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PSYC 211 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Where is language localized

A

Language is lateralized: for the vast majority of the people, language is almost entirely localized int he left hemisphere.

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2
Q

What is the role of the right hemisphere in language?

A

Relates more to how people use language, instead of what do words mean. The Prosody of speech: rhythm, tone or emphasis. Emotional state of the speaker. Recognizing people’s voices. Understanding metaphors.

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3
Q

What happens to language when the right hemisphere is damaged?

A

People get literal in their interpretation of language.

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4
Q

Phonagnosia

A

A disorder where people have great difficulty recognizing familiar voices. Result of damage to right hemisphere.

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5
Q

Posterior Language Area

A

It is near the junction of the temporal, occipital, and parietal lobes. It is a hub where the perception of a word is linked up to the concept it represents. It is critical for language comprehension.

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6
Q

Wernicke’s Area

A

Could also be called: posterior aphasia, sensory aphasia, receptive aphasia, or fluent aphasia. Location in the superior gyrus of the left hemisphere (region of the auditory association cortex). Involved in the analysis of speech sounds and in recognition of spoken words. Important for comprehending words and producing meaningful speech.

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7
Q

Broca’s Area

A

Could also be referred to as anterior aphasia, motor aphasia, expressive aphasia, or non-fluent aphasia. Location in the frontal lobe. Involved in speech production.

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8
Q

Disorders of language: Aphasia

A

Important for studying the neural basis of language in humans. Aphasia is the disturbance in understanding, repeating or producing meaningful speech, caused by brain damage. Difficulty patients experience cannot be due to sensory or motor deficits or lack of motivation. Not all language disturbances are aphasias.

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9
Q

2 broad categories of aphasia depending on the location of the brain damage:

A
  1. Damage to the frontal lobe:
    anterior aphasia, motor aphasia, non-fluent aphasia, Broca’s aphasia, expressive aphasia (difficulty producing language).
  2. Damage to the sensory association cortex: posterior aphasia, sensory aphasia, fluent aphasia, Wernicke’s aphasia, receptive aphasia (difficulty comprehending language).
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10
Q

Transcortical Sensory Aphasia

A

Caused by damage to the posterior language area. Patients fail to comprehend the meaning of words and they are unable to express their thoughts in meaningful speech. They are able to perceive and recognize words as well as speak fluently. They can repeat words back to you, read, and write without understanding. Suggests that there might be a direct connection between Wernicke’s area (recognizing words) and Broca’s area (speech production) that bypasses the posterior language area.

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11
Q

Conduction Aphasia

A

Caused by damage to and around the connections between Wernicke’s and Broca’s area known as the arcuate fasiculus. Patients are unable to repeat the words they hear. They have meaningful, fluid speech as well as intact speech comprehension. Especially impaired at repeating nonsense words or novel sounds. Disrupts short term working memory.

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12
Q

Pure Word Deafness

A

Caused by damage to Wernicke’s area or disruption of auditory input to this region. Patients are unable to recognize the words they hear. In addition, they are unable to comprehend or repeat spoken words. They speak intelligently at first but over time their speech becomes a bit awkward. They are able to hear, read lips, read and write and interpret non-speech sounds (door bell).

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13
Q

Wernicke’s Aphasia

A

Caused by damage to both Wernicke’s area and the posterior language area. Patients have features of both transcortical aphasia and pure word deafness. Patients have poor language comprehension. What they say is meaningless and filled with function words (a, the, in). Patients have natural and fluent speech, with intact prosody.

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14
Q

Brocca’s Aphasia

A

Caused by damage to Broca’s area. Patients are unable to express themselves. The speed is slow, laborious, and confluent. They understand language. They are well-aware of their deficits - makes them frustrated.

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15
Q

3 Distinct Issues of Broca’s Aphasia

A
  1. Articulation Problems: Patients have issues with engaging in the coordinated movements necessary to make appropriate speech sounds (moving lips, tongue, jaw). A related problem is sequencing the sounds properly (saying LIKSTIP instead of LIPSTICK).
  2. Agrammatism: Difficulty using and understanding grammar. Grammar is important to understand when the action is happening or who is doing it.
  3. Anomia: Patients have a hard time coming up with the appropriate word. They think about the word, but it remains at the tip of their tongue. They describe things in a roundabout way (circumlocution).
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16
Q

Facial Paresis: Volitional vs Emotion

A

Volitional: Difficulty moving facial muscles on command. Able to move muscles in response to emotion. Damage to primary motor cortex.
Emotional: Able to move facial muscles on command. Difficulty moving muscles in response to emotion. Damage to thalamus / insular cortex.

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17
Q

How are emotions measured? (Behavioural, Autonomic, Hormonal)

A

Behavioural: Movements, Facial expression, Body language.
Autonomic: Signalling through PNS, Fight or flight response.
Hormonal: Signalling through bloodstream, e.g., endorphins linked with relaxation and lower stress.

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18
Q

Common Sense Theory

A

Perceive emotional event / stimulus –> Emotion occurs –> Physiological response

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19
Q

James-Lange Theory

A

Perceive emotional event / stimulus –> Physiological response –> Emotion occurs

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20
Q

Limbic System

A

Group of brain structures involved in feeling, perceiving, and regulating emotion. Central nucleus of the amygdala: important for inducing fear, important for recognizing emotions in others. People with bilateral amygdala damage can still feel fear, it’s just much harder to find things that will induce this.

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21
Q

Ventromedial Prefrontal Cortex (vmPFC)

A

Important for regulation of emotion: inhibition of emotion expression, fear extinction learning depends on vmPFC. Damage to vmPFC: impulsive (sometimes violently), outwardly emotional, childlike. Serotonin inhibits emotional outbursts: riskier behaviour in rhesus monkeys with low serotonin.

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22
Q

Strokes

A

Sudden interruption of blood supply to the brain.
Cause: Atherosclerosis. Plaque buildup in arteries. Often form an internal carotid artery. Risk factors: Age, high blood pressure, high cholesterol. Decreases blood flow. Increases blood pressure.

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23
Q

Ischemic Stroke

A

Blocked artery: blocks blood flow in artery in brain. Thrombus: Clot forms within blood vessel. Embolus: Clot breaks away from origin & occludes artery.

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24
Q

Hemorrhagic Stroke

A

Ruptured artery: bleeding around the brain (i.e., hemorrhage). High blood pressure: pressure in artery builds up, causes wall of blood vessel to rupture.

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25
Q

Ischemic Stroke Treatments

A
  1. “Clot-busting” drugs (thrombolytics): Dissolve clot & restore blood flow. Tissue plasminogen activator (tPA). Short time window (3-4 hours).
  2. “Clot removal”: thrombectomy.
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26
Q

Hemorrhagic Stroke Treatments

A
  1. Surgery: Repair the blood vessel.
  2. Blood Pressure Management: Lowering blood pressure. Decreasing pressure in the brain.
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27
Q

Stroke: Prognosis & Recovery

A

Strokes often cause permanent brain damage: depends on size of blood vessel, time-lapse from blockage/rupture until treatment. Improvement of function over time: physical therapy, occupation therapy, speech therapy, constraint-induced movement therapy.

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28
Q

Closed-Head Injuries (Concussions)

A

Caused by a blow to head with blunt object: brain moves inside skull due to impact.
1. Coup: Brain contacts inside of skull on the same side as the impact. Direct injury at point of contact.
2. Countercoup: Brain contacts inside of skull on the opposite side of the impact. Secondary injury brain bouncing back.

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29
Q

Open-Head injuries

A

Caused by penetrating brain injuries. Damaged blood vessels, increases pressure, leads to inflammation.

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30
Q

Traumatic Brain Injuries Results cycle

A

Inflammation –> Glial Cells increase (esp. astrocytes) –> Pressure increases –> Apoptosis (neuron death) –> Scarring Plaque Residue –> Seizure Disorders, Alzheimer’s Disease, Parkinson’s.

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31
Q

TBIs: Treatment & Prognosis

A

Rest!. Avoid other hits in future. Multiple hits can lead to Mild TBI. Greater risk of developing brain problems: Seizure disorders, Neurodegenerative diseases. Alzheimer’s, Parkinson’s.

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32
Q

Seizure Disorders

A

Sudden, uncontrolled, electrical disturbances in the brain. Have many causes.

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33
Q

Causes of seizures

A

Scarring: Relates to stroke, injury, tumor. Can lead to: withdrawal or reduced function of GABA receptors. This leads to Withdrawal of GABA Agonist: GABA - regulate neuronal excitability by inhibiting neuronal firing. Example Cases: alcohol, barbiturates )(sleeping aids).
Idiopathic (unkown cause). Gene Mutations (causes neural network instability). High Fevers (in children).

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34
Q

Seizure Disorders - GABA & Alcohol: Alcohol consumption

A

Higher activity of GABA receptors –> Higher inhibition in the brain –> Neurons less likely to fire

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35
Q

Seizure Disorders - GABA & Alcohol: Long-term alcohol abuse

A

Brain adapts to constant increase in GABA activity.
Reduced GABA receptor activity –> Increased excitatory neurotransmitters –> Counteract sedative effects; maintain normal brain function.

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36
Q

Seizure Disorders - GABA & Alcohol: Alcohol withdrawal

A

GABA system no longer overstimulated; compensatory changes remain. Decreased GABA receptor activity –> Increased excitatory neurotransmitters –> Imbalance (hyper-excitable state).

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37
Q

Partial Seizures

A

Begins & remains in an identifiable part of the brain (clear focus/focal area). A simple one does not lead to loss of consciousness, but a complex one does.

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38
Q

Generalized Seizures

A

Begins & involves most of the brain (no clear focus/focal area).
Grand Mal (tonic-clonic): Aura (sensation preceding seizure), Tonic (Loss of consciousness, Intense muscular contraction), Clonic (Violent, rhythmic contractions).
Petit Mal (absent): ‘Less violent’, ‘Spells of absence’ (stare into distance, blinking repeatedly), Short, More common in children.

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39
Q

Seizure Disorders: Treatment & Prognosis

A

Anticonvulsant Drugs: Benzodiazepines - increase GABA’s inhibitory effects on the brain (increases inhibitory synapses).
Most respond well to medications.
In few cases, medication doesn’t work: surgery (if seizure foci located).

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40
Q

Non-Malignant Brain Tumours

A

Has a distinct border: “Benign”. Encapsulated: Can be removed. Cannot metastasize (spread).

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41
Q

Malignant Brain Tumours

A

Does not have distinct borders. Is cancerous. Infiltrates surrounding tissues: difficult to remove, remaining cells with reproduce. Can metastasize (ie., spread).

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42
Q

Brain Tumours damage brain tissue in two main ways

A

Compression and Infiltration

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43
Q

Meningioma Brain Tumours

A

Non-malignant. Arise within tissues of the meninges. Dura mater. Arachnoid membrane - easier to remove.

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44
Q

Glioma Tumors

A

Malignant. Arise from neural stem cells that give rise to glial cells. Grow & Divide quickly: difficult to remove. More resistant to: chemotherapy and radiation. Poor prognosis: aggressive, treatment resistant.

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45
Q

Infections of the Brain

A

Certain bacteria & viruses circumvent the blood-brain barrier. This can cause encephalitis and/or meningitis. Both are brain infections, but they affect different parts of then brain.

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46
Q

Meningitis

A

Inflammation of the meninges. Due to: Bacteria, Virus. First symptoms: Headache, Stiff neck.

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47
Q

Encephalitis

A

Inflammation of the brain itself. Due to: Bacteria, Virus, Toxic chemicals, Allergic reactions. First symptoms: Headache, Nausea, Fever.
Polio, Rabies, Herpes Simplex.

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48
Q

Polio

A

Viral Disease. Causes: Destruction of motor neurone in the brain stem and spinal cord. Can lead to: muscle weakness, paralysis. Largely eradicated: vaccines.

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49
Q

Rabies

A

Viral Disease. Causes: Widespread brain damage - enter motor neurons, spread to brain. Transmitted through: Bite of infected animal.

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50
Q

Herpes Simplex

A

Common Virus (cold sores). Causes: rare cases - enters brain, causing encephalitis, and brain damage.

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51
Q

Developmental Disorders - Toxins, Viruses, Drugs

A

Insecticides, Heavy metals (lead, mercury). Impairs fetal development: intellectual disability. Fetal Alcohol Syndrome: alcohol consumption in 3rd & 4th week of pregnancy - born prematurely, smaller birth size, distinct facial features, delayed development.

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52
Q

Developmental Disorders: Inherited Metabolic Disorders

A

“Inborn errors in metabolism”. Caused by: Gene mutations that disrupt the code (‘recipe’) for enzyme synthesis - enzyme not produced. Phenylketonuria (PKU): Absence of enzyme that converts phenylalanine to tyrosine. Tay-Sachs Disease: Absence of enzyme in lysosomes - waste buildup, cell & brain swelling.

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53
Q

Developmental Disorders - Congenital

A

Present at birth. Down syndrome: caused by extra 21st chromosome, impairs fetal development - intellectual disability, distance facial features. Increased Risk Alzehimers: after age 30, extra chromosome: overproduction amyloid-beta, forms plaques, cognitive decline.

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54
Q

Autoimmune Disease: Multiple Sclerosis - Characteristics

A

Damages myelin sheath (white matter in brain & spinal cord). Leads to: Scarring, plaques, interrupts action potentials. Sporadic disease: no obvious genetic predisposition, more prevalent in northern climates. Two hypotheses:
1. Infections Hypothesis: Childhood infections trigger immune system disruption, causing it to later attack healthy myelin.
2. Hygiene Hypothesis: Lack of early viral/bacterial exposure leads to immune system confusion, causing it to later misinterpret own myelin as harmful.

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55
Q

Autoimmune Disease: Multiple Sclerosis - Symptoms

A

Remitting-relapse MS: Cycles - symptoms false up (get worse) and recede (get better); gradually worse over time.
Progressive MS: Slow, continuous increase in symptoms and disease progression.

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56
Q

Autoimmune Disease: Multiple Sclerosis - Treatment

A

Currently no cure, but some drugs help:
Interferon b: Protein modulates (reduces during flare ups) immune response.
Glatiramer Acetate: Synthetic peptide that mimics myelin, acts as a ‘decoy’, immune s system attacks them instead of myelin.

57
Q

Neurodegenerative Diseases

A

Result of cellular apoptosis. Triggered by: aggregates of misfolded proteins. Normally: proteins fold into specific 3D structure. Diseases: proteins misfold & aggregate (clump together).

58
Q

Alzheimer’s Disease: Characteristics

A

Beta-amyloid plaques: clumps of beta-amyloid protein accumulate outside neurone –> interfere synapses (blocks communication). Neurofibrillary Tangles: Twisted fibres of tau protein form inside neurone (in cell body) –> disrupts intracellular transport.

59
Q

Alzheimer’s Disease: Characteristics - Amyloid Precursor Protein (APP)

A

Transmembrane protein. Precursor fo b-amyloid protein. Gene for this protein on chromosome 21. Can be ‘cut’ into smaller pieces by enzymes (secretase).

60
Q

Alzheimer’s Disease: Characteristics - Secretase

A

Enzymes that ‘cut’ APP into smaller pieces. In Alzheimer’s: Cuts create beta-amyloid protein.

61
Q

Alzheimer’s Disease: Characteristics - Different Mutations Linked to AD (Presenilin, ApoE)

A

Presenilin: Affect gamma-secretase. Cuts long from beta-amyloid protein. Early onset AD.
ApoE: Protein involved in moving lipids. Has three alleles. Presence of the E4 allele –> increased risk late-onset AD.

62
Q

Alzheimer’s Disease: Prognosis

A

Currently no cure. Treatment mostly consists of slowing progression. Other than age, strongest risk factor is TBI. Less prevalent in well-educated people.

63
Q

Parkinson’s Disease: Characteristics

A

Lewy Bodies: clumps of alpha-synuclein protein aciculate inside neurone (in cell body) –> interfere dopaminergic synapses (blocks communication).
Cell apoptosis: brain produces less dopamine –> motor symptoms: tremors. muscle stiffness, difficulty with balance & walking.

64
Q

Parkinson’s Disease: Characteristics - Parkin, Ubiquitin, Proteasome

A

Parkin: Identifies & “tags” misfiled protein with Ubiquitin.
Ubiquitin: Protein that is added to misfolded protein.
Proteasome: Breaks misfolded protein into amino acids.

65
Q

Parkinson’s Disease: Characteristics - Mutation in alpha-synuclein

A

Misfolded protein not recognized by Parkin. Alpha-synuclein ‘gained a toxic function’.

66
Q

Parkinson’s Disease: Characteristics - Mutation in Parkin

A

Parkin does not “tag” misfolded protein with Ubiquitin. Parkin ‘loss of function’.

67
Q

Parkinson’s Disease: Prognosis

A

Currently no cure. Drug treatments: Focus on L-DOPA - precursor of dopamine, can cross blood-brain barrier, converted to dopamine.
Deep brain Stimulation: used when no responding to L-DOPA. Targets: globus pallidus, subthalamic nucleus. Reduces abnormal activity in those regions: alleviates symptoms.

68
Q

Huntingon’s Disease: Characteristics

A

Mutation in Huntington Gene: “Long” version of Huntington gene - greater than 39 repeats, accumulate inside neurons –> Degeneratio of neurone in caudate nucleus & putamen (basal ganglia). Leads to Motor symptoms: Uncontrollable jerky movements.

69
Q

Huntington’s Disease: Prognosis

A

Currently no cure or efficient treatment. Antisense Therapy: antisense DNA to ‘bind’ to mRNA - blocks translation of mRNA into protein, breaks it down.

70
Q

Prion Protein Disease: Characteristics

A

Transmissible Spongiform Encephalopathy, Mad Cow Disease, Scrapie Disease. Transmissible Neurodegenerative Disease: Misfiling of prion proteins, spreads from cell-to-cell –> Widespread brain damage. Very Rare: Contaminated surgical instruments, tissue transplants, blood transfusions.

71
Q

ALS: Characteristics

A

Affects motor neurons: spinal cord, cranial nerves. Protein misfolding: Unclear - “handful of mutations”, variability. 90% of cases are sporadic (known cause). No cure - variability (2-4 years… 50 years).

72
Q

Autism

A

Spectrum disorder characterized by: challenges with social interaction & communication, restricted & repetitive behaviour.
Prevalence: nearly 2% of the world’s population. Predominantly genetic disorder: Gene mutations - associated with brain development. Symptoms first noticed in first 2-3 years of a child’s life.

73
Q

Autism Symptoms - Social Interaction & Communication

A

Difficulty Communicating: Abnormal or nonexistent speech - using few words, echo, referring to oneself in third person.
Challenges in Social Dynamics: Struggles interpreting social cues - “Reading the room”, tone of voice, body language.
Sensory Processing Issues: Sensory overload impacting interactions - lights too bright, sounds too loud.

74
Q

Autism Symptoms - Restricted & Repetitive Behaviour

A

Repetitive Movements: Simple repetitive motor actions - rocking back-and-forth.
Ritualistic Behaviours: Compulsive need for routine “has to be exactly like this”
Extreme Narrow Interests: Interested in very specific subjects - know everything about model trains.

75
Q

Autism Symptoms - Comorbidities

A

Intellectual disability. Seizure disorder. ADHD. OCD. Depression. Anxiety.

76
Q

Autism: Brain Development Abnormalities

A

Often abnormalities in brain development: Growth trajectory slightly differ from average - too quickly. Around age 2-3: Brain volume 10% larger than average. Adulthood: Falls back into normative range.
Abnormalities in brain function: Reduced activity in the fusiform gyrus (specialized area for faces).

77
Q

Autism: Treatment

A

Goals: Lessen impact of associated deficits, increase daily functioning & quality of life, functional independence.
Intensive special education programs & behavioural therapy: Self-care, communication, general life skills.
Supplemented with medication: Don’t usually address core symptoms, help reduce symptoms associated with comorbidities (e.g., irritability & attention).

78
Q

Most mental disorders have a genetic basis

A

Some gene variants are protective. Some gene variants increase risk.

79
Q

Gene-Environment Interaction

A

Tend to be shown in common disorders. Prevalence fluctuates across cultures & history. (E.g., Asthma, obesity, drug addiction). Not the case for some disorders: Schizophrenia & Autism.

80
Q

Schizophrenia: Gene-Environment “Paradox”

A

If Schizophrenia is predominantly a genetic disorder, why hasn’t natural selection eliminated the “bad genes”? Combination of gene variants associated with Schizophrenia are also associated with the risk o developing other disorders (ASD, OCD, etc.)

81
Q

Balance between natural selection & gene mutation

A

Harmful mutations get eliminated over time. But gene mutations arise in each generation. Around 10k protein-encoded genes in human genome expressed in brain. Mutations in any of those 10k genes strain brain development & function. Combination of gene mutations across genome –> disrupt neural network dynamics.

82
Q

Schizophrenia

A

Characterized by: social withdrawal, disorganized thinking, abnormal speech, inability to understand reality. Prevalence: nearly 1% of the world’s population. Gradual symptom onset: beginning of young adulthood.

83
Q

Schizophrenia Symptoms - Negative

A

Absence of “wanted” behaviours:
Social withdrawal, reduced emotional expression, poverty of speech, reduced motivation. Account for large part of long-term disability & poor functional outcomes. Emerges first.

84
Q

Schizophrenia Symptoms - Cognitive

A

Disorganized & irrational thinking:
Deficits in learning & memory
Poor abstract thinking
Poor problem solving. Emerges second.

85
Q

Schizophrenia Symptoms - Positive

A

Presence of “unwanted” behaviours:
Delusions (i.e., contradict reality) - persecution, grandeur, control.
Hallucinations - perception of stimuli that is not actually there (often auditory - critical). Emerges third.

86
Q

Schizophrenia Symptoms - Age at Onset

A

Differs across sexes. Most common onset of symptoms: periods of change.
Within the body: during teens -puberty, during 40’s - menopause (for females).
Outside body: during 20’s - move out, new job.

87
Q

Schizophrenia: Genetic Heritability

A

It is predominantly a genetic disorder. Concordance rates:
Identical twin: 50%
Both parents: 50%
One parent: 13%
Sibling: 8%

88
Q

Schizophrenia: Environmental Risk Factors

A

Small influence. Predominantly relate to the developing embryo. Environment in womb & developing embryo: Pregnancy “issues” - mothers’ nutrition, stress, infections. Birth month - seasonality effect: higher rates in February-may, hypothesis: viral infection –> embryo –> brain development. Raised in city: 3x more prevalent than rural areas, hypothesis: virus propagation densely populated environments.
Perinatal hypoxia/brain damage
Childhood trauma
Social isolation

89
Q

Schizophrenia Treatment

A

No cure. Main treatment: Medication + psychological and social support. Focus: alleviating symptoms.

90
Q

Schizophrenia Treatment - Dopamine hypothesis of schizophrenia

A

Excessive dopamine D2 receptor activity in the basal ganglia underlies positive symptoms: Antipsychotics & Neuroleptic Drugs - Primarily work by blocking dopamine D2 receptors –> Relieves positive symptoms. Challenges - Cannot measure dopamine signalling in living humans, does not help reduce negative symptoms.
Hypofrontality (decreased activity in frontal lobes) underlies negative symptoms: Decreased activity in dorsolateral PFC may relate to hyperactivity of local dopamine D1 receptors.

91
Q

Schizophrenia may be associated with

A

Too much dopamine in basal ganglia. To little dopamine in prefrontal cortex. Need a drug that simultaneously adjusts dopamine levels in basal ganglia & prefrontal cortex.

92
Q

Schizophrenia Treatment - Atypical Antipsychotic Medication

A

Aim to reduce both positive and negative symptoms of Schizophrenia. Typically affect several neurotransmitter receptors - not just dopamine D2 receptors. Aripiprazole: acts as partial agonist at dopamine D2 and D3 & serotonin 1A receptors.

93
Q

Schizophrenia Treatment - Partial Agonist

A

Aripiprazole. Once partial agonist binds to serotonin 1A receptors –> receptor partially activated. Functions as a “balance drug”. Too much dopamine in basal ganglia: When PA binds to receptor –> Reduces receptor activity. Alleviates Positive symptoms.
Too little dopamine in prefrontal cortex: When PA binds to receptor –> Increases receptor activity. Alleviates negative symptoms.

94
Q

Attention-Deficit/Hyperactivity Disorder (ADHD)

A

Mental disorder characterized by: problems paying attention, difficulty controlling behaviour in age-appropriate manner, hyperactivity. Usually first identified in classroom (before age 12); often comorbidities. Prevalence rate varies, but is largely genetic, and 3x more commonly diagnosed in men.

95
Q

Attention-Deficit/Hyperactivity Disorder (ADHD) Treatments

A

Management of ADHD involves counselling and medication (stimulants) or antidepressants. Medication can also lead to side effects, such as sleeping too much or too little, or eating too much or too little.

96
Q

Major Affective Disorders (Mood Disorders)

A

Characterized by disordered feelings. Disconnect between feelings and environment. There are two principal types of mood disorders: bipolar disorder, major depressive disorder. Prevalent and dangerous: people with mood disorders have high risk of self-harm and suicide ideations.

97
Q

Bipolar Disorder

A

A serious disorder characterized by cyclical periods of mani and depression. Largely genetic - around 80% of the risk is attributed to genes. Genes associated with BDP overlap a lot with genes associated with schizophrenia and autism. It affects around 2% of the population.

98
Q

Bipolar Disorder - Mania / Depression

A

Sense of euphoria that is not justified by the circumstance (inflated self-esteem). Symptoms include nonstop speech and motor activity (reduced need for sleep). Impulsive and reckless behaviour (e.g., shopping spree, sexual indiscretions). Lasts days or weeks (at least 1 week DSM5). Often followed by…
Depression: Sad & hopeless; loss of interest and pleasure in most activities.

99
Q

Bipolar Disorder Treatment

A

Lithium (used as a mood stabilizer): Most effective for treating manic phase. Once mania is eliminated, depression usually does not follow. Rapid therapeutic effect. We don’t really understand mechanism of action (like Tylenol), typically because it’s administered at high doses. Know how it works; may be decreasing presynaptic dopamine activity to reduce excitatory neurotransmission in the brain. Some anticonvulsant drugs are also prescribed as mood stabilizers. Antipsychotics and antidepressants may also be prescribed, often in combination with a mood stabilizer.

100
Q

Major Depressive Disorder (MDD)

A

Characterized by: Low mood for at least two weeks, for most of the day, every day. Feelings of hopelessness, unworthiness, guilt. High risk of self-harm and suicide. Depression affects approximately 7% of women and 3% of men. 40% of risk is attributed to genetics. Environment plays a big role (e.g., traumatic/abusive childhood).

101
Q

Treatments for MDD

A

Medications: Increase serotonin and/or norepinephrine signalling (by inhibiting their breakdown or blocking their reuptake). Ketamine, ECT (highly effective, but people don’t like it), Deep brain stimulation, Transcranial magnetic stimulation, Vagusnerve stimulation, Bright-light therapy (phototherapy), Sleep deprivation - total or REM.

102
Q

Treatments for MDD - Tricyclic antidepressants

A

Inhibit serotonin and norepinephrine reuptake but also affect other neurotransmitters.

103
Q

Treatments for MDD - Serotonin specific reuptake inhibitors (SSRIs)

A

Class of drugs that inhibit reuptake of serotonin only (E.g., Prozac, Celexa, Paxil, Zoloft).

104
Q

Serotonin and norepinephrine reuptake inhibitors (SNRIs)

A

Inhibits reuptake of serotonin and norepinephrine only. Success of treatments led to Monoamine Hypothesis.

105
Q

Monoamine Hypothesis

A

Developed largely based on the success of tricyclic and SSRI treatments. Suggests that depression is caused by insufficient monoamine receptor activity. If we raise levels, depression will go away. Additional evidence: tryptophan/serotonin depletion can elicit depressive episode in those susceptible to depression.

106
Q

Challenges of Monoamine Hypothesis

A

Trouble monitoring serotonin levels in living humans; difficult to model depression in animals.

107
Q

Evidence against Monoamine Hypothesis

A

SSRIs and SNRIs increase serotonin & norepinephrine very quickly (30 min), but symptoms do not remit for several weeks. Suggests something other than simple increase in monoamine levels is responsible for AD effects.

108
Q

Functional Imaging

A

Few (if any) correlations have emerged, except: one area of the anterior cingulate cortex becomes less active after successful treatments.

109
Q

Role of Sleep

A

One of the most prominent symptoms of depression is disordered sleep. People with depression tend not to enter slow deep state, and wake more frequently. Staying up all night tends to have an immediate antidepressant effect (but it also leads to some degree of mania) - this does not have a lasting effect.

110
Q

Stress

A

Physiological reaction caused by the perception of aversive or threatening situations. Prepares people for fight or flight situations. Involves autonomic (sympathetic branch) and endocrine (epinephrine, norepinephrine, glucocorticoids) responses that mobilize the body for action. Can have negative effects on health over time if repeatedly activated for prolonged period of time.

111
Q

Stress vs Anxiety

A

Stress can lead to anxiety (feeling of worry, fear, unease), but anxiety can also occur without any obvious trigger. Anxiety is characterized by a persistent feeling of apprehension or dread - judged in relation to others. Often feels more intense than stress.

112
Q

Physiological of Stress Response

A

Stress activates sympathetic branch of the autonomic nervous system - causes adrenal glands to release epinephrine and norepinephrine into the blood stream.

113
Q

Physiological of Stress Response - Stress activates HPA axis

A
  1. Stress triggers hypothalamus to release corticotropin-releasing hormone (CRH)
  2. CRH stimulate pituitary to secrete adrenocorticotropic hormone (ACTH).
  3. ACTH stimulates adrenal glands to release glucocorticoids (name cortisol)
  4. Result: High levels of cortisol in blood, increased HR, BP, and blood flow to muscles.
114
Q

Glucocorticoids

A

Hormones (e.g., cortisol) that are necessary for survival: prepare body for immediate action, making glucose and fat available for immediate use, increases blood flow and arousal, can also suppress secretion of sex hormones, growth hormone & immune function.

115
Q

Persistent glucocorticoid signalling can

A

Increase BP, damage muscle tissue, inhibit growth, suppress immune system, cause infertility (suppression of sex hormones), cause steroid diabetes.

116
Q

Posttraumatic Stress Disorder (PTSD)

A

A mental disorder that can develop after a traumatic event. Symptoms: Disturbing thoughts, feelings or dreams related to event. Mental or physical distress or trauma-related cues (and attempts to avoid them). Increased fight or flight response (hyperactive HPA & cortisol signalling). Symptoms can interfere with functioning & lead to hopelessness and risk of suicide. Most people exposed to trauma don’t develop PTSD. 30% of variance in PTSD is related to genetics.

117
Q

PTSD Treatment

A

CBT, group therapy, supplemented by medication (e.g., SSRIs)

118
Q

Anxiety Disorders

A

A variety of disorders characterized by unrealistic and unfounded fear and anxiety. Often include: muscle tension, expectation of impending disaster, continuous vigilance for danger.

119
Q

Generalized anxiety disorder (GAD)

A

Excessive anxiety and worry that impairs functioning.

120
Q

Social anxiety disorder

A

Excessive fear of being exposed to scrutiny/judgment of other people; leads to avoidance.

121
Q

Panic disorder

A

Episodic periods of severe & unremitting terror (intense fear); shortness of breath, heart palpitations, & other physical symptoms.

122
Q

Anticipatory Anxiety

A

Fear of having a panic attack. Sometimes leads to the development of agoraphobia.

123
Q

Agoraphobia

A

Fear of being away from home or other protected places.

124
Q

Causes of anxiety disorders

A

Combination of genetic and environmental factors (e.g., child abuse, poverty). Brain circuits involved are not well known: older people with dementia struggle with anxiety, amygdala (increased activation) and PFC (decreased activation) may be involved.

125
Q

Anxiety Disorders Treatments

A

Lifestyle changes: exercise, socialize, sleep, diet, reduce caffeine & smoking. CBT: First line of treatment. Medications: SSRIs - long term treatment, Benzodiazepines - emergency use, but risk of abuse.

126
Q

Obsessive-Compulsive Disorder (OCD)

A

Characterized by:
1. Obsessions: intrusive/repetitive thoughts.
2. Rituals/Compulsions: repeatedly engaging in certain behaviours/routines to deal with the obsessions (e.g., handwashing, checking if door is locked, stove is off); performed to seek relief.
Significant distress and impairment.

127
Q

OCD Symptoms

A

Symptoms usually characterized into 4 groups:
1. Symmetry
2. Cleaning (germs, contamination)
3. Hoarding
4. Forbidden thoughts (violation, religious, or sexual nature).
People with OCD are unable to control obsessions and compulsions.

128
Q

OCD Prevalence

A

Affects <2% of population. Nearly twice as common in females than males. Onset typically before age 25. 50% of risk attributed to genetics, 50% to environmental factors - environmental risk factors can include a history of child abuse, brain damage, or infections.

129
Q

OCD Treatment

A

Cognitive Behavioural Therapy: exposure & response prevention (ERP) - increase exposure to what causes the problems without engaging in compulsive behaviour.
Not great pharmacological treatments; SSRIs sometimes.
Severe cases: cingulotomy (cutting a fibre bundle between PFC & anterior cingulate).
Without treatment, condition can last decades.

130
Q

Substance Abuse Disorders

A

Extremely serious debilitating disorder. Big players: alcohol, opiates, cocaine & meth, nicotine, barbiturates, & benzos. Some gene variants predispose people to becoming addicted to a specific drug, while others increase the risk of developing addiction in general.

131
Q

Substance Abuse Disorders - Reinforcement Learning

A

Addictive drugs positively reinforce behaviour. Reinforcement is most “effective” when consequence of action are immediate (e.g., heroin versus morphine). The most addictive drugs rapidly increase dopamine signalling.

132
Q

Substance Abuse Disorders - Tolerance / Withdrawal

A

Tolerance: Drug effects get smaller with repeated use; need greater doses to achieve the same effect.
Withdrawal: Appearance of symptoms opposite of those produced by drugs when the drug is not taken.

133
Q

Substance Abuse Disorder - Negative Reinforcement

A

Referred to (in psychology) when a behaviour is reinforced by the removal of an aversive stimulus.

134
Q

Substance Abuse Disorder Treatments - Naltrexone

A

Opioid receptor antagonist (slow onset; long-acting); reduces the high produced by opiates.

135
Q

Substance Abuse Disorder Treatments - Naloxone (Narcan)

A

Opioid receptor antagonist (rapid onset; short-lived); reverses effects of opiate overdose.

136
Q

Substance Abuse Disorder Treatments - Methadone

A

Administered in clinics. Strong opiate but slower onset & offset (no rush like with heroine; similar concept to nicotine patches).

137
Q

Substance Abuse Disorder Treatments - Buprenorphine

A

Partial opioid receptor agonist (blocks effects of other opiates and produces weak effect).

138
Q

Substance Abuse Disorder Treatments - Varenicline

A

Partial agonist at nicotinic (acetylcholine) receptors; used for nicotine addiction

PSYC 211 (4 decks)

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