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Cognitive Neuroscience (Subject) / Emotion (Lesson)

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• Patients with focal bilateral amygdala lesions or Urbach-Wiethe disease do not have an amygdala. Name and explain three studies that explored the effects on fear learning and fear responses. Feinstein et al. (2011): After watching fear inducing film clips ppt SM with FBA lesion subjectively reported less arousal than controls. Ppt SM also scored lower on fear, anxiety, panic and distress in trait questionnaires. Feinstein et al. (2013): The anticipatory physiological response before CO2-Inhalation measured via SCR (skin conductance response) and heart rate was significantly lower or not present at all (as for heart rate) for subjects with no amygdala. Klumpers et al. (2014): Patient with BLA lesion had a significantly lower startle magnitude following a fear conditioned stimulus than controls.
• What do you know about neural activation and PTSD (two studies)? Name and describe (methods and results) a study that compares veterans with PTSD to veterans without PTSD and normal controls. Shin et al. (2005): In PTSD patients the activation of the amygdala was higher than in the control group when fearful and happy faces were presented. This leads to the question of a general hyperarousal of the amygdala in patients with PTSD. Hayes et al. (2012): In general the neural activation of the midACC was found to be higher in PTSD patients than in normal controls. The neural activation in vmPFC and IFG seems to be lower in PTSD patients than in normal controls. Liberzon et al. (1999): Combat sounds provocated significantly more anxiety symptoms (measured via anxiety ratings and skin conductance) in veterans with PTSD than in veterans and normal controls without PTSD. Additionally, the activation in limbic regions was higher in PTSD veterans compared to the activation in both control groups.
• Name the "three routes to fear". Direct experience Observation Instruction
• Name scientific evidence (one study) supporting the following statement: "One can 'learn' fear through observation". Olsson et al. (2007): When watching a model receiving electric shocks after a conditioned stimulus, subjects' skin conductance response (to the conditioned stimulus) was equally as high as when they themselves were the ones receiving the electric shocks. The same was true for amygdala activation.
• What is the relationship between serotonin transporter expression level and serotonin in the synaptic cleft? Describe studies that looked at differences between carriers of the s-allele or l-allele for serotonin transporter expression level (5-HTT). l/l-allele carriers generate more transporter, which leads to a more efficient uptake of serotonin from the synaptic cleft and thus, less serotonin in cleft. Lonsdorf et al. (2009): After classical fear conditioning, s-allele carriers show a higher fear response (measured via startle blink magnitude) to conditioned stimuli (CS+) and CS- than l/l-allele carriers. This is also true for trials following a 24h-delayed extinction.Mean item scores on PDSS and MADRS are also highest for s/s-allele carriers, medium for s/l-allele carriers and lowest for l/l-allele carriers. Crisan et al. (2009): When observing models receiving an electric shock after CS+ and when tested themselves, s-carriers show a greater skin conducatnce response than l-carriers. For the test phase, this difference reaches significance as the skin conductance response in s-allele carriers is higher than during observation. Klumpers et al. (2011): The fear potentiated startle is lower in l/l-allele carriers than in s/l- and s/s-allele carriers following instructed fear (fear expression).
• Describe the difference in neurocircuitry between pathologic and healthy anxiety (LeDoux). In pathological anxiety a direct pathway between thalamus (e.g. audotory, sensorimotor) and Amygdala exist, leading to a direct, fast anxiety response to stimuli (shortcut) without the information being evaluated by sensory cortices (e.g. sensorimotor cortex or auditory cortex). However, this finding still has to be validated in humans.
• Adults who have experienced child maltreatment show higher STAI trait scores than controls. This was also true in comparison to controls experiencing resent stressful events. How can this be explained? Comparing the structure of grey matter in the brain, Kuhn et al. (2015) found that the amygdala volume in healthy adults who have experienced childhood maltreatment was larger.
• An aversive stimuli may activate the fear system in the brain eliciting an emotional response. Name aversive stimuli used in experimental settings to induce fear, brain regions involved in the fear system and measurements for the emotional response. Aversive Stimuli: electric shock, fear inducing pictures and film clips, conditioned stimuli, observation and instruction. Fear system: Amygdala, striatal areas, dorsal anterior cingular cortex (dacc) Emotional response: pupil dilatation, skin condictance response, heart rate and blood pressure, fear potentiated startle/startle blink magnitude (eye blink more & higher amplitude), questionnaires on anxiety, fear, distress etc.
• Name the four different regions the central nucleus of the amygdala connects to. What emotional Response are they associated with? Central Grey (PAG): Freezing Lateral Hypothalamus: Blood pressure Paraventral Hypothalamus: Stress Hormones Reticulopontis caudalis: Startle reflex
• Explain the relationship between mOFC (medial orbito-frontal cortex) thickness and extinction. Milad et al. (2005): Cortical thickness in mOFC correlates with the extinction retention index.
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• Explain the relationship between Catechol-o-methyl-transferase (COMT), its encoding alleles (met/val) and effects on extinction learning. Expression of COMT causes the degradation/inactivation of dopamine in the synaptic cleft. As val-allele carriers express more COMT, dopamine is less active in val-allele carriers. Lonsdorf et al. (2009): met/met-allele carriers (more dopamine) profit less from extinction learning . Lonsdorf et al. (2010): For val-allele carriers (less dopamine) exposure-based cognitive-behavioral treatment in panic disorer is associated with more symptom relief than for met/met-allele carriers.
• What are therapygenetics? Describe two studies that looked at the relationship between 5HTTLPR and response to CBT. Therapygenetics is the idea that treatment can be optimized via adaptation of procedures to genetic differences in individuals. Eley et al. (2011): Children (6-13 years) suffering from anxiety disorder were found to respond better to CBT in the six-month-follow up when they were homozygotic carriers of the s-allele. Bryant et al.: s/s-allele PTSD patients profit less than l-carriers from exposure-based CBT. This difference is significant in the follow up.
• How could extinction memory consolidation be enhanced in therapy (name studies). What is the problem with implementation in clinical settings? Ledgerwood et al. (2003): The NMDA-Agonist D-Cycloserin (cognitive enhancer) enhances consolidation and makes extinction more efficient, which was seen in less freezing in animals in response to the cs. Hofmann et al. (2006): The same effect was shown for social phobics receiving D-Cycloserin during CBT (decrease of total SPAI score). De Quervain (2011): The same effect was shown for acrophobics receiving cortisol before extinction-based psychotherapy. However, these methods are not implemented in clinical practice, as they also enhance memory consolidation for fearful experiences and failure during exposure/therapy.
• Explain the efeccts of L-Dopa on extinction memories and brain activation. What would be needed to enhance extinction memory in therapy pharmacologically? Haaker et al. (2013): L-Dopa enhances extinction learning. It was found that activation in vmPFC increases while it decreases in the amygdala (mirrors safety learning). Medication is needed that has the same effects, but can be given after the session, depending on whether it was good and successful.
• Name and explain a study that looked at the role of social groups in the persistence of learned fear. Olsson et al. (2005): Fear-relevant stimuli (e.g. a snake) are more readily associated with negative outcomes and extinction is less successful than for fear-irrelevant stimuli (e.g. birds). This was measured via SCR. The same holds true for racial outgroups. Extinction learning was successful for the racial ingroup, but not for the racial outgroup.
• Name non-linguistic functions related to Broca’s region. Action perception (mirror system), working memory, memory retrieval control
• Name language-specific functions related to Broca’s region. Syntactic complexity, syntactic movement, syntactic structure building, thematic role assignment, unification of syntactic and semantic cues.
• Name and describe three syntactic phenomena (Grodzinski & Santi, 2008). Describe the related study on patients with Broca’s Aphasia. Merge: allocation of symbols to syntactic structures Movement: syntactically marked elements can be moved to non-canonical positions Binding: flexible concatenation of new elements with anaphoric reference. Patients with Broca’s Aphasia and controls had to allocate pictures to sentences. Patients were not able to correctly allocate object relative clauses (e.g. the cat that the dog chased was very big) and passive clauses (e.g. the girl was dried by the mother), but correctly allocated subject relative clauses and active clauses. Hence, patients had difficulties in understanding complex grammatical structures.
• Describe the fMRI study’s result of Santi and Grodzinski (2007). They found that the BOLD-activation in the LIFG increased with the number of intervening noun phrases between co-dependent elements (noun-verb) of a sentence.  

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