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Neuro Flashcards

0
Q

What divides the pre and post central gyrus

A

The central sulcus

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1
Q

What is the gap that divides the two hemispheres called? What runs down it?

A

Longitudinal fissure

Falx cerebri

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2
Q

What divides the temporal lobe from the frontal and parietal?

A

Lateral cerebral sulcus

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3
Q

What divides the cerebellum from the cerebrum?

A

The transverse fissure

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4
Q

What connects the lateral ventricles to the third ventricle?

A

Intraventricular foramen

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5
Q

What connects the third and fourth ventricle?

A

Cerebral aqueduct

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6
Q

How do the white and grey matter change in the spinal cord in c,t,l and s?

A

C - big white, small grey
T - smaller white, small grey, lat grey horns
L - big white, big grey
S - small white, big grey

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7
Q

What is at the end of the spinal cord

What are they made of?

A

Conus medularis

Flium terminale - extension of the pia blended with arachnoid and dura)

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8
Q

Where do the periosteal and meningeal dura mater separate?

A

Falx cerebri
Falx cerebelli
Tentorum cerebeli
Diaphragm sellae

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9
Q

What covers the pituitary gland?

A

Diaphragm sellae

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10
Q

What are the three ways the brain can herniate with increased icp?

A

Uncal - the uncus of the temporal lobe is pushed round the tentorum cerebeli
Subfacal - the cingulate gyrus is pushed between the falx cerebri and the corpus callosum
Tonsillar - cerebellar tonsils and brainstem pushed through foramen magnum

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11
Q

Which layer of dura persists in around the spinal cord?

A

Meningeal

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12
Q

What is the difference between the epidural and extradural space?

A

Extradural is around the brain. It is potential as the dura is adhered to the bone
Epidural is around the spine. It is real consisting of fat and connective tissue

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13
Q

Why is a basal skull fracture more likely to cause csf leakage?

A

The dura is not surgically seperable from the bone

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14
Q

At what point do the neuropores fuse?

A

25 and 28 days cranial and caudal respectivly

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15
Q

What occurs if the neuropores fail to fuse?

A

Spina bifida

Anencephaly

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16
Q

What might be suggestive of a neuropore deficit whilst the fetus is in utero? What else could cause this?

A

A raised alpha fetoprotein level

Omphalocele, gastroschisis

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17
Q

When should folic acid be taken to reduce chance of neuropore deformity?

A

3 months before and during 1st trimester

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18
Q

What are the cranial regions of the neural tube - how do they divide?

A

Procencephalon - telencephalon, diencephalon
Mesencephalon - mesencephalon
Rhomboencephalon - metencephalon, mylencephalon

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19
Q

Why is the axis of the brain different to the axis of the brainstem?

A

As the tube grows it runs out of space so folds. This creates a cervical flexure and a cephalic flexure

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20
Q

In which regions of the embryonic brain are the ventricles?

A

Telencephalon (lateral)
Diencephalon (third)
Metencephalon (fourth)

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21
Q

What is the derviative of the metencephalon?

A

Pons and cerebellum

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22
Q

What are the types of spina bifida?

A

Occulta
Meningocele
Mylomeningocele

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23
Q

How is the neural tube organised?

A

Dorsal alar plate (sensory)

Ventral basal plate (motor)

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24
Q

How are the alar and basal plates of the neural tube regualted?

A

Signalling from (dorsal) roof and (ventral) floor plates

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25
Q

What do neural crest cells contribute to?

A 
Adrenal glands
Sympathetic ganglion
Enteric ganglion
Schwann cells
Melanocytes
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26
Q

What disrupts neural crest cell migration?

A

Alcohol

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27
Q

What are the functions of astrocytes?

A 
Formationof bbb by foot processes (glia limitans) 
Structural support
Nutrition (glucose lactate shuttle)
Removal of neurotransmitters
Maintain ionic environment
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28
Q

What is the glucose lactate shuttle?

A

Neurones cant store glycogen so astrocytes break theirs down to lactate, transport it to neurones where it is used to create pyruvate.

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29
Q

What would happen if K+ rose around the brains neurones? What stops this?

A

Decreased k gradient so decreased efflux so cell moves closer to membrane potential so increased excitability of neurones
Astrocytes

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30
Q

When does mylination of cns begin? When does it end?

A

4 months gestation until 1 - though not complete until maturity

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31
Q

How can the brain respond to damage?

A

Plasticity (forming new pathways)

Oligodendrocyte precursors to replace myelin lost in disease

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32
Q

How is the bbb formed around penetrating capillaries?

A

Foot processes of astrocytes inducing tight junctions between endothelial cells using occludins

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33
Q

Where is the bbb missing?

A

Choroid plexuses
Vomiting centre
Pituitary
Pineal gland

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34
Q

What does the bbb stop?
What does the bbb slow?
What does the bbb allow?

A

Stops proteins
Slows creatine, urea, ions
Allows glucose, lipid soluble substances

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35
Q

Why is it that csf glucose can be controlled?

A

They are actively transported

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36
Q

Why is the cns immunprivilaged?

A

Enclosed therefore inflammation would increase icp

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37
Q

What is the major excitatory and inhibitory neurotransmitters of the brain and spine?

A

Brain - ex = glutamate, in = gaba

Spine - ex = glutamate, in = glycine

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38
Q

What sorts of glutamate receptors are there?

A

Metabotrophic - Gaq or Gai

Ionotrophic - Kainate, AMPA and NMDA

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39
Q

What is required for NMDA receptor activation?

A

Binding of glutamate

Degree of depolarisation to move Mg ion

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40
Q

What process is involved in the long term potentiation of glutamate receptors?

A 
Activation of AMPA
Depolarisation
Activation of NMDA
Calcium influx
Upregulation of AMPA
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41
Q

What is the mechanism for glutamate excitotoxicity?

A

Ischemia - decreased atp therefore decreased na/k ATPase therefore decreased ecf sodium ions, therefore decreased or reversed na glutamate synporting increasing extracellular glutamate

Trauma or injury resulting in glutamate release

Increased glutamate causes increased intercellular calcium and cell death

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42
Q

What are the different sorts of gaba receptors?

A 
GABAa = ionotrophic cl- channels
GABAb = metabotrophic GPCRs decreasing GABA and glutamate release
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43
Q

What is the term for one sided weakness?

A

Hemiparesis

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44
Q

What is the term for one sided paralysis?

A

Hemiplegia

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45
Q

What is ataxia?

A

Uncoordianted movement

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46
Q

What is dysarthria?

A

Slurred speech due to lack of coordination of vocal muscles

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47
Q

What is dysphasia?

A

Difficulty in using language

  • expressive
  • receptive
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48
Q

What is agnosia?

A

No object perception

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49
Q

What is apraxia?

A

Unable to execute purposeful movement that is already learnt in spite of good power, sensation and coordination

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50
Q

Where is ACh released from in the brain? What are its effects?

A

Nucleus basalis and brainstem

Generally excitatory

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51
Q

What are the dopaminergic pathways in the cns? What do they do?

A 
Negrostriatal (control of movement)
Mesocortical (arousal and mood)
Mesolimbic (emotion)
Tuberohypophesal (inhibition of prolactin secretion) 
D1 = GalphaS 
D2 = GalphaI
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52
Q

What are the na pathways of the cns? What do they do?

A

Pons and medulla right through the cns

Effects arousal and mood

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53
Q

Where do 5ht neurones originate, what do they do?

A

Raphe nucleus in the brainstem
Widely distributed
Effects mood and wakefulness

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54
Q

What cell type covers choroid plexuses? What makes them special?

A

Ependymal - tight junctions with occludins allowing specific filtering

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55
Q

What is the rate of csf turnover.

A

20ml/hour

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56
Q

Describe the root of csf circulation

A 
Lateral ventricles
Interventricular foramen
Third ventricle
Cerebral aqueduct
Fourth ventricle 
Central canal / medial/lateral apatures
Subarachnoid space
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57
Q

Where is csf reabsorbed? How?

A

arachnoid granulations at the venous sinuses that have arachnoid matter that protrudes through the meningeal dura

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58
Q

What are the functions of csf?

A 
Mechanical protection - shock absorber 
Maintains icp
Reduces weight of brain preventing crushing of own blood vessels
Chemical protection
Circulation of nutrients
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59
Q

What is the pathogen, glucose and cellular composition of csf?

A

Sterile
Glucose 2/3rds of blood
Low numbers of WBC (no polymorphs)
No erythrocytes

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60
Q

What (grossly) can cause hydrocephalus?

A

Overproduction of csf
Blockage of csf flow
Under reabsorption of csf

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61
Q

Differentiate communicating and non communicating hydrocephalus

A

Communicating - free flowing csf but inadequate reabsorption

Non communicating - blockage to csf flow

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62
Q

What is the most common site of csf flow blockage?

A

Cerebral aqueduct

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63
Q

Give 2 examples of communicating hydrocephalus

A

Congenital absence of arachnoid granulations

Blockage of arachnoid granulations due to RBCs in SAH

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64
Q

Give two examples of non communicating hydrocephalus

A 
Tumour compressing cerebral aqueduct 
Spina bifida (aquaductal stenosis, open myleomeningoceal)
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65
Q

What is the main arterial supply to the meningies?

A

Middle meningeal artery as a branch of the maxillary artery

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66
Q

Where does the middle meningeal artery enter the cranium?

What happens then?

A

Foramen spinosum

Branches to anterior and posterior

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67
Q

Where do the meningies drain?

A

Through paired middle meningeal veins through the foramen spinosum into the pterygoid venous plexus

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68
Q

Where do the vertebral arteries pass?

A

Up the transverse foramen of the top 6 cervical vertebra then through the foramen magnum

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69
Q

What are the branches of the vertebral and basilar artery from posterior to anterior?

A 
Posterior inferior cerebellar arteries
Anterior inferior cerebellar arteries
Pontine arteries
Superior cerebellar arteries
Posterior cerebral arteries
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70
Q

What are the branches of the internal carotid artery?

A

The anterior cerebral, middle cerebral and the posterior communicating

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71
Q

Where does the posterior cerebral artery span?

A

Ica to posterior cerebral

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72
Q

Where does the anterior cerebral artery supply?

A

Medial and anterior surface of the hemisphere

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73
Q

Where does the middle cerebral artery supply?

A

The lateral surface of the hemispheres

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74
Q

Where does the posterior cerebral artery supply?

A

Inferior hemisphere and occipital lobe

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75
Q

How does blood drain from the brain?

A

Small veins pass through arachnoid and meningeal dura into dural venous sinus
Emissary veins into extracranial veins
Through the dural venous sinuses into then ijv

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76
Q

What is the order of drainage through the sagittal dural venous sinuses?

A

Superior sagittal sinus joins straight sinus (from inferior sagittal sinus and great cerebral vein) at the confluence of sinuses

Confluence of sinuses splits bilaterally into the transverse sinuses into the sigmoid sinus then the ijv

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77
Q

What is the drainage into and out of the cavernous sinus?

A

Superior opthalmic veins and spenoparietal sinus drain in anteriorly

Drains out posteriorly via the superior and inferior petrosal sinus into the transverse and sigmoid sinus respectively

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78
Q

How can blood move through the emissary veins?

A

In both directions - though usually out away from the brain

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79
Q

What is sensation?

A

A conscious or unconscious awareness of an internal or external stimuli

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80
Q

What are the neurones of general sensation?

A

1st order - contain or link to sensory receptor
2nd order - link 1st to thalamus
3rd order - link thalamus to cerebral cortex

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81
Q

Where do third order sensory neurones travel?

A

Through the internal capsule

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82
Q

What is the advantage of having multiple neurones in the sensory pathways?

A

Allow for divergence, convergence and modification from external neurones

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83
Q

What are the three general types of sensory receptors? Give an example of what each detects

A

Free nerve endings - e.g. Cold
Encapsulated nerve endings - e.g. Pressure
Synapse with specialised cell - e.g. Vision

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84
Q

Are sensory receptors totally specific for one stimuli type?

A

No - large input from another modality can cause stimulation e.g. Seeing stars when hit in the eye

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85
Q

What is the term for different types of one sensation (e.g. Sweet and sour taste)?

A

Qualities

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86
Q

What sensory receptors are present in muscles? What do they do?

A

Spindle fibres - detect change in muscle length

Golgi tendon organs - detect change in muscle tension

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87
Q

What do we need to know about a sensory stimuli?

A

What type
Where
How long
How strong

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88
Q

How can we determine stimuli strength?

A

Rate of firing of action potentials (frequency coding)

Activation of neighbouring cells

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89
Q

How can neurones encode a time frame for a stimuli?

A

Phasic response - rapidly adapting, only fire for a short time when stimuli changes - i.e. an on and off signal

Tonic response - slowly adapting, fires for the entire time the stimulus is active

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90
Q

What methods does the ns use to localise a sensory stimuli?

A

Lateral inhibition
Two point discrimination
Convergence and divergence

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91
Q

What is the process of lateral inhibition?

A

Each first order neurone sends inhibitory interneurones to neighbouring second order neurones localising a stimulus.

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92
Q

What is two point discrimination?

What does it depend on?

A

The distance at which you can distinguish two stimuli as distinct

Depends on receptive field of the neurones and the degree of convergence of 1st orders on 2nd orders and 2nd orders on 3rd orders.

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93
Q

What does neurone divergence cause in sensory pathways?

A

Amplification of signal

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94
Q

Where in the cns do we convert afferent sensory impulses into the feeling of sensation?

A

Thalamus - crude localisation and modality

Post central gyrus (somatosensory cortex) - sharp localisation

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95
Q

After reaching the somatosensory cortex where are sensory inputs relayed too?

A 
Cortical association areas (combining multiple modalities into a general picture)
Subcortical areas (movement alteration)
Limbic system (emotion)
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96
Q

How does then limbic system associate with sensation?

A

Pain is unpleasant and upsetting

Same touch can be nice from a partner but nasty from a stranger

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97
Q

What are the ascending tracts of the spinal cord?

What modalities do they convey?

A

Posterior column medial leminiscal - fine touch (light touch, vibration, hair movement), conscious proprioception

Anteriolateral system - pain, crude touch, temperature

Spinocerebellar - unconscious proprioception

Cuneocerebellar - unconscious proprioception from upper c-spine

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98
Q

Where does the posterior column medial leminiscus tract run?

A

First order enters spinal cord, passes into gracile or cuneate nucleus, ascends to medulla and synapses in cuneate or gracile nucleus.

Second order decussate and ascend the medial leminiscus pathway to the ventral posterior lateral nucleus of the thalamus

Third order ascend through the internal capsule to the somatosensory cortex

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99
Q

What is the route of the anteriolateral system?

A

1st order enter spinal cord and ascend or descend up to 3 segments in the dorsolateral tract of lissauer. They then synapse in lamina I, II, or V

2nd order neurones decussate immediately crossing in the anterior grey commiseur before ascending in the anteriolateral system to the ventral posteriolateral nucleus of the thalamus

3rd order neurones pass through the internal capsule to the somatosensory cortex

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100
Q

What is the route of the spinocerebellar tract?

A

First order enter the spine. These are the same neurones as the dorsal column medial leminiscal. They branch giving two synapses in the dorsal horn.

Second order neurones ascend in two different ways. The anterior set decussate ascending contralaterally before decussating again syanpsing at the ipsolateral cerebellum. The posterior set ascend ipsolaterally and do not decussate at all

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101
Q

Where do lower motor neurones have their cell bodies?

A

Lamina IX of the ventral horn

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102
Q

What is a motor unit?

A

A combination of a lower motor neurone and the muscle fibres it supplys

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103
Q

What are the classifications of nerve fibres based on speed of conduction? What is an example of each?

A 
A alpha - LMN, proprioception 
A beta - touch
A delta - sharp pain, temperature 
B - preganglionic autonomic 
C - dull pain
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104
Q

How can lmn be activated?

A

Input from higher centres

Reflex

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105
Q

What is a reflex?

A

An involuntary, unlearned, automatic repeatable response to a specific stimuli that does not require the brain

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106
Q

What must a reflex involve?

A 
A receptor
Afferent neurone
Integration centre
Efferent neurone
Effector
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107
Q

Describe the process of a stretch reflex

A

Tendon hammer stretches tendon
Spindle fibre stretched
Afferent impulse to spinal cord
Afferent impulse up spinocerbellar and DCML (proprioception to brain)
Synapse in cord lamina IX with LMN - excitatory to muscle to contract and inhibits antagonistic muscle causing relaxation

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108
Q

What muscles maintain tone during sleep?

A

Respiratory
Extraoccular
Urinary and anal sphincters

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109
Q

What are typical signs of LMN lesion? How are they distributed?

A 
Weakness
Muscle wasting 
Loss of tone
Decreased or absent weakness
Initial fasiculations

Tend to be localised to a specific peripheral nerve

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110
Q

What two broad groups can UMNs be classified into?

A

Pyramidal tracts from cortex to effector (CN and spine)

Extrapyramidal tracts from brainstem to effector

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111
Q

What are the pyramidal tracts motor tracts? What do they supply?

A

Corticospial - cortex to spinal lmns

Corticobulbar - cortex to CN lmns

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112
Q

Where do the corticospinal and corticobulbar tracts origionate

A

30% in the precentral gyrus (motor cortex)
30% in the premotor cortex and supplementary motor area
40% in the somatosensory cortex

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113
Q

After origination where do the UMNs of the corticospinal tract travel?

A

Internal capsule
Brainstem
Decussation of pyramids in medulla
85% decussate into the contralateral lateral corticospinal tract
15% remain ipsolateral in the anterior corticospinal tract
All synapse in lamina IX (most via an interneurone)

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114
Q

How many of the fibres of the corticospinal tract decussate? Which part of it do they entre?

A

85%

The lateral section

115
Q

Where do the fibres of the corticobulbar UMN travel?

A

Through the internal capsule, most decussating and not decussating giving bilateral innervation synapsing with the CN nuclei. The exception to this is the UMN to the facial nerve supplying the muscles of facial expression

116
Q

What is the function of the motor cortex and premotor cortex with supplimentary motor area?

A

Motor cortex - coordinates action

PMC and SMA - formulating a plan and organising supplementary muscle activation

117
Q

What is the process of altering the state of the other muscles around the body prior to a movement called? What coordinates this?

A

Body set

PMC and SMA

118
Q

What are the extrapyramidal motor pathways?

A

Tectospinal
Rubrospinal
Reticulospinal
Vestibulospinal

119
Q

Which extrapyramidal pathways decussate? What do they do?

A

Tectospinal - decussates, controls head and eye movement to visual and audible stimuli. Stops in upper thoracic spine.

Rubrospinal - decussates, controls upper limb flexor tone. Stops in upper thoracic spine

120
Q

Which extrapyramidal tracts do not decussate? What do they do?

A

Reticulospinal - posture and rhythmic movements by facilitation and inhibition of LMNs

Vestibulospinal - balance and antigravity msulces

121
Q

What are signs of upper motor neurone lesions? Where are they found?

A 
Hypertonia
Hyperreflexia
Clonus
Babinskis sign
Movement weakness
Clasp knife reflex

Tend to be widespread

122
Q

What are the three regions of the cerebellum? What do they do?

A

Vestibulocerebellum - coordination of balance via vestibulospinal and reticulospinal tracts. Occular reflex allowing eyes to tract object as head turns
Spinocerebellum - receives proprioceptive info and a copy of the motor plan in order to predict errors in movement and correct them before they occur
Cerebrocerebellum - hand eye coordination, motor learning and memory, predicts sensory consequence of actions

123
Q

Signs of cerebellar dysfunction?

A 
Dysdidochokinesia
Ataxia 
Nystagmus
Intenetion tremor
Speech problems
Hypotonia
Past pointing
124
Q

What are the functions of the basal ganglia?

A

Decision to move
Direction of movement
Amplitude of movement
Motor expression of emotion

125
Q

What makes up the basal ganglia?

A 
The caudate nucleus
The putamen
The globus pallidus
The substantia nigra
The subthalmic nucleus
126
Q

What comprises the striatum?

A

The caudate nucleus

The putamen

127
Q

What comprises the lenticular nucleus?

A

The putamen and globus pallidus

128
Q

What are the pathways of the basal ganglia? What do they achieve?

A

Direct pathway - increase movement

Indirect pathway - decreased movement

129
Q

When the cortex wants to move what is the effect on the direct pathway of the basal ganglia?

A

Stimulation of the striatum
Inhibits the GPi/SNr
Reduced inhibition of the thalamus
Increased positive feedback to the cerebral cortex affirming the movement

130
Q

When the cortex signals for movement what is the effect on the indirect pathway?

A

Increased stimulation of the striatum
Increased inhibition of the GPe
Decreased inhibition of the subthalmic nucleus
Increased inhibition of the thalamus
Decreased positive feedback to the cerebral cortex dampening movement

131
Q

What does the nigostriatal pathway do to the direct and indirect pathways? Which receptors are involved?

A

Direct, D1 receptor - increased stimulation - increases excitation of thalamus
Indirect D2 receptor - decreased stimulation - decreases inhibition of thalamus

132
Q

What are the effects of parkinsons disease?

A

Resting tremor
Increased tone
Bradykinesia
Mask facies

133
Q

What is the effect of huntingdons disease?

A

Damage to the striatum removing inhibition on the GPe causing decreased inhbition of the thalamus

134
Q

What is pain?

A

An unpleasant sensation and emotional experience associated with actual or potential tissue damage

135
Q

What are the two parts to pain?

A

Nociception (detection of stimuli from actual or potential damage causing ascending unconscious neural traffic)

Conscious perception of pain - the sensation

136
Q

What varies in people who deal with pain differently, what doesn’t?

A

Tollerance varies

Threshold does not!

137
Q

What alters pain tolerance?

A

Environment (e.g. Better tolerance with adrenaline post accident)
Emotion (worse tolerance if upset, depressed)
Age (better tolerance in elderly)
Distracting injury

138
Q

Where do pain fibres ascend?

A

Ascend in the lateral part of the anteriolateral system to the ventral posteriolateral nucleus of the thalamus

139
Q

What are the contents of the anteriolateral system?

A 
Spinothalmic - perception of pain
Spinoreticular - arousal to pain
Spinotectal - looking at source
Spinohypothalmic - autonomic response
Spinomesencephalic - descending inhibition and emotion
140
Q

What are the four stages of pain?

A

Transduction - the activation of the receptor
Transmission - relay
Modulation
Perception

141
Q

What is pain transduction?

A

Release of k, serotonin, bradykinin, h, prostaglandins from damaged tissue activating nociceptors

142
Q

What fibres convey pain? What activates them?

A

A delta - mechanical

C - mechanical, thermal, chemical

143
Q

What sort of pain do different nerve fibres produce?

A

A delta - sharp stabbing localised pain

C - dull throbbing poorly localised pain

144
Q

Which lamina do primary pain fibres terminate?

A

I, II, V

145
Q

Where does the anteriolateral system arise (lamina)

A

Lamina I and V

146
Q

How can pain be modulated physiologically?

A

The gate control theory

Descending inhibition

147
Q

What is the gate control theory of pain?

A

Stimulation of A beta fibres by rubbing causes stimulation of interneurones in lamina II which cause inhibition of lamina I and V

148
Q

What effects do A delta and C fibres have on lamina II?

A

Inhibition of interneurones that inhibit lamina I and V thus decreasing own inhibition

149
Q

What substances do A dela and C fibres relase in the 1 st and second lamina? What about the inhibitory synapses?

A

Substance P and glutamate

Glycine

150
Q

What is the decending inhibition of pain?

A

Direct - spinothalmic tract to periaquiducal grey matter to raphae nucleus
Indirect - spinomesencephalic to raphae nucleus

Raphae nucleus releases 5HT, enkephalins and noradrenaline into lamina I and V inhibiting the spinothalmic tract

151
Q

Where is pain percieved?

A

Third order neurones to primary sensory areas but also limbic system and hypothalamus for emotional and stress response

152
Q

Differentiate hyperalgesia from allodynia

A

Hyperalgesia - increased pain at normal threshold stimulus due to peripheral and central sensitisation
Allodynia - pain from stimuli that are not normally painful or pain in an area not stimulated

153
Q

What is peripheral sensitisation?

A

Painful stimuli (5HT, K, PGE etc) trigger c fibre. C fibre releases substance P that activates mast cells releasing histamine and other chemicals. These cause vasodilation and also reactivate the original fibre in a vicious cycle.

154
Q

What is central sensitisation?

A

Glutamate released at first order synaptic bulbs activate AMPA receptors, depolarising second order neurones. Depolarisation allows for opening of NMDA receptors allowing calcium influx. Calcium influx up regulates expression of AMPA. This occurs with long term stimulation.

155
Q

What is the general cut off for a pain to be chronic? What is the usual aetiology of chronic pain?

A

3 months

Often not known

156
Q

What is the mechanism behind neuropathic pain?

A

Of neuronal origin, no nociception

Occurs due to increased excitability post injury (ectopic) and activation of neighbouring fibres (ephapatic)

157
Q

What is phantom limb sensation caused by?

A

Not fully understood but may be cortical remodelling

158
Q

What is complex regional pain syndrome? What are the two types?

A 
No history of trauma - type 1
History of trauma (often minor) - type 2
1) initiation of pain 
2) sympathetic and inflammatory response
3) increase pain
4) sympathetic and inflammatory response 
And so on

Causes pain, oedema, vasomotor disturbance, movement limitation, muscle waisting, skin thickening

159
Q

What can cause pain in cancer?

A

The disease

The treatment!

160
Q

Differentiate opiate and opioid

A

Opiate from a poppy

161
Q

How does the inner ear form?

A

Otic placode on ectoderm

Sinks and pinches off forming ottic vesicle

162
Q

What forms the middle ear and eustachian tube?

A

Expansion of the 1st pharangeal pouch

163
Q

What forms the ossicles of the ear?

A

Merckels and reicherts cartilage

164
Q

What forms the external aucoustic meatus?

A

1st pharangeal cleft

165
Q

What forms the auricle?

A

Proliferation of the first and second arches

166
Q

Where does the ear form?

A

The embryonic neck

167
Q

Which part of the ear is most susceptible to teratogenesis?

A

Inner ear from the otic vesicle

168
Q

What is the first stage of eye formation?

A

Formation of the optic placode and outpouching of the proencephalon towards it

169
Q

How does the lens of the eye form?

A

Invagination of placode forming vesical

170
Q

How is the embyonic lens of the eye supplies with blood?

A

The hyaloid artery that runs up the optic stalk (from the proencephalon)

171
Q

How does the hyaloid artery fit in the optic stalk? What does persistance of this feature cause?

A

The stalk contains a fissure, the choroid fissure. Persistence causes a coloboma

172
Q

How does the central artery of the retina form?

A

Degeneration of distal hyaloid artery (proximal remnants becoming the central artery)

173
Q

How does the proencephalon outpouching go on to form the optic nerve and retina

A

Stalk becomes optic nerve
End envelopes the lens forming a double layered cup
Outer layer becomes the pigment layer and inner layer becomes the sensory layer of the retina

174
Q

How does the retina detach in pathology?

A

Opening of the intraretinal space between the pigment layer and the neural layer of the retina

175
Q

How does the iris of the eye form?

A

Lining of the optic cup buckles forming the ciliary body and iris.

176
Q

Hw doe the extraoccular muscles form?

A

From preotic myotomes

177
Q

Where do the eyes develop?

A

Side of the embryonic head

178
Q

What is the structure of the retina from back to front?

A

Pigment cells - absorb scattering light
Photoreceptive cells - rods and cones
Bipolar neurones
Ganglion cells

179
Q

What is special about the fova?

A

Concentrated cone cells

Overlying neurones displaced

180
Q

Difference between rods and cones inc. neural wireing

A

Rods - high sensitivity, many rods into one bipolar neurone, low acuity
Cones - low sensitivity, high acuity, one rod to one bipolar neurone , colour

181
Q

Where is the fova?

A

Lateral to the optic disk

182
Q

Which regions of the retina (and vision) form the left optic tract?

A

Left temporal retina (left nasal vision) and right nasal retina (right temporal vision)

183
Q

Where do fibres of the optic tract go?

A

90% to lgn

10 % superior colliculus - edinger westphal - CNIII

184
Q

What are the optic radiations?

A

inferior half of each retina - meyers loop

superior half of each retina - baums loop

185
Q

Which optic radiation is direct?

A

Baums loop - superior retina (inferior visual field)

186
Q

Where do fibres of the lgn go?

A

Primary visual cortex

187
Q

In the primary visual cortex what patterns are maintained from the retina?

A

Spacial

Magnocellular vs parvocellular

188
Q

How do fibres leave the primary visual cortex?

A

Ventral stream - to temporal - object recognition

Dorsal stream - to parietal - object location and motion

189
Q

What are the four types of strabismus?

A

Esotropia - defective eye looks in
Exotropia - defective eye looks out
Hypertropia - defective eye looks up
Hypotropia - defective eye looks down

190
Q

Why dont kids with strabismus have double vision?

A

Plasticity in nerves allows supression of vision

191
Q

Why do occipital lesions spare the macular?

A

Dual blood supply to the regions that detect macular vision

192
Q

Pupil reflex pathway

A

Light - retina - optic nerve - optic tract - pretectal nuculus - superior colliculus - edinger westphal nucleus - cniii, cillary ganglion, constrictor pupillae

193
Q

Why is the pupil reflex pathway bilateral?

A

Optic tract contains fibres from both retina

Neurones from superior colliculus innervate both edinger westphal nuclei

194
Q

What two parameters of sound are detectable?

A

Frequency and volume

195
Q

What is the decibel scale?

A

A measure of volume

dB = log10 (P2/P1)

196
Q

How do louder sounds get detected as being louder?

A

More intense vibrations of sensory hairs and activation of neighbouring fibres

197
Q

What are the three chambers of the cochlea?

A

Scala vestibuli
Scala media
Scala tympani

198
Q

Where are the cells that detect sound located in the cochlea?

A

In the scala media

199
Q

What is the membrane that sits above the hair cells in the ear?

A

Tectoral membrane

200
Q

What are the membranes between the cavities of the cochlea?

A 
Scala vestibuli
VESTIBULAR MEMBRANE
Scala media
BASALAR MEMBRANE
Scala tympani
201
Q

What fluid is found in the cavities of the cochlea?

A

Scala vestibuli and scala tympani = perilymph

Scala media = endolymph

202
Q

What windows border the cavities of the cochlea?

A

Scala vestibuli - oval window

Scala tympani - round window

203
Q

What are the distribution of the hair cells in the cochlea? Which is more sensitive? What is the function of the others?

A

1x inner hair cell = most sensitive

3x outer hair cells = vibrate with the sound alternating the tension on the tectoral membrane

204
Q

How is movement of the oval window translated into movement of the hair cells of the cochlea?

A

Pressure wave in perilymph, deformation of vestibular membrane, pressure wave in endolymph, deformation of basilar membrane, hair cells move against tectoral membrane

205
Q

What happens to the hair cells on movement?

A

Bending of steriocillia opens K+ channels, K+ diffuses into the cell due to high conc. in endolymph, cell depolarises, calcium flows. Through vgCa channels, neurotransmitter released

206
Q

What are the ganglia of the cochlear nerve termed?

A

Spiral ganglia

207
Q

How do the ears detect changes in frequency?

A

Activation of hair cells at specific points down scala media

208
Q

Where in the scala media are high frequencies detected

A

Near the oval and round windows?

209
Q

Where in the scala media are the low frequencies detected?

A

Near the heicotrema

210
Q

What is the range of frequencies in normal human hearing?

A

20-20000 Hz

211
Q

What is the nervous propergation of sound from the hair cells to the brain?

A 
Hair cell
Spiral ganglion cell
CNVIII
Cochlear nucleus (medulla) 
Superior olivary complex
Inferior colliculus
Medial geniculate nucleus
Auditory cortex
212
Q

What can cause hearing impairment?

A 
Loud noise
Congenital defect
Infection
Ototoxic compounds
Trauma 
Age
213
Q

What are the three types of hearing impairment?

A

Conductive (blockage, rupture of membrane)
Sensory (hair cell destruction, hair cell death)
Neural (spiral ganglion damage, tinnitus)

214
Q

What test can be used to quantify a degree of hearing loss? How does it work?

A

Audiogram

Sensitivity vs frequency

215
Q

How can the function of the outer hair cells be measured?

A

Otoacoustic emissions

216
Q

Treatments for hearing loss

A

Hearing aids

Cochlear implant

217
Q

What are primary and secondary haemorrhagic strokes?

A

Primary - no structural lesion
Secondary - following a lesion (tumour, aneurysm, malformations, thrombotic disease). These abnormalities may themselves be secondary to diseases such as htn or dm

218
Q

What could be effected by a frontal stroke?

A

Expressive dysphasia - brocca’s area
Motor disturbance - motor cortex and premotor areas
Disinhibition - cortical association areas
Incontinence - micturition inhibition centre

219
Q

What could be caused by a temporal stroke?

A

Receptive aphasia - wernicke’s area
Memory problems - hippocampus
Superior quadrantanopia - meyers loop

220
Q

What could a parietal stroke cause?

A

Inferior quadrantanopia or hemianopia - baums loop
Somatosensory deficits - somatosensory cortex
Nominal aphasia - angular gyrus

221
Q

What could an occipital stroke cause?

A

Visual disturbance

222
Q

What are the different grades of stroke?

A

Total anterior circulation (TACS)
Partial anterior circulation (PACS)
Lacunar (LACS)
Posterior circulation (POCS)

223
Q

What is a lacunar stroke?

A

A stroke effecting a single perforating artery

Usually asymptomatic - if symptomatic single system signs

224
Q

Differentials of stroke

A 
Hypoglycemia 
Seizure
Migrain
Space occupying lesion
Demylination
225
Q

Blood tests in a stroke

A

Bm, fbc, inr, u+e

226
Q

Scanning in a stroke

A

Ct, mri, carotid us, cxr, echo, holter, ecg

227
Q

What is the blood supply to the spine?

A

Single anterior artery, duel posterior arteries

228
Q

What sort of arterial occlusion is most serious in the spine? How does it present?

A

Anterior as no anastamosis

Acute painful with sensory loss and progression to upper motor neurone signs.

229
Q

First signs of raised icp

A 
Behaviour changes
Decreased gcs
Localising signs
Pupil reactions
Cushings triad
230
Q

What is the shape of a epidural haematoma on imaging

A

Lentiform

231
Q

What is the shape of a subdural haemotoma on imaging

A

Follows skull contours

232
Q

What does cat stand for?

A

Computer axial tomography

233
Q

How does bone appear on CT.

A

White

234
Q

What is seen in a T1 MRI?

A

Fatty tissues (cortex)

235
Q

What is seen in a T2 MRI.

A

Watery tissues (oedema, lesions)

236
Q

Indications for ct head?

A

Gcs 1 vomiting post trauma
>65 with LOC or amnesia
Dangerous MOI

237
Q

Complications of a skull fracture

A

Neuronal damage
Blood vessel damage
Infection risk

238
Q

Signs of a SAH on CT

A

Blood in ventricles

239
Q

What are the components of a TACS

A

Hemiparesis / hemianaesthesia
Hemianopia
High cerebral dysfunction (dysphasia, dyspraxia, cortical signs)

240
Q

What are the componenets of a PACS?

A

2 of TACS

241
Q

Which sort of stroke is most likely fatal?

Which sort of stroke has a high reoccurance rate ?

A

TACS

PACS

242
Q

Where does a TACS effect

A

ICA or proximal MCA

243
Q

Where does a PACS effect

A

Distal MCA or branch of MCA

244
Q

Why do we need sleep?

A

Cns resetting
Toxin clearance
Long term memory

245
Q

What are the two types of sleep? Differentiate appearance / dreaming / obs

A

REM - active brain (dreaming), body still (inhibition of motor neurones), difficult to disturb, erection, irregular pulse and rr

NonREM - low brain activity, body mobile (rolling over, sleep walking), decreased bp, spo2, rr,

246
Q

Differentiate rem/nonrem sleep in terms of bmr

A

Increase bmr in rem

Decrease bmr in non rem

247
Q

Differentiate rem / nonrem in terms of eeg

A

Rem - eeg as awake (beta)

Non rem - eeg alpha to theta to delta

248
Q

How does the pattern of sleep change through the night?

A

Start into non rem
Duration and frequency of rem increases during the night
Tend to awake naturally from rem

249
Q

What is the change in neurotransmitters during rem/nonrem sleep?

A

In rem ach increases and 5ht/na decrease

In non-rem all of ach, 5ht and na decrease

250
Q

What are the different eeg wave types in order of decresing frequency?
When are they seen?

A

Beta - awake eyes open
Alpha - awake eyes shut
Theta - children, mediating adults
Delta - deep sleep, coma

251
Q

Where in the brain would closing eyes cause a decrease in eeg wave frequency from beta to alpha with an increase in amplitude?

A

Occiput as its sending ‘im not seeing anything signals

252
Q

Two types of parasomnia

A

Sleep paralysis

Acting out dreams

253
Q

Two types of hypersomnia

A

Narcolepsy

Obstructive sleep apneoa

254
Q

What activates RAS

A

Sensation - auditory, visual, nociception, viceral

255
Q

What inhibits ras?

A

Alcohol,
Sedatives
Sleep centre

256
Q

Where is the reticular formation? Why?

A

In the white matter of the pons where it can sense ascending tracts

257
Q

Functions of the reticular formation?

A

Sleep regulation
Motor control
Motivation and reward
Cvs and rs control and autonomics

258
Q

Functions of reticular activating system?

A 
Raises conciousness (depresses hypothalmic sleep centre)
Filters incoming signals (removing response to background stimulation)
259
Q

What generates eeg loops ?

A

Thalmocoritcal loops - stimulation from thalamus to cortex is reinforced by positive feedback from cortex to thalamus - staying awake!

260
Q

What happens in the different layers of the cortex?

A

1/2/3 - signals too and from other areas of cortex
4 - input from body
5/6 - output too body

261
Q

What are the functional classifications of the areas of the cortex (generally)?

A

Primary sensory / primary motor areas
Secondary sensory / supplementary motor areas
Tertiary areas
Association cortex

262
Q

Which areas of the brain deals with more than one modality of sense?

A

Association areas

263
Q 
What are the functions of the 
Frontal
Parietal 
Temporal
Occipital 
Association areas?
A

Frontal - interlect, personality, mood
Parietal - language, calculation, visiospacial
Temporal - memory, language
Occipital - vision

264
Q

Lesions of the association areas of the parietal cause…

A

Attention deficites

Contralateral neglect

265
Q

Lesions of the association areas of the temporal lobe cause

A

Agnosia

266
Q

In a left handed person which hemisphere is more likely to be dominant?

A

Left!

267
Q

What processes in the brain are effected by lateralisation?

A

Dominant - language, maths, logic, motor skill

Non dominant - visiospacial, music, art, emotion, body awareness

268
Q

What connects the hemispheres?

A

Corpus callosum

Anterior and posterior commissure

269
Q

What is the function of broccas area?

Dysfunction?

A

Formulation of language components

Expressive dysphasia - poorly constructed disjointed speech

270
Q

What does wernicks area do?

Dysfunction?

A

Interpretation of written and spoken word

Receptive dysphasia - lack of comprehension and with fluid but nonsensical speech

271
Q

Define the two categories of memories. What major brain areas are associated with each?

A

Declarative - things you can state - hippocampus

Procedural - motor memories - cerebellum, premotor cortex, basal ganglia

272
Q

What is needed to transfer memories from short to long term memory?

A

Rehersal
Emotion
Association
Automatic (trivia!)

273
Q

Where are memories ‘stored’?

A

Each modality in its appropriate cortical area - then combined by the hippocampus

274
Q

What brain functions are vital in memory formation?

A

Neuronal plasticity

Long term potentiation

275
Q

Why dont we remember everything

A

Long term depression

276
Q

What pathology causes anterograde amnesia?

A

Hippocampal damage

277
Q

What disease may cause reterograde amnesia”

A

Alzheimers

278
Q

What is dementia?

A

Aquired loss of cognitive ability sufficiently severe to interfere with daily function and quality of life
Can be direct (neuronal damage) or indirect (vascular)

279
Q

What is the cut off age for presenile demetia?

A

65

280
Q

Causes of dementia and differentiating factors

A 
Cjd -  young
Picks disease - personality change
Vascular - stepwise progression
Alzheimers - senile onset
Lewis body - parkinsonism
281
Q

What are the effects of sub cortical damage in dementia?

A

Slowness and forgetfulness

282
Q

What are the effects of anterior cortical damage in dementia?

A

Decreased inhibition
Antisocial behaviour
Irresponsibility

283
Q

Effects of posterior cortical damage in dementia?

A

Loss of memory

Disturbed language

284
Q

What structural changes occur in dementia?

What happens to csf pressure?

A

Cortical atrophy with ventriculomegaly

Csf pressure normal (normal pressure hydrocephalus)

285
Q 
What are the types of the following nerve fibres:
Light touch
Proprioception
Pain
Temperature
Muscle fibre motor
Muscle spindle motor
A 
Light touch - A alpha
Proprioception - A alpha
Pain - C
Temperature - A delta
Muscle fibre motor - A alpha 
Muscle spindle motor - A beta

PPE (12 decks)

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