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second year > Neurovascular Physiology > Flashcards

Neurovascular Physiology Flashcards

1
Q

Where is the vestibular system found?

A

Inner ear

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2
Q

What does the vestibular system consist of?

A

Fluid filled membranous tubes embedded in the temporal bones (labrinyths) - three semi circular canals (at right angles) connected to ampulla and the utricle and sacule.

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3
Q

What are the utricle and saccule collectively known as?

A

Otolith organs.

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4
Q

What is the function of the vestibular system?

A

Control of balance and posture and proprioception of head.

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5
Q

In which parts of the vestibular system are movement detected?

A

Cristae of semi-circular canals

Maculae of otolith organs

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6
Q

What sort of movement do the semicircular canals detect?

A

Rotation movement.

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7
Q

What sort of movement do the otolith organs detect?

A

Utricle - horizontal acceleration

Sacule - vertical acceleration, or head position when lying down

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8
Q

The vestibular centres of the medulla have strong associations with where and why?

A

Cerebellar centres to coordinate postural muscles to maintain balance.

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9
Q

To which three things does the vestibular nuclei connect the vestibular system with?

A

Descending motor pathways of the EOM of eye.

Receives input from proprioceptors signalling limb and body, neck and eye muscles position.

Via thalamus to cerebral cortex to signal perception of movement and body position = kinaesthesia.

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10
Q

What are the swellings at the end of the semicircular canals known as and what is their structure?

A

Ampulla - inside are cristae. Cristae are composed of a gelatinous structure (cupula) which has cilia in it (which synapse directly on to sensory neurone of vestibular nerve).

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11
Q

How do the cristae function to detect rotation acceleration?

A

Skull is rotated to right, endolymph doesn’t move initially due to inertia, but ampulla moves as it is embedded in skull, produces drag which bends cupola and cilia in opposite direction of movement.

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12
Q

What is the structure of the cilia within the cristae?

A

A single, large kinocilium and many stereocilia.

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13
Q

Distortion of cilia in direction of kinocilium causes what?

A

Depolarisation and increased discharge of APs in vestibular nerve.

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14
Q

Where is the sensory information from the vestibular system mostly integrated?

A

Cerebellum.

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15
Q

What are the structure of the maculae?

A

Kinocilium and series of stereocilium which protrude into a gelatinous mass (otolith membrane), embedded in the otolith membrane are otoliths (calcium carbonate crystals).

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16
Q

How do the maculae detect linear acceleration?

A

Otoliths have greater density than endolymph and thus are move affected by gravity and this causes them to move in the otolith membrane which distorts the jelly and moves fo the cilia. E.g. backward tilt moves otolith in direction of kinocilium causing depolarisation and increased discharge of APs, opposite for forward tilt.

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17
Q

What tracts do the vestibular system reflexes involve?

A

Vestibulocortical and vestibulospinal.

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18
Q

What are the main vestibular system reflexes?

A

Tonic labyrinthine reflexes - keep axis of head in constant relationship with rest of body (involves maculae and neck proprioceptors)

Dynamic righting reflexes - rapid postural adjustments made to stop falling when tripping (involves long reflexes, and extension of limbs)

Vestibular ocular reflex - associations with vestibular apparatus, visual apparatus and postural control that influence eye movement and balance.

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19
Q

What are the two vestibular ocular reflexes?

A

Static reflex - when you tilt your head your eyes intort/extort

Dynamic vestibular nystagmus - saccadic eye movements that rotate the eye against direction of rotation to maintain gaze (restricted so flicks back)

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20
Q

If someone is rotated what type of nystagmus will they get during and after the rotation?

A

During - same side nystagmus.

After - opposite side nystagmus due to endolymph catching up and pushing cupula in opposite direction.

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21
Q

Inserting warm fluid into the ear causes what?

A

Nystagmus towards the affected side (convection currents affect endolymph).

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22
Q

Inserting cold fluid into the ear causes what?

A

Nystagmus away from the opposite side (COWS - cold opposite, warm same).

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23
Q

Define sleep.

A

Stage of unconsciousness from which an individual can be roused by normal stimuli, light touch, sound etc.

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24
Q

What causes sleep?

A

Active inhibitory processes in the pons.

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25
Q

What chemical is thought to be essential to sleep initiation? And why is it thought to be involved?

A

Seratonin, precursor of melatonin (assoc. with see).

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26
Q

What place in the brain is thought to be linked to the induction of sleep?

A

Suprachiasmastic nuclei of the hypothalamus.

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27
Q

What is the SCN responsible for other than sleep induction?

A

Controlling Circadian rhythm as it is entrained by light (cells in back of retina send signals to this to entrain it).

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28
Q

What does activity in the SCN stimulate?

A

Release of melatonin from the pineal gland –> feelings of sleepiness.

When more light hits back of retina –> less melatonin

When less light hits back of eye –> more melatonin

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29
Q

What is orexin?

A

Aka hypocretin

Excitatory neurotransmitter that is required for wakefulness.

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30
Q

What does defective orexin signalling cause?

A

Nacrolepsy.

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31
Q

So, during wakefulness what, in summary, is occurring?

A

Excitatory neurons in ascending reticular activating system are released from inhibition from sleep centres (all in reticular formation).

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32
Q

What is thought to occur to create a sleep-wakefulness cycle?

A

Active cells become fatigued and excitatory signals dafe, so inhibitory peptide signals from sleep enters in reticular formation take over (and vice versa, inhibitory cells fatigue, and excitatory cells are reinvigorated).

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33
Q

How can EEG waves be analysed?

A

Amplitude

Frequency (increases with neuronal excitation)

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34
Q

What are different lengths of wavelengths associated with?

A

Very long - unconciousness
Shorter - awake and relaxed
V. short - alert
Shortest - epileptic seizures

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35
Q

What are the different classifications of EEG waves?

A

Alpha - awake, relaxed = high amplitude, high frequency, waves synchronous

Beta - awake, alert, higher frequency, low amplitude, waves asynchronous

Theta - low frequency, varying amplitude

Delta - very low frequency (occur in deep sleep)

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36
Q

Why are beta waves of a lower amplitude despite a higher level of awareness?

A

Waves are asynchronous meaning that there are loads of inputs to the brain which may involve negative and positive waves, which cancel each other out, leading to a lower amplitude.

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37
Q

When are theta waves common?

A

More common in children and during times of stress in adults. Dominate early part of sleep.

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38
Q

What are the 5 stages of sleep?

A

Stage 1 - slow wave, non-REM S-sleep - slow eye movements, easily roused. Theta waves.

Stage 2 - no eye movement. Frequency slows but burst of rapid waves (sleep spindles)

Stage 3 - high amplitude, v slow delta waves and episode of faster waves

Stage 4 - exclusively delta waves

REM sleep - rapid eye movements, on EEG appears similar to awake state. Dreams occur.

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39
Q

Is it easy to be roused from stage 3 and 4 sleep?

A

Deep sleep stages - so no.

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40
Q

In which stages does sleep walking and talking occur?

A

3 and 4.

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41
Q

How long does one sleep cycle tend to last?

A

90 mins.

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42
Q

How does your sleep change throughout the night?

A

More deep sleep initially, then more REM sleep at the end.

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43
Q

Waking during which stage will increase chance of remembering dreams?

A

REM.

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44
Q

What is the most restful type of sleep?

A

Deep sleep.

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45
Q

In which type of sleep is their decreased vascular tone, BP, respiratory and basal metabolic rate (and therefore temp)?

A

Deep sleep.

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46
Q

How long does REM sleep tend to last for every cycle?

A

5-30 mins.

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47
Q

In REM there is profound inhibition of what and why?

A

Skeletal muscles due to inhibitory projections from pons to spinal cord to prevent us acting out our dreams.

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48
Q

REM sleep is dependent on what kind of pathways?

A

Cholingeric pathways in the reticular formation and their projections to the thalamus, hypothalamus and cortex.

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49
Q

What kind of drug increases time spent in REM sleep?

A

Anticholinesterases.

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50
Q

What waves are seen in REM sleep on EEG?

A

Beta waves.

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51
Q

Do heart rate/resp rate slow in REM sleep?

A

No, they become irregular and brain metabolism also increases.

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52
Q

How easy is it to rouse someone from REM sleep?

A

Very difficult.

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53
Q

Is REM sleep important?

A

Very. Unknown why.

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54
Q

What are symptoms of sleep deprivation?

A

Impaired cognitive function, impaired physical performance, sluggishness, irritability….

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55
Q

What activities in the brain does sleep support?

A

Neuronal plasticity, memory, learning, cognition, clearance of waste products from the CNS, conservation of whole body energy and immune function.

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56
Q

How does sleep change with age?

A

More REM sleep in children, may be absent in 80+. Total time asleep in development, where brain maturation and synaptic formation occurring rapidly.

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57
Q

What is cognition?

A

Highest order of brain function, includes thought processing via integration of sensory information and learning from it. Requires consciousness.

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58
Q

What does learning and memory require?

A

Motivation.

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59
Q

What concept explains our ability to learn and remember?

A

Neuronal plasticiity - the ability of central neurone to adapt their neuronal connections in response to new experiences (synapses change chemically and physically).

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60
Q

Where does learning occur in the brain?

A

Spread out over whole brain and involves several association areas.

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61
Q

What are the three key components of learning and memory?

A

Hippocampus - formation of memories
Cortex - storage of memories
Thalamus - searches and assesses memories

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62
Q

In order to store memories, we need a —— component.

A

Emotional.

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63
Q

What creates the emotional component required for the formation of memories?

A

The limbic system.

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64
Q

What does the limbic system consist of?

A

Cingulate gyrus, hippocampus and amygdala and hypothalamus.

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65
Q

Is the thalamus considered as part of the limbic system?

A

No, but it is crucial to memory.

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66
Q

What is the oldest part of the cortex?

A

Limbic system.

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67
Q

What is the hypothalamus associated with?

A

ANS responses.

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68
Q

Collectively, what are the components of the limbic system responsible for?

A

Our instinctive behaviours, e.g. thirst, sex, hunger… and emotive behaviour.

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69
Q

What is emotive behaviour driven by?

A

Seeing reward or avoiding punishment (reward and punishment areas are distinct areas in the limbic system).

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70
Q

What does motivation require?

A

Reward or punishment to give a task significance.

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71
Q

What deems the significance of an experience and whether it should be stored or not?

A

The frontal cortex and its association with the reward/punishment areas in the limbic system.

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72
Q

What structure is essential for the formation of new memories?

A

Hippocampus.

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73
Q

What are the different types of memory?

A

Immediate/sensory
Short term
Immediate long-term
Long-term

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74
Q

How long does your immediate/sensory memory hold information for?

A

A few seconds, holding experiences in the mind for a few seconds.
Visual memories decay faster (<1s) than auditory memories (4s).

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75
Q

How long does your short term memory hold information for? What is it associated with?

A

Seconds-hours, aka. working memory, allows small tasks to be carried out, e.g. reading a sentence.

Associated with reverberating circuits.

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76
Q

How long does your immediate long-term memory hold information for? What is it associated with?

A

Weeks-hours.
Associated with chemical adaptations at presynaptic terminal - - increased Ca entry into presynaptic terminals which increases NT release (i.e. more NT released for the same stimuli).

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77
Q

How long does your long-term memory hold information for? What is it associated with?

A

Lifelong.

Associated with structural changes in synaptic connections.

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78
Q

Describe the electrical phenomenon behind short term memory.

A

Maintenance of excitation from reverberating circuits, i.e. neurones in the circuit are constantly excited.

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79
Q

If something is deemed significant in short term memory, how is it moved into long term memory?

A

Consolidation - selective strengthening of the synaptic connections through repetition. This process takes time (during which electrical activity vulnerable to being wiped out).

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80
Q

If a short term memory is deemed insignificant what occurs?

A

Reverberation fades away.

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81
Q

What are the structural changes involved in long term memory?

A

Increase in NT release sites on presynaptic membrane
Increase in NT vesicles stored and released
Increase in no. of presynaptic terminals.

This leads to greater amplitude in EPSP in post-synaptic cell, strengthening the synapse = long-term potentiation.

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82
Q

Long term memory is basically a well-established, well-rehearsed —- – —– —– unique to that particular —— and they are stored in different parts of the brain.

A

Pattern of neural firing

Memory

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83
Q

What are the two main types of long term memory?

A
  1. Declarative/explicit - memory for events/words/rule/language. RELIES HEAVILY ON HIPPOCAMPUS.
  2. Procedural/reflexive/implicit memory - acquired slowly through repetition, incl. motor memory. Mainly based in cerebellum, INDEPENDENT of hippocampus.
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84
Q

What is the difference between semantic and episodic memory?

A

Semantic - not drawing from personal experiences, e.g. common knowledge, colours, alphabet etc.

Episodic - autobiographical events.

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85
Q

How are memories stored?

A

They are coded and then stored in sensory association areas of the brain (coding allows similar memories to be grouped together).

Different parts of memory are laid down in different parts of cortex, e.g. visual component in visual cortex.

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86
Q

What is the Papez circuit?

A

The structures through which the reverberating circuit flows - includes hippocampus, maxillary body, anterior thalamus and cingulate gyrus.

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87
Q

If deemed significant information, where does the reverberating circuit extend to to allow consolidation?

A

Reverberating activity continues between Papez circuit, frontal cortex and sensory and association areas until consolidation complete.

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88
Q

Why are olfactory stimuli powerful in evoking long term memories?

A

Substantial connections between amygdala and hippocampus and the primary olfactory cortex.

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89
Q

Describe the sequence of events in synaptic transmission.

A
  1. Synthesis/packaging of NTs
  2. Na AP invades terminal
  3. Activates voltage gated Ca channels
  4. Triggers Ca-dependent exocytosis of NTs
  5. NT diffuses across cleft and binds to inotropic/metabotrophci receptors on post-synaptic cell
  6. Presynaptic autoreceptors inhibit more NT release
  7. NT inactivated by uptake into glia/neurons/extracellular breakdown (ACh)
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90
Q

What methods could you use to reduce synaptic transmission?

A

Block Na channels, e.g. local anaesthetics
Block Ca channels, e.g. spider toxin
Block release machinery, e.g. botox
Block post-synaptic receptors, e.g. receptor antagonists
Activate presynaptic inhibitor receptors
Increase NT breakdown/uptake
Inhibit NT synthesis/packaging

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91
Q

What is the issue with using botox, spider toxin and local anaesthetics to reduce transmission?

A

They affect all the neurones (are not specific).

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92
Q

What methods could you use to increased synaptic transmission?

A

Flow cells with appropriate precursors
Use agonist to activate postsynaptic receptor
Allosteric drug activating receptor on its own
Block transmitter breakdown
Block uptake of transmitter

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93
Q

Give examples of monoamine NTs?

A

Noradrenaline, dopamine, serotonin.

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94
Q

Give examples of amino acid NTs.

A

Glutamate, GABA, glycine.

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95
Q

Give examples of purine NTs.

A

ATP, adenosine.

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96
Q

Give examples of neuropeptide NTs,

A

Endorphins, CCK, substance P.

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97
Q

Give example of noradrenaline reuptake blockers.

A

Tricyclic drugs, e.g. antidepressants.

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98
Q

What are MOA inhibitors?

A

Antidepressants.

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99
Q

What are selective serotonin uptake inhibitors?

A

Antidepressants.

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100
Q

What can GABA analogues be used to treat?

A

Epilepsy and anxiety.

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101
Q

What germ layer does the nervous system develop from and how?

A

Ectoderm (wk3). It thickens and forms a neural plate, neural folds migrate towards each other to form neural tube (initially remains open at cranial (anterior) end and posterior (caudal) end.

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102
Q

When does the anterior neuropore close?

A

25 days (18-20 somite stage).

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103
Q

When does the posterior neuropore close?

A

27th day.

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104
Q

What can failure of the neuropores cause?

A

Neural tube defects, e.g. anencephaly, encephalocoele, spina bifida.

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105
Q

When does development of the brain vesicles begin?

A

With closure of anterior neuropore (25th day).

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106
Q

Where is the cephalic flexure and when does it form?

A

End of third week, it is between the midbrain (mesencephalon) and hindbrain (rhombencephalon).

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107
Q

Where is the cervical flexure and when does it form?

A

End of 4th week, between the spinal cord and hindbrain.

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108
Q

Where does the pontine flexure form and when does it form?

A

5th week and between metecephalon and myelencephalon.

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109
Q

What are the initial 3 brain vesicles?

A

Prosencephalon (forebrain)
Mesenecephalon (midbrain)
Rhombencephalon (hindbrain)

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110
Q

What does the forebrain develop into?

A

Telecephalon and diencephalon.

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111
Q

What does the rhombencephalon develop into?

A

Metechephalon and myelencephalon.

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112
Q 
From where do: 
1. lateral ventricles
2. 3rd ventricle
3. cerebral aqueduct 
4. 4th ventricle
Form?
A
  1. telecephalon
  2. telencephalon and diencephalon
  3. mesencephalon
  4. metecenaphlon and myeloencephalon
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113
Q

When does CSF production begin?

A

5th week.

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114
Q

Where is CSF predominantly produced from?

A

Choroid plexus (3rd and 4th ventricles).

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115
Q

Neural tube is initially a single layer of what?

A

Rapidly dividing neuroepithelial cells (pseudo stratified epithelium dividing at ventral surface).

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116
Q

Which cells are not produced by neuroepithelium?

A

Microglia, mesenchymal cells (macrophages) that migrate into the CNS.

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117
Q

What are neural crest cells and where do they come from?

A

Cells from dorsal part of neural tube migrate, e.g. some to between somites to form dorsal root ganglia, or close to organs to form ganglia or to gut to form ENS ec.

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118
Q

What sort of information do the cranial nerves carry?

A

Somatic motor fibres, visceral motor fibres, visceral sensory fibres, general sensory fibres, special sensory fibres.

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119
Q

What is the function of the olfactory nerve?

A

Smell.

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120
Q

Where does CN I emerge from and where does it emerge from the skull?

A

Receptors in olfactory epithelium from olfactory nerve, pass through foramina in cribriform plate and enter olfactory bulb in anterior cranial fossa.

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121
Q

Where does CN II emerge from?

A

Enters optic canal.

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122
Q

What is the function of CN II?

A

Optic nerve - conveys vision.

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123
Q

Where does CN III emerge from and where does it emerge from the skull?

A

Emerges from midbrain and exits superior orbital fissure.

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124
Q

Where does CN IV emerge from and where does it emerge from the skull?

A

Emerges from dorsal surface of midbrain and exits superior orbital fissure.

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125
Q

Where does CN V emerge from and where does it emerge from the skull?

A

Emerges from pons, travels through trigeminal ganglion (stacked cell bodies) then splits into V1, V2 and V3.

V1 - exits via superior orbital fissure.

V2 - exits via formanen rotundum.

V3 - exits via formanen ovale.

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126
Q

Where does CN VI emerge from and where does it emerge from the skull?

A

Emerges between pons and medulla and exits via superior orbital fissure.

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127
Q

Where does CN VII emerge from and where does it emerge from the skull?

A

Emerges between pons and medulla and exits via internal acoustic meatus, facial canal and stylomastoid foramen.

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128
Q

Where does CN VIII emerge from and where does it emerge from the skull?

A

Emerges between pons and medulla and exits via internal acoustic meatus dividing into vestibular and cochlear nerves.

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129
Q

Where does CN IX emerge from and where does it emerge from the skull?

A

Emerges from medulla and exits via jugular foramen.

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130
Q

Where does CN X emerge from and where does it emerge from the skull?

A

Emerges from medulla and exits from jugular foramen.

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131
Q

Where does CN XI emerge from and where does it emerge from the skull?

A

Emerges from medulla and exits via jugular foramen.

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132
Q

Where does CN XII emerge from and where does it emerge from the skull?

A

Emerges from medulla and exits via hypoglossal canal.

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133
Q

What is the function of CN III?

A

Oculomotor Nerve
EOMs and LPS motor innervation. Parasympathetic supply to pupil causing constriction (carries PS fibres from EWN which synapse at ciliary ganglion and travel in short ciliary nerves to innervate sphincter papillae and cilliaris muscle).

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134
Q

What is the function of CNVI?

A

Abducens Nerve

Innervates lateral rectus

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135
Q

What is the function of CNIV?

A

Trochlear Nerve

Innervates superior oblique (turns eye downwards)

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136
Q

What is the function of V1?

A

Ophthalmic division of trigeminal nerve

Sensory - cornea, forehead, scalp, eyelids, nose, mucosa of nasal cavity and sinuses

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137
Q

What is the function of V2?

A

Maxillary division of trigeminal nerve

Sensory - face, maxilla, teeth, TMJ, mucosa of nose, maxillary sinuses and palate

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138
Q

What is the function of V3?

A

Mandibular division of trigeminal nerve
Sensory - face over mandible, teeth, TMJ, mucosa of mouth and anterior 2/3rd of tongue

Motor - muscles of mastication, part of digastric, tensor veli palatini, tensor tympani

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139
Q

What is the function of CN VII?

A

Facial Nerve
Motor - muscles of facial expression, scalp, stapedius, part of digastric

PS to submandibular, sublingual salivary glands, lacrimal glands and glands of the nose and palate

Taste from anterior 2/3rd of tongue and palate

Sensory - external acoustic meatus

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140
Q

What is the function of CN VIII?

A

Vestibulocochlear Nerve

Vestibular sensation from semicircular canals and otolith organs

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141
Q

What is the function of CN IX?

A

Glossopharyngeal Nerve
Taste from posterior 1/3rd of the tongue.

Sensation from middle and posterior oral cavity
Sensation from carotid body and carotid sinus

PS to parotid gland

Motor to stylopharyngeus

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142
Q

What is the function of CN X?

A

Vagus Nerve
Taste from epiglottis and palate

Sensation from auricle, EAC

Sensory - pharynx, larynx, trachea, bronchi, heart, oesophagus, stomach, small intestine

PS to smooth muscle in bronchi, gut heart

Motor - pharynx, larynx, palate and oesophagus

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143
Q

What is the function of CN XI?

A

Accessory Nerve

Motor - SCM and trapezius.

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144
Q

What is the function of CN XII?

A

Hypoglossal Nerve

Motor - muscles of tongue.

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145
Q

Problems with the trochlear nerve can cause what?

A

Diplopia when looking down.

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146
Q

What can damage to the hypoglossal nerve cause?

A

Paralysis and atrophy of ipsilateral half of tongue (tip deviates towards affected side).

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147
Q

What nerves are involved in the pupillary light reaction?

A

Afferent - II

Efferent - III

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148
Q

What nerves are involved in the corneal reflex?

A

Afferent - V

Efferent - VII

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149
Q

What nerves are involved in the jaw jerk reflex?

A

Just trigeminal.

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150
Q

What nerves are involved in the gag reflex?

A

Afferent - I

Efferent - X

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151
Q

Loss of parasympathetic supply to the eye causes what?

A

Fixed, dilated pupil.

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152
Q

What can cause small pupils?

A

Old age, bright light, miotic eye drops, opiate OD, Horner’s.

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153
Q

What can cause dilated pupils?

A

Youth, dim lighting, excitement, anxiety, mydriatric eye drops, third nerve palsy, brain death…

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154
Q

Interruption to the sympathetic supply to the eye causes what sort of pupil?

A

Constricted pupil.

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155
Q

What are the depressions of the cerebrum known as?

A

Sulci.

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156
Q

What are the elevations of the cerebrum known as?

A

Gryri.

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157
Q

What does the longitudinal fissure separate?

A

Two hemispheres.

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158
Q

What does the corpus callosum do?

A

Connects the two hemispheres, and contains commissural white mater fibres.

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159
Q

Where does the lateral sulcus separate?

A

Frontal and parietal lobe from temporal lobe.

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160
Q

Where does the central sulcus separate?

A

Starts from lateral sulcus and separates parietal and frontal cortices.

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161
Q

What does the parieto-occipital sulcus separate?

A

Parietal and occipital lobe.

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162
Q

What is the cingulate gyrus responsible for?

A

Receiving information and memory etc.

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163
Q

Where is the hippocampus?

A

Medial surface of temporal lobe.

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164
Q

What are the features of the frontal lobe?

A

Precentral gyrus, superior, middle and inferior frontal gyri.

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165
Q

What are the features of the parietal lobe?

A

Superior and inferior parietal lobules and postcentral gyrus.

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166
Q

What are the features of the temporal lobe?

A

Superior, middle and inferior temporal gyri.

167
Q

What is the insular cortex?

A

Consists of insula and insular lobe. Portion of cerebral cortex tucked deep within lateral sulcus. Involved in consciousness, emotions and body homeostasis.

168
Q

What is the role of the hippocampus?

A

Part of limbic system. Involved in consolidation of short-term memory to long-term memory.

169
Q

How many Broadmann areas are there?

A

52

170
Q

What are ‘primary’ areas in the brain?

A

Where the information comes to.

171
Q

What are ‘association’ areas in the brain?

A

What makes sense of sensory information.

172
Q

What are the functions of the frontal lobe?

A

Motor, intellect, speech, saccadic eye movements, bladder control, gait, higher order.

173
Q

What is meant by higher order?

A

Restraint, initiative and order.

174
Q

Where is gait controlled?

A

Periventricular area.

175
Q

Where is bladder control?

A

Paracentral lobule.

176
Q

Where is saccadic eye movements controlled?

A

Frontal eye field.

177
Q

Where is speech controlled?

A

Pars opercularis, pars triangularis.

178
Q

What is area 4?

A

Precentral gyrus - primary motor complex, it is the motor homunculus.

179
Q

What is area 6?

A

Consist of premotor area and supplementary motor area.

SMA innervates distal motor units directly. PMA connects with reticulospinal neurones innervating proximal motor units.

180
Q

What is area 44-45 on the inferior frontal gyrus?

A

Broca’s area - where muscles used for speech are represented, language processing thought to occur here.

181
Q

What functions take place in the prefrontal cortex?

A

Cognitive functions of higher order (intellect, judgement, prediction, planning).

182
Q

TRUE OR FALSE:

The larger an organ is the more space it takes up on the motor homunculus.

A

FALSE

Amount of area taken up is dependent on the required dexterity of a limb/organ.

183
Q

What is mental image of the body in space generated by?

A

Somatosensory, proprioceptive and visual inputs to posterior parietal cortex.

184
Q

What’s the difference between area 4 and 6?

A

Area 6 is for imagining carrying out movements and planning them. Area 4 is for carrying out said movements by activation of the CST and RST.

185
Q

Explain directional tuning in the primary motor cortex?

A

Neuron discharge will be greatest in a preferred direction. Each neurone has a preferred direction and the overall movement direction is encoded by integrated activity of these neurones.

186
Q

What is the main functions of the parietal lobe?

A

Somatosensory - body image representation, multimodality assimilation, visuospatial coordination language numeracy.

187
Q

What are areas 1, 2, and 3?

A

Post-central gyrus - primary sensory area. Receives general sensations from contralateral half of body (sensory homunculus).

188
Q

What can lesions of the parietal cortex lead to?

A

Hemisensory neglects and if dominant side can lead to acalculus or agraphic.

189
Q

What are the functions of the temporal lobe?

A

Hearing, smelling, encoding memories, emotion (amygdala).

190
Q

What are areas 41 and 42?

A

Heschl’s convolutions - primary auditory areas.

191
Q

What is Wernicke’s area?

A

Auditory association area - crucial for understanding spoken words. Connected to Broca’s area. ONLY on dominant lobe.

192
Q

What is the function of the occipital lobe?

A

Vision.

193
Q

Where is the primary visual cortex located?

A

Area 17 - calcimine sulcus/fissure.

194
Q

Apart from the primary visual cortex, what is the rest of the occipital lobe composed of?

A

Visual association areas that interpret visual images.

195
Q

What does the limbic lobe consist of?

A

Cingulate gyrus, hippocampus, parahippocampus gyrus, amygdala.

196
Q

Where is the amygdala found?

A

Tip of hippocampus.

197
Q

What is aphasia?

A

Problem with speech due to damage to one or more speech areas in the brain.

198
Q

What is the difference between Broca’s and Wernicke’s aphasia?

A 
Broca's = knows what to say just can't get the words out. 
Wernicke's = speech area is fine but doesn't hear what he is speaking or understand what you are saying.
199
Q

What are the three type of myelinated axon fibres bundled into tracts?

A

Commissural fibres - connect two hemispheres (corpus callosum)
Association fibres - connect one part of cortex with another in same hemisphere
Projection fibres - run between cerebral cortex and various subcortical centres (pass through internal capsule)

200
Q

What is the internal capsule?

A

V shaped tract dense with projection fibres.

201
Q

Where does the internal capsule derive its blood supply from?

A

Middle cerebral artery.

202
Q

What are the different parts of the internal capsule?

A

Anterior limb, knee (genu) and posterior limb.

203
Q

Name the basal ganglia.

A

Caudate nucleus, putamen, globus pallidus, subthalamic nuclei and substantia nigra.

204
Q

What are the basal ganglia?

A

Subcortical nuclei (collections of neuronal cell bodies).

205
Q

What makes up the corpus striatum?

A

Globus pallidus and caudate nucleus and putamen.

206
Q

What makes up the lentiform nucleus?

A

Globus pallidys and putamen.

207
Q

Where is the caudate nucleus?

A

It is always applied to the lateral ventricle.

208
Q

What does the substantia nigra do?

A

Plays a role in reward and movement.

209
Q

Why is substantia nigra so called?

A

It is black in colour due to high levels of neuromelatonin in dopaminergic neurone.

210
Q

What is the substantia nigra part of?

A

Extrapyramidal system.

211
Q

What is the function of the red nucleus?

A

Involved in motor coordination and gate.

212
Q

Why is the red nucleus red in colour?

A

Iron.

213
Q

What is the red nucleus part of?

A

Extrapyramidal motor system.

214
Q

What is the role of the basal ganglia?

A

Major function is to help initiate and terminate movement of the extrapyramidal system.

215
Q

What is the major subcortical input to area 6?

A

Ventral lateral nucleus in dorsal thalamus.

216
Q

What is input into area 6 by the ventral lateral nucleus called? Where does it arise from?

A

VLo, arises from basal ganglia.

217
Q

Where does the corpus striatum receive information from and what is this pathway called?

A

All over the cortex, corticostriatal pathway.

218
Q

What sort of signals do the caudate and putamen receive? What do they then do?

A

Excitatory (glutamatergic) cortical inputs.

So they integrate somatosensory, premotor and motor inputs and send in inhibitory (GABAergic) signals to globus pallidus and substantia nigra pars reticulata.

219
Q

What does the putamen fire before?

A

Limb/trunk movement.

220
Q

What does the caudate fire before?

A

Eye movements.

221
Q

Describe the signals sent in the motor loop (cortex –> basal ganglia –> cortex).

How does this process initiate movement?

A

Cortex to putamen = excitatory
Putamen to globus pallidus = inhibitory
Globus pallidus to VLo neurons = inhibitory
VLo to SMA = excitatory

So functional consequence of cortical activation of putamen is excitation.

This occurs at rest as globus pallidus neurones spontaneously excited and inhibit VLo - acts as negative feedback loop (GO signal for voluntary movement occurs when SMA excited over threshold)

222
Q

Describe the direct and indirect loops through basal ganglia.

A

Direct - acts as positive feedback loop, GO signals to SMA and enhances ignition of movement.

Indirect - antagonises direct route (striatum inhibits globus pallidus external which inhibits globus pallidus internal and sub thalamic nuclei, cortex excites STN and this excites GPi which inhibits the thalamus.

223
Q

What is the function of the cerebellum?

A

Controls balance, coordination, posture and fine tune motor activity.

224
Q

What information does the cerebellum use to create a picture of the body and its position in space?

A

Pyramidal tracts, ipsilateral proprioceptors from periphery, vestibular nuclei.

225
Q

What does the cerebellum calculate?

A

Best way to coordinate force, direct ad extent of muscle contraction to maintain posture and prevent overshoot and ensure a smooth co-ordinated muscle contraction.

226
Q

Planned movements from the cerebellum are then what?

A

Sent back to superior cortex by superior cerebellar peduncle.

227
Q

Lesions to the cerebellum cause what?

A

Ataxia - lack of voluntary co-ordinated muscle movements.

228
Q

How can you test ataxia?

A

Finger-nose test, shin-heel test, walking in a straight line

229
Q

What structures are involved in the portico-cerebellar projection?

A

Cortex, pontine nuclei, cerebellum.

Cerebellum communicates back to cortex via the ventrolateral thalamus (indicating direction and force of movement).

230
Q

What is motor learning in the cerebellum?

A

Predictions, calculations and experiences what compared what was intended with what happened to allow compensations.

Involves feedback loop through pons, cerebellum an thalamus back to cortex.

231
Q

How is the cerebellum attached to the brain?

A

Brainstem.

232
Q

What are the right and left hemispheres of the cerebellum separated by?

A

The vermis.

233
Q

What lobes are present on each of the cerebellar lobes?

A

Anterior, posterior and flocculondular lobes.

234
Q

What does the surface of the cerebellar lobes appear like?

A

Sulci and folia (sheet like gyri).

235
Q

What are the pyramids of the medulla oblongata caused by?

A

Tracts of fibres coming from the motor cortex.

236
Q

Where do motor fibres cross in the pyramids of the medulla?

A

At the decussation of the pyramids.

237
Q

What are the more lateral structures on the medulla?

A

Olives contain olivary nuclei.

238
Q

What cranial nerves emerge from the medulla?

A

9-12.

239
Q

What connects the cerebellum to the medulla?

A

Inferior cerebellar peduncles.

240
Q

Are the caudal and cranial parts of the medulla oblongata closed?

A

Caudal part closed around IV ventricle and cranial part open with IV ventricle posteriorly.

241
Q

What are the white matter structures in the medulla oblongata?

A

Pyramidal tracts, medial lemniscus, inferior cerebellar peduncle and other tracts.

242
Q

What grey matter structures are in the medulla oblongata?

A

Cranial nerve nuclei, inferior olivary nuclei, nuclei of the reticular formation and sensory nuclei (gracile and cuneate).

243
Q

How many cerebellar peduncles are there and what do they connect?

A

2 inferior cerebellar peduncles - connect medulla and cerebellum.

2 middle cerebellar peduncles - connect pons and cerebellum.

2 superior cerebellar pentacles - midbrain.

244
Q

What type of fibres does the superior cerebellar peduncle contain?

A

White matter.

245
Q

What type of fibres does the middle cerebellar peduncle contain?

A

Centripetal fibres.

246
Q

What are the cerebral peduncles?

A

Structures at the front of the midbrain, arising from pons and containing efferent/afferent nerve tracts running to and from cerebellum and pons.

247
Q

What cranial nerve arises from surface of pons?

A

CN V.

248
Q

What cranial nerves arise from the ponto-medullary junction?

A

CN VI-VIII.

249
Q

What does the midbrain develop from?

A

Mesencephalon.

250
Q

What does the midbrain’s central cavity contain?

A

CSF - known as cerebral aqueduct, which allows CSF to flow from the third to the fourth ventricle.

251
Q

What are the corpora quadrigemnia?

A

Inferior and superior colliculi, reflex centres involving vision and hearing.

252
Q

What cranial nerves arise from the midbrain?

A

III and IV.

253
Q

What grey matter structures are in the midbrain?

A

Nuclei of III and IV CNs.

254
Q

Where is the diencephalon found?

A

Deep within the cerebral hemispheres, around III ventricle.

255
Q

What does the diencephalon develop from?

A

Diencephalic vesicle (part of forebrain).

256
Q

What structures are considered part of the diencephalon?

A

Thalamus, hypothalamus, epithalamus (mainly grey matter).

257
Q

What does the thalamus mainly contain?

A

Nuclei (anterior, medial and lateral group).

258
Q

What are the lateral group of nuclei mostly involved in processing?

A

Sensory information.

259
Q

Any sensory information passing to go to conscious level must synapse at what structure?

A

Thalamus.

260
Q

What is the role of the hypothalamus?

A

Body homeostasis and endocrine functions (temperature, thirst, food intake, sleep-awake cycle…).

261
Q

What structure connects the lateral ventricles with the 3rd ventricle?

A

Interventricular foramen.

262
Q

Where does the 4th ventricle lie?

A

Behind the brainstem (b/w pons, medulla and cerebellum).

263
Q

Between which meninges in the brain and spinal cord is CSF present? Where else is it present.

A

Subarachnoid space (between pia and arachnoid).

Central canal of spinal cord and inside cavity of the brain.

264
Q

Where is the CSF reabsorbed?

A

Into arachnoid villi into the sagittal sinus.

265
Q

What can arachnoid villi form if they group together?

A

Arachnoid granulations (seen as depressions in the skull).

266
Q

What does the subdural space transversed by?

A

Transversed by BVs penetrating into the CNS.

267
Q

What are the dura matter folds?

A

Falx cerebri - separates two hemispheres of the brain.

Tentorium cerebelli - separates cerebellum from occipital lobes.

Falx cerebelli - seperates two cerebellar hemispheres.

Diaphragma sellae - surrounds pituitary gland.

268
Q

What is the function of the blood brain barrier?

A

Prevents harmful amino acids and ions from entering brain.

269
Q

In which structures of the brain is the BBB not present?

A

Parts of the hypothalamus, posterior pituitary.

270
Q

What is the BBB composed of?

A

Astrocytic foot processes wrapping around capillary endothelium connected by tight junctions.

271
Q

How are substances transported across the BBB?

A

If lipid soluble may penetrate all capillary endothelial cell membranes passively.

Amino acids/sugars transpired by capillary endothelium specific carrier-mediated transport mechanisms.

272
Q

Where do the two ICAs enter the skull?

A

Carotid canal (foramen lacerum).

273
Q

Where do the vertebral arteries pass through?

A

Transverse foramen of the cervical vertebrae and through the foramen magnum.

274
Q

What three branches do the ICAs give off?

A

Anterior and middle cerebral and posterior communicating arteries.

275
Q

What do the vertebral arteries unite to form?

A

Basilar artery.

276
Q

What does the vertebra-basilar artery supply?

A

Brainstem and cerebellum.

277
Q

How is the circle of willis a protective measure?

A

Gives alternative ways of oxygenating the brain if one of the main arteries gets obstructed.

278
Q

Downstream of the circle of willis are all end arteries, why does this increase vulnerability to stroke?

A

No alternative supply of blood.

279
Q

What does the anterior cerebral artery supply?

A

Medial aspect of cerebral lobes, not incl. occipital lobe.

280
Q

What do the middle cerebral arteries supply?

A

Lateral aspects of cerebral hemispheres. Right one supplies left body strength and sensation. Left one supplies right body strength, sensation and language.

281
Q

What do the posterior cerebral arteries supply?

A

Inferior aspect of cerebral hemisphere and occipital lobe.

Contralateral visual field.

282
Q

What arteries supply the cerebellum?

A

Posterior inferior, anterior inferior and superior cerebellar arteries.

283
Q

What signs are present in cerebellar strokes?

A

Ataxia/nystagmus.

284
Q

Why does damage to the basilar artery lead to such a high mortality?

A

As it leads to damage of brainstem, where all major centres, including breathing centre is.

285
Q

What is the most significant factor determining cerebral blood flow?

A

Cerebral perfusion pressure.

286
Q

What is CPP?

A

Net pressure gradient causing cerebral blood flow to the brain.
CPP = MAP - ICP.

287
Q

How does an increase in ICP affect CPP?

A

Causes cerebral perfusion to decrease.

288
Q

What factors regulate cerebral blood flow under physiological conditions?

A

CPP, concentration of arterial CO2 and arterial PO2.

289
Q

What is cerebral auto regulation?

A

Ability to maintain constant blood flow to the brain over a wide range of CPP (50-150mmHg).

290
Q

When CPP is low, how do the cerebral arterioles compensate?

A

Dilate to allow adequate flow at that decreased pressure.

291
Q

When CPP is high, how do the cerebral arterioles compensate?

A

Constrict.

292
Q

Is CPP exceeds 150mmHg, what is it known as?

A

Hypertensive crisis and autoregulatory system fails.

293
Q

Introduction of new intracranial masses leads to what compensatory mechanisms to maintain a constant intracranial pressure?

A

Reciprocal decrease in venous blood or CSF (Monro-Kelly Doctrine).

Venous system collapses and squeezes venous blood out via jugular veins/emissary veins. CSF displaced from ventricular system through foramina of Luschka/Magendie into spinal SA space.

294
Q

Define compliance.

A

Change in volume for a given change in pressure.

295
Q

Define elastance.

A

Inverse of compliance. Change in pressure observed for a given change in volume (accommodation to outward expansion of a cranial mass).

296
Q

After mechanisms to compensate for intracranial masses have been exhausted, small changes in volume lead to what?

A

Significant increases in pressure and intracranial hypertension ensues.

297
Q

What are the three ICP waveforms (Lundberg waves)?

A

A - abrupt elevation in ICP for 5-20 mins followed by rapid fall in pressure to resting levels.

B - Frequency of 0.5-2 waves per minute, related to rhythmic variants in breathing.

C - rhythmic variations related to waves of systemic BP and have smaller amplitude.

298
Q

What is cushing’s reflex?

A

Physiological nervous system response to increased ICP that leads to Cushing’s triad of HTN, irregular breathing and bradycardia.

Indicative of arteriolar compression. So ICP > MAP.

Decreased CBF leads to activation of ANS (alpha-adrenerfix receptors –> HTN and tachycardia. Aortic baroreceptors stimulate vagus –> bradycardia.

299
Q

Where do the superficial and deep veins of the brain drain into?

A

Dural venous sinuses which lie between the 2 layers of dura mater.

300
Q

What produces CSF?

A

Choroid plexus (process req ATP whereby sodium is pumped into SA and water fro BVs follows (NaK-ATPase).

301
Q

Where is choroid plexus mostly located?

A

Lateral ventricles (temporal horn roofs and floor of bodies), posterior 3rd ventricle roof, caudal 4th ventricle rood.

302
Q

Describe the flow of CSF.

A

Lateral ventricles –> foramen of Munro –> third ventricle –> cerebral aqueduct –> foramina of Luschka and Magnedie –> SA space –> arachnoid villi –> dural venous sinuses (mostly superior sagittal sinus).

303
Q

How do the arachnoid villi function?

A

As pressure dependent one way valves that open when ICP is around 3-5cm water greater than dural venous sinus pressure. CSF resorption is passive driven by P gradient between ICP and venous system.

304
Q

What two things does consciousness depend on?

A

Intact ascending reticular activating system (alertness) and function cerebral cortex of both hemispheres (content of consciousness).

305
Q

What symptoms would the patient experience if there is a lesion to the CST and RST?

A

Loss of fine movements of the hands and arms - cannot move shoulders, elbows, wrists and fingers independently.

306
Q

If there is a lesion of the CST and not the RST what will the patient experience?

A

Loss of fine movement etc. again but after a few months, function reappears as RST takes over (normally dominated by CST).

307
Q

What is a reflex?

A

Involuntary stereotyped pattern of response brought about by a sensory stimulus.

308
Q

What are spinal reflexes?

A

Reflexes mediated at level of spinal cord.

309
Q

Give an example of a monosynaptic reflex.

A

Stretch reflex.

310
Q

Give an example of a polysynaptic reflex.

A

Flexor reflex.

311
Q

Can reflexes be overridden consciously?

A

Yes, as alpha-motoneurons controlling muscles have inputs from descending pathways, and continually integrates EPSPs and IPSPs. Strong descending inhibit hyper polarises alpha-motoneurons and reflex will not take place.

312
Q

What does activity of the gamma-motoneurons depend on?

A

Entirely depends on descending pathways. High gamma-motoneuron activation can lead to muscle spindle fibres becoming extremely resistant to stretch and becoming spastic.

313
Q

Where is the stretch reflex found?

A

In every muscle.

314
Q

Describe what happens in the stretch reflex.

A
  1. Tendon stretched
  2. Infrafusal muscle fibres stimulated
  3. Sensory neuron activated
  4. Synapses directly with motoneuron
  5. Motoneuron causes contraction of muscle
  6. Polysynaptic arch to inhibitory interneuron
  7. Reciprocal innervation

Remember the UMNs from the pyramidal tract will act on the same LMN as involved in this reflex arc.

315
Q

What is the stretch reflex important for?

A

Maintaining normal muscle tone and posture.

316
Q

What is the role of flexor reflex?

A

Helps protect body from painful stimuli but withdrawing the body part away from the stimulus and into the body.

317
Q

Describe the flexor reflex.

A
  1. Painful stimulus (increased APs from receptors)
  2. Sensory neurones activated
  3. Polysynaptic reflex arc
  4. Flexion and withdrawal from noxious stimulus
  5. Crossed extensor response to contralateral limb (in weight bearing limbs)
318
Q

To prevent falling over during the flexor reflex what occurs?

A

Small excitatory interneurons cross spinal cord and excite contralateral extensors and several interneurons inhibit the contralateral flexors.

Helps maintain upright posture.

319
Q

How does sensory information from the painful stimuli reach the brain?

A

Spinothalamic tract.

320
Q

Which of the reflexes (stretch or flexor) is faster?

A

Flexor-crossed extensor reflex much slower than stretch reflex as nociceptive sensory fibres have a small diameter than muscle spindle afferents and so conduct more slowly.

321
Q

What spinal cord segments are crucial for the bicep jerk reflex?

A

C6.

322
Q

What spinal cord segments are crucial for the tricep jerk reflex?

A

C7.

323
Q

What spinal cord segments are crucial for the patellar tendon jerk reflex?

A

L4.

324
Q

What spinal cord segments are crucial for the achilles tendon reflex?

A

S1.

325
Q

What are the differences in the flexor and stretch reflex in terms of how diffuse they are in the spinal cord?

A

Stretch - muscle spindle fibre input highly localised, affecting only alpha-motoneurons of 1/2 spinal segments.

Flexor - pain input diffuse and spreads through several spinal segments.

326
Q

How does the intensity of a painful stimulus affect how diffusely it spreads within the spinal cord?

A

Greater spread with increased intensity –> larger response.

NB - can also occur between similar inputs, e.g. pain fibre input facilitates action of muscle spindles by maintaining alpha-motoneurons in more depolarised state.

327
Q

What is Babinski’s sign?

A

Babinski positive if stroking of sole of foot causes upward curling of toe (seen in those with CST damage, in children under 1 (not fully developed yet) and after epileptic fits (transient cortical function disruption).

328
Q

What is spinal shock?

A

Transection of spinal cord leads to immediate sensory, autonomic effects (bowel, bladder, sexual problems) and aflexia/hyporeflexia (which gradually return after 2-6 weeks).

329
Q

What is clonus?

A

A series of involuntary, rhythmic muscle contractions and relaxations (associated with UMN damage).

330
Q

Direct control of muscles is via which neurones?

A

Alpha-motoneurons in the spinal cord.

331
Q

What are the four systems controlling movement?

A

Descending control pathways (cortex, basal ganglia, cerebellum)

Basal ganglia

Cerebellum

Local spinal cord and brainstem circuits

332
Q

How does the brainstem nuclei control spinal reflexes and control posture and balance?

A

Via innervation of trunk and limb muscles by the vestibulospinal and reticulospinal tracts.

333
Q

The spinal cord receives descending input from neurone from where via which tracts?

A

Brainstem and direct cortical input via corticospinal tract and pyramidal tract.

334
Q

What is the highest level of motor control?

A

Strategy - goal and movement strategy to achieve it - by neocortex, basal ganglia.

335
Q

What is the middle level of motor control?

A

Tactics - sequence of spatiotemporal muscle contraction to achieve goal. By motor cortex and cerebellum.

336
Q

What is the lowest level of motor control?

A

Execution - activation of motoneurons and interneurons to generate directed movement. By brainstem and spinal cord.

337
Q

What do the lateral pathways control?

A

Voluntary movements of distal muscles directly under cortical control.

338
Q

What do ventromedial pathways control?

A

Posture and locomotion under brainstem control.

339
Q

What does the tectospinal tact pathway do?

A

Brings visual information down spinal cord.

340
Q

Change in body position initiates rapid compensatory feedback messages from where to do what?

Before these movements even begin what occurs?

A

Brainstem vestibular nuclei to spinal cord neurons to correct postural instability.

Brainstem reticular formation nuclei initiate feedforward anticipatory mechanisms to stabilise posture.

341
Q

If there is damage to the cortex and the UMN what signs will be seen?

A

Flaccidity of contralateral muscles, initial hypotonia (spinal shock, but will regain some function through strengthening of spared connections/production of new ones), Babinski’s sign, spasticity, hyperreflexia, hypertonicity clonus.

342
Q

What information do small sensory axons contain?

A

Pain and temperature.

343
Q

What do large sensory axons contain?

A

Proprioception and vibration.

344
Q

What is the function of LMNs?

A

At spinal cord level directly innervate muscle to initiate reflex and voluntary movements.

345
Q

What signs appear with LMN lesion?

A

Flaccid paralysis, muscle atrophy, weakness, hyporeflexia, hypotonicity, fasciculations.

346
Q

On the spinal cord how are muscles represented?

A

Distal limb muscles (e.g. arm and leg muscles, fingers etc represented most laterally) and proximal limb muscles represented most medially (e.g. shoulders).

347
Q

If there is a lesion to the corticospinal tract will there be paralysis?

A

Only weakness.

348
Q

Can damage to sensory inputs (at spinal level) cause muscle weakness?

A

Can lead to paralysis, as though the motoneurons themselves had been damaged.

349
Q

What are the components involved in muscle converting chemical energy into mechanical energy?

A

Excitation-contraction coupling at NMJ
Contractile mechanism (fibres shorten)
Structural components
Energy system (anaerobic vs aerobic)

350
Q

What muscle relates to the C5 myotome?

A

Elbow flexors.

351
Q

What muscle relates to the C6 myotome?

A

Wrist extensors.

352
Q

What muscle relates to the C7 myotome?

A

Elbow extensors.

353
Q

What muscle relates to the C8 myotome?

A

Finger extensors.

354
Q

What muscle relates to the T1 myotome?

A

Intrinsic hand muscles.

355
Q

What muscle relates to the L2 myotome?

A

Hip flexor.

356
Q

What muscle relates to the L3 myotome?

A

Knee extensors

357
Q

What muscle relates to the L4 myotome?

A

Ankle dorsiflexors.

358
Q

What muscle relates to the L5 myotome?

A

Long toe extensors.

359
Q

What muscle relates to the S1 myotome?

A

Ankle plantar flexors.

360
Q

Define pain.

A

Unpleasant sensory and emotional experience which we primarily associated with tissue damage. Not a stimulus but a final product of a complex information processing network.

361
Q

What picks up different sensory information?

A

Receptors, e.g. mechanoreceptors, chemoreceptors, thermoreceptors, nociceptors, proprioceptors.

362
Q

What is the receptive field?

A

The specific area over which a sensory receptor will respond to a stimulus.

363
Q

Adequate stimuli on the sensory receptors causes what?

A

The receptor to depolarise (receptor generator potential), which evokes firing of APs.

364
Q

What does size of receptor potential encode?

A

Intensity of stimulus.

365
Q

What does frequency of APs from a sensory receptor encode?

A

Intensity of stimulus.

366
Q

What does the receptive field encode?

A

The location of stimulus and gives information about the modality and intensity of sensation.

367
Q

What determines acuity of a sensory stimulus?

A

Density of innervation, size of receptive fields.

368
Q

What are the three types of primary afferent fibres and what do each transmit?

A

Abeta - large myelinated - touch, pressure and vibration

Adelta - small myelinated - cold, fast pain, pressure

C - unmyelinated fibres - warmth, slow pain

369
Q

What type of fibres are in the dorsal column and what sort of information do they carry?

A

Aalpha and Abeta fibres - carry proprioception, vibration.

370
Q

Describe the path taken by the dorsal column fibres.

A

Project up ipsilateral dorsal column, synapse in cuneate and gracile nuclei and 2nd order neurone decussate in brainstem and project to reticular formation, thalamus and cortex.

371
Q

What sort of fibres are in the spinothalamic tract and what sort of information do they carry?

A

Adelta and C fibres.

Pain and temperature.

372
Q

Define nociception.

A

Detection of tissue damage by specialised transducers connected to Adelta and C fibres (responding to chemical, thermal, mechanical and noxious stimuli).

373
Q

Describe the path taken by the spinothalamic tract fibres.

A

Synapse in dorsal horn, 2nd order neurone cross midline in spinal cord, project up contralateral spinothalamic (anterolateral) tract to reticular formation, thalamus and cortex.

374
Q

How is grey matter split up in the spinal cord?

A

Split into ventral, lateral or dorsal horns.

Rexed divided the grey matter into 10 layers.

375
Q

What are the three predominant neurone types in the grey matter of the spinal cord?

A

Low threshold mechanoreceptor neurone (layer 3 and 4) receiving input from A beta fibres.

Nociceptive specific neurone (layer 1 and 2) receiving input from C and Adelta fibres.

Wide dynamic range neurone (layer 5) receiving input mainly from Abeta but responds to noxious and non-noxious stimuli via interneurons.

376
Q

Where do primary nociceptive afferent impulses end?

A

In dorsal horn of spinal cord.

377
Q

What is the major tract sending impulses to the thalamus?

A

Spinothalamic.

378
Q

Where are the cell bodies for the spinothalamic tract mostly located?

A

Rexed lamina 1, 2 and 5.

379
Q

What are the two different spinothalamic tracts?

What do each do? What path do they follow?

A

Lateral and ventral.

Lateral terminates in ventroposterior thalamic nuclei (feeds spatial, temporal and intensity of noxious stimuli to somatosensory cortex).

Ventral feeds information to medial thalamic nuclei (which projects to cortical regions, e.g. cingulate and insular cortex and other parts of limbic system).

380
Q

What is thought to contribute to the affective ocomponent of pain?

A

Anterior cingulate cortex.

381
Q

Where does pain perception primarily occur?

A

Somatosensory cortex.

382
Q

What is the pain matrix?

A

Connections between different brain centres to perceive pain.

383
Q

What are the different components of the brain matrix?

A

Somatosensory cortex, ventral posteriomedial nuclei of the thalamus, amygdala, hippocampus, cingulate gyrus, insular, prefrontal cortex which all feed back and forward with brainstem centres for affective component as well as descending control of pain.

384
Q

What are the descending pathways controlling pain?

A

From brain to dorsal horn via periaqueductal grey matter and usually decreases pain system (nor-adrenergic system).

385
Q

What does damage to the dorsal column of the spinal cord lead to?

A

Loss of touch, vibration, proprioception below lesion on ipsilateral side.

386
Q

What does damage to the anterolateral quadrant result in?

A

Loss of nociceptive and temperature sensation in contralateral side of lesion.

387
Q

What is adaptation in terms of sensory stimulation?

A

Change overtime in responsiveness of a sensory system to a constant stimulus.

388
Q

What is convergence of neurone (in context of sensory stimulation)?

A

Saves neurones but reduces acuity (may underlie referred pain).

389
Q

What is lateral inhibition of neurones?

A

Activation of one sensory input causes synaptic inhibition of its neighbours - gives better boundaries and cleans up sensory info.

390
Q

What fibres convey first/fast/sharp pain?

A

Adelta fibres (lightly myelinated medium diameter fibres).

391
Q

When the first pain transforms into a dull pain, what fibres convey this?

A

C fibres (myelinated small diameter fibres).

392
Q

What is acute pain?

A 
Lasting <1 month (resolution after healing) 
Physiological
Noxious stimuli
Protective function
Usually nociceptive
393
Q

What is chronic pain?

A 
Lasting 3-6+ months (beyond healing)
Pathological
May not be noxious stimuli
Not protective/purposeful
Nociceptive/neuropathic/mixed
394
Q

Define visceral pain.

A

Pain resulting from activation of nociceptors in organs (organs particularly sensitive to stretch, ischaemia, inflammation and insensitive to cutting/burning).

395
Q

Define referred pain.

A

Pain felt in another part of body, other than its actual source.

396
Q

Define phantom limb pain.

A

Pain left from a limb that has been amputated.

397
Q

Define nociceptive pain.

A

Sensory experience that occurs when specific peripheral sensory neurone respond to noxious stimuli (typically at site of injury and time limited, although can be acute/chronic).

398
Q

How do you treat nociceptive pain?

A

Responds to conventional analgesics.

399
Q

Define neuropathic pain.

A

Pain initiated by primary lesion in somatosensory nervous system but painful region may not be same as site of injury (occurs in neurological territory of affected structure - usually chronic).

400
Q

Can you use conventional analgesics to treat neuropathic pain?

A

Usually ineffective.

401
Q

How can nociceptors be activated?

A

Low pH, heat (via ASIC, TRPV1 etc.)

Local chemical mediators, e.g. bradykinin, histamine, prostaglandins.

402
Q

How can transmitter release from Adelta/C fibres be inhibited?

A

Inhibitory ibternueorns releasing opioid peptides (endorphins) inhibit Adelta/C fibres.

403
Q

What is the gate control theory?

A

Suggested that non-painful stimuli closes gate to noxious stimuli to prevent it from reaching CNS and thereby suppressing pain.

Thought to occur by activity in Aalpha and Abeta fibres activating inhibitory interneurons.

404
Q

Define allodynia.

A

Decreased threshold for pain (can cause pain for non-noxious stimuli).

405
Q

Define hyperalgesia.

A

Increased sensitivity for pain (for normally painful stimuli).

406
Q

What causes spontaneous pain?

A

Spontaneous activity in nerve cells.

407
Q

What is central sensitisation?

A

Condition of nervous system associated with the development and maintenance of chronic pain.

408
Q

What are the three main components of central sensitisation? What do each involve?

A

Wind-up: involves activated synapses (those in contact with primary afferent fibre synapses). Homosynaptic activity dependent progressive increase in response of neurone (terminates with stimuli). Involves neurotransmitters substance P and CGRP.

Classical: opening up new synapses (silent nociceptors in dorsal horn). Heterosynaptic activity dependent plasticity. Immediate onset with (v. strong) appropriate stimuli (outlasts stimuli nutation). Involves NMDA receptor activation by glutamate. Leads to secondary hyperalgesia.

Long-term potentiation: involves activated synapses mostly. Occurs if v intense stimuli. Mechanism involves AMPA and NMDA receptor activation by glutamate.

409
Q

How do NSAIDs function as analgesics?

A

Inhibit cycle-oxygenase which converts arachidonic acid to prostaglandins (which sensitise nociceptors to bradykinins). Work well for pain assoc. with inflammation.

410
Q

What methods are there of reducing pain?

A

Blocking transduction, transmission, descending modulation or changing perception of pain.

411
Q

How do you block transduction of pain?

A

NSAIDs
Ice
Rest
Local anaesthetics - block Na ion action potential
Transcutaneous electrical nerve stimulation (TENS)

412
Q

How do you block transmission of pain?

A

Opiates (e.g. morphine) - reduce sensitivity of nociceptors and block transmitter release in dorsal horn
Nerve blocks
Anti-convulsants
Surgery - DREZ, cordotomy

413
Q

How can you change perception of chain?

A

Education, CBT, distraction, relaxation, graded motor imagery, mirror box therapy.

414
Q

How can you blocking descending modulation of pain?

A

Placebos, drugs (opioids, antidepressants), surgery (spinal cord stimulation).

second year (9 decks)

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