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PSYCH 3410 > Lecture 8 - Brain Damage and Neuroplasticty > Flashcards

Lecture 8 - Brain Damage and Neuroplasticty Flashcards

1
Q

What is Encephalitis?

A

Inflammation of the brain caused by a microorganism (bacteria, fungi, parasite, viruses)

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2
Q

What are Abscesses?

A

Pockets of Pus

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3
Q

What is the Meningitis?

A

Inflammation of the Meninges

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4
Q

How is Meningitis treated?

A

By antibiotics

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5
Q

What is an example of meningitis

A

Syphilis

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6
Q

What do some bacterial infections do?

A

Attack neural tissue and affect host’s behaviour

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7
Q

What is an exogenous neurotoxin?

A

Comes from the environment, enters general circulation and crosses the blood-brain barrier

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8
Q

What are examples of exogenous neurotoxins?

A

Heavy metal and poison

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9
Q

What are Endogenous neurotoxins?

A

Coming from the inside - antibodies (autoimmune disorder) and excess excitatory neurotransmitters (glutamate in strokes)

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10
Q

What can heavy metals such as mercury and lead cause?

A

Toxic psychosis

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11
Q

What are examples of venoms?

A

Spiders, snake, bacterial toxins, Botox

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12
Q

What can venom cause?

A

Tardive dyskinesia

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13
Q

What is Tardive Dyskinesia?

A

Involuntary, repetitive movements

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14
Q

What are Genetic Factors for Brain damage disorders?

A

Mostly recessive genes (as one dominant would override the effects) and problems with cell division

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15
Q

What are examples of recessive disorders?

A

PKU, Beckner’s Dystrophy

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16
Q

What can there be for one disorder?

A

Mostly multiple gene mutations

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17
Q

What is the percentage of Down syndrome?

A

0.15% and increases with maternal age

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18
Q

What is Down syndrome Caused by?

A

Trisomy 21 (extra chromosome)

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19
Q

What is Epilepsy?

A

Common, reoccurring seizures of endogenous origin

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20
Q

What is the percentage of epilepsy?

A

Affecting about 4% of the population

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21
Q

What are the causes of epilepsy?

A
  • Brain Damage
  • Inflammatory Processes
  • Over 100 faulty genes
  • Issues with GABA signalling
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22
Q

What is the Diagnosis of Epislepy?

A

EEG

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23
Q

What does a seizure indicate?

A

The sudden bursting discharge of a neuron

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24
Q

What are some subtle behaviour changes of epilepsy?

A

Change in thought, mood, behaviour

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25
Q

What is a more severe behavioural change?

A

Convulsions

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26
Q

What are Convulsions?

A

Motor seizures with tremors, rigidity, loss of balance, loss of coordination

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27
Q

What are the Types of Seizures?

A

1.) Focal (partial) seizures

2.) Generalized seizures

28
Q

What do focal seizures consist of?

A

Simple and complex seizures

29
Q

What is a simple seizure?

A

Symptoms are sensory, motor or both

Symptoms spread as the discharge goes to different brain regions

30
Q

What is a complex seizure?

A

Restricted to the temporal lobe (temporal lobe seizures)

Patient engages in compulsive and repetitive behaviours

More complex behaviours (hallucinations, weirdness)

31
Q

What do Generalize Seizures consist of?

A
  1. Tonic-Clonic Seizures
  2. Absence Seizures
32
Q

What are Tonic Clonic Seizures?

A

Loss of balance and equilibrium

Violent tonic (rigidity) and clonic (tremors) convulsions

33
Q

What can Tonic-Clonic seizure result in?

A

Hypoxia - loss of oxygen in brain which can cause brain damage

34
Q

What are Absence seizures?

A

No convulsions

35
Q

What is an Absence?

A

Disruption of consciousness with ongoing behaviour (blink out or stare into space for a moment)

36
Q

What are Epileptic Auras?

A

Auras are partial or focal seizures that sometimes happen before a more severe seize occurs.

37
Q

What are the systems of an Aura?

A

Deja Vu, Euphoria, Impending Doom, Fear

38
Q

What can Auras help identify?

A

Where the seizure is originating (Aura’s nature suggests the site of epileptic focus)

39
Q

What can the frequency and severity of Epilepsy be treated with?

A

Anti-convulsant medication

40
Q

How else can you treat Epilepsy?

A

Stimulation of the Vagus Nerve deep brain stimulation

41
Q

What are newer interventions, that are still under investigation?

A
  • Transcranial Magnetic Stimulation
  • Ketogenic Diet
42
Q

What did the Kindling Model of Epislepy demonstrate?

A

The progressive development of convulsions with electrical or chemical brain stimulation

43
Q

What did the Kindling Model do?

A

Continued to stimulate the amygdala in mice, this produced temporal lobe seizures, when they stopped stimulating, these mice still produced seizures.

44
Q

What did Extensive Kindling cause?

A

Spontaneous Convulsions

45
Q

How did the Kindling model correlate to humans?

A

They found that humans have a similar progressive onset - after one epilepsy attack, seizures continue

46
Q

What is the percentage of people Parkinson’s affects?

A

Around 1% of the population (more common in males)

47
Q

What are the symptoms of Parkinson’s disease?

A

Motor: slow movements, tremor during inactivity, reduced facial expression

No dementia is seen

Pain and depression

48
Q

What is the cause of Parkinson’s ?

A

The loss of dopaminergic neurons (project to the striatum) in the substantia nigra

49
Q

What is the effect on dopamine for Parkinson’s?

A

Loss of dopamine release in the striatum of the basal ganglia

50
Q

What did Autopsies show with Parkinson’s?

A

Lewy bodies (protein clumps)

51
Q

What does the substantia nigra look like in Parkinson’s patients?

A

Diminished

52
Q

What do we see inside the striatum?

A

Lewy bodies

53
Q

What are the treatment used for Parkinson’s?

A

L-dopa (dopamine agonist)

Deep brain stimulation in the subthalamic nucleus

54
Q

What does DOPA do to a Parkinson’s patient?

A

Secretes more dopamine

55
Q

What have 80% of Parkinson’s been?

A

Idiopathic (no specific cause)

56
Q

What has 5% of Parkinson’s been?

A

Famililal

57
Q

What have the other 5% been knows as?

A

A known mutation
(SNCA, PRKN, LRRK2)

58
Q

What is Alpha-Synuclein (SNCA)?

A

Main component of Lewy bodies
2% of all familial cases

59
Q

What is Daddarian protein (LRRK2)?

A

5% of familial cases and 2% of sporadic cases

60
Q

What is Parkin (PRKN)?

A

18% of early onset (<40)
28% of recessive familial cases (<40)
80% of recessive juvenile cases (<20)

61
Q

What is MPTP model of Parkinsons?

A

Synthetic Heroin

62
Q

What is MPTP converted to?

A

The neurotoxin MPP+ in astrocytes

63
Q

What can MPP+ cause?

A

Cell lose in the substania nigra and reduced dopamine release in the striatum

64
Q

What does the MPTP model work on?

A

A primate model - hasn’t worked well on rodents

65
Q
A
66
Q
A

PSYCH 3410 (10 decks)

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