Quiz 5 Flashcards
1
Q
Neural basis of consciousness:
A
- The end product of all cortical areas, their connections, and their cognitive outputs
- Includes information from sensory systems, memory, imagination
- Emerges from neural circuits, not single neuron
- Greater degree of consciousness associated with greater complexity of neural circuitry
2
Q
Level of consciousness or alertness:
A
- Can vary over a continuum
- May be affected by metabolism, circadian rhythms, fatigue, drugs, medical conditions, brain lesions
- Precisely measured by EEG, ERP
- Observe changes in level in your clients (e.g., drugs, delirium)
3
Q
Consciousness requires 4 processes:
A
- Arousal/activation
- Perception
- Attention
- Working memory
4
Q
Arousal/activation
A
- Physiological and psychological state of being awake or reactive to stimuli.
- It involves the activation of the reticular activating system in the brain stem, the autonomic nervous system and the endocrine system, leading to increased heart rate and blood pressure and a condition of sensory alertness, mobility and readiness to respond.
5
Q
Perception:
A
• the organization, identification, and interpretation of sensory information in order to represent and understand the environment
6
Q
Attention underlies:
A
- Consciousness – Without attention, there is no awareness
- Other cognitive functions
- Therefore, it is critical to determine the extent to which an impairment in cognition is due to an impairment in attention.
7
Q
Attention:
A
Are several different aspects (components): • Attentional capacity • Selective (focused) attention • Sustained attention • Divided attention • Alternating attention
8
Q
Attentional capacity:
A
Refers to the extent that one can allocate their processing resources.
• May be diminished by:
• Fatigue, depression, or lesions
• Usually relatively resistant to aging & some disorders
• Measured by immediate span of attention (e.g., Digits Forward)
9
Q
Selective (focused) attention:
A
• The ability to maintain a cognitive set which requires activation and inhibition of responses dependent upon discrimination of stimuli.
- Bottom-up processes may bias attention by salient features of stimuli.
- Top-down processes from cortex helps to avoid distractions.
10
Q
Sustained attention (concentration) – Maintaining attention
A
• The ability to maintain a consistent behavioral response during continuous or repetitive activity.
11
Q
Divided attention
A
• The ability to simultaneously respond to multiple tasks.
12
Q
Alternating attention
A
• The capacity for mental flexibility which allows for moving between tasks having different cognitive requirements.
13
Q
Processing speed - Psychomotor speed:
A
The rate of information processing of cognitive, attentional, motor functions.
14
Q
Positive symptoms of Schiz.
A
Excess of normal functions • Delusions • Hallucinations • Distorted or disorganized language • Disorganized, catatonic, or agitated behavior
15
Q
Negative symptoms of Schiz.
A
- Affective blunting
- Alogia (restrictions in fluency/productivity of thought/speech)
- Avolition (restrictions in goal-directed behavior)
- Anhedonia
- Asociality
16
Q
Cognitive/Executive symptoms:
A
• Thought disorder including incoherence, loose associations, neologisms
• Impaired selective & sustained attention
• Impaired verbal fluency
• Impaired memory/learning
• Impaired executive functioning
- Difficulty making and maintaining goals
- Solving problems
- Monitoring behavior
17
Q
Cognitive/Executive symptoms are the strongest predictors of…
A
- real-world functioning in schizophrenia.
18
Q
Mesolimbic dopamine pathway
A
— From ventral tegmental area (VTA) to limbic brain, particularly nucleus accumbens
• Hyperactivity of D2 receptors in mesolimbic pathway causes positive sxs & psychosis.
• “Mesolimbic dopamine hypothesis of positive symptoms of schizophrenia”
19
Q
The NMDA hypofunction hypothesis of schizophrenia states that hypofunction of NMDA-Glu receptors causes:
A
A. Hypoactivity of the mesocortical pathway, resulting in cognitive, negative, and affective symptoms
B. Hyperactivity of the mesocortical pathway, resulting in cognitive, negative, and affective symptoms
C. Hyperactivity of the mesolimbic pathway, resulting in positive symptoms
D. Both A and C
(D)
20
Q
Mesocortical dopamine pathway
A
— From VTA to prefrontal cortices
• Deficiency of DA results in cognitive, negative, and affective sxs
• “Mesocortical dopamine hypothesis of cognitive, negative, and affective symptoms of schizophrenia”
• May be due to abnormal neurodevelopment
• May be due to blockade of D2 receptors by antipsychotics
21
Q
The strongest predictor of real-world functioning in patients suffering from schizophrenia:
A
A. Positive sxs
B. Cognitive/Executive sxs
C. Affective sxs
D. All the above are equally predictive
(B)
22
Q
Patients suffering from schizophrenia may have difficulty interpreting social cues and may have distortions in social judgment and reasoning partially because:
A
A. Their amygdalae are hyperactive when viewing scary faces.
B. Their amygdalae are hyperactive when viewing neutral faces.
C. Their amygdalae are hypoactive when viewing neutral faces.
D. Both A and C
(B)
23
Q
Neurodevelopmental Hypothesis
A
- There are at least 25 “risk” genes and the more one has, the greater the risk
- Certain combinations are worse than others and some appear to interact
- During pubescence & adolescence, there is massive competitive elimination & restructuring of synapses (reorganization)
- 33-50% of synapses are eliminated.
- Improper elimination of “weak” but critical synapses may occur in schizophrenia.
- Helps to explain why prodromal sxs, clinical sxs, and full syndrome may start during these years
24
Q
Epigenetics
A
• The epigenetics of schizophrenia is the study of how the inherited epigenetic changes is regulated and modified by the environment and external factors, and how these changes shape and influence the onset and development of, and vulnerability to disorder, schizophrenia.
25
Nature vs. Nurture: Genetics Plus Epigenetics as the Stress–Diathesis Model of Schizophrenia:
* too many genetic biases combined with too many stressors results in schizophrenia
* It is now recognized that single genes do not directly cause schizophrenia; rather, more than a dozen “susceptibility” genes code for subtle molecular abnormalities that hypothetically provide a genetic “bias” toward inefficient information processing in brain circuits that mediate the symptoms of schizophrenia.
26
*Multiple Susceptibility Genes Converge on NMDA Synapses in Schizophrenia
NMDA-R hypofunction =
• dysconnectivity
• abnormal LTP
• abnormal synaptic plasticity and connectivity
• inadequate synaptic strength
• dysregulation of AMPA-R
• abnormal competitive elimination of synapses
27
Choose the most correct statements(s):
A. Fear and panic attacks are associated with dysfunction of circuits that involve the cortex, basal ganglia (striatum), and thalamus.
B. Worry and obsession are associated with dysfunction of circuits that involve the cortex, basal ganglia (striatum), and thalamus.
C. Fear and panic attacks are associated with dysfunction of circuits that involve the amygdala
D. Both B and C
(D)
28
Medical causes of anxiety include:
A. Numerous neurological disorders
B. Many drugs, especially stimulating ones
C. Withdrawal from certain psychotropic drugs
D. All of the above
(D)
29
Anxiety: The Phenotype
Fear =
- panic
- phobia
Worry =
- anxious misery
- apprehension
- expectation
- obsession
30
Associate Symptoms of Anxiety With Brain Regions and Circuits That Regulate Them
* Fear = amygdala centered circuit
| * Worry = cortico-striatal-thalamic-cortical circuit
31
Chronic fear/anxiety is associated w/ increased risk of:
* Cardiovascular disorders, (strokes, heart attacks, hypertension)
* Type-2 diabetes
* Asthma
32
Associate Symptoms With Brain Regions, Circuits, and Neurotransmitters That Regulate Them (Fear)
* 5-HT usually decreases anxiety.
* May increase activation of ACC and prefrontal cortex
* Causes increased inhibition of amygdala via GABA interneuron
* May directly inhibit excessive activity in amygdala
* Norepinephrine (NE) may increase anxiety when excessive.
33
Associate Symptoms With Brain Regions, Circuits, and Neurotransmitters That Regulate Them (Worry)
* CSTC (cortico-striato-thalamo-cortical) loops are implicated in “worry.”
* This includes DLPFC & various neurotransmitters, such as DA.
* One reason for over-activation of DA may be a risk gene for COMT (catechol-O-methyl-transferase), an enzyme that metabolizes DA.
34
Met vs Val - Worry
* “Met” genotype has less enzyme activity, causing higher DA levels in areas such as DLPFC
* “Val” genotype has more enzyme activity, causing lower DA levels in areas such as DLPFC
* A person w/ Met when stressed may have excessive DA activity in CSTC loops, leading to inefficient processing, causing anxiety & worry - a “worrier”.
* A person w/ Val may be better able to cope - a “warrior”.
* But Val is a risk gene for schizophrenia since it may cause too little DA activity in cortex, especially DLPFC.
35
Neurological disorders producing anxiety:
* Stroke
* Parkinson’s disease
* When focal lesions, more likely if in temporal lobes (especially right)
* TBI, meningiomas, metastatic or primary brain tumors
36
CNS Disorders Producing Anxiety
* Epilepsy
* Common, especially if partial complex seizures in temporal lobes
* Ictal panic sxs are more stereotyped and are not recalled.
* Abnormal EEG is unusual in classical anxiety disorders.
37
Moral for therapists re: anxiety-
• Always consider medical causes of anxiety.
38
Drug-Induced Anxiety
```
Ilicit drugs producing anxiety:
• Cocaine (“crack,” etc)
• Amphetamine (“speed”)
• Cannabinoids (marijuana)
• Alcohol
• Ecstasy
```
39
Anxiety caused by withdrawal from drugs:
* CNS depressants (alcohol, opiates, benzodiazepines)
* Antidepressants (especially more anxiolytic ones)
* Stimulants
40
Low “level” of the dopamine system is associated with:
A. Increased “negative affect” (dysphoria, rumination, guilt/disgust, worthlessness, loneliness, fear/anxiety, irritability, hostility, suicidality).
B. Decreased “positive affect” (dysphoria, anhedonia, loss of motivation & enthusiasm, apathy, anergia or psychomotor retardation, impaired attention & cognition, decreased self-confidence).
C. Both A and B
D. None of the above
(B)
41
Neurochemicals Implicated in Depression
* Monoamines - Serotonin (5-HT), Dopamine, Norepinephrine
| * CRF (corticotropin releasing factor [or hormone]) - Cortisol
42
Monoamine Hypothesis of Depression
* Deficient monoamine signaling decreases BDNF:
* Decreases synaptogenesis, neuroplasticity, cell survival, neurogenesis
* Increases apoptosis
43
Stress & Depression
* Stress may decrease BDNF by:
* Decreasing 5-HT and acutely increasing and then depleting NE, DA
* Affecting the gene for BDNF
* Chronic stress may cause excessive levels of CRF (CRH) and cortisol:
* Neurons in hippocampus, amygdala, & anterior cingulate have receptors for cortisol.
* Stress damages these, leading to disinhibition of hypothalamic neurons that release CRF
* Damages the negative feedback loop of the HPA-axis and perpetuates “viscous cycle”
44
Hippocampal Atrophy and Hyperactive HPA in Depression
* Atrophy in hippocampus, amygdala, prefrontal cortex impairs:
* Memory, cognitive/executive functions, efficient emotional processing
45
Stress-Diathesis and Depression
* Example of a risk gene implicated in depression is the gene for SERT (serotonin transporter/pump), with 2 variants (“s” and “l”):
* If “s” is expressed:
* Greater risk for depressive sxs when exposed to multiple stressors
* More atrophy, cognitive sxs
* Poorer response to SSRIs, SNRIs
* Stronger activation of amygdala in response to fearful faces
46
Low “level” of the 5-HT system is associated with...
...increased “negative affect.”
• Dysphoria, rumination, guilt/disgust, worthlessness, loneliness, fear/anxiety, irritability, hostility, suicidality
• Particularly affects prefrontal cortex, amygdala, hypothalamus
47
Low “level” of the NE system is associated with...
...increased “negative affect” and decreased “positive affect.”
48
Low “level” of the DA system is associated with...
...decreased “positive affect.”
• Dysphoria, anhedonia, loss of motivation & enthusiasm, apathy, anergia or psychomotor retardation, impaired attention & cognition, decreased self-confidence
• Particularly affects prefrontal cortex, nucleus accumbens, basal ganglia, hypothalamus
49
Neurological disorders producing depression
* Depression is most common in disorders affecting basal ganglia, frontal cortex, or temporal cortex
* Dementias
* Basal ganglia diseases
* Cerebrovascular diseases (e.g., stroke)
* Cerebral neoplasms
* Cerebral trauma
50
Medical causes of Depression - Caution!
* Some neuropsychiatric conditions cause sxs that occur in MDD but do not cause dysphoria or anhedonia and, therefore, are not sxs of MDD
* Aphasia (e.g., aprosodia)
* Dementia (apathy, cognitive dysfunction, retardation, agitation, loss of appetite, insomnia)
51
Moral for therapists re: Depression
* Always consider medical causes of depression.
* Refer to PCP or other medical professional for medical workup prior to initiating psychotherapy, unless pt has gone recently and you have medical records.
52
Schizophrenia and Bipolar Disorder: Dichotomous Disease Model
The assumption that schizophrenia and bipolar disorder are separate disease entities with different underlying etiologies.
* Schizophrenia is schizophrenia
* Any hint of mood disorder = mood disorder
53
Schizophrenia and Bipolar Disorder Continuum Disease Model
Schizophrenia, bipolar, and schizoaffective exist on a continuum
• Schizophrenia - chronic unremitting psychosis, with poor outcomes expected. Bipolar – cyclical manic and other mood episodes and has better expected outcomes than schizophrenia.
• Schizoaffective – characterized by psychosis and mania as well as other mood sxs
54
That “kindling” may occur in mania and numerous other disorders implies that neuroplasticity may at times be pathological. (True or False)
True
55
Why is it critical to differentiate whether a depressive episode is unipolar or bipolar?
* Antidepressants for unrecognized bipolar depression may increase:
* Mood cycling, mixed states, and conversion to hypomania or mania
* Suicidality in younger pts
56
Two questions concerning Hx re: Bipolar
* “Who’s your daddy?”
* Family Hx of Dx, treatments
* “Where’s your mama?”
* Relatives may provide better Hx since bipolar pts often under-report hypomanic or manic episodes.
57
Hx of untreated illness prior to current sxs that suggest bipolar depression:
* Early age of onset
* High frequency of depressive sxs and lots of time being ill
* Acute onset or abatement of sxs
58
Identifying Bipolar Depression:
```
More:
• Time sleeping
• Overeating
• Comorbid anxiety
• Motor retardation
• Mood lability during episode
• Psychotic symptoms
• Suicidal thoughts
```
59
“Kindling”
Hypothesized to occur in:
• Bipolar mania, Bipolar depression, Schizophrenia, Chronic pain, “Unipolar” depression, Anxiety, Insomnia
* The name "kindling" was chosen because the process was likened to a log fire. The log itself, while it might be suitable fuel for a fire, is very hard to set afire in the first place. But surround it by smaller, easy to light pieces of wood - kindling - and set these blazing, and soon the log itself will catch fire.
* Initial periods of cycling may begin with an environmental stressor, but if the cycles continue or occur unchecked, the brain becomes kindled or sensitized - pathways inside the central nervous system are reinforced so to speak - and future episodes of depression, hypomania, or mania will occur by themselves (independently of an outside stimulus), with greater and greater frequency.
60
Moral: Treat these disorders/symptoms aggressively and appropriately w/ a biopsychosocial model to:
* Relieve suffering
* Increase well-being and productivity
* Prevent further episodes
* Lifelong Rx with multiple mood stabilizers is the norm.
61
Bipolar: Psychotherapy may be very valuable -
* Educating pt & significant others concerning:
* Adherence to drug regimen & labs
* Extremely harmful effects of drugs of abuse on functioning and on exacerbating sxs of bipolar
* Discriminating normal from abnormal mood swings
* Reporting pregnancy or intention of becoming pregnant to prescriber
* Helping pt cope with:
* Anger, denial and ambivalence
* Partial tx response
* SEs
* Loss of “benefits” of hyponamia/mania
* Lifelong treatment
* Psychosocial consequences of episodes
* Fear of recurring episodes & subsequent inhibition of normal psychosocial interaction
62
Early signs of an episode, especially decreased need for sleep, and importance of adequate sleep to prevent mania (give CBT if necessary)
* Sleep hygiene – regular hrs, avoiding sleep deprivation, avoiding drugs that interfere w/ sleep (stimulants, alcohol, benzodiazepines, decongestants)
* Avoid/limit shift work, traveling across time zones.
* Keep light stable throughout year.
63
Bipolar disorder may be conceptualized as...
...“out-of-tune,” unstable, dysfunctional circuits, especially those involving monoamines.
• Causes decreased efficiency of information processing in symptomatic circuits and increased sxs, whether manic or depressed
• Particularly affects prefrontal cortex and its role in modulating mood, thinking clearly, and inhibiting inappropriate behavior
• Also affects limbic system, basal ganglia, hypothalamus
64
Moral for therapists re: Bipolar
* Always consider medical causes of mania.
* Refer to PCP or other medical professional for medical workup prior to initiating psychotherapy, unless pt has gone recently and you have medical records.
