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JMP Y2S1 > Week 37- The Skull and an overview of Brain function > Flashcards

Week 37- The Skull and an overview of Brain function Flashcards

1
Q

What are the brains primary sources of fuel?

A

Glucose and oxygen

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2
Q

How does glucose and oxygen enter the brain?

A

Has to pass the blood brain barrier

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3
Q

What is Glucose and oxygen used for in the brain?

A

To produce ATP –> to support normal brain function

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4
Q

What is the potential pathologies associated with the brain not being able to utilise fuel?

A
  1. Supply reduction
  2. Altered BBB
  3. Decreased ATP production within cells
  4. Reduction in brain functionality
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5
Q

What % body weight is the brain?

A

2%

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6
Q

How much blood flow, glucose and O2 does the brain utilise?

A

15% blood flow output
20% of total O2 consumption
65% of blood glucose

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7
Q

What are the fuel types apart from glucose used by the brain?

A

Glucose is main fuel

  1. Lactate –> supplementary fuel source
  2. Ketone bodies –> minor/supplementary source
  3. Phosphocreatine (Emergency supply under anaerobic conditions)
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8
Q

What are the emergency fuels used by the brain?

A

Phosphocreatine (anaerobic)

Anaerobic metabolism of glucose to lactate for limited ATP

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9
Q

What is ATP required for within the brain?

A

Maintaining resting potential ion gradients:

Na+/K ATPase –> using ATP to pump Na+ and K+ against their concentration gradients

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10
Q

How is glucose transported across the BB and into neurons?

A

Facilitated diffusion

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11
Q

What transporters are used in the brain for glucose transport and what are the differences between them?

A
  1. GLUT1 –> present on BBB endothelial cells and astrocytes

2. GLUT3 –> present on neurons –> 5x the transport capacity than GLUT1

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12
Q

What happens in GLUT1 deficiency syndrome?

A

Defective glucose transport across BBB

  • -> low glucose in CSF when glycaemia levels are “normal”
  • -> leads to infantile seizures and developmental delay
  • -> chronic epilepsy
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13
Q

How can the affinity and capacity of glucose transport in the brain be described?

A

High affinity

High capacity

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14
Q

How is lactate transported across the BBB?

A

Across BBB epithelium down its concentration gradient via MCT1 facilitated diffusion

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15
Q

Where does the brain get its blood supply?

A

Four arteries:
Internal carotid arteries (80% of flow)
Vertebral arteries (20%)

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16
Q

Where do the four brain supplying arteries meet before the brain?

A

Circle of Willis –> base of the brain

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17
Q

How far are brain neurons from blood supply?

A

Within 20um of a capillary

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18
Q

What is the blood-brain barriers role?

A

is a dynamic and highly selective permeable interface between central nervous system (CNS) and periphery that regulates the brain homeostasis.

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19
Q

What exactly is the blood-brain barrier?

A

It is capillaries with many tight junctions that seal the endothelial cells along with a thick basement membrane around the capillaries.

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20
Q

What is the roles of the pericyte?

A
  1. Regulates endothelium tight junctions
  2. Secrete basement membrane (basal lamina)
  3. Contractile properties of the pericyte give it the ability to regulate capillary blood flow
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21
Q

What part of the astrocytes interacts with the capillaries of the blood-brain barrier?

A

The processes

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22
Q

What do astrocytes do in relation to the BBB?

A

Press processes up against the capillaries
Secrete chemicals to maintain the endothelial cell tight junctions
Therefore –> reinforces the highly-selective permeability nature of the endothelium

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23
Q

What does the BBB control the exchange of?

A

Ions
Molecules
Cells

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24
Q

Why does the BBB control the entrance of things coming into the brain?

A
  1. Insulate the brain from toxins and invading pathogens

2. Maintaining its status as a immune-privileged organ

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25
Q

What types of transport is allowed by the BBB?

A

Paracellular transport

Transcellular transport

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26
Q

What is paracellular transport and what regulates it within the brain?

A
  1. refers to the transfer of substances across anepithelium by passing through the intercellular spaceBETWEEN the cells.
  2. Within the brain this process is regulated by endothelium tight junctions
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27
Q

What is transcellular transport and what regulates it within the brain?

A
  1. where the substances travelTHROUGH the cell, passing through both theapical membrane andbasolateral membrane
  2. Within the brain this process is regulated by endothelium cell membrane transporters, pumps and receptors
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28
Q

What are some examples of channel mediated substance transport in the brain?

A

H2O, Na+, K+, Cl-

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29
Q

What are some examples of membrane transport in the brain?

A 
Small lipophilic molecules
Anaesthetics 
Ethanol 
Nicotine
Caffeine
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30
Q

What are some examples of carrier-mediated transport in the brain?

A

Energy transport systems:
1. Glucose –> Glut 1

  1. Lactate, monocarboxylates, pyruvate (MCT1)
  2. Creatine (CrT)
    Amino acid transport systems:
  3. Large neutral AAs –> (LAT1)
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31
Q

What are some receptor mediated transporter examples for the brain?

A 
Insulin
Transferrin
Leptin
IgG
TNF alpha
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32
Q

What are some examples of adsorption-mediated transcytosis systems in the brain?

A

Histone

Albumin

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33
Q

What are some active efflux transporters in the brain?

A

P-glycoprotein
BRCP
MRP 1,2,4,5

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34
Q

What happens during Anaerobic glycolysis?

A

Pyruvate and NADH build up
Drives lactate production
Too much lactate –> lactic acidosis
Low yield ATP production compared to aerobic

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35
Q

What is the mechanism of Creatine production and utilisation in the brain?

A
  1. Creatine synthesised –> two steps with AGAT and GMAT enzymes
  2. Taken up into cells via SLC6A8 transporter
  3. Allows ATP regeneration and high energy phosphate shuttling though the Cr/PCr/CK system
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36
Q

What is the main use of Creatine in the brain?

A

Alternative fuel –> used for ATP regeneration and high energy phosphate shuttling

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37
Q

When is Ketone bodies used as a fuel source in the brain?

A
  1. During hypoglycaemia

2. During situations of intense neural activity

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38
Q

Where is lactate generated for use in the brain?

A
  1. Astrocytes –> during glycogen breakdown (glycogenolysis)
  2. Muscles –> from muscle pyruvate during anaerobic glycolysis (cori cycle) –> lactate enters the blood –> uptaken in the brain
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39
Q

How long can lactate extend neuronal function during hypoglycaemia?

A

More than 20mins

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40
Q

What is the mechanism suspected for the astrocyte to neuron lactate shuttle hypothesis?

A
  1. Glucose into astrocytes via GLUT1
  2. Glucose converted to glucose-6-phosphate (Glc-6-P)
  3. Glucose-6-phosphate –> glycogen via glycogen synthase (GlyS)
  4. During greater energy demand glycogenolysis reforms Glc-6-P
  5. Synaptic transmission induces glycolysis and lactate production through glutamate uptake
  6. Astrocyte lactate is transported into the extracellular space by MCT1
  7. From extracellular space into neurons by MCT2
  8. Neurons convert lactate to pyruvate for oxidative phosphorylation
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41
Q

Does the brain store glucose?

A

No –> it requires continuous supply of glucose and O2 to generate ATP via aerobic glycolysis

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42
Q

What are the effects of altered blood supply in the brain?

A
  1. Sodium potassium (Na+/K+) exchanger maintains resting membrane potentials
  2. Runs on ATP –> no ATP production pump no longer active
  3. Sodium will begin to accumulate in the cells cause them to depolarise
  4. Depolarisation leads to action potentials
  5. Action potentials lead to neurotransmitter release:
    - Impaired cognition
    - Euphoria
    - Convulsions
    - Unconsciousness
    - Continued inappropriate excitation –> seizures
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43
Q

What is an Excitatory Amino Acid (EAA) injury?

A

Neuronal death and injury caused by overstimulation of excitatory amino acid receptors by glutamate –> also termed excitotoxicity

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44
Q

What is the mechanism behind EAA injury?

A
  1. Brain trauma –> ischaemia
  2. Ischaemic cascade
  3. Release of glutamate into extracellular space
  4. Glutamate binds to NMDA receptors
  5. Increase in intracellular calcium
  6. Intracellular enzymes released
  7. Cause neuronal injury and death
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45
Q

What are some effects of excessive glutamate?

A
  1. Altered cell permeability
  2. Release of toxic chemicals
  3. Increase in nerve damage from electrolyte imbalance (cation influx)
  4. Axon swells and bursts
  5. Protease activated –> further damage to neurons
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46
Q

What is vasogenic oedema caused by?

A

Increased permeability of the capillary epithelium

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47
Q

What is cytotoxic oedema caused by?

A

Increase permeability of the parenchyma

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48
Q

What is interstitial oedema caused by?

A

Increased permeability of the ependymal cells

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49
Q

What is Oncosis?

A

A process of cellular death characterised by cellular swelling caused by a failure in ion pump function

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50
Q

Define cerebral ischemia?

A

Condition where there is insufficient blood flow to the brain to meet metabolic demands

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51
Q

What is the difference between Hypoxia and Anoxia?

A

Hypoxia is an oxygen deficiency reaching tissues

Anoxia is an absence of oxygen reaching tissues (severe hypoxia)

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52
Q

What is the difference between hypoxic/anoxic ischaemia and anaemic ischaemia?

A 
Hypoxic = lack of oxygen reaching tissues 
Anaemic = lack of oxygen carrying capacity inducing hypoxic conditions at tissues
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53
Q

What is brain reperfusion?

A

Blood/oxygen is returned to the brain

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54
Q

What is a reperfusion injury mechanism?

A

Inflammatory response may occur

Phagocytic cells engulf damaged cells

BBB damaged by toxic chemicals

Cerebral oedema due to leakage of large molecules like proteins from blood vessels through BBB

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55
Q

What is a synapse?

A

Junction between two nerve cells consisting of a small gap in which impulses pass across via diffusion of neurotransmitters

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56
Q

What is pre-synaptic?

A

Relating to a nerve cell that releases a transmitter substance during transmission of an impulse

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57
Q

What is post-synaptic?

A

A neuron or cell body or dendrite of which the electrical impulse is transmitted across the synapse to from the presynaptic neuron

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58
Q

What is an example of an excitatory neurotransmitter?

A

Glutamate –> leads to opening of Na channels in the post synaptic neuron
–> Na in the post synaptic cell causes an action potential to continue the impulse transmission

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59
Q

What is an example of an inhibitory neurotransmitter?

A

GABA –> leads to flooding of the post synaptic end with negatively charged Cl- –> action potential is not generated to fire the post synaptic neuron

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60
Q

What is the other name for a neurons cell body?

A

Soma

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61
Q

What is the processes off cell bodies called?

A

Dendrites

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62
Q

What do neurons communicate with other neurons via?

A

Via the synapse using neurotransmitters

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63
Q

What is a synapse?

A

Chemical junction between neurons

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64
Q

What are the three types of synapses?

A

Axo-dendritic –> synapse joins to the dendrite of another neuron

Axo-somatic –> Synapse joins to the soma (cell body) of another neuron

Axo-axonic –> synapse joins to the axon of another neuron

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65
Q

What are the three major chemical groups that neurotransmitters are made from?

A

Amino acids –> GABA, glutamate, Glycine

Amines –> acetylcholine (ACh), Dopamine, Histamine, Serotonin, adrenalin, noradrenaline

Peptides –> cholecystokinin (CCK), Neuropeptide Y, substance P, Somatostatin

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66
Q

Where are small neurotransmitters synthesised?

A

Synaptic terminal

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67
Q

Where are neuropeptides synthesised?

A

Soma –> transported to the synaptic terminal

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68
Q

What is the mechanisms of neurotransmitter release?

A
  1. Action potential arrival –> initiates Ca2+ entry into the cell
  2. Ca+ entry –> stimulates exocytosis of neurotransmitter vesicles into the synaptic cleft
  3. Vesicle membranes recovered by endocytosis
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69
Q

What does excitatory neurotransmitters do to the post synaptic membrane?

A

Transient depolarisation

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70
Q

What does inhibitory neurotransmitters do to the post synaptic membrane?

A

Transient hyperpolarisation

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71
Q

What happens to the neurotransmitters after they have their action?

A
  1. Enzymatic degradation within the synapse
  2. Presynaptic uptake followed by degradation or recycling
  3. Uptake by glia
  4. Uptake by the post synaptic neuron and desensitisation
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72
Q

What glial cells are present in the synapse and what is their role?

A

Astrocytes –> neurotransmitter metabolism

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73
Q

How do astrocytes interact with neuroactive substances in the synapse?

A

They have receptors and uptake systems to quickly terminate the post synaptic effect

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74
Q

What is the action of astrocytes on glutamate for example?

A
  1. Glutamate is released to cause post synaptic effect
  2. Glutamate is taken up by astrocytes to terminate post synaptic effect
  3. Glutamate is inactivated by glutamine synthase with addition of ammonia to form glutamine
  4. Glutamine is released from the astrocytes and taken up by neurons
  5. Neurons reconvert glutamine to glutamate to future use
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75
Q

Can astrocytes themselves release neurotransmitters?

A

Yes

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76
Q

What is the effects of astrocytes secreting glutamate or d-serine?

A

Astrocytes secrete glutamate or d-serine in response to neural activity:
1. Binds to neuronal N-methyl-d-aspartate (NMDA) receptors

  1. Modulates long term synaptic activity:
    - long-term potentiation OR
    - long term depression
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77
Q

What are some other neurotransmitters released by astrocytes and what are their effects?

A
  1. GABA –> causes tonic inhibition of synapses in the surrounding area
  2. ATP –> metabolised into the neurotransmitter adenosine
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78
Q

How does Astrocytes modulate the environment of the synapse?

A
  1. Buffers ionic composition
  2. and pH of the extracellular fluid
  3. Propagate calcium waves –> to regulate secretory activity
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79
Q

How does Astrocytes modulate K+ levels in the extracellular fluid?

A
  1. K+ release during AP firing
  2. Astrocytes clear K+ with their plasma membrane ion channels
  3. Astrocytes are interconnected by gap junctions allowing them to shunt K+ ions to perivascular spaces to restore local balance after heavy local activity
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80
Q

What are neurons specialised for?

A

Computing and communication

Chemical or physical stimuli

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81
Q

What is the resting transmembrane potential of a neuron?

A

-70mV

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82
Q

What enables the propagation of the electric signal from soma –> synaptic terminal?

A

Axon

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83
Q

What is the difference between ICF and ECF?

A 
E = extracellular (outside)
I = intracellular (inside)
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84
Q

What is the relative proportion of common ions around neurons ECF vs ICF?

A

Sodium –> low inside, high outside
Potassium –> High inside, low outside
Calcium –> High inside, low outside
Chlorine –> low inside, high outside

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85
Q

What is Donnan’s equilibrium potential?

A

When diffusion gradient (pushing K+ out) is equal to electrical gradient (pushing K+ in).

Consequence of positive charge outside and negative charge inside

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86
Q

What is Donnan’s equilibrium determine?

A

The resting transmembrane potential (Vr)

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87
Q

What is some features of an action potential?

A
  1. Transient reversal of membrane potential
  2. Conducted at steady speed along the axon
  3. All or none response
  4. Has a refractory period
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88
Q

What is the steps in an Action potential generation?

A
  1. Cell is at resting membrane potential
  2. Stimulus causes depolarisation to threshold (small depolarisation)
  3. Voltage gated Na+ channels open (makes sure its an all response)
  4. Cell hits maximum depolarisation
  5. Voltage gated K+ channels open, Voltage gated Na+ channels are inactivating
  6. When membrane potential reaches back to threshold Voltage gated Na+ channels are in resting state and the open K+ channels return cell to resting potential (-70mV) after a small window of hyperpolarisation (small dip to more polarised than -70mV)
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89
Q

What is the difference between the Absolute refractory period and the relative refractory period for a neuron?

A

Absolute –> after the cell has depolarised and is returning to a potential a little above the threshold potential. After this point the cell can actually depolarise again without returning to the resting membrane potential

Relative –> the period after the absolute where the cell properly returns to the resting membrane potential

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90
Q

What is the simple key difference between the absolute and relative refractory periods?

A

Absolute –> cell cannot depolarise within

Relative –> cell can depolarise within

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91
Q

What are the two main types of glia in the (PNS) Peripheral nervous system?

A

Schwann cells –> provide myelination to PNS axons –> cover axons

Satellite cells –> cover nerve cell bodies (soma) –> gives nutrients and protection to soma

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92
Q

What is saltatory conduction and where does it occur?

A

Conduction in leaps/hops –> occurs in myelinated neurons

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93
Q

What are the main types of glial cells in the CNS?

A
  1. Microglia
  2. Astrocytes
  3. Oligodendrocytes
  4. Ependymal cells
94
Q

What are the role of microglia in the CNS?

A
  1. Equivalent to macrophages –> phagocytosis when CNS damaged or infected)
  2. Reuptake of neurotransmitters –> especially glutamate
  3. Synaptic plasticity –> important for memory/adaption
  4. Control of chemical environment –> release of inflammatory cytokines
95
Q

What happens to the microglia in stressed rats?

A

Highly connected –> overgrowth –> potential neuroinflammatory theory of depression

96
Q

What is the role of oligodendrocytes in the CNS?

A

Similar to Schwann cells –> myelinating glia

97
Q

What are some examples of demyelinating diseases?

A

Guillain Barre Syndrome –> autoimmune disorder that causes demyelination in the PNS

Multiple Sclerosis (MS)–> autoimmune disorder which causes demyelination in the CNS

98
Q

What is the role of Astrocytes in the CNS?

A
  1. Fill spaces between neurons
  2. Influence neurite growth –> guides neuronal migration during development
  3. Regulate chemical content of extracellular space
  4. Form blood-brain barrier –> astrocytes’ perivascular feet
  5. Most numerous glia in the brain
  6. Responds to CNS injury –> damaged space filled by proliferating and hypertrophy of astrocytes –> results in the formation of an astrocytic scar
99
Q

What are the two types of astrocyte in the CNS?

A

Fibrous astrocyte –> occur in white matter

Protoplasmic astrocyte –> occurs in grey matter

100
Q

What is the role of Ependymal glial cells in the CNS?

A

Lining the CSF-filled ventricles, theependymal cellsplay an importantrolein the production and regulation of CSF. Their apical surfaces are covered in a layer of cilia, which circulate CSF around the CNS.

101
Q

What is the first line of defence for the CNS?

A

The skeletal system:
1. Brain –> located within the skull –> formed by interlocking cranial bones

  1. Spinal cord –> enclosed within the vertebral column
102
Q

What is the second line of protection for the CNS?

A

The meninges:
1. Brain –> cranial meninges

  1. Spinal cord –> spinal meninges
103
Q

What is the three layers of the meninges?

A

Dura mater –> outer –> strong –> dense irregular connective tissue

Arachnoid mater –> middle –> avascular –> Interstitial fluid between arachnoid and Dura mater

Pia mater –> inner –> adheres to brain and spinal cord –> CSF is between pia and arachnoid

104
Q

What is the name of the spaces where ISF and CSF is?

A

ISF –> between dura and arachnoid –> subdural space

CSF –> between arachnoid and pia –> subarachnoid space

105
Q

What is the role of cerebrospinal fluid (CSF)?

A
  1. Mechanical protection –> shock absorbing medium –> allows brain to float and reduces impact of gravity on neural tissue
  2. Chemical protection –>provides optimal chemical for neuronal function
  3. Circulation –> provides medium for exchange of nutrients and wastes between the blood and the nervous tissues of the brain and spinal cord
106
Q

Do all brain regions have a blood brain barrier?

A

No some regions don’t –> eg postrema

107
Q

What is a Traumatic brain injury (TBI) normally characterised by?

A

An external mechanism of injury

–> eg assault to the head

108
Q

What is the difference between a primary and secondary brain injury?

A

Primary –> damage at the same time of injury –> tissue loss to trauma

Secondary –> post injury cause –>

–> extracranial causes –> hypoxia, hypotension or hypoglycaemia

–> intracranial causes –> eg haemorrhage, swelling, infection

109
Q

What type of injuries are considered to have the potential to cause damage to the brain?

A

Anything that causes loss of consciousness

110
Q

How do TBIs normally present?

A
  1. Confusion
  2. Altered level of conscious
  3. Seizure
  4. Coma
  5. Autonomic deregulation
  6. Neurological deficits
111
Q

What is an acquired brain injury (ABI)?

A

Commonly associated with misuse/ abuse of drugs and/or alcohol or a causative agent
Examples –> strokes, tumours, etc

112
Q

What are the three major physical mechanisms of traumatic brain injury (TBI)

A
  1. Impact loading –> collision of the head with a solid object at tangible speed –> contact/inertial forces strain brain beyond tolerances –> brain tissue deformed by compression, stretching or sheering force.
  2. Impulsive loading –> a sudden motion without significant physical contact
  3. Static loading –> slow moving object traps the head –> gradually squeezing the skull and causing fractures which can cause deformity in the skull and brain
113
Q

What are some common effects of primary traumatic brain injuries?

A
  1. Skull fractures
  2. Linear fractures –> fractures that pass through entire skull thickness
  3. Depression fractures –> bone fragmentation that cause depression in skull surface
  4. Base of skull fractures –> base or cribriform plate
  5. Concussion –> transient alteration in cerebral function
  6. Contusion –>bruising to the brain
  7. Haemorrhage
  8. Diffuse axonal injury –> tearing/disruption of axonal fibres
114
Q

What is concussion and how does it manifest?

A

Concussion is a transient alteration of cerebral function without structural defect
Manifests –> loss of consciousness with rapid recovery

115
Q

What is the typical causes of concussion?

A

Acceleration/deceleration force

Blunt forced trauma

116
Q

What is contusion?

A

Bruising to the brain tissue –> resulting in alteration of neurological function that may alter consciousness levels

117
Q

What is the two forms of contusion?

A

Coup –> the brain strikes the skull on the side of impact

Countercoup –> the brain strikes the skull at the opposite side of impact

118
Q

How long does it take for a secondary brain injury to occur (SBI)?

A

2-24 hours after the primary injury –> most prominent cause is impaired cerebral blood flow.

119
Q

Does a brain injury promote an inflammatory response?

A

Yes –> release of cytokines, free radicals and excitatory amino acids

120
Q

What happens during intracranial inflammation post brain injury?

A
  1. Capillary permeability is altered (just like in any inflammatory response)
    - BBB swelling
    - Glial cell swelling
    - The increase in BBB permeability may cause pharmaceutical agents to cross into the vertebral compartment and cause a further increase in intracranial pressure
121
Q

What are the main factors that can vary the manifestations of a TBI?

A
  1. The force of injury
  2. Mechanism of injury
  3. Developmental age of the skull
  4. Friability and structures of the vasculature
122
Q

What is Cerebral palsy?

A

A group of permanent disorders of the development of posture and movement, causing activity limitation associated with non-progressive disturbances in the developing foetus or infant brain.

123
Q

What are some risk factors for cerebral palsy?

A
  1. Low birth weight
  2. Prenatal –> intra uterine infections
  3. Perinatal –> instrument delivery, neonatal jaundice, asphyxia, neonatal convulsions, antepartum bleeding and neonatal infections
  4. Postnatal –> Asphyxia, infections
124
Q

What are the three main types of Cerebral Palsy?

A
  1. Spastic (75%) –> cerebral cortex damaged –> some muscles tight and some weak –> jerky movements, limb deformities
  2. Athetoid (24%) –> basal ganglia affected –> muscle change from floppy to tense –> involuntary flailing and contorted movements
  3. Ataxic (1%) –> cerebellum damaged –>unsteady movement, poor balance, shaky hand and feet movement and jerky speech
125
Q

What are the four affective type areas of cerebral palsy?

A
  1. Monoplegia –> affects one limb
  2. Hemiplegia –> affects one side of the body left/right
  3. Diplegia –> affects symmetrical parts of both eg arms or legs
  4. Quadriplegia –> affects all four limbs
126
Q

What does intracranial haemorrhage lead to in pretty much all cases?

A

Increased intracranial pressure

127
Q

What is some symptoms of intracranial haemorrhage and thus intracranial pressure increase?

A
  1. Budging fontanelles –> in infants
  2. Behavioural changes
  3. Altered level on consciousness
  4. Drowsiness
  5. Seizures
  6. Vomiting
  7. Headache
  8. BP changes
128
Q

What is an extradural (epidural) haemorrhage?

A

Blood collects in the extradural space –> between the skull and the dura mater

129
Q

What is the main cause of extradural (epidural) haemorrhage?

A

Impact loading to the skull with associated laceration of the Dural arteries or veins

130
Q

How does an extradural (epidural) haemorrhage classically present?

A
  1. Brief loss of consciousness –> followed by an increase in consciousness –> followed by a rapid decline into unconsciousness
  2. When in consciousness period –> lethargic, nauseated, confused and headaches
  3. Mortality rate of 20% if no surgical interventions available
131
Q

What is a subdural haematoma/haemorrhage?

A

Bleeding between the dura and the arachnoid layers of the meninges

132
Q

What is the main cause of subdural haematoma/haemorrhage?

A

Sudden acceleration then deceleration (severe blunt trauma) of the brain tissue with related tearing of the bridging veins

Generally venous in origin

133
Q

How do the incidence and mortality rates of extradural vs subdural haemorrhage compare?

A

Extra –> 2% of TBI –> 20% mortality untreated

Subdural –> 30% of TBI –> 50% mortality (as slow to cause symptoms)

134
Q

What is intracerebral bleeding?

A

Bleeding of the brain tissue itself

135
Q

What are the most common regions for intracerebral bleeding?

A

Temporal and frontal lobes

136
Q

What are intracerebral bleeds caused by?

A

Penetrating trauma or diffuse injury from blunt trauma

137
Q

What is a subarachnoid haemorrhage?

A

Trauma leading to haematoma in the subarachnoid space (between arachnoid and pia)

138
Q

What is an intraventricular haemorrhage?

A

Rupturing of the subependymal vessels –> mostly in premature babies
Blood fills the ventricles

139
Q

What is contained in the ventricles normally?

A

Cerebrospinal fluid (CSF)

140
Q

What is Meningitis?

A

Is an inflammatory process of the leptomeninges (membrane surrounding the brain and spinal cord) and the CSF caused by bacteria, viruses, fungi or parasites.

141
Q

What is Encephalitis?

A

Infection of the brain tissue or parenchyma

142
Q

What is a Brain abscess?

A

Is a localised focus of necrosis of brain tissue with accompanying inflammation, usually caused by a bacterial infection

143
Q

What is Brudzinski’s sign and what does it indicate?

A

A test for meningeal irritation.
Supine patient has neck flexed by the doctor –> positive sign is if the patient flexes their hips and knees to help them relieve pain/irritation

144
Q

What is Kernig’s sign and what does it indicate?

A

A test for meningitis or subarachnoid haemorrhage
The thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance).
Positive signs –> Generalised spinal pain, Resistance to the test, Involuntary hip flexion of the opposite hip

145
Q

What is the outcomes for viral vs bacterial meningitis?

A

Viral –> full recover normal

Bacterial –> can have lasting damage –> CNS damage by bacterial toxins, compressions herniation from inflammatory oedema leading to ischemia

146
Q

What are some symptoms of meningitis?

A
  1. Fever
  2. Nuchal rigidity (neck)
  3. Altered mental state
    (classic triad^^)
  4. Headache
  5. Photophobia
  6. Lethargy
  7. Vomiting
  8. Purpural or petechial rash
  9. Seizures
147
Q

What is Encephalitis?

A

Inflammation of the brain
–> Reservoirs for virus –> wild animals and domestic animals –> biosecurity and public health protocols in place to prevent and contain these viruses

148
Q

How does virus gain access to CNS to cause encephalitis?

A
  • Bloodstream
  • Direct from neighbouring structure –> nasal and middle ear
  • Retroaxonally –> from peripheral nerve endings
149
Q

What is the symptoms of Encephalitis?

A
  1. Fever
  2. Altered level of consciousness
  3. Cerebral dysfunction
  4. Seizures
  5. Headache
  6. Myalgia –> muscle pain/ache
  7. Weakness
  8. Paralysis
  9. Mild respiratory infection
150
Q

What is a brain abscess?

A

Collection of infected material at epidural or subdural locations

151
Q

What commonly causes brain abscesses?

A
  1. Bacterial cause is most common –> Commonly streptococcus infections but can also be staphylococci gram negative and Propionibacterium acnes
  2. Parasites
  3. Fungus

All of these are most likely to occur in immunocompromised patients

152
Q

How do brain abscesses most commonly arise?

A

From infections elsewhere in the body –> endocarditis, pulmonary infections, IV drug use
OR
Nearby areas –> teeth, ear, paranasal sinuses or mastoid bone

153
Q

What clinical information can a lumbar puncture assess?

A 
Causative agent
Leucocytes
Protein
Increased pressure
Changes in glucose levels
154
Q

What is some biographical information to attain first in the neurological history?

A 
Age
Place of birth
Left/right handedness
Occupation
Level of education
155
Q

What is an acute onset of neuro symptoms (seconds to minutes) suggestive of?

A

Vascular or Convulsive origins

156
Q

What is a key sign of subarachnoid haemorrhage?

A

Explosive severe headache “thunderclap headache”

157
Q

What may precede episodes of sudden neurological symptoms?

A

Precipitating events –> exercise or warning (aura)

158
Q

What is the aura that precedes a seizure?

A

Partial (focal seizure)

159
Q

What are the two kinds of auras preceding seizures and examples of their symptoms?

A

Localising –> auditory hallucinations, unusual smell/taste, loss of speech, motor changes

Non-localising –> feeling of apprehension

160
Q

Aura followed by sudden unconsciousness is very suggestive of what?

A

Diagnosis of complex partial seizure

161
Q

What is the normal time course for stroke symptom onset?

A

Seconds –> minutes before symptoms appear

However symptoms may appear when the patient wakes from sleep

162
Q

What is the hallmark of stroke?

A

Focal neurological dysfunction arising from a localised insult to the brain and symptomatic dysfunction reflects this area

163
Q

What are examples of focal neurological dysfunction in stroke?

A

Patient unable to move one side of their body (hemiplegia)

Difficulty with speech or swallowing

164
Q

What is it called when symptoms are resolved within completely post neurological dysfunction suspected from ischaemia

A

Transient ischaemic attack (TIA)

165
Q

How long does symptoms need to persist to be associated with abnormal imaging results?

A

1-2 hours –> These cases are typically termed a stroke

166
Q

What is the cause almost all cases of rapid focal neurological dysfunction without seizure?

A

Vascular causes –> infarction OR haemorrhage

167
Q

In patients exhibiting symptoms of focal neurological dysfunction and can reply to questioning what is the crucial information to obtain?

A

Onset of symptoms

Risk factors for stroke

168
Q

What is some examples of disease and time courses for subacute onset of neurological dysfunction?

A

Hours - days –> Infections (meningitis, encephalitis)

Days - weeks –> Inflammatory disorders (Guillian-Barre syndrome etc)

Weeks - months –> tumours

Months - Years –> degenerative processes

169
Q

What time courses can Metabolic or toxic disorders be expected to take?

A

Any time course –> wide variation

170
Q

What are some different types of headache and how can they present?

A

Migraine with aura –> unilateral headache preceded by flashing lights or “zig-zag” lines and is associated with light hurting eyes (photophobia)

Common migraine –> unilateral headache, no aura

Cluster headache –> pain over one eye lasting minutes to hours associated with, Lacrimation, Rhinorrhoea, flushing of the forehead –> occurring in bouts that last several weeks a few times a year or less.

Coital headache –> during intercourse, middle aged men, severe for 15 minutes and persist in a mild form for a few hours

171
Q

What is another name for cluster headache and why?

A

Alarm clock headache –> tend to wake patient from sleep at the same time each day during the cluster

172
Q

What does coital headache need to be distinguished from that can also occur during sexual intercourse?

A

Subarachnoid haemorrhage

173
Q

What is suggested by a generalised headache that is worse in the morning and is associated with drowsiness or vomiting?

A

Raised intracranial pressure

174
Q

What are some symptoms of meningitis?

A 
Generalised headache
Photophobia
Fever
Stiff neck
More gradual onset
175
Q

What kind of headache occurs in acute sinusitis?

A

Headache with pain or fullness behind the eyes or over the cheeks or forehead

176
Q

What may behind an instantaneous severe headache that is initially localised but then more general and associated with neck stiffness?

A

Subarachnoid haemorrhage

177
Q

What is the most frequent type of headache?

A

Episodic or chronic tension-type headache

178
Q

What is the presentation of a chronic tension-type headache?

A

Commonly bilateral

Occurs over frontal, occipital or temporal areas
Sensation of tightness that lasts for hours and reoccurs often

Not made worse by walking
No associated symptoms (nausea, weakness, tingling limbs)

Does not normally wake the patient from sleep

179
Q

What is the mnemonic for differentiating between a migraine headache from a tension one?

A 
P -->pulsatile headache
O --> hours duration (4-72hours)
U --> Unilateral, not bilateral
N --> Nausea and/or vomiting 
D --> Disabling headache
180
Q

What are the two major classes of seizure?

A

Focal

Generalized

181
Q

What are focal seizures?

A

Notable for symptoms localisable to a single part of the brain.

In “simple” forms –> no impaired consciousness

In “complex” forms –> consciousness is often lost from seizure activity spreading though the brain

182
Q

What intracranial haemorrhage subtype encapsulates epidural, subdural and sub arachnoid haemorrhages?

A

Extra-axial haemorrhage –> within the skull but outside the brain tissue

183
Q

What is the clinical pattern of presentation of epidural vs subdural haemorrhage?

A 
Epidural:
Commonly triphasic --> altered consciousness --> lucid --> sharp neural decline
Altered consciousness
Headache
Vomiting
Confusion/seizures
Aphagia

Subdural:
Very similar to epidural haemorrhage symptoms
Coma in 50% of cases
LESS common Triphasic/lucid interval

184
Q

What is difference in most common source of blood for epidural vs subdural haemorrhage?

A

Epidural –> arterial

Subdural –> venous

185
Q

What can be different about the presentation of epidural vs subdural haemorrhage?

A

Subdural can present in elderly with no obvious origin of trauma and be classed as chronic –> may present as a long term dementia before presentation

186
Q

What is the most common cause/ source of blood for sub arachnoid haemorrhage?

A

Rupturing of an aneurism –> in particular the cerebral arteries

187
Q

What is the clinical presentation of sub-arachnoid haemorrhage?

A

Similar to epi and subdural
Often occurs with a sudden “thunderclap headache”
Can cause symptoms of irritated meninges:
-nuchal rigidity etc

188
Q

What are the symptoms of increased intracranial pressure?

A 
Headache
Nausea
Vomiting
Increased BP
Altered cognition/ confusion
Double vision
Slow/ unresponsive pupils
Seizures
Coma
189
Q

What are some ways intracranial pressure is measured?

A
  • Intraventricular catheter –> hole drilled and catheter is inserted through the brain into the lateral ventricle
  • Subdural screw (bolt) –> (fast way) hollow screw through hole in the skull and dura mater
  • Epidural sensor –> epidural sensor is inserted through a drill hole in the skull
190
Q

What are some features of the three intracranial pressure measurements?

A
  • Intraventricular catheter –> most accurate, allows CSF sampling
  • Subdural screw –> fastest method, no CSF sampling
  • Epidural sensor –> least invasive, no CSF sampling
191
Q

What are some ways meningeal irritation is assessed?

A

Kernig’s sign –> hip and knee of patient flexed to 90 degrees –> Dr slowly extends the flexed knee –> will cause the patient to move their head up or be uncomfortable

Brudzinski’s test –> flex the patients neck –> they will flex their knees and or hip in response to pain

192
Q

What are some symptoms of meningitis?

A 
Nausea/vomiting
Fever
Headache
Nuchal rigidity 
Photosensitivity 
Confusion
193
Q

What is the effects of alcohol on the CNS?

A

Increases risk of ICH

Affects consciousness

194
Q

How is consciousness evaluated in a patient?

A

Glasgow coma scale (GCS)

195
Q

What is the Glasgow coma scale?

A 
is a neurological scale which aims to give a reliable and objective way of recording the state of a person's consciousness.
It assesses:
Eye movements/responses
Verbal ability
Motor ability
196
Q

What is pain sensitive in the brain?

A

Meningeal layers

197
Q

What does the epidural haemorrhage CT shape look like?

A

Biconvex –> near skull

198
Q

What does a subdural haemorrhage CT shape look like?

A

Crescent shaped

199
Q

What does a subarachnoid haemorrhage CT shape look like?

A

Amorphous substance that fills the normally dark, CSF-filledsubarachnoidspaces around the brain –> can spread further than epi or subdural haemorrhage

200
Q

Why does a epidural haemorrhage shoe up as biconvex on CT?

A

Cannot cross the sutures lines as the dura matter is tightly adhered there

201
Q

Why does a subdural haemorrhage present as crescent shaped on CT?

A

can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only atDural reflections like the tentorium cerebelli and falx cerebri.

202
Q

How is raised intracranial pressure treated?

A

Fluid draining through shunt in a small hole in skull or spine

Medications mannitol and hypertonic saline solution

Intubation and hyperventilation

203
Q

How does Hyperventilation assist raised ICP?

A

Cerebral blood flowislargely dependent on PaCO2.Hyperventilationcauses decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, andICP.

204
Q

What are the three essential findings for brain death?

A

Coma

Absence of brainstem reflexes

Apnoea –> not breathing

205
Q

What is encephalopathy?

A

a disease in which the functioning of the brain is affected by some agent or condition (such as viral infection or toxins in the blood).

206
Q

Why does encephalopathy cause confusion?

A

Impaired brain function –> altered mental state –> confusion

207
Q

What is the difference between depression, delirium and dementia?

A

Delirium –> reversible
Depression –> reversible
Dementia –> not reversible

208
Q

How does vit b12 deficiency cause confusion?

A
  • -> leads to pernicious anaemia
  • -> anaemia reduces rates of oxygen delivery
  • -> less oxygen to the brain
209
Q

What are some resp causes of confusion?

A

Hypoxia
Acidosis
Alkalosis

210
Q

What are symptoms of alcohol/drug withdrawal?

A 
Headaches
Nausea 
Anxiety 
Tremor
Vomiting 
Insomnia 
Sweating
211
Q

What is ketotic breathe and what is it a sign of?

A

describes the characteristic fruity smell ofbreathladen with ketones. It can occur in any condition associated withketosis

212
Q

What is ketosis and when does it occur?

A

Ketosis –> fat provides most of the fuel for the body

Happens in situations with limited glucose –> starvation or diet induced

213
Q

What direction are CT scans?

A

Its in the inferior –> superior direction

214
Q

What colour is blood on a CT?

A

White

215
Q

What is leads affect on RBC?

A

Haem production interference –> leads to anaemic

216
Q

What is the purpose of a randomized control trials/clinical trials?

A

is a type of scientific (often medical) experiment that aims to reduce certain sources of bias when testing the effectiveness of new treatments; this is accomplished byrandomly allocating subjects to two or more groups, treating them differently, and then comparing them with respect to a measured response.

217
Q

What are key design features of RCTs?

A

The only expected difference between the control and experiment group should be the outcome variable being tested if the randomization is good enough

218
Q

What are some other types of RCTs apart from clinical trials?

A

Superiority trials
Noninferiority trials
Equivalence trials

219
Q

What is the difference between an Randomized controlled trial and an observational study?

A

Observational studies –> no randomization –> difference in outcomes observed after a therapy has been selected

RCTs –> randomization –> patients are assigned a treatment/group

220
Q

What are some strengths of RCTs?

A
  • Good randomization will “wash out” any population bias
  • Easier to blind/mask than observational studies
  • Results can be analyzed with well known statistical tools
  • Populations of participating individuals are clearly identified
221
Q

What are some weaknesses of RCTs?

A
  • Expensive in terms of time and money
  • Volunteer biases: the population that participates may not be representative of the whole
  • Loss to follow-up attributed to treatment
222
Q

What is single blinding?

A

The subjects do not know if they are receiving treatment or placebo

223
Q

What is double blinding?

A

Subjects and experimenters do not know who is receiving treatment or placebo

224
Q

What is triple blinding?

A

Subjects, people administering treatment and experiment evaluators do not know who received treatment or placebo

225
Q

What is randomization in study design?

A

Process of assigning trial subjects to treatment or control using an element of chance –> to reduce bias

226
Q

What is loss to follow up?

A

Patients who are lost-to-follow-up lead to incomplete study results, which in turn can put abias on the result of the study as well as a bias on the investigational studymedication

227
Q

What is intention to treat?

A

means all patients who were enrolled and randomly allocated to treatment are included in the analysis and are analysed in the groups to which they were randomized

228
Q

What is the method used to minimise confounding in RCTs?

A

Randomization

229
Q

What proportion of strokes are ischaemic vs haemorrhagic?

A

Ischaemic –> 80%

Haemorrhagic –> 20%

230
Q

5 Major causes of strokes?

A

Atherosclerosis

Embolic (plugs of clotted material which have mobilised)

Small vessels or lacunar

Cryptogenic (unknown cause) (20%)

Rare but known causes

231
Q

Atherothrombosis is?

A

Thrombus superimposed on atherosclerosis

JMP Y2S1 (24 decks)

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