ions inside the cell increases

￬

Development of endplate potential

￬

Generate muscle action potential

￬

Muscle contraction takes place

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119
Q

Outline: “1. Acetylcholine release” stage of neuromuscluar transmission

A
  1. Acetylcholine release
    - Action potential opens voltage gated calcium channels . Ca2+ enters and move the presynaptic vesicles containing ACh to the presynaptic membrane which bursts the vesicles open. ACh released and diffuses through membrane and enters synaptic cleft through exocitosis
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120
Q

Outline “2. Acetylcholine’s action” step in neuromuscular transmission

A
  1. Acteylcholine’s action
    - at the synaptic cleft Ach interacts with nicotinic recpetors in the post synamptic membrane to form AchR complex which opens sodium channels. Na+ enters. this leads to 3.
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121
Q

Outline “3. Increasing end plate potential”

A
  1. Increasing end plate potential
    – due to sodium ions entering
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122
Q

Outline “4. Reaching the threshold for endplayte action potential” of neuromuscular transmission

A
  1. Reaching the threshold for endplate potential
    - small amount of Ach released from axon terminal, but not enough to reach the threshold required for muscle to develop action potential. more vesicles with more Ach arriving eventually produces an endplate postenial which results in an action potential in the muscle
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123
Q

Outline “5. Acetylcholine is destroyed” step of neuromusculatr transmission

A
  1. Acetylcholine is destroyed
    – Acetylcholinesterase enzyme quickly destroys the acetylcholine released into the synaptic cleft. This stops the muscle fibre from being excited repeatedly and enables the muscle to relax.
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124
Q

Patients with Myasthenia Gravis have variable weakness.

How can administering Acetyl Cholinesterase inhibitors improve muscle function?

A

Myasthenia Gravis is an autoimmune desease which attack the Ach receptors. = Not enough receptors to meet threshold to activate excitation.

Inhibit the breakdown of Acetylcholine (with Acetyl Cholinesterase inhibitors) so you will have more ACh for the receptors that are left (?)

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125
Q

Name thee fast neurotransmitters

A

Acetylcholine (ACh) - Excitory in skeletal muscle, inhibitory in heart
Glutamate (GLU) - excitory
Gamma-aminobutyric acid (GABA) - inhibitory

short term effects

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126
Q

name three neuromodulators

A

Dopamine (DA)
Noradrenalin (NA) (norepenephrine)
Serotonin (5HT) (5-hydroxytryptamine)

slower timescale

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127
Q

How do local anaesthetics work?

procain and lignocaine

A

Na+ channels blockers
Blocks progress of action potential

particularly well absorbed through mucous membranes, so can act on muscle too.

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128
Q

what can affect Ach?

A

Cigarettes (nicotine - agonist)
Poison arrows (curare - antagonist)
Spider toxins (black widow - release)
Nerve gas (WW-I – blocks break-down)

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129
Q

What can affect Noradrenaline?

Transmitter in peripheral (heart) and central nervous systems

A

Antidepressant drugs
Stimulants

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130
Q

what can affect dopamine?

Important transmitter in basal ganglia

A

Antipsychotic drugs
Stimulants
Anti-Parkinson drugs

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131
Q

what can affect serotonin (5-HT)?

Diverging projections in the brain – innervating many structures

A

Antidepressant drugs
Hallucinogens
Ecstasy

Hallucinogenic drugs include LSD, Magic Mushrooms, Ketamine

They mimic serotonin, and can activate numerous different serotonin receptor subtypes

But the hallucinogenic effect itself appears to be specifically related to the way they target the serotonin ‘2a’ receptor (5-HT2a

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132
Q

What can affect GABA (Gamma-aminobutyric Acid)

Main inhibitory transmitter

A

Anti-anxiety drugs
Anticonvulsant drugs
Anaesthetics

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133
Q

what are the main excitory and inhibitory neurotransmitters?

A

Glutamate - excitory
GABA - inhibitory

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134
Q

Each Schwann cell is responsible for [how many] segment[s] of myelin

A

Each Schwann cell is responsible for one segment of myelin

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135
Q

In the CNS 1 oligodendroctye myelinates =
In the PNS, 1 Schwann cell myelinates =

A

In the CNS 1 oligodendroctye myelinates = multiple axons
In the PNS, 1 Schwann cell myelinates = one axon

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136
Q

1 Schwan cell to how many unmyelinated axons?

A

1 schwann cell to multiple unmyelinated axons

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137
Q

At the nodes on ranvier, there are lots of [?]

A

ion channels

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138
Q

myelination allows [?] conduction

A

myelination allows solitary conduction which means jumping conduction.

more rapid conduction

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139
Q

Peripheral neuropathies can occur in which 3 ways?

A
  1. damage to motor/sesory neurons
  2. damage to axons
  3. demyelination
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140
Q

what happens when you cut/damage and axon

A

Distal fragmentation of axon
- myelin breaks down into globules (phagocytose by Schwann cell)
Proximal axon will try to regenerate/sprout
-multiple small axons which will grow along the oclumns of proliferating schwann cells - 1 remains
-regenerated axons will remyelinate

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141
Q

why does a remyelinated axon (after damage) conduct more slowly than the original axon.

A

tend to have shorter and thinner myelin sheaths and

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142
Q

MS is a demyelinating disorder of CNS.
This is distinct from PNS.

In PNS demyelination tends to be [?] because one schwann cell myelinates one segment

A

segmental

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143
Q

difference in remyelination between axon cutting and myelination disorders?

A

axonal = shorter regenerated myelin sgements
demyelination = thinner regenerated myelin segments

both slow conduction

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144
Q

Each spinal nerve is formed by the combination of nerve fibers from the dorsal and ventral roots of the spinal cord.

The dorsal roots carry what axons, while the ventral roots carry what axons.

A

Dorsal = afferent sensory axons (affected by the world)
- plus a “copy” to the brain so it knows whats going on

Ventral = Efferent Motor axons (effect on the world)

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145
Q

Ventral roots are Anterior or Posterior?

Dorsal Roots are Anterior or Posterior?

A

Ventral = Anterior
Dorsal = Posterior

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146
Q

what is the function of spinal nerves?

A

Receive sensory information from the periphery and pass them to the CNS
Recieve motor information from the CNS and pass them to the periphery

147
Q

what is the function of the medulla?

A
  • contain tracts carrying signals between the rest of the brain and the body
  • contain caudal part of reticular formation
    =low level sonsorimotor controle eg balance
    =involved in sleep, muscle tone, cardiac, circulatory, resp, excretory reflexes
148
Q

what is the function of the pons?

A
  • relay info from cortex and midbrain to cerebellum
  • Pontine retiular formation = pattern generators eg walking (cortex devolves this to the pons)
149
Q

What is the function of the cerebellum?

A

coordinating and corrrecting fine movement and balance. Also known as the “little brain,” it plays a vital role in language and attention and can assist people with vision and eye movement.

150
Q

What is the function of the colliuculi? (aka Tectum)

A

Superior Colliculus = sensitive to sensory change - orienting/defensive movements
Inferior Colliculus = similar, for auditory events

151
Q

colourful

What are the three structures that make up the tegmentum?

A

Periaquaductal grey
Red Nucleus
Substantia Nigra

152
Q

in the midbrain

what is the role of the periaquaductal grey?

A
  • defensive behavior
  • pain
  • reproduction
153
Q

What is the role of the red nucleus?

A
  • target of cortex and cerebellum - projects into spinal cord
  • role in pre-cortical motor control - arms/legs
154
Q

what is the role of the substantia nigra?

A
  • dopamine cells (Parkinson’s)
  • initiating movement
155
Q

what structures make up the diencephalon?

A

the thalamus, hypothalamus, subthalamus, and the epithalamus.

156
Q

function of the thalamus?

A

relay structure
relays signals for all sensations except smell
regulating sleep and arousal
relays from basal gamglia and cerebellum back to cortex

157
Q

function of hypothalamus?

A

regulates piutitary gland - interface between brain and hormones

role in hunger, pian, thirst, pleasure sex

158
Q

telencephalon = forebrain

Two portions of subcortical (under cortex) Telencephalon?

A

Basal Ganglia
Limbic system

159
Q

Function of the basal ganglia?

A

Group of structures organised in a loop, thought to be involved in motor function

involved in movement disorders. ?action selection and reinforcement?

160
Q

function of the limbic system?

A

group of structures involved in emtion, motivation and emotional association with memory.

161
Q

what structures make up the limbic system?

A

Amygdala
Hippocampus
Mammillary body
Septum
Fornix
Cingulate Gyrus

162
Q

function of amygdala?

A

fear
associating sensory stiumuli with emotions

163
Q

function of mammillary body?

A

formation of recollective memory

164
Q

function of hippocampus?

A

long term memory
spatial memory

165
Q

function of septum (in limbic system)

A

defense and aggression

166
Q

function of the fornix?

A

carries signals from hippocampus to mamillary bodies and septal nucleus

167
Q

function of the cingulate gyrus

A

linking behaviour outcomes to motivations and autonomic control

atrophied in schizophrenia

168
Q

3 steps in neuropathway of emotions?

A
  1. Identification (senses)
  2. Appraisal
  3. Reactivity
169
Q

What two structures are responsible for “2. Appraisal” of emotions pathway?

A

Amygdala (older)
Orbitofrontocortex (newer) - medial and lateral

170
Q

In the emotions pathway, what is the amygdala responsible for?

A

facial recognition and negative facial expressions
(more habitual and instinctive than the subjective orbitofrontocortex)
slower to “update”

171
Q

In the emotions pathway, what is the medial Orbitofronto Cortext responsible for?

A

assigns estimates of rewards.
gives an idea of how pleasurable something could be

172
Q

In the emotions pathway, what is the lateral Orbitofronto Cortext responsible for?

A

recognises potential punishment
recognises when an anticipated reward hasnt been recieved

173
Q

Which structures are responsible for “3. Reactivity” in the emotions pathway?

A
  • Mesolimbic pathway
  • cingulate cortex
  • Ventromedial Prefrontal cortex
  • Hypothalmus and Insula
174
Q

What does the mesolimbic pathway do in the emotional pathway?

A

dopamine to the ventral tegmental area
coordinate bahviour responses

175
Q

what does the cingulate cortex do in the emotional pathway (reactivity)?

A

action - outcome learning: aims to max reward and min punshment
Anterior = outcome
Posterior = action - inputs from orbitofrontal cortex; outputs to hippocampus

176
Q

what is the ventromedial prefrontal cortex responsible for in the emotional pathway (reactivity)?

A

reward related decision making

177
Q

Sensation =
Perception =

A

Sensation = delivery of raw data
Perception = interpretation of raw data

178
Q

what is your perceptual set?

A

The psychological factors that determine how you perceive your environment

context, culture, expectations, mood

179
Q

what structure goes through the foramen magnum?

A

medulla

not brainstem

180
Q

label the cisterns

A
181
Q

what structure here establishes that this is the midline of the brain?

A

the cerebral aqueduct

182
Q

colour of CSF in T1 and T2 weighted MRI?

A

T1: CSF black
T2: CSF white

183
Q

what do the colours in a colour FA map correspond to?

A

red = left/right
green = front/back
blue = head/foot

184
Q

?what is this an example of

A

Tractograph
-DWI Fibre Track Recontruction
- comuter generated map of best guess/fit of fibre tracks

185
Q

what is eustress and distress

A

good stress and bad stress

186
Q

what parts of the brain are involved in physical stressors?
what about psychological stressors?

A

Physical stressors (injury) - brainstem and hypothalamus
Psychological stressors (percieved threat) - PFC amygdala and hippocampus

187
Q

What are the three phases of stress response?

A
  1. Alarm - threat identified, fight/flight
  2. Adapation - body engages defensive countermeasures
  3. Exhaustion - Body runs out of defence resources
188
Q

What is Allostasis

A

complex homeostasis under stress conditions

189
Q

What kind of stress would hunger or a fire induce?

A

acute stress

(breif response to novel but short lived situation)

190
Q

what kind of stressor would poverty or bullying be?

A

chronic stress

continued or repeated exposure to threatening situation

191
Q

What are the 5 elements of human stress response?

A
  1. Biochemical - steroids and catecholamines
  2. Physiological - Fast and Chronic - rapid breathing, muscle tense, sweating, headache, low energy
  3. Behavioural - change in apetitie, sleep disturbances, withdrawal
  4. Cognitive - constant worrying, inability to focus
  5. Emotional - depression, irritability, tearfulness
192
Q

Explain the sympathomedullary pathway’s response to stress

A

ANS: acute fight/flight

193
Q

Explain the pituitary-adrenal system’s response to stress

A

HPA: slower/ long term

194
Q

what kinds of illness is stress most closely related to?

A

cardiovasular and Gi - those with strong ANS connections.

stress exacerbated physical illness, slows recovery and increased susceptibility to infection

195
Q

Traits that may have benefitted us in an ancesteral setting (hunter gatherer) that are “problematic” now is an example of what?

A

evolutionary psychiatry

take engineers view - how did the body get to be the way it is.

eg. sugary food now vs then, loneliness now vs then, anxiety now vs then, ADHD now vs then

196
Q

what is the smoke detector principle?

A

the idea that you would want a smoke detector to er on the side of caution. This may cause a few false alarms but we are prepared to pay that price to avoid missing a real fire.

apply this to anxiety

197
Q

in the sensorimotor system, what is in charge of WHAT to do, and what
is in charge of HOW to do it?

A

Basal Ganglia = WHAT to do
Cerebellum = HOW to do it

198
Q

Explain the decsending sensorimotor system.

A
199
Q

smalles muscle in the body?
largest?

A

smallest = strapedius
largest = gluteus maximus
strongest = masseter

200
Q

The activation of muscle fibres is all or none.
So how do we achieve such a range of movements and forces ??

A
  • Antagonistic arrangement – combined co-ordinated action
  • Recruitment of muscle fibres – fast/slow twitch, small and large motor units
201
Q

A skeletal muscle is attached to the bone by the [a]
A skeletal muscle comprises several muscle [b] (group of muscle fibres)
A muscle [b] comprises several [c] (= muscle cells)
A [c] is constituted of several [d]
[d] contain protein filaments: [e] and [f] myofilaments
When the muscle fibre is depolarised [e] and [f] slide against each other which produce muscle contraction

A

a. tendon
b. fasciculi
c. muscle fiber
d. myofibrils
e. actin
f. myosin

202
Q

how do muscles contract?

A

The release of acetylcholine causes a cascade of events resulting in the release of packets of calcium from inside the muscle cell (fibre)
This causes the myosin head to change shape, enabling it to bind with the actin filament
The rowing action of myosin pulls the Actin filaments closer together. This shortens sarcomeres within a fiber, causing it to contract.

203
Q

Why is ATP important for the The Sliding Filament Theory of muscle contraction?

A

ATP (provides energy for cells) is required to break the bond between the myosin head and the actin filament

ATP is produced by oxidative metabolism, which stops upon death

So the muscle become contracted and remain that way until enzymes begin to disrupt the actin/myosin (rigor mortis)

204
Q

What makes up the motor unit?

A

single alpha motor neuron + all the muscle fibres it innervates

205
Q

What would a motor neuron that innervates few fibres mean in terms of movement?

A

The fewer fibres a motor neuron innervates, the more fine tuned the movement.

eg the eye, few fibres

206
Q

What would a motor neuron that innervates many fibres mean in terms of movement?

A

If a neuron innervates many muscle fibre, less fine tuned but more power.

eg the leg muscles.

207
Q

what is a motor pool?

A

all the LMN that innervate a single muscle.
contains both alpha and gamma neurons.
often arranged in rod like shape withing ventral horn or spinal column§

208
Q

alpha motor neurons originate in the…?

A

spinal cord

209
Q

Ventral root = ?
Dorsal root = ?

A

Ventral = motor output
dorsal = sensory input

210
Q

what in the tendons/joints sense tension?

A

Golgi tendon organs
- Mostly, it sends ascending sensory information to the brain via the spinal cord about how much force there is in the muscle
- Critical for proprioception

Under conditions of extreme tension, it is possible that GTOs act to inhibit muscle fibres (via a circuit in the spinal cord) to prevent damage

211
Q

what in the muscle senses stretch?

A

muscle spindles
- Muscle spindles sense the length of muscles, i.e. the amount of stretch
- This information forms a key part of reflex circuits

212
Q

what type of muscle fibres are muscle spindles wrapped around?

A

Intrafusal Muscle Fibres

213
Q

what innervates intrafusal muscle fibres?

why is the separate innervation important?

A

Gamma (𝛾) motor neuron innervates intrafusal fibres
Alphal (𝛼) motor neurons innervate extrafusal fibres

If intrafusal muscle fibre is controlled by same motor neurons as extrafusals, when muscle is slack (or taught), the system won’t be sensitive to slight changes. They keep the intrafusal fibres set at a length that optimises muscle stretch detection, regardless of muscle length.

214
Q

What is Sherrington’s Law of reciprocal innervation?

A

Reciprocal innervation of antagonistic muscles explains why the contraction of one muscle induces the relaxation of the other.

-permits the execution of smooth movements

215
Q

the primary motor cortex exterts what kind of control obver muscular activity?

A

direc,t, top down control.
little as one synapse in the spine between cortical neuron and innervation of muscle cells.

216
Q

motor command orginates in which cells?

A

motor cortex pyramidal cells = UPPER MOTOR NEURONS

217
Q

where are pyramidal cells found?

A

layer 5-6 grey matter

218
Q

Pyramidal cell axons project directly or indirectly (e.g. via brainstem) to spinal cord, where they synapse with what?

A

lower motor neurons

219
Q

the axons of upper motor (pyramidal) nuerons form the?

A

pyramidal tract

220
Q

aside from the direct control of the motor cortex, what other systems are important for motor control modulations?

A

basal ganglia (inhibit)
cerebellum (excitatory)

(in a general sense, but actually much more complicated)

221
Q

Which descending motor tract is responsible for proximal muscle innervation (trunk, legs)

A

Anterior Corticospinal Tract

222
Q

what descending motor tract is responsible for fine movement of distal muscles

A

lateral contricospinal tract

223
Q

which corticospinal tracts deccussate an which are ipsilateral in the spinal chord?

A

lateral corticospinal - deccussate
anterior corticospinal - ipsilateral until ventrral horn

224
Q

the corticobulbar tracts innervate which muscles?
terminate where?
and bilaterally innervate except for which nerves?

A

Corticobulbar (brainstem)
- innervate head/neck
- terminate at CNs
- CNVII and CN XII controlateral innervation

225
Q

what are the four extrapyramidal descending tracts?

A
  1. Vestibulospinal (vesitublar nuclei)
  2. Retriculospinal (medial = pons, lateral = medulla)
  3. Rubrospinal (red nucleus)
  4. Tectospinal (superior colliculus)
226
Q

function of the medial and lateral retriculospinal tract?

A

medial reticulospinal = facilitates voluntary movement
lateral reticulospinal = inhibits voluntary movement

227
Q

which of the extrapyramidal descending tracts deccussate?

A

rubrospinal and tectospinal

228
Q

function of the vestibulospinal tract?

A

Balance

229
Q

function of the tectospinal tract?

A

visual stim

230
Q

what types of tracts are responsible for involuntary movement?

A

extrapyramidal (- ipsilateral)

231
Q

what is the default output of the basal ganglia?

A

inhibitory (GABA) - thalamus and superior colliculus and therefore the cortex

232
Q

what triggers the basal ganglia’s disinhibition (double negative) of the thalamus?

A

dopamine activation in substantia nigra.

i.e dopamine removes inhibition of movement/allows movement

233
Q

what is the point of the basal gangli’a ability to selectively inhibit/disinhibit

A

basal ganglia is gatekeeper for muscle control
(ancient system)

resolves what wins the competition between motor resource us. dont try to run away and drink at the same time.

234
Q

what are the three imputs of the cerebellum?

A

cortical - copies of motor commmands
spinal - proprioception
vestibular - roation/acceleratory

makes fine tuning of motor command.

235
Q

What is the IASP definition of pain?

A

Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.

old definition required being able to articulate their pain

236
Q

what is the purpose of immediate pain?

A

warns of imminent tissue damage _ withdraw from the source of injury

237
Q

what is the purpose of perisiting pain?

A

encourages us to immobilize the injured area, giving damaged tissue the best chance to heal.

238
Q

what is nociception?

A

describes the neural processes involved in producing the sensation of pain

239
Q

outline the nociceptive pathway

A

pain pathways.
transduction in the periphery, through transmission to the dorsal horn of the spinal cord, then on to the brain

240
Q

what is the difference between acute and chronic pain?

A

acute serves a purpose. <12 weeks

241
Q

what is nocicpetive pain?

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.

burning, stinging, sharp etc

242
Q

what is neuropathic pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system.

Trigeminal Neuralgia
Glossopharyngeal Neuralgia
Post Herpetic Neuralgia
Painful Diabetic Neuropathy
Complex Regional Pain Syndrome
Phantom limb pain
Pain due to spinal cord damage / stroke / brachial plexus avulsions

243
Q

what is nociplastic pain?

A

Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain.

244
Q

what is allodynia?

A

Pain due to a stimulus that does not normally provoke pain.

eg light touch causing pain –> sunburn?

245
Q

what is dysesthesia?

A

An unpleasant abnormal sensation, whether spontaneous or evoked

246
Q

what is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain.

pin prick on clavicle hurts 3/10. but on back 9/10 pain

247
Q

what is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus.

248
Q

name the four parts of the pain pathway

A

All modalities share a common pathway from the periphery to the brain

249
Q

which order neuron crosses over in the pain pathway?

A

second order neuron

crosses to the controlateral chors and ascends to the thalamus

250
Q

what are nociceptors?

A

Receptors that sense pain.
(the free nerve ending of primary afferent neuron)

Responsible for Transduction: Physical stimulus –> action potential

Most are poly-modal (can respond to thermal / chemical / mechanical)

251
Q

where can A𝞓 and c fibres of nociceptors be found?

A

anyway in thhe body than can sense pain, internally or externally.

252
Q

where do the cell bodies of primary afferent neurons reside?

A

in the body - dorsal root ganglion
in the fac/head/neck - trigeminal ganglion

253
Q

what is the dorsal root ganglion?

A

collection of first order sensory nerve fibre cell bodies. (afferent. from periephery to seond order neurons)

The role of DRG in chronic pain has been well established.

254
Q

which are the smallest nerve fibres?
which fibres have the quickest conduction speed?

A

c fibres = smalles and slowest (pain, unmyelinated)
A-alpha = fastest (proprioception)

255
Q
A
256
Q

where in the dorsal horn do pain pathways terminate and synapse with body second order neurons?

A

I - V

(can be done with intraneuron)

257
Q

what senesations do the lateral spinothalmic tract carry?

A

pain and temperature - made up of axons of second order neurons in the pain pathway

258
Q

all sensation except oflactory relay through which structure?

A

thalamus

259
Q

The main thalamic nuclei involved in pain processing are:

A

Lateral ventral posterolateral (VPL) nuclei
Medial midline group of nuclei

260
Q

where do third order neurons end?

A

post central gyrus - sensory cortex

261
Q

where is the degree of pain judged?

A

insula.
also involved in addiction.

262
Q

which area of brain is important brain center for the emotional-affective dimension of pain and for pain modulation

A

amygdala

263
Q

Which area of the brain is intricately linked with the limbic system which is associated with emotion formation and processing, learning and memory

Has recently been shown to be one of the areas activated by acupuncture

A

cingulate cortex

264
Q

what is the peri-aqueductal gray?

A

Grey matter located around the cerebral aqueduct
Receives input from cortical and sub-cortical areas
Projects onto neurons in the dorsal horn

NATURAL PAIN RELEIF CENTRE - SEND SIGNALS TO DORSAL HORN TO INFLUENCE HOW PAIN IS TRANSMITTED

265
Q

is the peri

explain how phantom limb pain can occur during particular activities.

A

hair brushing.
Another explanation for feeling in the limb when the face touched may be that the tactile and proprioceptive input from the face and tissues proximal to the stump takes over the brain area- so spontaneous discharges from these tissues would get misrepresented as arising from the missing limb (Figure 11) [Ramachandran & Hirstein, 1998].

266
Q

three (broad) ways we can treat pain?

A
  1. stimulate descending inhibitory pathway
  2. gate control
  3. pharmacotherpay
267
Q

why, in theory, does “rubbing something better’ work?

A

gate control theory. - peripheral control of pain

c fibres: transmit pain and inhibit pain inhibitors.

Rubbing - AB fibres: transmit crude touch (myelinates and faster than c fibres) faster. reduce activation and activate pain inhibitors.

red nerves firing

268
Q

what kind of pain can opioids treat?

A

acute. not chronic

opioid induced hyperalgesia

269
Q

three causes of cancer pain

A
  1. Pain associated with direct tumor (tumor infiltration, bone metastases)
  2. Pain associated with cancer therapy (chemo, surgery or radiation)
  3. Pain unrelated to cancer (RA, OA, headache or herpes zoster)

total pain (bio pyscho social and spiritual)

270
Q

what are the three layers of the eye?

A

Outer - sclera + cornea
Middle - Iris, Ciliary body, Choroid
Inner - Retina

271
Q

what are the two humours of the anterior segment of the eye?
what is their function?

A

anterior chamber = aqaueous humour
posterior chamber = vitreous humour
-maintain pressure in the eye

272
Q

why is the scalera white and cornea transparents

A

cornea extension of sclera, both made from collagen by collagen in sclera is crosslinked ∴ opaque, whereas cornea collagen runs parallel

273
Q

which structures in the eye are responsible for refractive power?

A

Cornea = 2/3 refractive power
lense = 1/3 refractive power

274
Q

what are the hisoogical layers of the outer eye. which layer is able to regenerate?

A

epithelium able to regenerate.

275
Q

function of the iris

A

contains dilator and sphincter pupillae muscles.
pupillary reflexes

276
Q

where in the eye is aqueous humour produced?

A

glandulary epithelium of the ciliary body

277
Q

function of the choroid?

A

blood supply to outer third of retina

278
Q

function of the retina?

A

Tranducer.
(turns image into electrical signals)

279
Q

what are the two types of photoreceptor cells in the retina?
what is the difference between them?

A

Rod cell = B+W, Low Res., Peripheral, low res
Cone cell = Colour, High Res. Central/fovea (macula lutia)

280
Q

What do photons do during phototransuduction?

A

chemically change to Rhodopsin molecule (rods) which changes Opsin molecular sturcture (cones) which triggers a cascade

11-cis-retinal cells (vit A)

281
Q
A
282
Q

what is myopia?

A

shortsightedness.
- lense overpowered so cant focus far objects onto retina
- too steep a lense curve or eyeball too long

283
Q

what is hypermetropia?

A

farsightedness
- underpowered lense so cant focus near objects onto retina
- lens not flexible enought
- corneal curvature too shallow
- axial eyeball too short

284
Q

What are the three layers of the tear film?

A

anterior lipid (prevent evapouration)
middle aqueous (lube)
posterior mucous

285
Q

Blood supply to the eye?

A

opthalmic artery (from internal carotid)

286
Q

Inner 2/3 of retina supplied by?

A

Inner 2/3 retina = central retinal artery
Outer 1/3 retina = choroid (from posterior cilliary)

287
Q

what are the lymphatic drainage routed from the globe?

A

no lymphatic drainage from the globe of eye
(conjunctiva and lids do have lymphatic drainage)

288
Q

Descibe Motor Neuron Disease

A

Progressive disorder of unknown aetiology

Onset usually after age 50. Males more likely to be affected.

Present with combination of both UMN and LMN signs without sensory involvement.

Symptoms include – limb weakness, cramps, disturbance of speech or swallowing.

Signs – wasting and fasciculation of muscles, pyramidal tract involvement causing spasticity and exaggerated tendon reflexes

Symptoms can start focally but become widespread with time

289
Q

A 42 year old woman suffers a violent headache followed by sudden collapse. You notice that her left pupil is fixed and dilated and her left eye is deviated laterally and downwards.

Which artery is likely to have been affected? Why?

A

Posterior Communicating Artery. (subarachnoid haemorrhage)
CNIII palsy - only SO and LR left

290
Q

Whilst examining an elderly lady on the stroke ward, it becomes apparent that she can only see one half of your face.

Where is the likely lesion?

A

Occipital lobe lesion:
Typically cause visual disturbances and depends on where the lesion is

These can include visual illusions and hallucinations

Trouble recognising objects or facial blindness

Being able to write but not read

When a lesion affects most of the occipital lobe on one side it can cause an homonymous hemianopia which means the patient is unable to see the visual field on the opposite side of the lesion

291
Q

As part of a neurological examination, you ask the patient to walk a few steps. When they do so they walk with a wide unsteady gait and appear uncoordinated. Their speech is slurred.

Where is the likely lesion?

A

Cerebellar lesions:

Patients have a wide unsteady gait

Impaired coordination

Uncontrolled repetitive eye movements

Difficulty with fine motor tasks

Intentional Tremor

Slurred speech

292
Q

An elderly patient has a stiff flexed arm, and a stiff extended leg (both on the left) which they find difficult to bend.

Where is the cause most likely to be located?

A

UMN

293
Q

An 89-year-old man presents with acute onset of weakness and numbness of his left lower leg and foot is unusually agitated and in an aggressive mood.

Which artery is likely to have been affected?

A

ACA

  • Supplies the anteromedial surface of the cerebral hemisphere.
  • Paraplegia usually affects the lower limbs sparing the upper limbs and face.
  • They may be incontinent.
  • They may display frontal lobe symptoms e.g. personality changes
294
Q

A 40-year-old woman felt immediate back pain and a popping sensation after lifting a heavy box. The next day she noticed she was tripping over her right foot as it was dragging along the floor. Where is the cause most likely to be located?

A

nerve root.

this is foot drop. paralysis of myscles that lift food.
Possible prolapsed vertebral disc.

295
Q

A 69-year-old lady was slurring her words at a coffee morning. At the same time her right arm began to feel heavy and weak. 24 hours later all her symptoms had resolved. Which of these is the likely cause?

A

Transient Ischaemic Attack

296
Q

A 30-year-old woman noticed both her eye lids becoming progressively droopier with time (ptosis). Weeks later she began to experience double vision and found it progressively more tiring and difficult to chew while eating. Which of these is the likely cause?

A

Myasthenia Gravis

  • Condition of the neuromuscular junction
  • Acetylcholine receptors are blocked by an auto immune reaction between the receptor protein and anti-acetylcholine receptor antibody.
  • Women more affected than men. Presents between 15 to 50 years.
  • Main symptom is abnormal fatigable weakness of muscles.
  • First symptoms are usually ptosis or diplopia.
  • Weakness of chewing, swallowing, speaking or limb movement can occur.
297
Q

A 30-year-old pregnant lady complains to the GP of progressive hand weakness. She is unable to open jars and even grip her tea cup. The GP noticed that the muscles around her thumb were wasting.Cause?

A

peripheral nerve - carpal tunnel.

  • This due to compression of the median nerve in the carpal tunnel.
  • Wasting of the abductor pollicis brevis can develop with the following distribution of numbness and pain.
298
Q

A 53-year-old man with hypertension is admitted following a sudden collapse and is unable to move any part of his body except for eye movements, he appears to understand your questions, but is unable to answer.

where is the likely lesion?

A

Brainstem

  • This is locked-in syndrome.
  • Patients cannot move or communicate verbally due to paralysis of nearly all voluntary muscles.
  • Blinking and vertical gaze may be preserved depending on the extent and level of the lesion within the brainstem
  • They are conscious and aware.
  • Complete recovery is rare.
299
Q

which CNs are considered extensions of the brain rather than specific ‘nerves”, making them CNS structures?

A

CNI CNII

300
Q

which CN’s are sensory only?

A

I, II VIII

301
Q

which CN’s are motor only?

A

III IV VI XI XII

302
Q

which CN’s are sensory and motor?

A

V VII IX X

303
Q

Which CN’s have parasympathetic innervation

A

III VII IX X

304
Q

CN I dysfunction

A

altered/loss of sense of smell

305
Q

CN II dysfunction?

A

altered/loss of vision

306
Q

dysfunction of CN III?

A

eye rests down and out.
Ptosis.
mydriasis

307
Q

dysfunction of CN IV?

A

eye unable to look down whilst adducted

308
Q

CN V1 skull base foramen?
dysfunction

A

SOF (sphenoid bone)
altered/absent sensation to upper 1/3 of face

309
Q

which CN is responsible for the sensory afferent pathway of the corneal reflex?

what about the motor effect?

A

sensory = opthalmic V1
motor = facial VII

310
Q

skull base foarmen of CN V2?
dysfunction?

A

forman rotundum

absent/altered sensation to middle 1/3 of face

311
Q

Skull base foramen of V3?
which muscles does it innervate?
dysfunction

A

CN V3 - mandiular branc
foramen ovale.
sensation to lower 1/3 of face.
muscles of mastication and tensor tympani
dysfunction = altere/absent sensation in lower 1/3 of face. weakness in mastication

312
Q

dysfunction of CN VI?

Bonus: origin and foramen

A

unable to abduct (LR)

Pons and SOF

313
Q

dysfunction of CN VII?

A

weakness, paralysis of facial muscles, reduced (not zero) salviation (not parotid), sensitive hearing, cant blink, no tearm, dry eyes. Reduced taste

314
Q

which nerves prodive taste sensation to the tongue?

A

Facial = Anterior 2/3
Glossopharyngeal = Posterior 1/3

315
Q

which nerve prodives motor sensation to the tongue?

A

hypoglossal

316
Q

which nerve prodives general senstation to the tongue?

A

CNV3

317
Q

dysfunction of CN VIII

A

vertigo, tinnitus or deafness

318
Q

dysfunction of CN IX?

foramen?

A

loss of gag reflex.
reduced salivation.

jugular foramen

319
Q

dysfunction of CN X

A

loss of gag reflex, absent rise of soft palate, weak/absent cough or swallow - parasym—>thorax/abdo

AWAY FROM AFFECTED SIDE

320
Q

what are the afferent and efferent nerves of the gag reflex?

A

afferent (sensory) = glossopharyngeal IX

efferent (motor) - vagus

321
Q

dysfunction of CN XI?

A

cant shrug (trapedius)
or turn head (Sternocleidomastoid)

322
Q

dysfunction of XII?

A

weakness/paralysis of tongue.
TOWARDS THE AFFECTED SIDE

323
Q

outline the HPA axis.

how is it altered in depression?

A

increased CRH enlarged adrenals and pituitar, reduced negative feedback, reduced glucocorticoid resistance

Corticotropin-releasing hormone
Adrenocorticotropic hormone

324
Q

how does stress impact neurogenesis?

A

stress reduced neurogenesis and therefore neuroplasticity.

325
Q

*

cortisol is neurotoxic.
which areas of the brain, in particular, does it affect?

A

Hippocampus - up to 20% volume loss in depression
Frontal Lobes - large volume loss of dorsolateral PFC
(working memory, porblem solving)

326
Q

why do antidepressents take so long to work?

A

they affect the gene expression, the tablet increases neuroplasiticity and increases BDNF synthatsis (connection)

tablet increases the likelihood of change, but doesn not initiaite change itself.

327
Q

what is the DMN and how is it affected in depression?

A

default mode network - the brain’s ‘screen saver’
Depressed people find it hard to appropriately switch off their DMN in response to a task.

328
Q

which CN carries general sensation to the middle ear?

A

glossopharyngeal - It carries general sensation
from the middle ear, auditory tube, majority of the pharynx and both general and taste sensation from the posterior 1/3 of the tongue.

facial = ear canal

329
Q

what are the features of upper motor neuron disorder?

A
  • Spasticity
  • Spastic paralysis
  • Brisk reflexes
  • Positive Babinski reflex

the corticospinal tract helps in the conscious inhibition of muscle. If we damage UMNs, there is a loss of inhibitory tone of muscles leading to constant contraction of muscles.

330
Q

With complete damage to CN VIII, when a tuning fork is placed in the middle of the forehead, the sound is heard best on which side?

A

Weber test – neurosensory = if damage to CNVIII hear best in normal ear;

if conductive issue conductive = hear best in abnormal ear

331
Q

what are some common causes of UMN damage?

A

Brain - strokes, tumours, demyelination (MS)
Spinal Chord - MS, cord compression, spinal chord degeneration- vit B12 deficiency

332
Q

what are the features of lower motor neuron disorder?

A
  • Weakness- flaccid
  • Reduced tone
  • Muscle wasting (due to lack of innervation)
  • Fasciculations (look as if twitching)
  • Absent deep tendon reflexes
333
Q

causes of lower motor neuron injuries?

A
  • Motor neuron- MND, Polio
  • Motor nerve roots- radiculopathy, Guillain
    Barre syndrome
  • Motor nerves – Neuropathies, radiculopathies
  • Neuro muscular junction disorder- Myasthenia
    gravis
  • Muscle disorders – Myositis, myopathies
334
Q

what are some features of peripheral nerve/neuromuscular junction impairment?

A
  • Numbness, tingling, burning, freezing pain (sensory)
    – Weakness and muscle wasting (motor)
    – Poor balance as a result
    – Deformities secondary to weakness
335
Q

what type of pathologies are possible in peripheral nerves?

A

axonal (or demyelination

336
Q

causes of peripheral nerve damage

A
  • diabetes
  • alcohol/toxins/drugs
  • hereditary
  • cancers
  • metabollic
337
Q

explain the major events in neuromuscular transmission as best you can.

A
  1. Motor neuron depolarization causes action potential to
    travel down the nerve fiber to the neuromuscular junction(1)
  2. Depolarization of the axon terminal causes opening of voltage gated** calcium** channels and an influx of
    Ca2+ (2) which triggers fusion of the synaptic vesicles (3)
    and release of neurotransmitter (Acetylcholine; ACh) (4).
  3. ACh diffuses across the synaptic cleft and binds to post- synaptic ACh receptor (AChR) located on the muscle fiber
    at the motor end-plate (5).
  • Binding of ACh to AChRs opens the intrinsic ion
    channel    , resulting in a cation entry locally. This results
    in a local depolarisation of the sarcolema.
  • Local sarcolemmal depolarisation results in opening
    of the sodium channels (VGSC) causing an influx of
    Na (5), depolarization of the sarcolemma that travelsdown the t-tubules (6) and ultimately causes the release of Ca2+ from the sarcoplasmic reticulum - CONTRACTION.
  • Unbound ACh in synaptic cleft defuses away or is
    hydrolyzed (inactivated) by acetylcholinesterase
    (AChE) (7).
338
Q

name three things that a required for smooth coordination of movement

A
  1. extra-pyramidal system (mainly basal ganglia - process afferent info)
  2. Cerebellum (fine tuning and learning)
  3. sensory input (yes you are smooth, carry on)
339
Q

clinical findings in PD?

A
  1. Tremor
  2. Rigidity
  3. Akinesia/ Bradykinesia
  4. Postural instability

unsteady gate, loss of sense of smell, sleep disorder,

340
Q

diagnostic investigations for parkinsons

A

DAT scan. asymmetrical basal ganglia.

slos just see if medication helps

341
Q

features of cerebellar disorders

A

like drunk - slurred speech, ataxic walk.
no smooth eye movement - nystagmus
finger nose test unsteady
heel shin test fail.
police drink/drive test - walk on line - struggle

342
Q

causes of cerebellar disorders

A

vascular (due to stroke, hemorrhage), idiopathic, iatrogenic (drug), traumatic, autoimmune, metabolic, infective, inflammatory, neoplastic, toxic, and rare genetic disorders.

343
Q

give some examples of motor circuit disorders

A

Parkinson’s, Huntongton’s, Dystonia, Tourette’s

344
Q

give some examples of limbic circuit disorders

A

OCD, ADHD

345
Q

give some exapmles of oculomotor circuit damage disorders

A

cerebral palsy, Wilson Disease

346
Q

What is dopamine synthesised from?

A

L-Tyrosine –[hydroxylase]–> L-DOPA —-[decarboxylase]—> Dopamine

L-DOPA = best parkinson’s drug

347
Q

how many types of dopamine receptors are there?

A

2

348
Q

3 pathological findings in PD

A
  1. loss of dopananinergic neurons.
  2. Lewy body’s
  3. DAT scan reduced signal
349
Q

pathological findings in huntington’s

A

CT head scan - enlarged ventricles due to shrinking of striatum

350
Q

How does PD cause “reduced” movement and HD cause “excess” movement

A
351
Q

clinical symptoms of PD

A

Brady/Akenesia
Tremor
Rigidity

352
Q

how does deep brain stimulation help the symptoms of PD?

A

IN PD, there is not enough inhibition of the subthalamic nucleus (inhibits action). Subthalamic nucleus overpowered and inhibts movement too much.
DBS Disinhibts the Subthalamic nucleus, to reduce inhibition of movement.

353
Q

clinical features of huntington’s?

A

Chorea
Dementia
Personality changes

354
Q

genetic features of huntington’s?

A

Autosomal Dominant
Fully penetrant
“Too many Repeats”

355
Q

A 48-year-old man with type 2 diabetes mellitus, who smokes 30 a day and is overweight presents with bilateral “glove and stocking” loss of pain, temperature and pin prick sensation.
which spinal tract is affected?

A

spinothalamic

356
Q

what makes up the CNS and what makes up the PNS?

A

CNS = brain and spinal chord
PNS = cranial nerves and spinal nerves

357
Q

what dermatone is the nipple at?

A

t4

358
Q

A sexually active 75-year-old gentlemen presents with a stamping gait. He is diagnosed with tabes dorsalis. On examination he has a loss of joint position sense and cannot feel the tuning fork (vibration) when placed on his medial malleolus.
which spinal tract is affected?

A

DCML pathway

359
Q

A 73 year old lady presents to her GP surgery with an intensely itchy vesicular rash in a horizontal line at the level of the nipple.

What is the most likely diagnosis?

A

shingles

  • Caused by Herpes Zoster virus
  • Commonly affects the elderly
  • Produces a rash that is usually unilateral and has a dermatomal distribution
360
Q

Which group of spinal nerves innervates the ankle reflex?

A

S1/S2

361
Q

The central nervous system is composed of many cell types each with a differing role.

Which cell type listed below is NOT found in the central nervous system?

Answers:
A.
Astrocytes

B.
Ependymal cells

C.
Microglia

D.
Oligodendrocytes

E.
Schwann cells

A

schwann cells

362
Q

what is the upstroke arise from and what does the downstroke arise from?

A

The upstroke is mediated by sodium ions rushing into the cell. The downstroke is mediated by potassium ions rushing out of the cell.

363
Q

Which group of spinal nerves innervates the biceps reflex?

A

C5/C6

364
Q

which types of neuron are myelinated and unmyelinated?

A

autonomic motor neurons

Medicine - Phase 1 (16 decks)

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