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Neuro > Cerebellum, Limbig, Sleep and Pain > Flashcards

Cerebellum, Limbig, Sleep and Pain Flashcards

1
Q

Difference between top down and bottom up attention

A

Top down is volunary attending, conscious decision to direct attention. Bottom up is stimulus reaction

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2
Q

Brain function localisation can be:

A 
In vitro (take sample and record response, but differnet environment)
Microelectrodes (can be done in vivo, but restricted to small number of neurons and is invasive)
MRI - > functional MRI can look at blood oxygenation to indicate areas of brain in use

Transcranial magnetic stimulation uses localised magnetic filed to interferen with superficial cortical processing

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3
Q

Damage to occipital lobe

A

Causes visual defects/cortical blindness

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4
Q

Parietal lobe damage

A 
Sensory impairment (contralateral) - BUT left only deals with right while right does left and right so righr lesion leads to left side neglect. 
Left parietal damage also affects verbal short term memory, also agraphia and dysclaculia.

Right parietal lobe - > constructional apraxia, impaired ST visual memory

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5
Q

Right parietal lobe lesion

A

Causes left sided neglect, but left lesion might not cause right neglect as right has both right and left inputs

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6
Q

Frontal lobe lesion

A

Has primary moror cortex, pre motor and prefrontal cortex, so motor issue, personality changes, aggression.

Right frontal damage is immature, childish, inappropriate.
Left frontal damage is depression, lack if divergent thought, stimulus bound

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7
Q

McGurk effect

A

Audio perception altered by visual input

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8
Q

Temporal lesion

A

Impaired recognition of complex visual information

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9
Q

Papez circuit

A

Hippocampus to fornix to mammillary body to anterior thalamus to cingulate gyrus to parahyippocampal gyrus to entorhinal cortex to subiculum.

Involved in episodic (contextual) memory formation -retrieval of memories with emotional/contextual component and in memory consolidation

Damaged in Alzheimers, Parkinsons and Korsakoff (B12)

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10
Q

Locus ceruleus

A

Pons
ne
Projects to limbic, posterior basal forebrain. Stimulates ACh release into cerebral cortex

Involved in arousal, vigilance, sleep waking

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11
Q

Raphe nuclei

A

Midbrain
Serotonin

Projects to Hippocampus, nucleus accumbens, HPA axis (hypothalamus) , prefrontal cortex

Involved in cortical arousal, mood, movement

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12
Q

Substantia nigra

A

Midbrain
DA
Nucleus accumbense, limbic, prefrontal cortex
Mood, excitement, arousal, reward

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13
Q

Acetylcholinergic neurons

A

Pons/basal forebrain
ACH
Projects to cerebral cortex, involved in cortical activity/arousal

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14
Q

Histamergenic system

A

Hypothalamus, histamine release (stimulates ACh).
Thalamus, locus ceruleus.
Involved in cortical activity, arousal, sleep/wake

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15
Q

Serotonin role in addiction

A

Reward due to feeling good

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16
Q

Dopamine in addiction

A

Seeking behaviour

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17
Q

NE in addition

A

Motivation beharious

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18
Q

Septal nuclei of limbic system

A

Pleasure (inc. sexual), eating drinking

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19
Q

Nucleus accumbens

A

DA activated reard around wellbeing/love

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20
Q

Kluver Bucy syndrome

A

Underactive amygdala - > docile (lack of fear/anger) but increased appetite and hypersexual behaviour. Excessive exploratory behaviours with mouth/hands

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21
Q

Overactive amygdala

A

Anxiety disorder, excess anger, excess aggression

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22
Q

Contents of limbic system

A

Rim of cortex (hippocampus, fornix, mammillary bodies), subcortical nuclei (amygdala, nucleus accumbens, septal area, hypothalamic nuclei) and limbic gyrus (cingulate, parahippocampus gyrus)

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23
Q

Anterior hippocampal lesion

A

No NEW memory formation, but can usually recall long term memories (doesn’ rely on hippocampus)

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24
Q

Long term memroy

A

Temporal lobes/association areas

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25
Q

posterior hippocampus

A

Encodes long term memory

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26
Q

Visual/amygdala connection

A

occipital areas can recognise faces/shapes, temporal lobe input can identify them and these areas project to amygdala to deal with threatening sights/faces

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27
Q

Anterograde amnesia

A

Can’t form new memories

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28
Q

Korsakoff’s psychosis

A

Metabolic damage/alcohol related thiamine deficiency.
Mammillary body damage, disrupts papez circuit - > anterograde/retrograde amnesia. Patients often confabulate. Lack of inight. May also have ataxia, nystagmus, ophthalmoplegia

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29
Q

Cingulate gyrus lesions

A

Indifference to pain/emotional stimuli

This is because it functions in emotional modulation of pain, involved in self awareness, memory processing

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30
Q

Tectospinal/vestibulospinal inputs?

A

Largely spinal systems, lrather thn cortical control

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31
Q

Locked in syndrome

A

Basilar pons lesion - sloss of corticobulbar and corticospinal tracts - only blink and vertical gaze retained

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32
Q

Pre-motor area

A

Lateral to SMA - initial motor planning with visual guidance

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33
Q

Supplementary motor cortex

A

Medial to PMA. planning movement. Coordinates volunary movement (input from basal ganglia and cerebellum)

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34
Q

Posteior parietal cortex

A

Lesions here involve apraxia and neglect

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35
Q

Corticospinal LMN lesion

A

Causes weakness, hypotonia and hyporeflexia. Will be ipsilateral to lesion site

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36
Q

Corticospinal UMN lesion

A

Hypertonia, babinksi, spasticity, paralysis, contralateral lesion

37
Q

Cerebellar cortex is made from?

A

Folia

38
Q

Cerebellar ouput does not go to?

A

LMN, goies back to motor cortex to direct movement

39
Q

Cerebellar Structure: anatomical lobes

A

Two cerebellar hemispheres connected at vermis
Primary fissure separates anterior and posterior lobes.
Floculonodular lobe and tonsils on anterior

40
Q

Cerebellar structure: functional lobes

A

Spinocerebellum, neocerebellum, vestibulocerebellum

41
Q

Spinocerebellum

A

Midline vermis + paravermis. Receives major spinal cord input (spinocerebellar tracts) to regulate axial muscle tone/posture. Somatotrophic

42
Q

Neocerebellum

A

Vast majority of hemispheres. Recevies pontocerebellar fibres. Muscle coordination/trajectory/force

43
Q

Vestibulocerebellum

A

F/N lobe and posterior vermis. Connects with vestibular/reticular nuclei (balance and equilibrium/head/eye control)

44
Q

Superior cerebellar peduncle

A

Mainly efferent, main output route. Goes to contralateral Red nucleus and ventrolateral nucleus of thalamus

45
Q

Middle cerebellar peduncle

A

Largest. Contains mainly afferents from cerebral cortex (via contralateral pontine nuclei)

46
Q

Inferior cerebellar peduncle

A

Mainly afferent, info from medulla/spinal cord.

47
Q

Dentate nuclei

A

Project to ventrolateral thalamus nucleus

48
Q

Interposed nuclei

A

Project to red nucleus

49
Q

Fastigial nuclei

A

Project to reticular formation/vesticular neurones

50
Q

Major/minor cerebellar inputs

A

Main is vis contralateral pontine nuclei, minor is vestibular/inferior olive and spinal cord.

51
Q

Ataxia

A

Tremor on movement, errors in direction/range/rate/force

52
Q

dysdiadochokinesia

A

no rapidly alternating movements

53
Q

Intenstion tremor

A

Tremor when coming to the end of determined/visually directed movement

54
Q

Dysmetria

A

Over/unddershoot

55
Q

Chairi type 1

A

Not usually life threatning. Malformation where skull is too small and structures displaced inferiorly. Often causes headache, visual distrubance, nystagmus, ataxia

56
Q

Chiari type 2

A

Displaces cerebellum and brainstem, compress resp/cardio centres

57
Q

neuomelanin found in

A

PC of SN

58
Q

D1 pathway

A

Direct, stimulation promotes movement

59
Q

D2 pathway

A

Inhibits D2 indirect so promotes movement

60
Q

Nocicpetors transmit via

A

Free nerve endings

61
Q

Primary hyperalgesia

A

/tissue damaged/inflammated and light stimulation causes pain at site of injury (secondary isin surrounding tissue)

62
Q

Fast pain/slow pain fibres

A

A delta are fast (lightly myelinated). C fibres are unmelinated (Slow pain - dull)
Synapse on different rexed lamina (C on susbstantia gelatinosa)

63
Q

What is lissauer’s tract

A

Ipsilateral tract that primary neurons can travel in before synapse/decussation

64
Q

Pain fibre synapse neurotransmission

A

First order release glutamate/substance P to activate second order

65
Q

Trigeminal synapse order

A

GSA cell bodies in trigeminal ganglia (not DRG). Branches of CNV first order synapse with chief/spinal, second order synapse with thalamus, 3rd order with somatosensory cortex.

66
Q

Chief CNV nucleus

A

Equivalent to Dorsal column - > conscious proprioception/fine touch/vibration

67
Q

Spinal nucleus of CNV

A

Equivalent to spinothlamic - > pain/temp

68
Q

Mesencephalic CNV

A

Unconscious proprioception from muscles of mastication

69
Q

Gate control pain theory

A

Non nociceptive mechanoceptor (A alpha/ beta axons) stimulate same second order that C fibres go, suppressing/diluting nociceptive signal

TENS works on this theory

70
Q

Descending mechanisms for pain controle?

A

inhibiting projection neurons in dorsal horn (via direct/indirect pathways).
PAG/locus coerus, hypothalamus involved, midbrain/pontine ES can provoke analgesia

71
Q

RVM in pain?

A

5HT and rostral ventral medulla involved in pain modulation. Off cells are antinociceptive, on cells promote pain. Opioids inhibit ‘on cells’

72
Q

Intrathecal NA

A

NA on alpha 1 excitatory, on alpha 2 is inhibitory. Inintrathecal NA, alpha 2 activated to give potent analgesia (ADE: hypertension, bradycardia, sedation)
Intra theca is subarachnoid

73
Q

Endogenous opioids

A

Endorphins/enkephalins

74
Q

Allodynia

A

Pain from normally not noxious stimulus

75
Q

Spontaneous pain

A

No stimulus

76
Q

awake EEG waves

A

Beta

77
Q

Drowsy EEG

A

alpha

78
Q

Stage 1 NREM

A

Theta (like beta, but slower)

79
Q

Stage 2 NREM

A

Sleep spindles

80
Q

Stage 3/4 EEG

A

Delta

81
Q

REM sleep EEG

A

beta wave like pattern

82
Q

Sleep oscillations

A

Thalamus is powerful pacemaker, thalamocortical axons stimulate cortex and cortical cells to oscillate at same rhythm.

83
Q

Circadian rhythm

A

Suprachiasmic nucleus in hypothalamus - input is light sensitive. But does not induce sleep

84
Q

Sleep cycles

A

90 minute NREM1->4 REM and repeat. REM gets longer as night progresses.

85
Q

NREM sleep

A

5HT, NA, ACh all decrease for NREM.
Thalamus is gated, so can’t respond to external stimuli (HR, RR, BP steady)
Fact based memory aided by NREM sleep, and memory retrieval

86
Q

REM sleep

A

NA/5HT decrease, but Ach rapidly increases in pons to induce REM
REM aids problem solving and creativity.
Thalamus is closed to external stimuli, but can respond to internal stimuli so BP/RR/HR fluctuate, although skeletal muscles relaxed)

87
Q

Sleep inducing chemical

A

adenosine.

Caffeine is adenosine receptor antagonist,

88
Q

Wakefulness

A

Ascending reticular formation (Locus ceruleus, raphe nucleus, ACh cells of forebrain/brainstem, midbrain nucleus (histamine, hypathalamus neurons with orexin)

89
Q

Sleep disorders

A

Insomnia, sleep apnoea, NArcolepsy (ass. with hypocretin loss), Rapid eye movement disorder (pontine reticulospinal inhibition defect)

Neuro (6 decks)

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