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PSY1003 SEMESTER 2 > PSY1003 SEMESTER 2 - WEEK 3 > Flashcards

PSY1003 SEMESTER 2 - WEEK 3 Flashcards

1
Q

name 2 types of epilepsy

A

partial and generalised

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2
Q

define epilepsy

A

chronic medical condition produced by temporary changes in electrical function of brain, causing seizures which affect awareness, movement or sensation

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3
Q

what 2 types of seizures in partial epilepsy

A

simple partial and complex partial

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4
Q

what 2 types of seizures in generalised epilepsy

A

grand mal and petit mal

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5
Q

name commonness of epilepsy?

A

0.5-1% population, mainly children and elderly

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6
Q

explain how epilepsy is idiopathic

A

theres no single cause, symptom depend on epileptic type or brain area affected

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7
Q

why is the diagnosis of epilepsy not that informative

A

due to heterogeneity of disease types, that will affect individual and require treatment/adjustment in different way

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8
Q

outline what partial/focal epilepsy is

A

not involving the whole brain,
epileptic neuron at focus begins to discharge together in bursts, producing EEG epileptic spike. tends to spread to other brain areas but not entire so no loss of conscious

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9
Q

outline simple partial seizures

A

localised to specific areas of brain, localised effect usually sensory or motor

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10
Q

give example of simple partial seizure

A

localised jerking beginning in right hand, progress to clonic movements = entire arms jerking, Jacksonian march. focal motor seizure, produced by epileptiform activity in motor cortex controlling that arm

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11
Q

explain complex partial seizure

A

also “temporal lobe epilepsy”- common localisation in the temporal lobe
associated with coordinated but inappropriate motor beh like running
compulsive, repetitive but simple (automatisms)
may be absent, lasts few minutes but no memories

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12
Q

how common are complex partial seizures

A

1/2 of all adult epilepsy

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13
Q

outline generalised epilepsy

A

entire brain
begin as either focal discharge spreading or discharge beginning simultaneously in all brain area
results from diffuse pathology or begin focally in brain structure such as thalamus that project to many brain areas

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14
Q

outline petit mal (absence) seizures

A

can involve entire brain = generalised
brief absence, disrupted consciousness (not know, vacant expression, fluterring eye)
bilaterally symmetrical 3persecond spike-and-wave discharges EEG
more common in children, and usually disappears with age

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15
Q

what are concerns around petit mal seizure in childrens

A

more common and widely underdiagnosed = education disruption, social development

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16
Q

outline grand mal (tonic-clonic) seizures

A

often involve whole brain
lose consciousness, go to ground, rigidly extends all limbs (tonic phase)
jerk of all extremities (clonic phase)
bites tongue, incontinence, cyanosis and hypoxia

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17
Q

what is cyanosis

A

turn blue due to excessive oxygen extractions from blood

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18
Q

outline hypoxia

A

shortage of oxygen supply to a tissues

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19
Q

explain auras

A

prededing partial seizure and abnormal sensation, due to early abnormal electrical activity originating from seizure focus, gives clues on epileptic focus location, warns patient of impending seizures

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20
Q

give some examples of aura

A

sense of fear,
rising feeling in abdomen,
strange tastes or smells: metalic
visual sensations akin to hallucinations

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21
Q

name what surgical option can be done in severe epilepsy

A

remove problematic tissue, cut corpus callosum (rare due to pharmalogical advance and severe impact on brain functions)

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22
Q

outline the role of EEG when a seizure occurs

A

detects synchronised activity of many neurons (field potentials), influences diagnosis. too much synchronisation from too many neurons

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23
Q

compare EEG from normal to epileptic

A

in non-epileptic, when put bright light, EEG waves shown visual cortex, but in epilepsy there are extensive synchronisation of firing across many neuron

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24
Q

what components of an EEG do we study in epilepsy?

A

frequency (speed of waveforms oscillations) and signal over time. 3Hz is associated with petit mal seizure

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25
how can you induce a seizure in an animal model
inject an excitatory agent into cortex of rat, recreates epileptic activity of a spreading seizure, used to investigate treatment option like focal cooling for seizure focus
26
name pharmacological drugs to treat epilepsy
carbamazepine, phenobarbital, phenytoin (Dilantin), valproic acid
27
explain how epilpesy drug operate
target Na+ channels or GABA (inhibitory NT), increasing rate of inhibition so reduce activity of neuronal excessive firing
28
why do epileptic drugs need to be tightly controlled?
act similar to anesthetics, but can solve epilspey though impairs concentration and function
29
name some other epilepsy treatments apart from pharmacological
surgery, vagus nerve stimulation, TMS, ketogenic diet
30
what is neuroplasticity?
changes to brain structure, connectivity and function over time in response to changing environment (internal or external)
31
why is neuroplasticity similar to evolution?
what already exists modified to better suit requiriemnt
32
why is neurodegeneration important, with statistics
1quadrillion synapse at 3, reduce 50-90% to 100-500 trill as adult. neurons don't due, but connections do as allows optomisatio
33
how many neurons in adult brain
100 billion
34
outline how grey matter volume neurodegenerate with age?
grey matter (soma) decline w age, due to reduced connections, number of other supporting cells
35
outline how white matter volume neurodegenerates over adulthood
white matter volume grows as connection better insulated w/ myelin, connections to and from frontal cortex amongst last to be full myelinated
36
outline retrograde transneuronal degeneration
"dying backward". if neuron 'cut' post some, past neuron can die
37
outline anterograde transneuronal degeneration
"dying forward". if neuron 'cut' pre soma, then next neurons in chain will not be used
38
how can neurodegeneration result from brain damages
disruption to homeostatic environment within and surrounding neuron
39
name 5 factors that can lead to neurodegeneration:
1. NT function disruption (input lost, excitotoxicity- releasing too much NT into synapse poisons next neurons) 2. loss of O2, glucose 3. attack from infection, toxin, own immune system 4. faulty genetic signalling 5. brain injury
40
name 2 things neuronal death can lead to
necrosis and apoptosis
41
define necrosis
death due to cellular ill health (unmanaged)
42
define apoptosis
adaptive cellular self destruct option
43
whereabouts in the process does neural regeneration happen?
after degeneration
44
outline neural regeneration in human and animals nervous system
chop limb off amphibians grow back clear capacity for regrowth and regeneration in PNS, but is more complex difficult for CNS (less common_
45
what impacts whether regeneration occurs
tissue environment, if cause of degeneration removed (disease, hypoxia)
46
if the cause of generation is removed, what can occur
in the PNS, schwann cell guide successful "rejoining" up of axons distance to target also key factor in occurance for effective regen but regrowth can be detrimental eg: phantom limb syndrome - schwann cell don't guide them properly
47
outline regenerating implications for spinal cord injury
part of CNS- no schwann cells. oligodendrocyte guide regeneration. target of spinal chord axons usually distant, so less success. however PNS target muscle, so increased success
48
outline neural reorganisation
after damage, brain maps can get reconfigured. few motor commands needs isolated activation of single muscle/small groups
49
outline how phantom limb pains work
neural systems lose input however cell are still intact and connected to rest of nervous system - in non-amputee sends signal to clench hand, feedback come back to unclench, but if no hand then no feedbacks sent meaning constant loop. use mirroring to treat
50
what happen to reorganisations when theres peripheral input
reorganisation involves intact area that expanding to take over tissue that recieves no input - in amputation, remapping of area for new function
51
what provide evidence that there is pressure for space in brain
continuous competing for brain space amongst neural circuit, map
52
what is prevalence of Huntingtons
rare 1/10,000
53
define Huntingtons
progressive motor disorder with simple genetic basis, and associated with severe dementia
54
outline first clinical signs for Huntingtons
increased fidgetiness, developing to rapid complex, jerky movements of entire limb and eventual motor and intellectual deterioration, causing individuals unable to control bowl, feed self, recognise important other
55
how soon does a Huntington patient die?
15 yr after the first symptom
56
what cause Huntington's
single mutated dominant gene "huntingtin" and protein which codes it (huntingtin protein) - all individuals carrying gene develop disorder, 1/2 of their offsprings
57
when does Huntington symptom emerge
40
58
what changes to huntingtin protein is thought to form Huntington
increased protein aggregations means accumulations of abnormal protein clump
59
describe MS
autoimmune, attack CNS axon myelin, emerges in early adulthood, microscopic areas of degeneration on myelin sheath, so severe associated axon ends up dysfunctional
60
why MS can be difficult diagnosis
severity is depending on factor (number, size, positions of sclerotic lesion). periods of remission (<2years) where patient appear normal,w
61
what cause MS
genetic factors play less of causal roles 25% concordance in MZ and 5% DZ twins. more common in women, risk factors of vitamin D deficiency and smoking

PSY1003 SEMESTER 2 (10 decks)

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