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NEUR 1203 > Midterm Slids > Flashcards

Midterm Slids Flashcards

1
Q

Diagnosis:

A

Distinguish one disease from another

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2
Q

Etiology:

A

What caused it –> The apparent causation and developmental history of an illness

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3
Q

Prognosis

A

Forecast the probably course of a disease

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4
Q

Idiopathic:

A

disorder of unknown origin

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5
Q

Incidence

A

the number of new cases of a disorder in the given time period

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6
Q

Prevalence

A

Percentage of the population that exhibits a disorder during a specific time period

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7
Q

Lifetime Prevalence

A

percentage of people who have been diagnosed with a specific disorder at any time in their lives

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8
Q

What allowed neurological diseases to be properly diagnosed in the 19th century? (3)

A
  • Development of tools for investigation
  • Imaging techniques
  • Better note taking which lead to the ability to make correlations
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9
Q

What makes diagnosing a disorder so complex?

A

Many symptoms occur in many disorders and there are no conclusive causes or tests

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10
Q

What 2 things are always done when trying to diagnose a disorder?

A

A complete medical history and a physical exam

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11
Q

What are additional tests that can be run for diagnosis

A
  • MRI
  • EEG
  • Lumbar puncture
  • Evoked potentials
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12
Q

The brain makes up _% of our body weight and take up _% of our energy

A

2

20

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13
Q

How did we historically find out about what parts of the brain do?

A

By patients having brain injuries and seeing the ramifications

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14
Q

What are the modern ways of determining what parts of the brain do

A
  • Montreal procedure
  • animal models
  • brain imaging
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15
Q

What part of the brain moderates most complex, higher order processing

A

Cerebral cortex

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16
Q

Deep grooves in the brain

A

Fissures

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17
Q

Which fissure separates the two hemispheres

A

Longitudinal

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18
Q

What connects the 2 hemispheres

A

corpus callosum

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19
Q

What is another word for the lateral fissure?

A

Sylvian

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20
Q

What does the lateral fissure separate?

A

The frontal and parietal lobes from the temporal lobe

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21
Q

CNS

A

Brain + spinal cord

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22
Q

PNS

A

Somatic NS

Autonomic NS

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23
Q

What is another word for the autonomic NS

A

Visceral

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24
Q

What does the autonomic NS control

A

Everything outside voluntary control:

  • Smooth muscles
  • Secretory functions (glands
  • Sympathetic and Parasympathetic NS
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25
Q

The spinal cord is responsible for what kind of movement?

A

Spinal reflexes

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26
Q

where is the CSF and what does it do?

A

In the sub-arachnoid space and it surrounds the brain and spinal cord and protects them by allowing them to float

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27
Q

What is the CSF made of?

A

The water, NA, Cl, and HCO3 it pulls from the blood

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28
Q

What are the functions of the CSF

A
  • Transports substances throughout the NS

- Removes cell waste

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29
Q

Where is the CSF made?

A

In the ventricles by the ependymal cells

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30
Q

What is the specific name for the cells that make CSF

A

Choroid plexus

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31
Q

What things cannot pass through the BBB

A
  • Large charge
  • Large size
  • Lipophobic/hydrophilic
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32
Q

What cells are the primary info processing units

A

neurons

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33
Q

What cells support and modulate activity of neurons

A

glia

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34
Q

3 types of neurons

A

Sensory, motor, inter

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35
Q

Nociceptors:

A

pain receptors

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36
Q

Is it pain or motor neurons that do not need to reach the brain to do their job? Why?

A

Motor

Spinal reflex

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37
Q

Where are neurons layered?

A

In the cortex

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38
Q

Where are neurons usually in nuclei

A

older parts of the brain

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39
Q

What defines a nucleus from other bundles of cells?

A

They are a cluster of neurons that form a functional group (use the same chemicals)

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40
Q

Organization of cortical networks, why?

A

Uniform and grid-like

Because there was limited space

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41
Q

Organization or sub-cortical and brainstem networks

A

Sporadic and irregular organization

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42
Q

Nerve = _NS

A

PNS

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43
Q

Tract = _NS

A

CNS

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44
Q

Which matter is rich in cell bodies and blood vessels

A

Grey matter

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45
Q

Which matter is rich in myelin

A

White matter

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46
Q

The forebrain divides into what 2 parts

A

Telencephalon and diencephalon

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47
Q

The midbrain becomes what?

A

Mesencephalon

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48
Q

The hindbrain becomes what 2 parts?

A

Metencephalon and Myelencephalon

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49
Q

The 2 hemspheres are part of what part of the brain?

A

Cerebrum

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50
Q

Lateralization:

A

Differences (specialization) of the hemispheres

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51
Q

The left brain controls which part of the body

A

right

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52
Q

The left brain is lateralized for what functions

A

language, math and logic

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53
Q

The right brain is lateralized for what functions

A

emotion, spatial orientation, facial recognition, art/music

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54
Q

Commisural tracts

A

allow the left and right side to communicate

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55
Q

Where do most commisural tracts pass through?

A

corpus callosum

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56
Q

Is the corpus callosum a commisual tract?

A

yes

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57
Q

Projection tracts:

A

extend vertically between the higher and lower brain regions, to carry info between cerebrum and body

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58
Q

Association tracts

A

connects regions within the same hemisphere

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59
Q

What are the 2 different association tracts

A

Short fibers: connect gyri within a lobe

Long Fibers : connect lobes within a hemisphere

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60
Q

2 subcortical structures

A

Basal ganglia and Limbic system

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61
Q

Precentral gyrus is the ___ cortex

A

Motor

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62
Q

Post central gyrus is the ____ cortex

A

Somatosensory

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63
Q

Functions of frontal lobe

A

problem solving
planning
emotion
voluntary motor activity

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64
Q

Functions of temporal lobe

A

Understanding language
memory
hearing

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65
Q

Functions of parietal lobe

A

Sensation
reading
body orientation
spatial sense

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66
Q

Functions of occipital lobe

A

vision

colour perception

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67
Q

What are the contributions of each love to cognition

A

Frontal - Planning responses + personality
Temporal - recognizing stimuli
Parietal - attending to stimuli
Occipital - processing visual stimuli

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68
Q

Role of the basal ganglia (3)

A

control or voluntary movement, procedural memory and habit formation

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69
Q

3 main parts of the basal ganglia

A

Caudate nucleus + putamen + striatum
Globus pallidus
Substantia nigra

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70
Q

What are 2 things that dopamine is involved in?

A

Reward and Parkinson’s

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71
Q

3 roles roles of limbic system

A

Emotion control
Learning
Memory

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72
Q

3 main parts of the limbic system

A

Cingulate cortex
Amygdala
Hippocampus

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73
Q

Cingulate cortex

A

Emotional processing and memory

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74
Q

Amygdala

A

Fear
Aggression
Emotionally charged memories
Decision making

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75
Q

Hippocampus

A

Learning and memory (short to long term)

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76
Q

Functions of the cerebellum

A

Balance
Coordination and control of voluntary movement
Fine muscle control

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77
Q

Brain stem

A

Breathing
Heart beat
Respiration

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78
Q

2 parts of the diencephalon

A

Thalamus and Hypothalamus

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79
Q

What is the midbrain

A

A small area with many important functions (substantia nigra)

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80
Q

What are the 2 parts of the hindbrain

A

Pons and Medulla

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81
Q

Function of pons

A

connects cerebellum to brainstem

- inhibits movement during sleep

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82
Q

Function of medulla

A

Controls breathing and heart rate

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83
Q

Function of Tegmentum

A

Modulates activities like sleep, attention and reward

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84
Q

Function of Tectum

A

Important in linking auditory and visual systems, controls orienting movement

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85
Q

Superior coliculi =

A

vision

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86
Q

Inferior colicili

A

hearing

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87
Q

What is the most important role of the cerebellim

A

Fine tuning movement

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88
Q

The cerebellum is __% of the brain’s volume and __% of its neurons

A

10

50

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89
Q

If you put things out of equalibrium, they will

A

equilibrate

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90
Q

Neurons maintain an electrical charge across their:

A

membrane

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91
Q

The tendancy for electrons to move represents their ability to do work and is called ___ measured in ___

A

Electrical potential

Volts

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92
Q

When the channels are shut the energy is all ____ energy

A

potential

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93
Q

What is outside the neuron?

A

CSF

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94
Q

Why is the inside of the neuron negative

A

Because the proteins in it are negatively charged

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95
Q

Who discovered boielectricity in the late 1700s

A

Galvani and Volta

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96
Q

At rest is the neuron polarized

A

yes

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97
Q

Threshold of excitation #

A

-55mV

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98
Q

4 properties of an action potential

A
  • fast
  • localized but spreading
  • all or nothing
  • involve a large reversal of membrane polarity
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99
Q

voltage gated sodium channels open at __ and close at __

A

-55mV

+30mV

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100
Q

voltage gated potassium channels open at ___ and close at ____

A

+30mV

-70mV

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101
Q

How does the action potential propagate?

A

depolarization in one region can stimulate adjacent areas to depolarize as well

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102
Q

what ensures that action potentials only go one way

A

refractory period

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103
Q

action potentials happen the ___ way for all behaviour

A

same

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104
Q

The synapse is the site of ____ transmission in the cell

A

chemical

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105
Q

What is the PNS parallel to NTs?

A

hormones

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106
Q

How many kinds of NT

A

more than 50 identified

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107
Q

3 categories of NT

A
  • Amines (dopamine, epinephrine, serotonin)
  • Amino Acids (glutamate, GABA)
  • Other
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108
Q

When the AP reaches the terminal, what ion enters the terminal

A

Calcium

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109
Q

What does calcium do in the terminal

A

releases the vesicles to dump NT into the synapse

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110
Q

Where can terminals connect

A

Anywhere

- dendrites, soma, axon

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111
Q

2 types of post synaptic potentials

A

IPSPs

EPSPs

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112
Q

What process allows the neuron to “decide” whether to fire or not

A

Integration of PSPs

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113
Q

NT are ____ for a specific ____

A

ligands

receptor

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114
Q

Ionotropic receptor

A

Fast –> directly triggers ion channels to open or close

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115
Q

Metabotropic receptors

A

Slow –> indirectly opens or closes ion channels through second messengers

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116
Q

What are 4 ways to deactivate NTs

A
  1. Diffusion
  2. Degradation
  3. Reuptake
  4. Glial cells
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117
Q

Hormones:

A

Chemical messengers that are released by one cell group and travel through thr blood stream to act on targets

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118
Q

What are endocrine glands and 3 examples

A

Release hormones throughout the body

- Testes, thyroid, adrenal glands

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119
Q

What are exocrine glans and 3 examples

A

Use ducts to secrete fluids outside the body

- Sweat, lacrimal (tears) and mammary

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120
Q

8 main endocrine glands

A
  • Hypothalamus
  • Pituitary
  • Thyroid
  • Adrenal
  • Parathyroid
  • Pancreas
  • Ovaries
  • Testes
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121
Q

Neuroendrocrine glands

A

Brain regions that can release NT into the blood stream

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122
Q

What type of synapse can dump NT into the blood stream

A

axosecretory synapses

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123
Q

What are the 2 glands are the major locus of neuroendocrine integratoin in the body and 3 examples

A

Hypothalamus and Pituitary

  • HPA
  • HPT
  • HPG
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124
Q

What are the 2 glands are the major locus of neuroendocrine integration in the body and 3 examples

A

Hypothalamus and Pituitary

  • HPA
  • HPT
  • HPG
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125
Q

5 Principles of Action of Hormones

A
  1. Act in a gradual fashion
  2. Change probability or intensity of behaviour (shift in homeostasis)
  3. Have a reciprocal relationship with behavour
  4. May have multiple effects
  5. Released in pulses or at e specific time
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126
Q

3 similarities between NT and hormones

A
  1. neurons and glands make and store chemicals and release them upon stimulation
  2. Bind to receptors that stimulate target cells
  3. Some chemicals can be both hormones and NT
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127
Q

4 differences between hormones and NT

A
  1. Local vs Distant
  2. Fast vs Slow
  3. Voluntary vs Involuntary
  4. Precice vs Imprecise
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128
Q

What types of receptors to hormones act on?

A

Metabotropic

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129
Q

What is the typical progression of glands in hormone release

A

Hypothalamus (neurohormones) –> Pituitary (releasing hormones) –> Target Endocrine Gland (target hormone) –> Target Tissue

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130
Q

What type of hormone is usually released from the pituitary gland

A

releasing hormones

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131
Q

Which glad is considered the master gland

A

Pituitary

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132
Q

What connects the pituitary gland to the hypothalamus

A

pituitary stalk

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133
Q

What are the 2 divisions of the pituitary gland and how are they connected to the hypothalamus?

A

Anterior - blood vessels

Posterior - directly by axons from the hypothalamus

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134
Q

What do the anterior and posterior pituitary release?

A

Anterior - releasing hormones (ACTH, TSH)

Posterior - Vasopressin and oxytocin

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135
Q

What is the function of the hormones synthesized and released from the hypothalamus?

A

To inhibit or stimulate the release of hormones from the pituitary

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136
Q

What is another word for releasing hormones?

A

Tropic

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137
Q

Where are vasopressin and oxytocin synthesized?

A

Hypothalamus

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138
Q

How does the endocrine system regulate itself?

A

Negative feedback loops

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139
Q

Can a system have both a positive and negative feedback loop?

A

Yes

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140
Q

Steps of the HPA axis

A

Hypothalamus (CRH) –> Pituitary (ACTH) –> Adrenal cortex (glucocorticoids) –> Increased cortisol induces metabolic changes

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141
Q

Stressor:

A

A stimuli that challenges the body’s homeostasis and triggers a response

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142
Q

Minor vs Major stressors

A 
Minor = may be acute or chronic 
Major = something that really rocks the foundation of a persons life
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143
Q

What 2 things does the stress response accomplish?

A
  1. Temporarily puts the brain and body into “overdrive” in order to deal with the stressor
  2. Suspends bodily repair and growth in order to conserve energy
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144
Q

What is the fast stress pathway and what does it respond to?

A

Sympatho-adrenomedulary axis (SAM)

The alarm response to a surprise (acute) stressor

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145
Q

What is the slow stress pathway and what activates it?

A 
Hypothalamic-pituitary axis (HPA) 
Long lasting (chronic) stressors
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146
Q

What are the 2 adrenal glands and what do they secrete

A 
Cortex = cortisol 
Medulla = epinephrine and norepinephrine
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147
Q

What is the ratio of epinephrine and norepinephrine released

A

80% epinephrine

20% norepinephrine

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148
Q

How does the SAM axis work

A

Hypothalamus send projections to the spinal cord –> directly stimulates the sympathetic nervous system –> release of epinephrine and norepinephrine

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149
Q

Epinephrine and norepinephrine are ____ hormones from _____ family

A

Peptide

Catecholamine

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150
Q

What receptors do epinephrine and norepinephrine bind to?

A

Adrenergic receptors

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151
Q

What type of hormone is cortisol

A

Steroid hormone

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152
Q

What receptors do cortisol bind to?

A

Glucocorticoid (GR) and mineralcorticoid (MR) receptors

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153
Q

What time is cortisol the highest in the body

A

in the morning

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154
Q

What are the 2 main areas of the body that cortisol affects?

A

Metabolism and immune system

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155
Q

What affect does cortisol have on metabolism (3)

A
  • More breakdown of lean body mass (non-fat tissue)
  • increased blood sugar
  • less bone and connective tissue formation
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156
Q

What 3 areas in the brain are sensitive to cortisol and help shut down the stress response

A
  • Hypothalamus
  • Anterior pituitary
  • Hippocampus
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157
Q

What happens to cognition when there is a stress response?

A

It is impaired

|&raquo_space; PFC shuts down and older brain regions take control

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158
Q

What is good stress called

A

Eustress

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159
Q

Psychological resilience

A

Ability to cope with stressors improved by regularly overcoming them

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160
Q

When is it important to encounter manageable stressors

A

Childhood to build resilience

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161
Q

Too much stress results in what?

A

Learned helplessness

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162
Q

What is a way of volitionally getting good moderate stress

A

exercise

163
Q

What are the physical effects of too much stress (4)

A
  1. Increase in resting and stress induced levels of GCs
  2. Increased CRH expression
  3. Larger adrenal cortex
  4. Less GRs in the hippocampus (decreased neg feedback ability)
164
Q

What are the changes in the hippocampus as a result of chronic stress (3)

A
  • Less spine density
  • less neurogenesis
  • impaired negative feedback ability
165
Q

Acute vs chronic stress

A 
Acute = sharpens cognition and mobilizes energy 
Chronic = impairs cognition and results in fatigue
166
Q

Which type of cell death always illicit an inflammatory response?

A

Necrosis

167
Q

Acquired Brain Injury

A

any brain injury that occurs after brith (not hereditary, congenital or degenerative

168
Q

What are 6 possible causes for ABI

A
  • anoxia
  • drug toxicity
  • poisoning
  • concussion
  • blast injury
  • penetrative trauma
169
Q

TBi includes only trauma to the brain caused by an ____ _____ force

A

External mechanical

170
Q

What is the #1 cause of death in children and youth

A

TBI

171
Q

2 biggest risk factors for TBI

A

age and sex

172
Q

Is a concussion a mild or severe TBI?

A

Mild to moderate

173
Q

What causes damage to the brain during an injury

A

When there is a collision between the brain and the skull

174
Q

What are the 3 steps of injury in TBI

A
  1. Site where the brain and skull make first contact = coup
  2. Pressure can cause the brain to rebound and contact the opposite side of the skull = contre-coup
  3. This motion continues until the energy dissipates
175
Q

What are the 3 possible directions of impact on the head

A

Linear, rotational or angular

|&raquo_space; Usually a combo

176
Q

Which direction of injury is worst

A

Rotational

The degree of rotational force determines the severity of the injury

177
Q

What leads to the generalized damage in the brain after an injury

A

The grey and white matter will move at different speeds and slide over each other

178
Q

What is the primary phase of a TBI

A

Damage caused by initial impact

Swelling and bleeding cause increased intracranial pressure

179
Q

WHat is the secondary phase of TBI

A

Damage arising from the primary injury

Energy crisis and possible infection

180
Q

What is the only case where there can be possible infection after TBI

A

When there is a penetrating injury

181
Q

What is the energy crisis

A

Lack of oxygen and glucose due to disrupted blood flow

182
Q

What is the process of excitotoxicity

A
  1. Necrosis results in excess glutamate
  2. Leads to continual firing of AP
  3. Results in lots of Ca in cell
  4. Excess Ca goes in the mitochondria and will lead to apoptosis
183
Q

What is the cellular damage at the site of impact of a TBI?

A

Necrotic cell death

> All cell types impacted

184
Q

What is a diffuse axonal injury

A

Twisting forces cause axon to me torn from cell body

185
Q

What is another word for the axon being torn from the soma

A

Axotomy

186
Q

What are the 2 things that cause the energy crisis

A
  1. Lack of glucose (less ATP)

2. Lack of oxygen –> causes anaerobic glucose metabolism

187
Q

What is the result of hypoglycaemia

A

Leads to cognitive deficits as neuronal activity decreases after mass excitation of exitotoxicity

188
Q

What is the bad result of the brain switching to anaerobic metabolism

A

it leads to the overproduction of lactic acid –> acidosis

|&raquo_space;Causes damage to BBB

189
Q

What possible further damage could arise from damaged BBB

A

It is more permeable so something from the periphery can cause an infection in the brain

190
Q

Is the brain immune privileged?

A

No

191
Q

The brain is immune protected, what does that mean?

A

the peripheral immune system cannot get into the brain generally speaking

192
Q

What does it mean to say that the immune system is decentralized

A

Immune cells circulate in the blood and act where they are needed

193
Q

where do all immune cells develop from?

A

bone marrow

194
Q

What are the 2 divisions of the immune system?

A

Innate and adaptive

195
Q

The immune system relies on _____ communication through ______

A

chemical

cytokines

196
Q

Are cytokines only secreted by immune cells?

A

No, they are secreted by other cells too

197
Q

What is the basal level of cytokines in relation to the basal level of hormones

A

Lower

198
Q

What is the main thing that differentiate cytokines from hormones

A

Cytokines can increase very rapidly

199
Q

Are cytokines pro or anti inflammatory?

A

There are both types of cytokines

200
Q

Are pro or anti inflammatory cytokines more harmful?

A

Neither, they are both beneficial as long as they are in balance

201
Q

What nerve provides parasympathetic innervation of heart and digestive tract

A

Vagus nerve

202
Q

Paraganglia cells

A

The cells on the vagus nerve that releases NT upon cytokine binding

203
Q

What nerve is the bridge between the CNS and PNS

A

Vagus nerve

204
Q

What cell type is the first on the scene when there is an immune response in the brain

A

Microglia

205
Q

What method does microglia use to clean up debris in the brain

A

Phagocytosis

206
Q

What type of cytokine do microglia secrete

A

pro-inflammatory

207
Q

Other than cytokines, what molecules do microglia secrete?

A

Neurotrophic Factors (promote cell survival)

208
Q

Microglia come in 2 forms. What are they and what do they mean?

A 
Star = nothing is wrong 
Ball = something is wrong
209
Q

What is another word for reactive oxygen species

A

Free radicals

210
Q

What makes reactive oxygen species

A

Regular cell metabolism

211
Q

When are ROS produced more?

A

During stress (like injuries)

212
Q

What is oxidative stress?

A

When there are more ROS than antioxidants

213
Q

What negative effects can ROS have on neurons

A

Can kill neurons

|&raquo_space;Disrupts the DNA, membrane and proteins

214
Q

Do people always lose consciousness when they get a consussion?

A

No

215
Q

How many concussions go unreported

A

25%

216
Q

Prior concussions _____ the likelihood of a second concussion and cause greater _____

A

increase

morbidity

217
Q

Repeated concussion have ______ effects, even if they are separated by years

A

cumulative

218
Q

What is CTE

A

Chronic Traumatic Encephalopathy

It is a progressive degenerative disease found in individuals with a history of multiple concussions

219
Q

Is CTE a concussion?

A

No, it is a distinct disease

220
Q

What brain changes are associated with CTE (4)?

A
  • lower brain weight
  • widespread atrophy
  • enlarged ventricles
  • tau aggregates and beta-amyloid plaques
221
Q

What are common symptoms of CTE?

A
  • memory impairments
  • depression
  • impulsive behaviour
  • suicidal thoughts and/ot behaviours
222
Q

What 2 sources of blood does the brain use?

A

Common carotid

Vertebral arteries

223
Q

The brain arteries form a common circles at the base of the brain called?

A

Circle of Willis

224
Q

What is the overlap of the arteries in the brain like?

A

Limited

225
Q

Stroke is the ___ leading cause of death

A

2nd

226
Q

Ischemia

A

Lack of blood flow to tissue or organ

227
Q

Stroke

A

interruption of blood flow to the brain

228
Q

2 types of stroke

A 
Ischemic = blockage in blood vessel 
Hemmorhagic = rupture in blood vessel
229
Q

What stroke is most common

A

Ischemic 80%

230
Q

Large vs small vessel thrombosis (ischemic)

A 
Large = blockage in one of the larger blood supply arteries 
Small = blockage in one of the smaller, but deeper, arteries
231
Q

What causes stroke (3)

A
  1. Narrowing of the artieries in the neck or brain (plaques)
  2. Genetic mutations
  3. Environmental/experiential factors (high BP, smoking, trauma)
232
Q

What is the common link between all causes of stroke?

A

Inflammation in the blood vessel walls

233
Q

What are the symptoms of stroke

A

Depend on the location of stroke

234
Q

A stroke where results in ataxia and motor problems

A

Cerebellar

235
Q

What is a rare but mostly fatal stroke region

A

brain stem

236
Q

Even though it is less common there are more _____ with hemorrhagic strokes

A

death

237
Q

What is the mortality rate of intracerebral hemorrhage

A

35%

238
Q

The swelling and increased pressure of a hemorrhage leads to what

A

cell death

239
Q

What are subarachnoid hemorrhages most often caused by? What is the mortality rate?

A

Aneurysm

40-50%

240
Q

Characteristics of a mild stroke

A
  • Transient ischemic attack
  • brief loss of perfusion
  • may affect whole brain or be region specific
241
Q

Characteristics of severe stroke

A
  • Global ischemia
  • complete loss of perfusion
  • often fatal
242
Q

Transient Ischemic Attack (TIA)

A

“mini stokes”

Causes and symptoms the same as strokes but they are shorter

243
Q

TIA come when in 15-13% of patients who have a severe stroke

A

Before

244
Q

How are TIAs protective

A

The brain gets to adapt to the lack of blood and oxygen more slowly. Can prime the brain for a larger later stroke

245
Q

What is the treatment for TIA

A

Anti-coagulants (blood thinners) to prevent clotting and a larger stroke

246
Q

Why is a stroke so serious?

A

Because the blood needs a constant supply of glucose and oxygen and it does not store its own

247
Q

How long can the brain go without oxygen before permanent cellular damage?

A

4 minutes

248
Q

Infarction

A

Ischemia-induced cell death

249
Q

Core of a stroke

A

The area directly fed by blocked vessel

<20% blood flow

250
Q

Penumbra of stroke

A

Outskirts of blockage still getting blood from other vessels
20-40% blood flow

251
Q

Apoptosis is caused by a lack of ____, why?

A

glucose

Cannot fuel Na/K pump –> glutamate rushes in –> excitotoxicity and exhaustion cause cell to self-destruct

252
Q

Necrosis is caused by a lack of ____, why?

A

Oxygen
Brain switches to anerobic metabolism –> acib build up, –> increases membrane permeability –> water rushes in –> cell bursts

253
Q

The core has what type of cell death

A

apoptosis and necrosis

254
Q

The penumbra has what type of cell death, why?

A

Apoptosis

Receiving the diffused death signals the dying cells from the core are sending out

255
Q

Should research focus on the core or the penumbra?

A

Penumbra, the core is a lost cause

256
Q

When there is a stroke the BBB is weakened. What does that mean for re-perfusion

A

Peripheral immune cells can enter the brain and exacerbate the swelling

257
Q

The heightened immune response that results from the weakened BBB can impede what?

A

recovery

258
Q

The increase in Ca after a stroke is bad in what 2 ways?

A
  1. Triggers release of more Glu (excitotoxicity)

2. Results in the produciton of ROS

259
Q

When there is too much Ca for the cell to handle, what happens?

A

The mitochondria triggers apoptosis

260
Q

Collateral circulation

A

the blood flow through secondary pathways after the obstruction to the principle pathway occurs

261
Q

Survival of the stroke affected region depends on (4)

A
  • degree of obstruction
  • How suddenly it happened
  • length of time without blood
  • degree of available collateral circulation
262
Q

What is the more important factor in the survival of the stroke brain region

A

Degree of collateral circulation

263
Q

What is the immediate treatment of an ischemic stroke (2)

A

TpA - clot buster

Neurothrombectomy - surgical removal of the clot

264
Q

Within what time period does TpA work

A

3-4.5 hours

265
Q

Do people recover after a stroke

A

Most people recover at least a portion of their neurological function

266
Q

How far can nearby neurons migrate to make up for cell death after a stroke?

A

5mm

267
Q

Axonal sprouting after a stroke

A

the axon makes new branched off connections to the surviving neurons

268
Q

Angiogenesis

A

vascular growth

269
Q

What does speech and physical therapy after a stoke facilitate

A

neuroplasticity

270
Q

Common impairments after a stroke (3)

A

Motor - upper limb use and might need an assistive device for walking
Cognitive - memory, learning, language
Sensory - tingling or pain

271
Q

Anosognosia

A

When you have something wrong with you but you do not know it

272
Q

Hemi-spatial neglect

A

Patients completely ignore one side of the world

273
Q

Which side most often gets neglected in hemineglect

A

Left side from right parietal damage

274
Q

pairs of chromosomes

A

23

275
Q

Proteins DNA gets wrapped around

A

histones

276
Q

What do histones help with

A

Control the activity of genes

277
Q

Alleles

A

variants of a gene

278
Q

Expression of any train depends on _______ production

A

protein

279
Q

3 roles of proteins

A

Structural
Enzymatic
Cell signalling

280
Q

Epigenetics changes the _____ of DNA

A

accessability

281
Q

Huntingtin is what type of disorder

A

heritable

282
Q

What pattern of inheritance does huntingtin follow

A

autosomal dominant

283
Q

The huntingtin gene is on what chromosome

A

4

284
Q

Huntingtins symptoms appear

A

mid 30s-40s

285
Q

Prevalence of huntingtins

A

5-10/100 000

>Most common inherited neurodegenerative disorder

286
Q

Short form for the huntingtin protein

A

htt

287
Q

Where is the huntingtin protein expressed

A

Everywhere in the CNS and peripheral tissues

288
Q

What is the normal htt protein called

A

Wild type (WP)

289
Q

When is the WT htt protein critical

A

Embryonic development

290
Q

The htt protein has repeats of what codon

A

CAG

291
Q

How many CAG repeats is ok and how many is huntingtin

A 
<35 = normal 
36-40 = uncreased risk 
>40 = Huntington will develop
292
Q

What is wrong with excess repeats of the CAG codon

A

It changes the conformation of the protein, leading to mis folding and toxic protein aggregates in the cell

293
Q

Can a deficincy in WT htt produce HD

A

no

294
Q

What combination of htt genes is necessary to produce HD

A

Increased mutant htt and loss of WT htt

295
Q

What are the symptoms of HD

A

progressing motor, cognitive and emotional symptoms

296
Q

Motor symptoms of HD

A

Chorea
Clumsiness
Repetative movements

297
Q

Cognitive symptoms of HD

A

Restlessness
Agitation
Lack of concentration
Short term memory problems

298
Q

Emotional symptoms of HD

A

Depression and apathy

Antisocial behaviour and aggression

299
Q

When do the emotional symptoms of HD start

A

Several years before the onset of motor symptoms

300
Q

What is the progression of the HD symptoms?

A

Usually gets wrose

301
Q

After a while the HD chorea subsides and starts to look more like ______

A

Parkinson’s (hypokinesis)

302
Q

Progressive dementia and death occur __ yeard after HD onset

A

15-20

303
Q

Neurons in what part of the brain are affected in HD

A

Basal ganglia and cerebral cortex

304
Q

Basal ganglia neurons are mostly

A

inhibitory

305
Q

2 pathways basal ganglia influences movement

A

Direct –>excitation of motor neurons –> movement

Indirect –> inhibition of motor neurons –> suppresses movement

306
Q

In HD, the neurons in the cortex that project to which 2 parts are most at risk

A

Motor cortex and limbic system

307
Q

Where in the cell is the htt protein foud

A

cytoplasm

308
Q

Intraneural inclusions

A

when the mutant htt accumulates on the nucleus of the neuron

309
Q

Aggregates of the htt are correlated with death in the ____ but not in the ______

A

cortex

striatum

310
Q

Its not the accumulation of the aggregates that causes cell death in HD but rather the

A

translocation of aggregates to the nucleus that induces pathology

311
Q

Where do aggregates in HD accumulate more quickly? What might this do?

A

Nucleus

Might alter gene expression

312
Q

How do the aggegates form in HD

A

The cell will recognize the mutated protein and cut it up. the cut up pieces will clump together
Can also be the result of abnormal splicing

313
Q

Is the molecular directionality of HD known?

A

No

314
Q

Why might the striatum be more at risk for HD damage than other brain regions?

A

Increased risk because of all the Glutamate projections to this brain region
»>higher excitotoxicity risk

315
Q

Long circuit loop implicated in HD

A

Basal ganglia-thalamo-cortical circuitry

316
Q

What NT is involved in HD? How is it affected?

A

GABA

80-90% decrease in GAD (GABA precursor)

317
Q

Why can dysregulated GABA be problematic in HD

A

Increase in GABA + Glu in the corticalstriatal circuit –> Disruption in the integrative processes by medium spiny neurons

318
Q

Why might there be an increase in GABA in HD?

A

To deal with the increase of Glu as a result of cell death

319
Q

Increase in ____ NT receptor stimulation may contribute to symptoms of HD

A

Glutamate (NMDA receptor)

320
Q

Excitotoxicity in HD might also result from a decrease in glial _____ of glutamate

A

uptake

321
Q

Is there a cure for HD?

A

No, it is fatal

322
Q

What is the treatment for HD

A

Symptom management

323
Q

Where do upper motor neurons originate

A

In the brainstem or motor cortex

324
Q

Lower motor neuron send messages to muscles and tell them what?

A

to start contracting

325
Q

Upper motor neurons have what 2 jobs

A
  1. Tell the lower motor neurons to carry start signals to the muscles
  2. Tell LMN when to stop sending signals to contract (end movement)
326
Q

Upper motor neurons can talk to LMT directly and indirectly, how?

A 
indirect =  Interneurons
Direct = UMN to LMN
327
Q

Upper motor neurons cannot leave the

A

CNS

328
Q

Where are the cell bodies of the LMN

A

Brain stem or spinal cord

329
Q

Can the axons of LMN leave the CNS

A

Yes

330
Q

What are the 2 types of LMN

A

Spinal or cranial

331
Q

UMP can pass through what two regions via what pathways to synapse with the LMN

A

Brainstem = corticobulbar tract

Spinal cord = corticospinal tract

332
Q

How is the corticobulbar pathway protected from complete loss of function from damage

A

Some of the neurons stay on the ipsilateral side and some decussate

333
Q

Damage to UMN and LMN can both lead to what?

A

weakness

334
Q

What happens when there is damage to the upper motor neurons? (5)

A 
Spasticity 
hypertonia 
Hyperreflexia 
clonus 
Babinski reflex
335
Q

Why do we see those symptoms when there is damage to the UMN

A

Without inhibition, the LMN keeps telling the muscles to contract and this leads to sustained contraction and rigidity

336
Q

Why do we see the symptoms with LMN damage?

A

The LMN are unable to tell the muscles to start contracting, so the muscles are flaccid

337
Q

What symptoms are seen n LMN damage (5)

A 
Flaccidity 
Hyporeflecxia 
Hypotonia 
Muscle atrophy 
Fasciculations
338
Q

Upper motor neurons release what NT

A

glutamate

339
Q

lower motor neurons release what NT

A

Acetylcholine

340
Q

Is the cause for ALS known

A

No, it is idiopathic

341
Q

What is the mean age of diagnosis for ALS

A

~60

342
Q

What is the pattern of heredity for the familial form of ALS

A

Autosomal dominant

343
Q

The gene abnormalities of ALS lead to what?

A

protein aggregates

344
Q

ALS involves degredation of what

A

Upper and lower motor neurons

345
Q

What type of movement is damaged in ALS

A

Voluntary movement

346
Q

When muscles are not used they _____

A

atrophy

347
Q

Sensory neurons in ALS

A

they are not affected, people can still feel

348
Q

What does ALS not affect

A 
Sensation 
Heart 
Digestion 
Bladder 
Internal organs 
Cognitive processes
349
Q

What is the only voluntary movement that people with ALS can do

A

Move their eyes

350
Q

Where does weakness of ALS typically start

A

Arms or legs

351
Q

Loss of ___ function occurs first with sporadic ALS

Loss of ____ function occurs with familial ALS

A

arms

legs

352
Q

What are the later symptoms of ALS

A

loss of ability to:

  • walk
  • speak
  • hold up head
  • swallow
353
Q

There is an increased risk of what with ALS. What does this often lead to

A

Aspiration

Leads to infection, is often fatal

354
Q

What is the average life expectancy of ALS once diagnosis

A

2-5 years

355
Q

Is there a cue for ALS

A

no

356
Q

The only drug for ALS does what?

A

Slows the loss of muscle strength by blocking sodium channels and reducing glutamate release
» decreases excitotoxicity

357
Q

Other than drug, what are the 3 therapies for ALS

A

Physical - exercise and strength to keep mobility for as long as possible
Occupational - redesign environment
Speech-Language pathologist - keep speech and swallowing for as long as possible

358
Q

General pathology of Upper and lower motor neurons

A

Upper - spasms, hypertonia and hyper reflexia

Lower - muscle atrophy and fasciculations

359
Q

Necroptosis

A

Programmed necrosis

360
Q

Astrocytes in ppl with ALS

A

have been shown to release toxins that induce necroptosis

361
Q

What happens when you put motor neurons in a petri dish with ALS astrocytes
What type of study is this

A

they start dying

|&raquo_space; in vitro

362
Q

Underlying issues of how to fix astrocytes from killing motor neurons

A

How do astrocytes become toxic

How is this happening in vivo

363
Q

What does the drug Riluzole try to do in ALS

A

Block sodium channels to prevent neurotoxicity

364
Q

Under neormal circumstances, what do astrocytes do to protect neurons?
Via what ?

A

Remove excess glutamate

Glutamate transporters

365
Q

In ppl with ALS, what was discovered about the glutamate transporters on glial cells

A

there were less of them

366
Q

What are 5 ways we can experience what it is like to have ALS

A
  1. eat with a fork holding 10lb
  2. Sit, moving nothing but eyes
  3. Use wheelchair in store without speaking
  4. Climb 2 stairs at a time with weight on ankles
  5. talk with marshmallows in mouth
367
Q

Dementia

A

a set of symptoms that are caused by disorders that affect the brain

368
Q

Symptoms of dementia (4)

A

memory loss
Problems with thinking
problem solving problems
Language problems

369
Q

Does dementia affect daily life

A

yes

370
Q

Is dementia a specific disease?

A

no, it is caused by many things

371
Q

Neuron difference between dementia and normal aging

A

Normal aging = dysfunctioning of neurons

Dementia = dying neurons

372
Q

4 behavioural differneces between normal aging and dementia

A

Normal aging vs Dementia:

  1. Forgetting convo or event from last year vs forgetting recent events and convos
  2. Forgetting names of aquantences vs. forgetting lames of family and friends
  3. Occasional difficulty finding words vs frequent pauses and word substitutions
  4. Person worries but not family vs family worried but not person
373
Q

What is the leading cause of dementia

A

Alzheimers

374
Q

Mild cognitive impairment =

A

memory problems greater than expected for age, but does not impair daily function

375
Q

What puts people at greater risk for AD. What is it also known as?

A

mild cognitive impairment

|&raquo_space;dementia

376
Q

Mild AD (5)

A
  • memory loss
  • other cog deficits
  • impaired daily function
  • depression
  • apathy
377
Q

Moderate AD (3 main categories)

A
  • Impairment: language, reasoning, sensory processing, conscious thought
  • Unable to learn new things or do complex tasks
  • Hallucinations or paranoia
378
Q

Severe AD (4)

A
  • Massive cell loss
  • completely dependent
  • cannot communicate
  • body shuts down
379
Q

Cognitive And functional abilities in AD

A

Changes in ability to think, understand, remember and communicate

380
Q

Emotions and mood in AD

A
  • Apathy, depression and anhedonia

- withdrawl from people

381
Q

Behaviour in AD

A
  • Out of character behaviours
  • restless
  • repetative
382
Q

Physical abilities in AD

A

Impaired coordination and mobility influence ability for daily tasks

383
Q

2 forms of AD

A

Sporadic and familial

384
Q

Causes of sproadic AD

A

Unknown but age is biggest risk factor

385
Q

What gene (and number) is associated with sporadic AD

A

APOE e4
1 allel = risk
2 alleles = higher risk

386
Q

What does APOE do?

A

Helps break down a protein called beta amyloid which forms aggregates in AD

387
Q

Casue of familial AAD

A

A dominant gene that speeds up the progression of the disease

388
Q

What other disease is highly comorbid with AD

A

Down syndrome

389
Q

When can AD be diagnosed for sure

A

After death

390
Q

Degradation starts where in the brain in AD and spreads where

A

Hippocampus

spreads to rest of cortex

391
Q

4 structural signs of AD

A
  • brain atrophy
  • narrow gyri
  • wide sulci
  • enlarged ventricles
392
Q

2 key pathological features of AD

A

Beta amyloid plaques

Neurofibrillary tanges

393
Q

Beta amyloid plaques do what in in brain

A

illicit immune response

Collect around blood vessels, weakening them and increases the risk of hemorrhage

394
Q

Beta amyloid plaques increase the risk of what

A

hemorrhage

395
Q

Fibrillary tangles lead to what

A

dysfunctional axons which causes apoptosis

396
Q

Microglia in AD

A

Usually they take up amyloid plaques, but they are also activated by plaques, so they initiate an immune response and cause damage

397
Q

Astrocytes in AD

A

Start to atrophy, cause excitotoxicity, and contribute to the inflammatory response

398
Q

ROS in AD

A

they build up during normal aging and makes the brain more vulnerable to oxidative stress

399
Q

Is there a cure for AD

A

No cure and no treatment to stop or delay symptoms

400
Q

What is a main issue for making drugs for AD

A

Need something that can cross BBB

401
Q

What is the prognosis for AD

A

Death within 8-10 years of onset

402
Q

How do people with AD usually die

A

infection

403
Q

Can we prevent AD

A

No

But good nutrition, physical activity and stimulating brain can help you stay healthy

404
Q

Our ability to develop effective therapies is limited by

A

our understanding of the disease

NEUR 1203 (2 decks)

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