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
Dorsal SCT
Proprioception | No decussation
26
Where is the fastigial nucleus found?
Vermis
27
Where is the interpose nucleus found?
Anterior lobe
28
What males up the interpose nuclei
Globose | Emboliform
29
Where is the dentate nucleus found?
Posterior lobe
30
What is the nucleus for the flocculonodular lobe?
Lateral vestibular nucleus
31
What tracts does the spinocerebellum use?
Lateral vestibulospinal | Reticulospinal
32
Which lobe is the spinocerebellum?
Anterior lobe | Vermis
33
Which lobe is the cerebrocerebellum?
Posterior
34
Which lobe is the vestibulocerebellum?
FN
35
What are the inputs and outputs of the cerebrocerebellum?
``` Input = MCP Output = SCP ```
36
Medial vs lateral vestibulospinal tracts
``` Medial = head and neck Lateral = postural muscles ```
37
What does medulloblastoma commonly cause?
FN syndrome
38
Symptoms of FN syndrome
Nystagmus Ataxic gait Fall towards side of lesion Axial hypotonia
39
Symptoms of anterior lobe syndrome
``` Incoordination of the limbs Ataxic gait Hypotonia Dysdiadochokinesia Altered reflexes ```
40
Neocerebellar syndrome symptoms
Dysmetrria Intention tremor Slurred speech Loss of eye scanning
41
Which cerebellar syndrome does alcoholism cause?
Anterior lobe syndrome
42
What does the premotor cortex do?
Integrates information from the more anterior parts of the frontal lobe and forms motor programs that are sent to the primary motor cortex
43
What does damage to the premotor cortex cause?
Apraxia
44
What does damage to the FEFs produce?
Problems with cognitive eye movements | Saccades, smooth pursuit, vergence
45
What does the dorsalprefrontal cortex do?
Planning of movements where we evaluate possible actions | Executive function
46
What does the orbitofrontal cortex do?
Inhibition of motor responses associated with the limbic system
47
Where does the CST decussate?
Spino-medullary junction
48
What does the reticulospinal tract drive?
Sympathetic preganglionic neurones | Phrenic nerve
49
Where does the rubrospinal tract originate from?
Red nucleus
50
Where does the tectospinal tract originate from?
Superior colliculus
51
What does the tectospinal tract control?
Reflex head movements in response to auditory and visual stimuli
52
Arms in decorticate vs decerebrate
``` Decorticate = arms adducted and flexed Decerebrate = arms adducted and extended ```
53
Which lamina is innervated by Ad fibres?
V
54
Which lamina is innervated by C fibres?
I and some interneurones in II
55
What substances do peptidergic C fibres release?
Substance P | CGRP
56
Anterior spinothalamic pathway
``` Mostly Ad fibres From lamina V and IV Fast pain Discrimination and localisation Projects to VPL, VPM, VPI, CL ```
57
Lateral spinothalamic pathway
``` Mostly C fibres From lamina I Slow pain Emotionally punishing aspects of pain Projects to MDvc, POs, VMpo --> anterior cingulate cortex and insula ```
58
Input to BG
Cortex --> striatum | Via glutamate
59
Output from BG
GPI SNr --> VA/VL thalamus Via GABA
60
Input to medium spiny neurones
Cortical via spines | SNpc --> spines, dendritic shafts, cell body
61
Cardinal signs of PD
Tremor at rest Rigidity Bradykinesia Loss of postural reflexes
62
Cardinal signs of Huntingdon's
Hyperkinesis Ballismus = jerky Athetosis = smooth
63
APOE in AD
``` E4 = greatest risk E2 = protective ```
64
Amyloidogenic pathway
Beta and gamma secretases
65
CSF markers of AD
Raised Tau | Decreased beta amyloid
66
Signs of subfalcine herniation
Leg weakness
67
Signs of transtentorial herniation
CN III damage Midbrain damage Often fatal
68
Signs of tonsillar herniation
Reduced respiratory drive Unconscious Death
69
Rostral vs caudal ACC
``` Rostral = actions in response to pain Caudal = registers quality of pain ```
70
Posterior cingulate cortex function
Visuo-spatial memory
71
Orbitofrontal cortex function
What acts to take in response to pain
72
Symptoms of Wernicke-Korsakoff syndrome
Anterograde amnesia Some retrograde amnesia Confabulation Apathy
73
Kluver Bucy syndrome
Bilateral removal of amygdala Psychic blindness Oral tendancies Altered sexual behaviour emotional changes
74
Pre-synaptic changes in LTP
``` Early = increase in glutamate release in response to anterograde transmitters (NO, CO) Late = increase in number of glutamate release sites ```
75
Post-synaptic changes in LTP
``` Early = increased number and sensitivity of AMPA receptors Late = increased number of synapses ```
76
NMDA antagonists
``` Memantine = near to where Mg binds Ketamine = allosteric site ```
77
Persistent vs permanent vegetative state
``` Persistent = >1 month Permanent = >1 year ```
78
DBS for persistent vegetative state
Thalamus
79
Drugs for reduced consciousness
Amantadine | Zolpidem
80
Chemicals in the blood affecting sleep
``` Promote awake - ghrelin - low glucose Promote sleep - CCK - adenosine ```
81
Where are sleep chemicals detected?
Preoptic nuclei
82
Where are diurnal rhythms detected?
Suprachiasmatic nucleus
83
Where do the preoptic and suprachiasmatic nuclei project?
Tuberomamillary nucleus
84
What does the tuberomamillary nucleus release?
Histamine
85
Where are orexins released from?
Posterior thalamus
86
Which NT system is active during REM sleep/
ACh
87
Which NT is thought to be involved in remembering dreams?
NA
88
Time limit for thrombolysis
4.5 hours
89
Percent of strokes that are ischaemic
70-80%
90
TOAST stroke classification
``` 1 = large artery atherosclerosis 2 = cardioembolism 3 = small vessel occlusion 4 = other origin 5 = undetermined ```
91
ABCD2 score for TIA
``` 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
Utricle
Horizontal tilting Detect side to side movement and acceleration High activity lying down
93
Saccule
Vertical tilting Detect activity forwards and backwards and up and down High activity standing up
94
Endolymph vs perilymph
``` Endo = high K+, low Na+ Peri = high Na+, low K+ ```
95
What do the semicircular canals detect?
Angular acceleration
96
How is each semicircular canal activated?
``` Lateral = side to side rotation Anterior/superior = neck flexion Posterior/inferior = neck extension ```
97
Which was around are the striola directions in the otolithic organs?
``` Utricle = towards striola Saccula = away from striola ```
98
What does the striola divide the otoliths into?
``` Utricle = medial and lateral halves Saccule = anterior and posterior halves ```
99
Which direction will nystagmus occur with warm irrigation?
Same side
100
Which direction will nystagmus occur with cold irrigation?
Opposite
101
BPPV
Benign paroxysmal positional vertigo Otoliths displaced Can be detected by Hallpike manoeuvre
102
Meniere's disease
Dysfunctional production of endolymph | Can lead to rupture