bio sci 41 aspects of mood disorder final

Generalized Anxiety Disorder (GAD)

Excessive, frequent, unrealistic worry about everyday things (ex: job, health, chores)

TREATMENT: first-line (SSRIs)

Social Anxiety Disorder (SAD)

Intense and ongoing fear of being judged negatively and/or watched by others.

TREATMENT: first-line (SSRIs, SNRIs, CBT); second-line (benzodiazepines)

Specific Phobia

When a specific something causes a person to feel fear and anxiety so severe it disrupts life

TREATMENT: first-line (SSRIs)

Panic Disorder

Multiple unexpected panic attacks; anticipation and fear of future panic attacks

TREATMENT: first-line (SSRIs, SNRIs); second-line (benzodiazepines)

Agoraphobia

Fear of being overwhelmed/unable to escape or get help; avoid new places & unfamiliar situations

TREATMENT: first-line (SSRIs, SNRIs, CBT); second-line (benzodiazepines)

Obsessive-Compulsive Disorder (OCD)

Frequent unwanted thoughts (obsessions) that causes someone to perform repetitive, ritualistic behaviors (compulsions)

TREATMENT: first-line (SSRIs, CBT); second-line (antipsychotics)

Post-Traumatic Stress Disorder (PTSD)

Develops after a traumatic event; longterm. Symptoms-- flashbacks, anxiety, negative beliefs, hypervigilance, etc.

TREATMENT: first-line (SSRIs, SNRIs, CBT); second-line (antipsychotics)

Acute Stress Disorder (ASD)

Develops within a month of experiencing traumatic event. Closely related to PTSD but is not as severe.

Positron emission tomography (PET) scans

Measure blood flow/glucose metabolism to measure body's metabolic activity.

- Look at what parts of brain use more glucose

PTSD patients: greater amygdala response, smaller medial frontal cortex response, deactivation in frontal cortical

- PET scan study: decreased GABA-benzodiazepine binding in panic disorder patients

Single Photon Emission Computed Tomography (SPECT)

Uses a radioactive substance & special camera to create 3D pics

- Measures blood flow

Functional Magnetic Resonance Imaging (fMRI)

Measures blood flow and blood oxygen level-dependent (BOLD) signal/voxel changes (like an earthquake graph)

Study: using fMRI in masked face studies, PTSD subjects had amygdala hyperactivity (more blood oxygen), smaller response in frontal cortex, deactivation in some frontal cortex areas

Traumatic script PTSD (verbal) study

Normal control (NC): left amygdala activation & deactivate vmPFC

Combat control (CC): deactivated amygdala & vmPFC

PTSD (PP): no change in amygdala activity, deactivated ACC (feeling)

- High baseline amygdala activity to begin with or amygdala isn't responding-- wiring is different

Face masks fMRI (quick image flashes) study -- aversive odors vs neutral human faces

Healthy controls: respond differently between odor and faces

SAD patients: same response to odor and faces; RIGHT amygdala hyperresponsiveness (fear response) to human faces

CCK-4

Induces panic attacks via brainstem and activates both sides of the amygdala.

CCK-4 study on panic attacks and panic disorder

Findings: activating the amygdala was not enough to induce significant activated voxel differences between controls and panic disorder patients

- Yet panic disorder patients still had different reactions

Conclusion: The problem with panic disorder is not the panic itself, but rather the anticipation of panic

- When test subjects with panic disorder were waiting for the next CCK-4 injection, their ACC was activated

Neural activation role in anxiety disorders

Different types of anxiety disorders reveal varying degrees of activation in different parts of the brain

Glutamate (neurotransmitter)

Primary EXCITATORY neurotransmitter

- There's a relationship between glutamate-related genes & risk for mood disorders & treatment response

- Good for increased glucose to regulate mood

GABA (neurotransmitter)

Primary INHIBITORY neurotransmitter

- When GABA is activated, it inhibits neural firing

- Benzodiazepine activates GABA, thus inhibiting neural firing

- People with panic disorders and PTSD have less GABA-binding & GABA receptors

- GABA desensitization can occur --> excitation, anxiety

Amygdala & disorders

Overactive amygdala affects brain and peripheral nervous system (ex: racing heart)

Anterior Cingulate Cortex (ACC) & stress

ACC: anticipation & fear

dACC: mediates fear expression

vmPFC: mediates fear inhibition

There is decreased ability to inhibit fear expression in PTSD/anxiety patients

dACC & vmPFC can be dysfunctional in anxiety disorders

Extinction Context

when a learned behavior (conditioned response) is extinguished when the previously reinforcing stimulus is gone

SSRIs

Effective for all anxiety disorders; possible adverse effects

Use as first-line treatment:

- 5-HT1A receptors are a type of serotonin receptor

- So, less binding of 5-HT1S in social anxiety & PTSD --> amygdala is more excitatory

- So, SSRIs QUIET amygdala & ENHANCE feedback loop (frontal cortex calms ACC & amygdala)

Benzodiazepines aka Anti-Anxiety meds

Effective in many anxiety disorders; short-term and second-line treatment

Possible side effects and dependence

Activate GABA (inhibition)

- Good for if not enough GABA in brain

Tricyclic antidepressants, MAOIs, antipsychotics, anticonvulsants

Only for specific conditions; must weigh risks & benefits

Amanita muscaria

Mushroom containing muscimol-- agonist/activator for GABA

SNPs

Variations in single base pair in DNA (in genomes)

Disorders in genome analysis & SNPs study

Specific SNPs & mutations are associated with mood disorders

- Specific SNPs are more prevalent in those with specific mood disorders

- Use -log of pValues to determine significance of SNPs

Allostatic load

Concept that describes the cumulative physiological and psychological effects of chronic stress on the body

Normal allostatic load (healthy controls)

TRANSIENT activation of immune system-- normal flux of glucose & brain activity, neuroplasticity

Low allostatic load (mood disorder patients)

EPISODIC activation of inflammation in response to mood episodes-- episodic demand for glucose & neurotoxicity

High allostatic load (mood disorder patients)

LONG-STANDING activation of inflammation in response to chronic stress & toxicity-- high persistent demand for glucose & neurotoxicity

Selfish Brain Theory

Brain will prioritize itself and its needs over the rest of the body

- Leads to immune dysregulation and inflammation

Calcium channels

Open due to action potential-- activate proteins --> allow vesicles to release --> allow neurotransmitters to release

- When not open there is more excitation in brain