Neuropsychological Diseases Flashcards

(54 cards)

1
Q

What are 5 neuropsychological diseases?

A
  • Epilepsy
  • Parkinson’s Disease
  • Huntingdon’s Disease
  • Multiple Sclerosis
  • Alzheimer’s disease
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2
Q

What is the primary symptom of epilepsy?

A
  • Recurrent seizures (intense neurological activity that originates in a specific region of brain) of endogenous pain
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3
Q

What is the prevalence of epilepsy?

A
  • Affects about 3.8% of population
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4
Q

What are 4 causes of epilepsy?

A
  • Brain damage
  • Inflammatory processes
  • Genes (over 100 known so far)
  • Faults at inhibitory synapses (GABA, specifically GABAb receptors) -> excessive excitation
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5
Q

How is epilepsy diagnosed?

A
  • Electroencephalogram (EEG)

- See bursts of high amplitude spikes during seizures; single spikes between attacks

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6
Q

What is a seizure?

A
  • Sudden synchronous bursting discharge of neurons
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7
Q

What are 2 types of behavioural changes with epilepsy?

A
  • Convulsions: motor seizures with clonus (tremors), tonus (rigidity), loss of balance, loss of consciousness
  • Subtle: changes in mood, thought, behaviour
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8
Q

What are focal seizures?

A
  • Specific focus of origin

- Simple vs. complex

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9
Q

What are generalized seizures?

A
  • Originates in multiple sites

- Absence (petit mal) vs. Tonic-clonic (grand mal)

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10
Q

Describe simple focal seizures?

A
  • AKA Jacksonian seizures
  • Symptoms are primarily sensory or motor or both
  • Symptoms spread as epileptic discharge spreads through different brain regions
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11
Q

Describe complex focal seizures?

A
  • Often restricted to temporal lobes
  • Patient engages in compulsive and repetitive simple behaviours (automatisms)
  • More complex behaviours almost normal
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12
Q

What are 6 examples of symptoms in simple partial seizures?

A
  • Somatosensory: tingling of contralateral limb, face, or side of body
  • Focal motor: tonic-clonic movements of upper/lower limb
  • Contraversive: head/eyes turned to opposite side
  • Autonomic: sweating, flushing, nausea
  • Auditory: hears ringing, hissing or noises
  • Visual: sees flashes of light, scotomas, blurring
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13
Q

What do the symptoms of complex partial seizures look like?

A
  • Multiple symptoms of simple partial seizures
  • Complex hallucination
  • Undoing buttons of shirt
  • Loss of consciousness
  • Whole videos replaying in mind
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14
Q

Describe tonic-clonic seizures?

A
  • Loss of consciousness and equilibrium
  • Violent tonic (rigidity) - clonic (tremors) convulsions
  • Resulting hypoxia may cause brain damage (loss of consciousness)
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15
Q

What are absence seizures?

A
  • Not associated with convulsions
  • Absences: disruption of consciousness with cessation of ongoing behaviour
  • Bilaterally symmetrical EEG
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16
Q

What are auras?

A
  • Peculiar subjective experiences (e.g. smell, hallucination, feeling)
  • Often precede seizures (warning)
  • Nature suggests site of epileptic focus (ex. olfactory)
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17
Q

What is kindling?

A
  • The progressive development of convulsions with a series of periodic electric or chemical brain stimulations
  • Currents that induce some degree of stimulation locally
  • Neural changes are permanent
  • Produced by stimulation distributed over time
  • Extensive kindling -> spontaneous convulsions
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18
Q

How can kindling be used as a model for epilepsy?

A
  • Convulsions are similar to human’s
  • Human post-traumatic epilepsy follows a similar progressive onset
  • BUT it is not spontaneous
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19
Q

How prevalent is Parkinson’s disease?

A
  • About 1% of population (higher in males)

- Mostly middle and old age (#1 risk factor)

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20
Q

What are some symptoms of Parkinson’s disease?

A
  • Slow movements, tremor during inactivity (disappears with voluntary movements), difficulty initiating movements, muscle rigidity, reduced facial expression
  • Pain and depression are common
  • No single cause
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21
Q

What is Parkinson’s disease?

A
  • Degeneration of dopaminergic neurons in substantia nigra
  • Loss of dopamine release (and therefore loss of neurons) in the striatum of basal ganglia
  • Autopsies reveal Lewy bodies (protein clumps) in substantia nigra
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22
Q

What are some treatments of Parkinson’s disease?

A
  • L-dopa, DA agonists
  • > for early stages
  • > dyskinesia is a possible side effect
  • Deep brain stimulation of STN
  • > buys time
  • > mitigate symptoms
23
Q

Which dopaminergic tract tends to be affected in Parkinson’s disease?

A
  • Nigrostriatal tract
24
Q

How do genetics influence Parkinson’s disease?

A
  • 80% idiopathic (no known cause)
  • 15% familial/inherited
  • 5% a known mutation
25
What is Alpha-synuclein?
- Main component of Lewy bodies - Single nucleotide mutations are uncommon - Multiplication mutations = 2% of familial cases
26
Which 3 mutations have had the most research in the genetics of Parkinson's disease?
- Alpha-synuclein - Dardarin protein - Parkin
27
What is the MPTP model of Parkinson's disease?
- 'synthetic heroin' - MPTP causes cell loss in substantia nigra, and reduced dopamine release in the striatum - MPTP is mostly a primate model - MPTP used to develop dopaminergic drugs for PD
28
What is Huntington's disease?
- A rare progressive motor disorder of middle/old age with a strong genetic basis - AKA Chorea - Begins with fidgetiness and progresses to jerky movements of entire limbs and severe dementia - Death usually occurs within 15 years - Clumps of proteins within brain - No cure
29
What causes Huntington's disease?
- Caused be a single dominant gene | - Huntingtin gene -> Huntingtin protein
30
When do the first symptoms of Huntington's disease usually appear?
- Age 40
31
Where does Huntington's disease originate?
- Basal ganglia | - Leads to tissue loss in brain (see larger ventricles)
32
What does 'multiple sclerosis' mean?
- Multiple hardenings
33
What is multiple sclerosis?
- Progressive loss of CNS myelin (autoimmune) - Eventually neuronal degradation - Early onset -> progressive - Periods of remission are common
34
What are some advanced symptoms of multiple sclerosis?
- Visual disturbances - Muscle weakness - Numbness - Tremor - Loss of motor coordination (ataxia)
35
Is there a cure for MS?
- No cure | - Drugs (mostly immunomodulators) may retard progression/block symptoms
36
What are some causes of multiple sclerosis?
- Genetic predisposition - Environmental factors - Epigenetic influences
37
Describe the genetic factors of MS?
- 25% concordance in monozygotic twins - 3x higher in females - 0.15% greater in Caucasians - Several genes - Several non-coding RNAs (regulation of genes)
38
What environmental factors contribute to MS?
- Climatic zone (> childhood in cold climates) - Viral or bacterial infections (e.g. Epstein-Barr virus for mononucleosis) - Life style (smoke, diet, sun exposure)
39
What epigenetic influences may play a role in MS?
- Vitamin D and other chemicals | - Vit D seems to help symptoms in some studies
40
Where is the highest rates of MS in the world?
- Orkney islands off of Scotland
41
What is the most common cause of dementia?
- Alzheimer's disease
42
Describe Alzheimer's disease?
- Age-related (10% over 65 and 35% over 85) - Progressive - Microbleeds also common
43
What are some early symptoms of Alzheimer's?
- Confusion | - Selective decline in memory and attention
44
What are some late symptoms of Alzheimer's?
- Massive neurological impairment (e.g. bladder, motor control)
45
How is Alzheimer's disease diagnosed?
- Definitive diagnosis only at autopsy - Loss of neurons - Neurofibrillary (tau) tangles - Amyloid plaques
46
Where does Alzheimer's disease begin?
- Regions involved in learning/memory | - Ex. Posterior parietal cortex, Inferior temporal cortex, hippocampus, entorhinal cortex, amygdala, prefrontal cortex
47
Describe the neurobiology of early onset/familial Alzheimer's disease?
- Mutations in 3 specific genes for variants of amyloid proteins or their regulators
48
Why is Alzheimer's disease more common in those with Down syndrome?
- Beta-amyloid gene is found on chromosome 21, which there is a trisomy of in Down syndrome
49
How does late-onset Alzheimer's disease occur?
- Mutations in several (15+) genes for amyloid or tau proteins
50
What is the pathogenic spread hypothesis?
- Can tau-neuron transfer to healthy neuron? | - Begin in temporal lobe and spread
51
What are some treatments for Alzheimer's disease? Can Alzheimer's disease be cured?
- No cure (reduce symptoms) - Decline in ACh levels (ACh agonists help) - Immunotherapy (against amyloid proteins) - Reducing inflammation has been effective in animal models
52
What does 'transgenic' mean?
- Animals with the genes of another species
53
What is the transgenic mouse model of Alzheimer's disease?
- Only humans and a few related primates spontaneously develop amyloid plaques - Genes for rapid human amyloid synthesis introduced in mice - Genes for human tau protein into mice - Some can express both (which is the best model) - Individually, can help explain contributions of each
54
How does the proximity to amyloid plaques affect neuronal response?
- Neurons found closer to amyloid plaques have altered activity - Farther = more normal neurons