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PSYC 351D > Chapter 16 > Flashcards

Chapter 16 Flashcards

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1
Q

What kind of disorder is schizophrenia?

A

Psychiatric disorder

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2
Q

What is a positive symptom?

A

appearance of abnormal
behaviours

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3
Q

What is a negative symptom?

A

loss of
normal behaviour

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4
Q

What are the 6 symptoms of schizophrenia?

A

Delusions
Hallucinations
Disorganized speech
Disorganized behaviour or excessive agitation
Psychomotor symptom: Catatonic behaviour
Negative symptoms: blunted emotions or less or interest or drive

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5
Q

What is a delusion?

A

Belief that distorts reality - believing you are god

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6
Q

What are hallucinations?

A

distorted perceptions

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7
Q

What is catatonic behaviour? How to fix it?

A

Muscle rigidity and immobility. Benzos

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8
Q

What are the three correlates of schizophrenia?

A

Genetics, development, brain correlates

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9
Q

What are the genetic correlates of schizophrenia?

A

High concordance of schizophrenia in identical twins: ~80%
Mutations on several known genes is associated with predisposition

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10
Q

What are the developmental correlates of schizophrenia?

A

Diagnosed in young adulthood, but likely begins early in development
Environmental factors acting through epigenetic mechanisms may influence brain
development, leading to disorder.

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11
Q

What are the brain correlates of schizophrenia?

A

Enlarged ventricles and thinner cortex in the medial temporal and frontal regions
Abnormal dendritic fields in cells of the dorsal prefrontal regions, hippocampus, and
entorhinal cortex (disorganized)

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12
Q

What is the dopamine theory of schizophrenia?

A

Caused by too much dopamine

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13
Q

What is the support for the dopamine theory?

A

Dopamine agonists (amphetamines) can produce psychotic symptoms and give rise to tardive dyskneisia - motor rigidity
Neuroleptics/antipsychootics are dopamine antagonisrs used to treat schizophrenia

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14
Q

What shows that the dopamine hypothesis is too simple?

A

Many other neurochemical abnormalities are associated with schizophrenia

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15
Q

What are the three types of mood disorders (psychiatric disorders)?

A

Major depression
Mania
Bipolar disorder

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16
Q

What is major depression?

A

Prolonged feelings of worthlessness; sleep disturbances; general
slowing of behavior; frequent thoughts of suicide

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17
Q

What is mania?

A

Characterized by excessive euphoria; affected person often formulates
grandiose plans and is uncontrollably hyperactive
Person feels very in control

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18
Q

What is bipolar disorder?

A

alternating periods of depression & mania

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19
Q

What are some predisposing factors to depression?

A

neurological (brain injury), stress, vitamin deficiency, others are psychological or experiential

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20
Q

What do predisposing factors activate in depression?

A

HPA axis

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21
Q

How is prolonged stress related to depression?

A

Predisposes individuals to brain injury and neuroinflammation –> triggers immune response
Decrease activity in serotonergic and noradrenergic systems (systems that regulate mood)
Overactivity in HPA axis –> excess cortisol release –> damage to hippocampus

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22
Q

Is cortisol for short or long stress?

A

Long-term stress (moving houses)

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23
Q

Explain the stress response in the brain?

A

Hypothalamus releases corticotropin releasing hormone –> pituitary releases ACTH –> causes adrenal to release cortisol
cortisol goes to brain and give feedsback to hypothalamus to stop releasing cortisol

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24
Q

What happens to the stress response in someone with depression?

A

The high cortisol degenerates hippocampus cells which makes the feedback loop to the hypothalamus fail –> leads to chronic release of cortisol

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25
What are 4 treatment options for depression?
Antidepressant drugs Potential for anti-inflammatory drugs Ketamine (glutamate antagonist) for treatment resistant depression CBT
26
What do antidepressant drugs do?
Increase NE and serotonin --> stabilize levels Promote neurogenesis and pathway rewiring in brain
27
If someone is naturally low in NE and 5HT are they predisposed to depression?
NO
28
What is CBT? Is it the most effective?
problem focused and action orientated. Helps deal with dysfunctional thoughts and maladaptive behaviours Most effective
29
What happens in rat hippocampus during chronic stress?
neuronal degeneration
30
What is an example electrophysiological treatments for depression?
Electroconvulsive therapy (ETC) Transcranial magnetic stimulation (TMS)
31
What is ECT?
Uses electrical current to produce seizures as a treatment for severe depression Last resort
32
How does ETC work?
Stimulates production of neurotrophic factors (e.g., BDNF) that in turn restore inactive cells to a more active mode
33
What are the issues with ETC?
Need to medicate person to avoid the massive convulsions caused by the electrical stimulation ECT leads to memory loss that can show a cumulative effect with repeated treatments.
34
What is Transcranial magnetic stimulation (TMS)? How is it used for depression?
A magnetic coil placed over the scalp induces an electrical current in underlying brain regions. Can be applied to focal areas thought to be implicated in specific disorders TMS promising treatment for depression
35
What is Repetitive TMS?
continuous stimulation for up to several minutes (teaches areas to fire)
36
What are anxiety disorders? What are three examples?
characterized by excessive anxiety or fear reactivity GAD, phobia, panic
37
Are OCD and PSTD anxiety disorders?
Not any more
38
What percentage of the population has an anxiety disorder?
15-35%
39
What are three mechanisms for anxiety?
increased activation in the cingulate cortex and parahippocampal gyrus * Enhanced baseline activity in the amygdala and prefrontal cortex * Excessive excitatory neurotransmission may enhance anxiety -glutamate
40
How is the cingulate cortex involved in anxiety?
involved in error detection and emotional regulation --> leads to worry
41
How is the parahippocampal gyrus involved in anxiety
generalizes anxiety to everything
42
How is the amygdala involved in anxiety?
sees threat everywhere
43
What are some treatments for anxiety?
GABAergic drugs; SSRIs CBT – as effective as medications in treating chronic anxiety disorders
44
What are the three psychiatric disorders?
Schizophrenia, mood disorders, anxiety disorders
45
What are the 5 neurological disorders?
TBI an CTE Stroke Epilepsy Parkinson's disease
46
What is a TBI?
Wound to brain from head hitting other objects
47
What are the two possible behavioural effects of TBI?
Specific impairments result from coup and/or contrecoup lesion More generalized impairments may be due to widespread damage throughout the brain (e.g. diffuse axonal shearing)
48
What is coup and contrecoup?
Coup is at site of impact and contecoup is opposite side of impact
49
What is axonal shearing?
axons connecting brain areas are severed
50
What are the immediate and more long term effects of TBI? what shows the poorest recovery?
Impaired cognitive function -immediate Memory, social skills and personality show poorest recovery
51
Can you see chronic effects of injuries of TBI on CT or MRI scans?
NO
52
What is chronic traumatic encephalopathy?
A series of concussions or sub-concussive impacts
53
What is CTE characterized by?
Characterized by neurofibrillary tangles (caused by tau protein build-up), plaques, neuronal death and enlarged ventricles
54
When do symptoms of CTE appear and what do they resemble?
10-20 years later and resemble alzheimers and parkinsons
55
What are signs and symptoms of CTE?
Changes in thinking & memory --> confusion Changes in personality & behaviour --> impulsive Difficulty with balance & motor skills
56
What is a stroke?
An interruption of blood flow from either blockage (ischemic) or bleeding (hemorrhagic) of a vessel that sets off a sequence of damage
57
How to test for stroke?
FAST Face Ask for a smile to check both understanding and muscle control. Arms Check if one arm is weak by asking the person to raise both arms. Speech Listen for slurred speech Time If you see any symptom, call 911 or the local emergency services number right away.
58
What are the five effects of stroke?
1. Release of massive amounts of glutamate; prolonged opening of calcium channels 2. Toxic levels of calcium produce direct toxicity and instigate various second messenger pathways & altered protein production --> leads to cell death 3. Brain inflammation occurs, threatening neurons distant from the damaged site 4. Neural shock (diaschisis): Areas distant from the damage are functionally depressed (partially through lack of input) 5. May be followed by changes in metabolism of the injured hemisphere, glucose utilization, or both, which may persist for days -> less energy and neuron activity
59
Is diaschisis permanent?
temporary panic in the brain --> no structural damage
60
What are the overall effects of stroke?
chain reaction that leads to cell death and disrupted activity
61
What are treatments for stroke?
Clot-busting drugs for ischemic stroke Neuroprotectant Therapies are often used to facilitate plastic changes in the brain following a stroke
62
How fast do clot-busting drugs need to be administered?
3-5 hours
63
What are neuroprotectants?
Drug used to block the cascade of poststroke neural events
64
What are some post-stroke therapies?
speech, physical, constrained- induced therapy
65
What is epilepsy? What are the brain waves like? Can they occur while sleeping?
recurrent seizures highly synchronized, but abnormal, EEG waves Yes
66
What are some causes of epilepsy?
Genetic epilepsy Structural/metabolic epilepsy - tumor or brain defect Unknown
67
What is a Focal Seizure?
- arise from a synchronous, hyperactive activity in local brain region
68
How are focal seizures subdivided?
based on whether awareness is retained or altered (dyscognitive seizure) - Focal aware and focal impaired aware
69
What are focal aware seizures?
e.g., spatial distortions, laboured speech, unusual sensations --> fully conscious and aware, no memory impairment
70
What are focal impaired aware seizures?
consciousness impaired or lost; automatisms (simple repetitive behaviours), won't remember it
71
What is a generalized seizure?
Start focally, then spread bilaterally to distributed networks where you lose consciousness
72
What are the stages of generalized seizures?
1. Normal EEG record before onset 2. Onset and tonic phase, in which the body stiffens and loses consciousness 3. Clonic phase, in which the person makes rhythmic movements in time with the large, highly synchronized discharges 4. A depression period after the seizure --> confused, sleepy, no response --> slow brain waves
73
What is the name for seizures that do not self terminate?
Status epilepticus
74
How to treat Status epilepticus?
Drug intervention with a fast-acting GABA agonist or glutamate antagonist is required to end a seizure --> raise seizure thresholds by enhancing action of inhibitory NT GABA
75
What is it called when antiseizure drugs can't control epilepsy? What percent of people?
intractable epilepsy 37-40%
76
What are treatments for intractable epilepsy in adults? What is the success rate?
surgical resection of epileptogenic tissue. 70%
77
What is Parkinson Disease related to?
degeneration of substantia nigra (dopamine neurons) and loss of the dopamine released in the striatum
78
How long does it take to notice parkinson's?
Insidious - 10-20 years to cause serious impairment.
79
What are symptoms patterns for parkinson's?
Many symptoms resemble normal changes in motor activity that take place with aging. On-again–off-again quality: symptoms may appear or disappear suddenly.
80
What are the positive symptoms of parkinson's?
Tremor at rest Muscular rigidity (cogwheel rigidity) --> force it to move then it stops Involuntary movements (akathesia, or cruel restlessness)
81
What are the negative symptoms of parkinson's?
Disorders of posture: of fixation (hold body in a place) and of equilibrium Disorders of righting (hold body upright) Disorders of locomotion Speech disturbance Hypokinesia (general movement slowing)
82
Are there treatments to cure parkinson's?
No --> support and comfort
83
What are two Pharmacological treatments for parkinson's?
* Increasing activity in remaining dopamine synapses - L-Dopa * Cholinergic antagonist
84
What are two neurosurgical treatments for parkinson's?
DBS: Hyperactivity of GPi neurons can be reduced by electrically stimulating Subthalamic neurons A lesion of the internal part of the globus pallidus (GPi) can reduce rigidity and tremor.
85
How does DBS effect the basal ganglia pathway?
Causes the GPi to stop sending inhibitory signals to the thalamus --> allows for movement
86
How does deep brain stimulation work?
one or more electrodes implanted in the brain stimulate an area with low-voltage current to facilitate behavioral change. Stimulation may also make brain tissue more plastic and receptive to other treatments
87
What is DBS used to treat?
Parkinson, TBI, OCD, depression
88
How long does DBS last?
No permanent but electrodes can remain implanted for years

PSYC 351D (9 decks)

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