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Conditions + definitions > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

What is the function of the vestibulospinal tract?

A

Stabilises H&N

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2
Q

Where does the corticospinal tract start?

A

Areas 4-6 of frontal motor cortex

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3
Q

Where does the rubrospinal tract start?

A

red nucleus of brain

Has same cortical inputs but much smaller

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4
Q

What happens with a lesion in the RST/CST? (cortico/rubrospinal tracts)

A

If both affected - loss of fine movements of arms + hands
>Cannot move shoulders, elbows, wrists/fingers independently

If only lesion in CST you have same deficits, however after a few months they disappear as RST has taken over

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5
Q

What are the pontine/medullary reticulospinal tracts?

A

Originate in brain stem
Use sensory information about balance, body position and vision
Reflexly maintain balance and body position
Innervate trunk and antigravity muscles in limbs

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6
Q

What happens when motor cortex innervates spinal neurones?

A

Frees them from reflex control by communicating via nuclei of ventromedial pathways
All voluntary movement requires input from motor cortex via lateral pathways

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7
Q

How does the brain coordinate body movements?

A

Mental image of body in space generated by somatosensory, proprioceptive + visual inputs to posterior parietal cortex - areas 5+7
>Damage in one of these areas may lead to neglect in one side of body
Prefrontal + parietal cortex - decisions about movements/actions + likely outcomes
Axons converge on area 6. Junction where signals encoding desired actions

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8
Q

What are mirror neurones?

A

They are decision making neurones in command centres specific neurones in area 6 fire when movement is made and when movement is imagined
– rehearsed mentally they also fire when others make the same specific movement:
>allows understanding of actions or intentions of others so same motor circuits plan our movements and allow understanding of actions/goals of others
mirror neurones may underpin emotions and empathy – and they may be dysfunctional in autism

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9
Q

How is direction with movement decided?

A

Each neurone has a “preferred” direction
When activity increases in that direction the other directions are slightly supressed
All neurones work together to create a directional vector, giving the overall movement

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10
Q

What is feedback? (motor control)

A

Change in body position leading to messages from brainstem vestibular nuclei to spinal cord to correct instability

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11
Q

What is feedforward (motor control)

A

Brainstem reticular formation nuclei (cortex controlled) initiate anticipatory adjustments before movements begin, to stablise posture

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12
Q

Where does the subcortical input to area 6 come from?

A

From ventral lateral nucleus in dorsal thalamus
Called VLO - arises from basal ganglion
Basal ganglia receives input from frontal, prefrontal and parietal cortex
Results in loop in information Cortex to basal gangla –> thalamus –> supplmentary motor area (SMA)

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13
Q

How is the basal ganglia innervated?

A

Medium spiny neurones in putamen and caudate receive excitatory cortical inputs from dendrites
>Large dendritic trees - integrate somatosensory, premotor + motor cortical inputs
>Axons are inhibitory
>Project to globus palladus + substantia nigra pars reticula
Putamen fires before limb/trunk movements
Caudate fires before eye movements
>Both predictive of movements

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14
Q

What is Huntington’s?

A

Characterised chorea - spontaneous uncontrolled rapid flicks + movements with no purpose
Caused by substantial loss of caudate, putamen + globus pallidus
Loss of inhibitory function

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15
Q

What are the two motor loop pathways?

A

Direct - which is excitatory

Indirect - which antagonises direct pathway ie inhibtory

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16
Q

How is the cerebellum involved in motor control?

A

Controls direction, timing + force
Uses motor learning within cerebellum, based on predictions, calculations, experience (too fast for feedback control directly) – compares what intended w/ what happened and compensates
Lesions in cerebellum cause uncoordinated inaccurate movements
>Ataxia, failure to touch nose when eyes shut (similar to alcohol)

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17
Q

What is the vestibular system?

A

Sensory system essential for control of posture + balance
Found in inner ear - series of fluid filled membranous tubes (labyrinths)
Imbedded in temporal bone

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18
Q

What does the vestibular system consist of?

A

Consists of 3 semi-circular canals, utricle + the saccule

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19
Q

What are the utricle and saccule?

A

otolith organs - detect linear acceleration + encode about position of head in space -
back/front tilt by utricle.
Vertcial - saccule

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20
Q

What are the semi-circular canals?

A

Semi-circular canals at right angles to each other (3 dimensions)
Semi-circular canals - detect rotational acceleration

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21
Q

How is movement detected?

A

Ampulla contain sensory receptors cristae
>Contain flexible gelatinous structure - cupula
>Embedded within gelatinous cupula are hair cells - synapse to vestibular nerve
»Responds to endolymph fluid within canals - rotational acceleration
»Fluid moves slower than the bony structures because of inertia

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22
Q

What is the effect of inertia?

A

The endolymph produces drag against the hair cells, bending the cupula in opposite direction to movement
If rotating at same velocity, endolymph catches up + rotates at same speed (removing shearing forces) but takes a few seconds
Sudden stop won’t cause endolymph to stop as well, and so it crease a continuing sense of movement + dizziness

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23
Q

What are the types of cilia hair cells in the cupula?

A

Kinocilium - large

Stereocilia - progressively smaller

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24
Q

How to the hair cells in the ear convert the movement into an action potential?

A

Distortion of cilia towards kinocilium causes depolarisation + increased discharge of Aps in vestibular nerve
Distortion away from kinocilium leads to hyperpolarisation + decreased discharge of APs in vestibular nerve
>Allows for body to determine mvement in time and space
>Orientation of cupula slightly different so can create 3D image of body position using pattern of APs

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25
Q

What are the sensory receptors of the otolich organs?

A

Sensory apparatus of utricle + saccule = maculae
Macula in utricle orientated in horizontal plane
>Saccule - vertical plane
Maculae also have set of cilia, protruding into otolith membrane
>Embedded within this membrane are CaCO3 crystals - otoliths

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26
Q

How do the maculae detect movement?

A

Tilt of head
Otoliths greater density than endolymp, moves otoliths first + the otolith membrane in which they are embedded
>Distorts jelly + moves cillia
Backward - direction of kinocilium - depolarisation
Forwards away, hyperpolarisation, decreased APs

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27
Q

How does the brain recieve the information form the otolith?

A

Projections from vestibular nuclei on one side project ipsilaterally, bilaterally and contralaterally to desc motor pathways (+extraocular nuclei - from muscles)
Vestibular nuclei receive input from proprioceptors signalling limb + body position, also from neck and eye muscles
Vestibular nuclei then project via thalamus to cerebral cortex kinaesthesia
(the perception of movement + body position)

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28
Q

What are the reflexes of the vestibular system?

A

Tonic labryinthe reflexes
Dynamic righting reflexes
Vestibulo-occular reflexes

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29
Q

What is the function of the tonic larynthine reflexes?

A

Keep axis of head in a constant relationship with the rest of the body.
Use information from maculae and neck proprioceptors.

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30
Q

What are the vestibulooccular reflexes?

A

Afferents from semi-circular canals project and connect (within the vestibular nuclei) to afferent fibres travelling to the extraocular nuclei
>have strong input to influencing eye movement.
visual system sends powerful descending projections which control posture.
>demonstrated by increased difficulty experienced with balance with closed eyes

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31
Q

What is the clinical significance of the vestibuloocular reflexes?

A

People with destruction of vestibular apparatus can still maintain good balance if movement is relatively slow and eyes are open. But lost immediately on closing eyes.

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32
Q

What are the types of vestibuloocular reflexes?

A

Static

Dynamic

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33
Q

What is the static vestibuloocular reflex?

A

Tilted head, eyes intort/extort to compensate, so that over a certain range, the image stays the right way up.

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34
Q

What is the dynamic vestibular vestibulo occular reflex?

A

series of saccadic eye movements that rotate eye against direction of rotation of head and body so original direction of gaze is preserved despite head rotating.

The extent of eye movement is restricted; when eyeball comes to the end of its range of movement, rapidly flicks back to the zero position i.e. straight ahead.
If rotation continues the slow phase starts again, then flicks back.
By convention, direction of nystagmus is the direction of the rapid flick back R rotation = R nystagmus

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35
Q

How can you test nystagmus?

A

Post rotatory

Caloric stimulation

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36
Q

What is post rotatory nystagmus?

A

Subjects rotated in Barany chair.
If rotate to left - during acceleration get left nystagmus.
At end of rotation, for ~20 seconds, during deceleration get a right nystagmus.
Due to endolymph catching up - now pushing cupula in opposite direction.

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37
Q

What is caloric stimulation?

A

When outer ear washed with cold or warm fluid, temperature difference from core gets through thin bone and sets up convection currents which affect the endolymph.
Warm fluid causes nystagmus towards affected side, cold away from affected
>(COWS – Cold Opposite, Warm Same).
Stimulation without movement can cause nausea + vomiting

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38
Q

How does motion sickness arise?

A

Powerful maintained stimulation of the vestibular system - can give rise to kinetosis
Motion sickness is most likely to occur if visual and vestibular system inputs to the cerebellum are in conflict e.g. if the vestibular system indicates rotation but the visual system does not.
cerebellum generates a “sickness signal” to hypothalamus to bring about ANS changes
>BP decrease, dizziness, sweating + pallor

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39
Q

How does sleep occur?

A

Unknown exactly
Something below level of mid pons actively sending inhibitory impulses to cortex
Suggested that reticular formation at brain stem (associated with state of conciousness)
>Sends projections to thalamus + higher cortical areas
>Drugs blocking serotonin inhibit sleep, unknown how
Some sort of compound, probably peptide, in CSF contributes towards sleep

40
Q

How does the hypothalamus contribute towards sleep?

A

Suprachiasmatic nuclei (SCN) in thalamus role in induction of sleep
Electrical stimulation of SCN can promote sleep
Damage to SCN disrupts sleep/wake cycle

41
Q

What is orexin?

A

Hypothalamus releases orexin (hypocretin) - excitory neurotransmitter needed for wakefulness
Orexin active in waking state
Stop firing during sleep
Defective causes narcolepsy

42
Q

How can you assess the level of consciousness?

A

Look at behaviour, speech patterns, content, writing, calculating skills
Brain activity - EEG (Electroencephalogram)

43
Q

What are the types of brain waves?

A

Alpha
Beta
Theta
Delta

44
Q

When are alpha waves present, what are their features?

A

Alpha - relaxed awake

High frequency, high amplitude

45
Q

When are beta waves present, what are their features?

A

alert awake

Higher frequency, lower amplitude

46
Q

When are theta waves present, what are their features?

A

Deep sleep; Awake: common in children , emotional stress + frustration in adults
low frequency, vary in amplitude

47
Q

When are delta waves present, what are their features?

A

deep sleep

Low frequency, high amplitude

48
Q

Why are beta waves low amplitude?

A

Asyncrhnous waves due to multiple processes

NOT due to low activity

49
Q

What is the sleep cycle?

A

5 stages: 1-4, 4-3-2-5, back and forwards
1 slow wave, non REM sleep. Slow eye movements, light sleep easily roused.
>High amplitude low frequency theta waves
2 Eye movements stop, frequency gets slower
>Rapid waves called sleep spindles (occur in burts) - cluster of 12-14hz
3 High amplitude, very slow (2hz) delta waves interspersed with short episodes of faster waves, spindle activity slows
4 Exclusively delta waves
>3+4 = deep sleep
5 (REM sleep - dreams occur. Fast waves - like when being awake

50
Q

What are the characteristics of deep sleep?

A

Sleep in first few hours
Most restful
Associated with decreased vascular tone (and BP), respiratory + basal metabolic rates (decrease in BP)
Dreams occur but rarely remembered

51
Q

What are the characteristics of REM sleep?

A

5-30 mins every 90 min, often more frequent later
Dreams mostly occur in REM
Eye muscles show burst of rapid activity - profound inhibition of all other skeletal muscles due to inhibitory projections from pons to spinal cord.
>Prevents acting out
REM sleep dependent on cholinergic pathways within reticular formation + their projections to thalamus, hypothalamus + cortex. Anticholinesterases increase amount of time in REM sleep
>HR/RR irregular, brain metabolism increases
>EEG mimics beta waves
Very difficult to arouse person from them

52
Q

Why is sleep important?

A

Impairment results in: Loss of cognitive function
Loss of physical performance
Sluggishness
Irritability

53
Q

What is sleep necessary for?

A 
Neuronal plasticity
		Learning + memory
		Cognition
		Clearance of waste products from CNS
		Conservation of whole body energy
Immune function
54
Q

What are the common sleep disorders?

A 
Insommnia
	Sleep terrors
	Nightmares
	Somnambulism (sleep walking)
	Narcolepsy
55
Q

What is insomnia?

A

Chronic inability to obtrain necessary quality/amount of sleep for daytime behavious

a) Chronic, primary - no identifiable cause
b) Temporary, secondary insommnia - response to pain, bereavment or other crisis

56
Q

What are nightmatres + sleep terrors?

A

Strong visual component seen in REM. Waking will result in nightmare stopping
Terror - occur in deep delta sleep, common in ages 3-8
>Occur early in night
>Children thrash + scream - may sit/stand up with eyes open but not awake
>Often fail to recognise parents
>Child doesn’t remember episode next morning

57
Q

What is somnambulism?

A

Occurs only in non-REM often 4, more common in children/young adults
Walk with eyes open, can see + avoid objects, carry out complex tasks
No memory of episode

58
Q

What is narcolepsy?

A

Enter directly into REM with little warning
Very dangerous
Linked to dysfunctional orexin release

59
Q

What is circadian rhythm?

A

Biological body clock ~ 24hrs
Entrained, with light having effect
Nerve fibres pass through SCN - potential cause, but not only factor as blind people still have same body clock
If SCN destroyed, body clock rhythm lost

60
Q

What is cognition?

A

Thought processing
Integration of all sensory information to make sense of situation
Requires ability to remember
Requires motivation

61
Q

Where are memories formed?

A

Limbic system

62
Q

What is the limbic system?

A

Most primitive part of cortex
Four areas - hypothalamus, hippocampus (associated with memory), cingulate gyrus, amygdala
Collectively responsible for instinctive behaviour, and emotive - driven by reward, punishment`

63
Q

What are the reward/punishment areas?

A

Electrical stimulation of certain areas in limbic system in conscious patients -> intense feelings of wellbeing, euphoria + sexual arosual (reward areas)
Other areas terror anger, pain - punishment areas
Central spects to learning - form affective components of sensory experiences

64
Q

What is the significance of reward/punishment areas?

A

Experiences neither rewarding or punishment barely remembered - habitation
Rewarding/punishing remembered

65
Q

What is the hippocampus important for?

A

Central to learning + formation of memories
People with bilateral hippocampal damage - both immediate (sensory) memory but unable to form long term memories
Reflexive memory intact

66
Q

What are the types of memory?

A

Immediate/sensory
Short-term
Intermediate
Long-term

67
Q

What is immediate memory?

A

ability to hold experiences in the mind for a few seconds.
Based on different sensory modalities.
Visual memories decay fastest (<1s), auditory ones slowest (<4s).

68
Q

What is short term memory?

A

seconds - hours. “Working Memory”
short term tasks such as dialling a number, mental arithmetic, reading a sentence.
Associated with reverberating circuits.

69
Q

What is intermediate long-term memory?

A

hours to weeks e.g. what you did last weekend.

Associated with chemical adaptation at the presynaptic terminal.

70
Q

What is long term memory?

A

hours to lifetime.
e.g. where you grew up and your childhood friends.
Associated with structural changes in synaptic connections.

71
Q

What are reverberating circuits?

A

Short-term memory is an electrical phenomenon. It depends on maintained excitation from reverberating circuits i.e. they need to be constantly refreshed.
Reverberating circuit keeps memory alive. If deemed significant, consolidation of memory
If insignificant, reverberation fades
If refreshing effect disrupted, presents as amnesia

72
Q

What are the types of amnesia?

A

Anterograde

Retrograde

73
Q

What is anterograde amnesia?

A

Inability to recall events following injury
>Either short lived or permenant
Destruction of hippocampus results in permanent inability to form new memories

74
Q

What is retrograde amnesia?

A

Can’t remember events leading up to event (short term, long term normally unaffected)
>Often presents with anterograde
If thalamus damaged, hippocampus spared, only retrograde amnesia seen

75
Q

What changes allow for intermediate long-term memory?

A

Chemical changes in presynaptic neuron
Increasing Ca2+ entry to presynaptic terminals,
Increases neurotransmitter release (“strengthens” synapse”

76
Q

What changes allow for long-term memory?

A

Structural changes at synapses
>Increase in NT release sites on presynaptic membrane.
>Increase in number of NT vesicles stored and released.
>Increase in number of presynaptic terminals
At same time greater change in graded membrane potential in post-synaptic cell (EPSP) is often observed.
This “strengthens the synapse”, is called Long Term Potentiation
forms basis of much learning and memory.

77
Q

What are the types of long term memory?

A

Declarative

Procedural/ Reflexive/Implicit Memory:

78
Q

What is declarative memory?

A

Abstract memory for events (episodic memory)
words, rules and language (semantic memory).
Is based mainly in the hippocampus.

79
Q

What is Procedural/ Reflexive/Implicit Memory?

A

Acquired slowly through repetition. Includes motor memory for acquired motor skills (tennis), and rules based learning such as, in the UK, always driving on the left.
Thinking about these skills (“memories”) often impairs performance!
Is based mainly in the cerebellum.
Is independent of hippocampus

80
Q

What is consolidation?

A

Similar process in cerebellum during motor learning
Selective strengthening of synaptic connections through repetition (minutes –> hours)
>During which, simply exists as electrical activity
General anaesthesia or electrical convulsion, prevent memories of experiences immediately before event being consolidated (memories will be lost)
Requires attention
New memories coded, then stored in sensory association areas of cortex
Stored alongside similar memories

81
Q

How is information stored (if deemed useful)?

A

Frontal cortex gates a papez circuit
Reverberating activity then continues between the Papez circuit, frontal cortex, sensory and association areas until the consolidation process is complete.
Different components of the memory are laid down in different parts of the cortex, eg visual component in the visual cortex, auditory in auditory cortex, etc.
As such, recall can be evoked by multiple associations. Many memories have strong emotional components to them, ie pleasant or unpleasant.

82
Q

What are the types of sensory receptors?

A 
Mechanoreceptor
	Chemoreceptor
	Thermoreceptor
	Nocioreceptors
Proprioreceptors
83
Q

How do receptors make the brain aware of the stimuli?

A

They transduce their adequate stimulis into depolarisation (receptor (generator) potential
Size of receptor potential encodes intensity of stimulus
receptor potential then evokes firing of action potentials for long distance transmission
>frequency of action potentials encodes intensity of stimulus
receptive field encodes location of stimulus
gives information on the modality, intensity & location of the stimulus

84
Q

What determines acuity?

A

Density of innervation + size of receptive fields

85
Q

What fibres carry proprioception?

A

Aα & Aβ eg muscle spindles, golgi tendon organs etc

86
Q

What is the mechanism of mechanoreceptors?

A

project straight up through ipsilateral dorsal columns
synapse in cuneate & gracile nuclei
the 2nd order fibres cross over midline (decussate) in the brain stem & project to reticular formation, thalamus and cortex

87
Q

What is the mechanism of thermo/nocioceptors?

A

synapse in the dorsal horn
the 2nd order fibres cross over the midline in the spinal cord
project up through the contralateral spinothalamic (anterolateral) tract to reticular formation, thalamus and cortex

88
Q

What does damage to dorsal column lead to?

A

causes loss of touch, vibration, proprioception below lesion on ipsilateral side

89
Q

What does damage to the anterolateral column lead to?

A

causes loss of nociceptive & temperature sensation below lesion on contralateral side

90
Q

What is adaptation?

A

How the receptors respond to the stimuli
In rapidly adapting receptors, they stimulate lots to start with, and then stop firing until the stimulus is removed (with a few as it gets removed)
In slowly adapting receptors, action potentials are fired for the duration of the stimulus

91
Q

What is convergence?

A

Where multiple neurones feed into a single neurone
>saves on neurones
>but reduces acuity
>may underlie referred pain
>May also result in multiple stimuli triggering a single neurone - nonspecific pathways
Will know there is stimulus, but not sure which it is

92
Q

What is lateral inhibtion?

A

activation of one sensory input causes synaptic inhibition of its neighbours
gives better definition of boundaries
cleans up sensory information

93
Q

What activates signal conduction in nocioceptors?

A

Activated by
low pH, heat (via ASIC, TRPV1 etc)
local chemical mediators (eg bradykinin, histamine, prostaglandins)

94
Q

What are the three analgesia pathways?

A

NSAIDs
TENS - trans cutaneous electric nerve stimulation
Opiates

95
Q

How do opiates work?

A

reduce sensitivity of nociceptors
block transmitter release in dorsal horn (hence epidural administration)
activate descending inhibitory pathways

96
Q

How do NSAIDs work?

A

prostaglandins sensitise nociceptors to bradykinin
NSAIDs are analgesic (and antipiretic & anti-inflammatory) because they inhibit cyclo-oxygenase which converts arachidonic acid to prostaglandins
so NSAIDs work well against pain associated with inflammation

Conditions + definitions (68 decks)

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