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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
Q

how can you induce a seizure in an animal model

A

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
Q

name pharmacological drugs to treat epilepsy

A

carbamazepine, phenobarbital, phenytoin (Dilantin), valproic acid

27
Q

explain how epilpesy drug operate

A

target Na+ channels or GABA (inhibitory NT), increasing rate of inhibition so reduce activity of neuronal excessive firing

28
Q

why do epileptic drugs need to be tightly controlled?

A

act similar to anesthetics, but can solve epilspey though impairs concentration and function

29
Q

name some other epilepsy treatments apart from pharmacological

A

surgery, vagus nerve stimulation, TMS, ketogenic diet

30
Q

what is neuroplasticity?

A

changes to brain structure, connectivity and function over time in response to changing environment (internal or external)

31
Q

why is neuroplasticity similar to evolution?

A

what already exists modified to better suit requiriemnt

32
Q

why is neurodegeneration important, with statistics

A

1quadrillion synapse at 3, reduce 50-90% to 100-500 trill as adult. neurons don’t due, but connections do as allows optomisatio

33
Q

how many neurons in adult brain

A

100 billion

34
Q

outline how grey matter volume neurodegenerate with age?

A

grey matter (soma) decline w age, due to reduced connections, number of other supporting cells

35
Q

outline how white matter volume neurodegenerates over adulthood

A

white matter volume grows as connection better insulated w/ myelin, connections to and from frontal cortex amongst last to be full myelinated

36
Q

outline retrograde transneuronal degeneration

A

“dying backward”. if neuron ‘cut’ post some, past neuron can die

37
Q

outline anterograde transneuronal degeneration

A

“dying forward”. if neuron ‘cut’ pre soma, then next neurons in chain will not be used

38
Q

how can neurodegeneration result from brain damages

A

disruption to homeostatic environment within and surrounding neuron

39
Q

name 5 factors that can lead to neurodegeneration:

A
  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
Q

name 2 things neuronal death can lead to

A

necrosis and apoptosis

41
Q

define necrosis

A

death due to cellular ill health (unmanaged)

42
Q

define apoptosis

A

adaptive cellular self destruct option

43
Q

whereabouts in the process does neural regeneration happen?

A

after degeneration

44
Q

outline neural regeneration in human and animals nervous system

A

chop limb off amphibians grow back
clear capacity for regrowth and regeneration in PNS, but is more complex difficult for CNS (less common_

45
Q

what impacts whether regeneration occurs

A

tissue environment, if cause of degeneration removed (disease, hypoxia)

46
Q

if the cause of generation is removed, what can occur

A

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
Q

outline regenerating implications for spinal cord injury

A

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
Q

outline neural reorganisation

A

after damage, brain maps can get reconfigured. few motor commands needs isolated activation of single muscle/small groups

49
Q

outline how phantom limb pains work

A

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
Q

what happen to reorganisations when theres peripheral input

A

reorganisation involves intact area that expanding to take over tissue that recieves no input - in amputation, remapping of area for new function

51
Q

what provide evidence that there is pressure for space in brain

A

continuous competing for brain space amongst neural circuit, map

52
Q

what is prevalence of Huntingtons

A

rare 1/10,000

53
Q

define Huntingtons

A

progressive motor disorder with simple genetic basis, and associated with severe dementia

54
Q

outline first clinical signs for Huntingtons

A

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
Q

how soon does a Huntington patient die?

A

15 yr after the first symptom

56
Q

what cause Huntington’s

A

single mutated dominant gene “huntingtin” and protein which codes it (huntingtin protein) - all individuals carrying gene develop disorder, 1/2 of their offsprings

57
Q

when does Huntington symptom emerge

A

40

58
Q

what changes to huntingtin protein is thought to form Huntington

A

increased protein aggregations means accumulations of abnormal protein clump

59
Q

describe MS

A

autoimmune, attack CNS axon myelin, emerges in early adulthood, microscopic areas of degeneration on myelin sheath, so severe associated axon ends up dysfunctional

60
Q

why MS can be difficult diagnosis

A

severity is depending on factor (number, size, positions of sclerotic lesion). periods of remission (<2years) where patient appear normal,w

61
Q

what cause MS

A

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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