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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
posterior hippocampus
Encodes long term memory
26
Visual/amygdala connection
occipital areas can recognise faces/shapes, temporal lobe input can identify them and these areas project to amygdala to deal with threatening sights/faces
27
Anterograde amnesia
Can't form new memories
28
Korsakoff's psychosis
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
29
Cingulate gyrus lesions
Indifference to pain/emotional stimuli | This is because it functions in emotional modulation of pain, involved in self awareness, memory processing
30
Tectospinal/vestibulospinal inputs?
Largely spinal systems, lrather thn cortical control
31
Locked in syndrome
Basilar pons lesion - sloss of corticobulbar and corticospinal tracts - only blink and vertical gaze retained
32
Pre-motor area
Lateral to SMA - initial motor planning with visual guidance
33
Supplementary motor cortex
Medial to PMA. planning movement. Coordinates volunary movement (input from basal ganglia and cerebellum)
34
Posteior parietal cortex
Lesions here involve apraxia and neglect
35
Corticospinal LMN lesion
Causes weakness, hypotonia and hyporeflexia. Will be ipsilateral to lesion site
36
Corticospinal UMN lesion
Hypertonia, babinksi, spasticity, paralysis, contralateral lesion
37
Cerebellar cortex is made from?
Folia
38
Cerebellar ouput does not go to?
LMN, goies back to motor cortex to direct movement
39
Cerebellar Structure: anatomical lobes
Two cerebellar hemispheres connected at vermis Primary fissure separates anterior and posterior lobes. Floculonodular lobe and tonsils on anterior
40
Cerebellar structure: functional lobes
Spinocerebellum, neocerebellum, vestibulocerebellum
41
Spinocerebellum
Midline vermis + paravermis. Receives major spinal cord input (spinocerebellar tracts) to regulate axial muscle tone/posture. Somatotrophic
42
Neocerebellum
Vast majority of hemispheres. Recevies pontocerebellar fibres. Muscle coordination/trajectory/force
43
Vestibulocerebellum
F/N lobe and posterior vermis. Connects with vestibular/reticular nuclei (balance and equilibrium/head/eye control)
44
Superior cerebellar peduncle
Mainly efferent, main output route. Goes to contralateral Red nucleus and ventrolateral nucleus of thalamus
45
Middle cerebellar peduncle
Largest. Contains mainly afferents from cerebral cortex (via contralateral pontine nuclei)
46
Inferior cerebellar peduncle
Mainly afferent, info from medulla/spinal cord.
47
Dentate nuclei
Project to ventrolateral thalamus nucleus
48
Interposed nuclei
Project to red nucleus
49
Fastigial nuclei
Project to reticular formation/vesticular neurones
50
Major/minor cerebellar inputs
Main is vis contralateral pontine nuclei, minor is vestibular/inferior olive and spinal cord.
51
Ataxia
Tremor on movement, errors in direction/range/rate/force
52
dysdiadochokinesia
no rapidly alternating movements
53
Intenstion tremor
Tremor when coming to the end of determined/visually directed movement
54
Dysmetria
Over/unddershoot
55
Chairi type 1
Not usually life threatning. Malformation where skull is too small and structures displaced inferiorly. Often causes headache, visual distrubance, nystagmus, ataxia
56
Chiari type 2
Displaces cerebellum and brainstem, compress resp/cardio centres
57
neuomelanin found in
PC of SN
58
D1 pathway
Direct, stimulation promotes movement
59
D2 pathway
Inhibits D2 indirect so promotes movement
60
Nocicpetors transmit via
Free nerve endings
61
Primary hyperalgesia
/tissue damaged/inflammated and light stimulation causes pain at site of injury (secondary isin surrounding tissue)
62
Fast pain/slow pain fibres
A delta are fast (lightly myelinated). C fibres are unmelinated (Slow pain - dull) Synapse on different rexed lamina (C on susbstantia gelatinosa)
63
What is lissauer's tract
Ipsilateral tract that primary neurons can travel in before synapse/decussation
64
Pain fibre synapse neurotransmission
First order release glutamate/substance P to activate second order
65
Trigeminal synapse order
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
Chief CNV nucleus
Equivalent to Dorsal column - > conscious proprioception/fine touch/vibration
67
Spinal nucleus of CNV
Equivalent to spinothlamic - > pain/temp
68
Mesencephalic CNV
Unconscious proprioception from muscles of mastication
69
Gate control pain theory
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
Descending mechanisms for pain controle?
inhibiting projection neurons in dorsal horn (via direct/indirect pathways). PAG/locus coerus, hypothalamus involved, midbrain/pontine ES can provoke analgesia
71
RVM in pain?
5HT and rostral ventral medulla involved in pain modulation. Off cells are antinociceptive, on cells promote pain. Opioids inhibit 'on cells'
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Intrathecal NA
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
Endogenous opioids
Endorphins/enkephalins
74
Allodynia
Pain from normally not noxious stimulus
75
Spontaneous pain
No stimulus
76
awake EEG waves
Beta
77
Drowsy EEG
alpha
78
Stage 1 NREM
Theta (like beta, but slower)
79
Stage 2 NREM
Sleep spindles
80
Stage 3/4 EEG
Delta
81
REM sleep EEG
beta wave like pattern
82
Sleep oscillations
Thalamus is powerful pacemaker, thalamocortical axons stimulate cortex and cortical cells to oscillate at same rhythm.
83
Circadian rhythm
Suprachiasmic nucleus in hypothalamus - input is light sensitive. But does not induce sleep
84
Sleep cycles
90 minute NREM1->4 REM and repeat. REM gets longer as night progresses.
85
NREM sleep
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
REM sleep
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
Sleep inducing chemical
adenosine. | Caffeine is adenosine receptor antagonist,
88
Wakefulness
Ascending reticular formation (Locus ceruleus, raphe nucleus, ACh cells of forebrain/brainstem, midbrain nucleus (histamine, hypathalamus neurons with orexin)
89
Sleep disorders
Insomnia, sleep apnoea, NArcolepsy (ass. with hypocretin loss), Rapid eye movement disorder (pontine reticulospinal inhibition defect)

Neuro (6 decks)

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