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2 - BB/HD > BB physiology > Flashcards

BB physiology Flashcards

1
Q

Structural changes in epilepsy

A

Loss of CA2 and 3 cells in the hippocampus

Temporal lobe and hippocampal sclerosis

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2
Q

Causes of secondary epilepsy

A 
Craniotomy 
Brain injury 
Stroke 
Aneurysm 
Tumour 
CNS infection
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3
Q

Cellular mechanisms of epilepsy

A

Abnormal neuronal excitability
Increased excitation
Decreased inhibition

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4
Q

What is the paroxysmal depolarising shift?

A

Depolarisation of the membrane causes a sustained burst of action potentials involving activation of NMDA receptors

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5
Q

Which drugs are used for tonic clonic seizures?

A

Carbamazepine
Soldium valporate
Lamotrigine

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6
Q

Which drugs are used for absence seizures?

A

Ethosuzimide

Sodium valprotate

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7
Q

Which drugs are used for myoclonic seizures?

A

Sodium valprotate
Clonazepam
Levatiracetam

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8
Q

Which area is used for DBS in epilepsy?

A

Anterior nucleus of the thalamus

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9
Q

What diet can be used for epilepsy?

A

Ketogenic diet

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10
Q

What is optic neuritis?

A

Inflammation of the optic nerve

Seen in MS

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11
Q

What is internuclear ophthalmoplegia?

A

Damage to the MLF resulting in impaired adduction of the eye during head rotation
Seen in MS

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12
Q

What is Lhermitte’s symptom?

A

Electric shock sensation down the back of the leg

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13
Q

What is Uhthoff’s phenomenon?

A

Worsening of neurological symptoms in increased temperature due to increased velocity of nerve conduction

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14
Q

Where are MS lesions commonly found?

A 
Corpus callosum 
Periventricular 
Cervical spinal cord 
Optic nerve 
Brainstem and cerebellar connections
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15
Q

MS lesions enhance with what?

A

Gadolinium

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16
Q

What does the McDonald’s criteria state for MS diagnosis?

A

Presence of neurological symptoms
Dissemination in time
Dissemnination in space
Exclusion of other causes

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17
Q

HLA molecule implicated in MS

A

HLA-DRB1

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18
Q

No evidence of disease activity in MS

A

No relapses
No increase in disability
No new or active lesions on MRI

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19
Q

Which artery is most commonly occluded in the posterior circulation?

A

PCA

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20
Q

3 layers of the cerebellar grey matter?

A

Outer molecular layer = axons and densrites
Single middle Purkinje cell layer
Inner thick granule layer

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21
Q

What is within the SCPs?

A

Output fibres to the thalamus and cortex

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22
Q

What is within the MCPs?

A

Input fibres from the contralateral cerebral cortex and cranial nerve nuclei

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23
Q

What is within the ICPs?

A

Input fibres from the spinocerebellar tract

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24
Q

Ventral SCT

A

State of reflexes and interneurones

Decussates twice

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25
Q

Dorsal SCT

A

Proprioception

No decussation

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26
Q

Where is the fastigial nucleus found?

A

Vermis

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27
Q

Where is the interpose nucleus found?

A

Anterior lobe

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28
Q

What males up the interpose nuclei

A

Globose

Emboliform

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29
Q

Where is the dentate nucleus found?

A

Posterior lobe

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30
Q

What is the nucleus for the flocculonodular lobe?

A

Lateral vestibular nucleus

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31
Q

What tracts does the spinocerebellum use?

A

Lateral vestibulospinal

Reticulospinal

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32
Q

Which lobe is the spinocerebellum?

A

Anterior lobe

Vermis

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33
Q

Which lobe is the cerebrocerebellum?

A

Posterior

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34
Q

Which lobe is the vestibulocerebellum?

A

FN

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35
Q

What are the inputs and outputs of the cerebrocerebellum?

A 
Input = MCP 
Output = SCP
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36
Q

Medial vs lateral vestibulospinal tracts

A 
Medial = head and neck 
Lateral = postural muscles
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37
Q

What does medulloblastoma commonly cause?

A

FN syndrome

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38
Q

Symptoms of FN syndrome

A

Nystagmus
Ataxic gait
Fall towards side of lesion
Axial hypotonia

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39
Q

Symptoms of anterior lobe syndrome

A 
Incoordination of the limbs 
Ataxic gait 
Hypotonia 
Dysdiadochokinesia 
Altered reflexes
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40
Q

Neocerebellar syndrome symptoms

A

Dysmetrria
Intention tremor
Slurred speech
Loss of eye scanning

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41
Q

Which cerebellar syndrome does alcoholism cause?

A

Anterior lobe syndrome

42
Q

What does the premotor cortex do?

A

Integrates information from the more anterior parts of the frontal lobe and forms motor programs that are sent to the primary motor cortex

43
Q

What does damage to the premotor cortex cause?

A

Apraxia

44
Q

What does damage to the FEFs produce?

A

Problems with cognitive eye movements

Saccades, smooth pursuit, vergence

45
Q

What does the dorsalprefrontal cortex do?

A

Planning of movements where we evaluate possible actions

Executive function

46
Q

What does the orbitofrontal cortex do?

A

Inhibition of motor responses associated with the limbic system

47
Q

Where does the CST decussate?

A

Spino-medullary junction

48
Q

What does the reticulospinal tract drive?

A

Sympathetic preganglionic neurones

Phrenic nerve

49
Q

Where does the rubrospinal tract originate from?

A

Red nucleus

50
Q

Where does the tectospinal tract originate from?

A

Superior colliculus

51
Q

What does the tectospinal tract control?

A

Reflex head movements in response to auditory and visual stimuli

52
Q

Arms in decorticate vs decerebrate

A 
Decorticate = arms adducted and flexed 
Decerebrate = arms adducted and extended
53
Q

Which lamina is innervated by Ad fibres?

A

V

54
Q

Which lamina is innervated by C fibres?

A

I and some interneurones in II

55
Q

What substances do peptidergic C fibres release?

A

Substance P

CGRP

56
Q

Anterior spinothalamic pathway

A 
Mostly Ad fibres 
From lamina V and IV 
Fast pain 
Discrimination and localisation 
Projects to VPL, VPM, VPI, CL
57
Q

Lateral spinothalamic pathway

A 
Mostly C fibres 
From lamina I 
Slow pain 
Emotionally punishing aspects of pain 
Projects to MDvc, POs, VMpo --> anterior cingulate cortex and insula
58
Q

Input to BG

A

Cortex –> striatum

Via glutamate

59
Q

Output from BG

A

GPI
SNr
–> VA/VL thalamus
Via GABA

60
Q

Input to medium spiny neurones

A

Cortical via spines

SNpc –> spines, dendritic shafts, cell body

61
Q

Cardinal signs of PD

A

Tremor at rest
Rigidity
Bradykinesia
Loss of postural reflexes

62
Q

Cardinal signs of Huntingdon’s

A

Hyperkinesis
Ballismus = jerky
Athetosis = smooth

63
Q

APOE in AD

A 
E4 = greatest risk 
E2 = protective
64
Q

Amyloidogenic pathway

A

Beta and gamma secretases

65
Q

CSF markers of AD

A

Raised Tau

Decreased beta amyloid

66
Q

Signs of subfalcine herniation

A

Leg weakness

67
Q

Signs of transtentorial herniation

A

CN III damage
Midbrain damage
Often fatal

68
Q

Signs of tonsillar herniation

A

Reduced respiratory drive
Unconscious
Death

69
Q

Rostral vs caudal ACC

A 
Rostral = actions in response to pain 
Caudal = registers quality of pain
70
Q

Posterior cingulate cortex function

A

Visuo-spatial memory

71
Q

Orbitofrontal cortex function

A

What acts to take in response to pain

72
Q

Symptoms of Wernicke-Korsakoff syndrome

A

Anterograde amnesia
Some retrograde amnesia
Confabulation
Apathy

73
Q

Kluver Bucy syndrome

A

Bilateral removal of amygdala
Psychic blindness
Oral tendancies
Altered sexual behaviour emotional changes

74
Q

Pre-synaptic changes in LTP

A 
Early = increase in glutamate release in response to anterograde transmitters (NO, CO) 
Late = increase in number of glutamate release sites
75
Q

Post-synaptic changes in LTP

A 
Early = increased number and sensitivity of AMPA receptors 
Late = increased number of synapses
76
Q

NMDA antagonists

A 
Memantine = near to where Mg binds
Ketamine = allosteric site
77
Q

Persistent vs permanent vegetative state

A 
Persistent = >1 month 
Permanent = >1 year
78
Q

DBS for persistent vegetative state

A

Thalamus

79
Q

Drugs for reduced consciousness

A

Amantadine

Zolpidem

80
Q

Chemicals in the blood affecting sleep

A 
Promote awake 
- ghrelin 
- low glucose 
Promote sleep 
- CCK 
- adenosine
81
Q

Where are sleep chemicals detected?

A

Preoptic nuclei

82
Q

Where are diurnal rhythms detected?

A

Suprachiasmatic nucleus

83
Q

Where do the preoptic and suprachiasmatic nuclei project?

A

Tuberomamillary nucleus

84
Q

What does the tuberomamillary nucleus release?

A

Histamine

85
Q

Where are orexins released from?

A

Posterior thalamus

86
Q

Which NT system is active during REM sleep/

A

ACh

87
Q

Which NT is thought to be involved in remembering dreams?

A

NA

88
Q

Time limit for thrombolysis

A

4.5 hours

89
Q

Percent of strokes that are ischaemic

A

70-80%

90
Q

TOAST stroke classification

A 
1 = large artery atherosclerosis 
2 = cardioembolism 
3 = small vessel occlusion 
4 = other origin 
5 = undetermined
91
Q

ABCD2 score for TIA

A 
Predicts risk of stroke 
A = age>60 (1)
B = BP>140/90 (1)
C = clinical features --> hemiparesis (2), speech alone (1)
D = duration --> <1h (1) >1h (2)
D = diabetes (1) 
Hospitalise if >4
92
Q

Utricle

A

Horizontal tilting
Detect side to side movement and acceleration
High activity lying down

93
Q

Saccule

A

Vertical tilting
Detect activity forwards and backwards and up and down
High activity standing up

94
Q

Endolymph vs perilymph

A 
Endo = high K+, low Na+ 
Peri = high Na+, low K+
95
Q

What do the semicircular canals detect?

A

Angular acceleration

96
Q

How is each semicircular canal activated?

A 
Lateral = side to side rotation 
Anterior/superior = neck flexion 
Posterior/inferior = neck extension
97
Q

Which was around are the striola directions in the otolithic organs?

A 
Utricle = towards striola 
Saccula = away from striola
98
Q

What does the striola divide the otoliths into?

A 
Utricle = medial and lateral halves 
Saccule = anterior and posterior halves
99
Q

Which direction will nystagmus occur with warm irrigation?

A

Same side

100
Q

Which direction will nystagmus occur with cold irrigation?

A

Opposite

101
Q

BPPV

A

Benign paroxysmal positional vertigo
Otoliths displaced
Can be detected by Hallpike manoeuvre

102
Q

Meniere’s disease

A

Dysfunctional production of endolymph

Can lead to rupture

2 - BB/HD (8 decks)

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