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Intro to behavioural neuroscience > neurological disorders > Flashcards

neurological disorders Flashcards

1
Q

Difference between neurological and psychological disorders

A

In neurological disorders you can point to a problem

Psychological disorders a problem with pathways

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2
Q

closed head injuries

A

caused by low to the head by blunt surface.

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3
Q

open head injury

A

injury to the parts damaged by the object

there is damage to blood vessels which may deprive parts of the brain from blood

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4
Q

Do you always notice when you have . TBI

A

Not always immedietely

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5
Q

survivors of TBI will normally have

A

Scarring and seizures

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6
Q

seizure disorders

A

runaway excitation in the brain. When there is no balance in excitation and inhibitio

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7
Q

causes of seizure disorders

A

hit to the head, strokes
Genetic mutations in ion channels that makes neurons more excitable
In children, running a high temperature may cause seizures
- low depressants eg alcohol

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8
Q

why is alcohol withdrawal life threatening

A

because the body has gotten used to operating with alcohol in the body

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9
Q

is there always brain damage when a seizure occurs

A

there could be because excitsbility leads to aoptoid

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10
Q

partial seizures/ focal seizure

A

restricted to a small part of the brain
Simple
complex: produces loss of consciousness

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11
Q

Generalized

A

involves most of the brain

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12
Q

Where in the brain can seizures occur

A

anywhere in the brain.
Visual cortex: see lights
Temporal cortex: hearing sounds and smelling things
prirital cortex: out of body experiences

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13
Q

tonic-clonic seizure

A

Seizure in the whole brain
might starts with an aura
tonic phase_ muscle contracts
Clonic phase- convlusions

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14
Q

Absence seizures

A

they stop what they are doing and just stare off into the distance.

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15
Q

ways in the seizures are treated

A

by taking anticonvulsant drugs .These increase the effectiveness of inhibitory synapses.

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16
Q

what other method other than drugs do the treat focal seizures

A

They trigger a seizure and find where the seizuree affects and they cut out that part..

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17
Q

Why will a person with focal seizures after having that part cut out will sometimes have better cognitive funnction

A

Because parts of the brain that were working to inhibit the excitory neurons of the focal point are now free to be used for other cognitive tasks

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18
Q

Tumor

A

mass of cells growing uncontrollably and they serve no function

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19
Q

non malignant tumors

A

have distinct borders and they dont spread

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20
Q

malignant tumors

A

dont have distinct border and their cells metasticize aka spread

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21
Q

which tumor is more life threatening

A

they are both

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22
Q

why are neurons rarely cancerous

A

they do not divide

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23
Q

Why do you have brain tumors then?

A

its all the non neuronal cells that support brain function

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24
Q

Gliomas

A

they are a malignant brain tumor.

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25
how they treat gliomas
radiation therapy: use lasers to cause DNA damage to kill of the affected cells Chemotherapy: kill dividing cells. Target replication to cause mutations resulting in apoptosis.
26
Meningioma
Non-malignant. They grow slow and eventually manifest as a seizure
27
strokes
loss of blood to an area in the brain.
28
types of strokes
Hemarrhagic stroke: tear in blood vessel | Ischemic strokes: blockage in capillary in the brain
29
atherosclerosis
linings of the arteries develop layers of plaque. Connected to high cholesteral. It is a precursor to heart attacks and strokes.
30
Thrombus
blood clots that form within blood vessels
31
embolus
piece of blood clot that breaks off and goes to block another part of the circulatory system
32
How are we dealing with reducing clots
administration of tPA which dissolves clots. | But if there is a tear in the brain it is an neural toxin
33
What other solutions are being proposed for blood clots
using a protein found in vampire bats. These dissolve clots.
34
what normally cause disorders in development u
toxins and viruses and drugs taken during gestation
35
drinking during pregnancy can lead to
early birth small birth weight slow development But also there is a critical fay where a certain concentration of alcohol will lead to severe brain development problem
36
Inherited metabolic errors
errors of metabolism that can result in disturbed brain function
37
examples Inherited metabolic errors
PKU: disorder in which you cannot produce the enzyme that breaks down
38
encephalitis
inflammation in the brain caused by bacterial or viral infections
39
Meningitis
inflammation of meninges
40
Polio
viral infection that destoys neurons of the brain and spinal cord
41
rabies
viral infection that cause brain damage transmitted through bites
42
Herpes
virus that causes cold sores but can also cause brain damage.
43
autoimmune disorders
over active immune system and starts affecting body proteins
44
MS
immune system degrading myeline
45
What happens with MS
Neural transmition is disturbed
46
progressive MS
Increasing symptoms
47
remitting-relapsing MS
Starts-stops-starts common in people who live far from the equator. Might be due to previous viral attacks
48
treating MS
Interferons beta: protein that makes the immune system back off myelin Glatiramer acetate: blood the with the this decoy the immune system .
49
Neurodegenerative diseases
Neurons in the brain just start to die. Different cells depending on the disease.
50
How are proteins meant to interact with each other
they are meant to have purposeful interaction not aggregating
51
what is the driving force for neurodegenerative diseases
proteins starting to clamp up and building up over time
52
Transmissible spongiform encephalopathy
contagious disease. it causes a degeneration that causes spongelike appearances caused bu protein called prion
53
prion
a protein that exist in two forms that differ in their 3D shape.
54
how prion protein causes other proteins to fold abnormally
when they touch other proteins
55
sporadic disease
not obviously hereditary or an infectious agent
56
huntington disease
inherited gene disorder. Degeneration of the basal ganglia | An increasing loss of coordinations and then later jerky movements
57
the onset of huntington disease
where are many CAG repeats in the huntington protein the cell cuts it in half and then half starts to aggregate and form clamps and eventually where it is happening will start to die off.
58
how to treat huntington disese
no cure
59
trial for cures for huntington disease
Antisense therapy: injecting antisense DNA that bind to the extra long huntingtons proteins and they are destroted
60
parkinsons disease
also called a movement disorder. Slowness of movement and difficulty initiating movement
61
causes of parkinsons disease
death of dopamine neurons in the midbrain ie substantia nigra.
62
proteins affected
aggregation of alpha-synuclein: Dopamines are affected because they express this protein. Build up over time.
63
manifestation of parkinsons
slow movement and trouble initiating movement
64
Lewy body
alpha-synuclein accumulation into little balls.
65
enzyme parkin
enzyme parkin: floats around monitoring for misfolded proteins. It then adds ubiquitin molecules and proteosomes are meant to break it down
66
On set of parkinsons
mutation on parkin made dopamine sensitive and it produced more alpha-synucei
67
toxic gain on function
Dominant gene produces things that shouldnt be there
68
loss of function
2 recessive proteins resulting in the lack of a certain function
69
Treatment for parkinsons
administering L-dopa that will help make dopamine as soon as the symptoms shows
70
other characteristics of parkinsons
Subthalamic nucleus globus pallidus internal show hyper activity when there is little dopamine Deep brain stimulation: subthalamic nucleus, you stimulate at 130 times per second and the neurons stop having action potentials you can up or down regulate the frequency.
71
dementia
loss of cognitive abilities associated with old age
72
alzheimers
caused by misfolding of beta-amyloid protein. | causes memory loss, motor deficit
73
amyloid plaques
clamp of amyloid beta proteins
74
APP
precursor for amyloid beta proteins
75
secratases
cuts APP to fregments 3 parts
76
on set of alzheimers
secretase can cut in the long position resulting in longer APP which then aggregates and forms plaques
77
presenilin
protein that forms secretases. When mutated cause secretases to cut longer APP which leads to aggregation
78
Apolipoprotein
regulates cholesteral in the blood. A change in cholesterol levels in the cell also affects the action of secretases
79
who are at less risk
people who are active | well educated people
80
Treatments
giving Ach estarase inhibitors to keep ach longer at synapses. This helps because Ach does off faster NMDA receptor antagonist, activation which slows down cell death. which will keep them
81
immunotherapy
making antibodies to destroy proteins in the body eg Beta amyloid
82
why is it that clearing Beta Amyloid not working to stop alzheimers
Tau proteins which are microtubules which are involved in cell transport. These are hyperphosphorylated in alzheimers and tangle up
83
neurofibriliary tangles
hyperphosphorylated tau proteins
84
ALS aka Lou Gehrigs disease
attacks the spinal cord and cranial nerve motor neurons
85
causes of ALS
there is not just one protein that is acting up. Usually 2 or more genes required for this to ocur The ones that are hereditary
86
why are motor neurons vulnerable
because they are so long
87
treatments for ALS
Not much- riluzole which reduces glutamate reduced
88
what determines what mutations survive
how they affect survival. smaller effect mutations die off less. The family line continues with good genes
89
psychiatric illnesses
they are common | harmful to reproductive success
90
how psychiatric illnesses survive in gene line
- Maybe they were neutral but todays conditions are causing them to be active.
91
schizophrenia
Caused by many genes and so are manny other psychiatric illinesses

Intro to behavioural neuroscience (6 decks)

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