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Questions and Answers
What role does the hypothalamus play in the stress response related to MDD?
What role does the hypothalamus play in the stress response related to MDD?
The hypothalamus signals the pituitary gland to release adrenocorticotropic hormone (ACTH), which then prompts the adrenal glands to release cortisol and adrenaline.
How do high levels of cortisol affect brain function in individuals with MDD?
How do high levels of cortisol affect brain function in individuals with MDD?
High levels of cortisol negatively impact brain cells and inhibit neuroplasticity, which can worsen the symptoms of depression.
What are the key structural changes observed in the brains of individuals with depression?
What are the key structural changes observed in the brains of individuals with depression?
Individuals with depression often show decreased dendritic branching and reduced volume in areas such as the prefrontal cortex, hippocampus, and amygdala.
What is a significant risk associated with tricyclic antidepressants?
What is a significant risk associated with tricyclic antidepressants?
Describe a major limitation of Electroconvulsive Therapy (ECT) for treating MDD.
Describe a major limitation of Electroconvulsive Therapy (ECT) for treating MDD.
Flashcards
Major Depressive Disorder (MDD) symptoms
Major Depressive Disorder (MDD) symptoms
Prolonged sadness, feelings of helplessness and worthlessness, sleep and concentration problems, loss of interest in activities (anhedonia), physical pain, and symptoms impairing daily life.
HPA Axis
HPA Axis
The body's stress response system, involving the amygdala, hypothalamus, pituitary gland and adrenal glands. It releases hormones like cortisol and adrenaline to prepare for a challenge, (fight-or-flight response).
Brain-Derived Neurotrophic Factor (BDNF)
Brain-Derived Neurotrophic Factor (BDNF)
A protein vital for the health and survival of nerve cells in the brain, and is involved in brain development and plasticity. Its levels are linked/correlated with mood regulation.
Antidepressant: Tricyclics
Antidepressant: Tricyclics
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Electroconvulsive Therapy (ECT)
Electroconvulsive Therapy (ECT)
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Study Notes
Major Depressive Disorder (MDD) Treatment
- Symptoms: Lasting weeks/months. Involve sadness, helplessness, worthlessness, impaired sleep & concentration, anhedonia (loss of pleasure), physical pain, multiple symptoms impacting daily life.
Stress Response (HPA Axis)
- Mechanism: The amygdala detects stress, alerting the hypothalamus. The hypothalamus prompts the pituitary to release ACTH, signaling the adrenal glands to release cortisol & adrenaline for "fight or flight" response. This is controlled by the sympathetic nervous system (SNS).
- MDD Connection: High cortisol levels negatively impact brain cells and plasticity, potentially contributing to the condition.
Depressed Brain Changes
- Chemical Imbalances: High cortisol levels, low levels of Brain-Derived Neurotrophic Factor (BDNF), and increased inflammation are linked to MDD.
- Neurological Changes: Structural differences, including decreased dendritic branching (especially in the prefrontal cortex, hippocampus, & amygdala), decreased hippocampus volume and neurogenesis (birth of new cells), are observed. This leads to decreased plasticity and the brain's ability to regulate the HPA axis.
- Dexamethasone Suppression Test: Used to assess cortisol levels.
Antidepressant Treatments
Electroconvulsive Therapy (ECT)
- Mechanism: Induces seizures through electrical stimulation, potentially rebooting the brain.
- Pros: Fast-acting and effective.
- Cons: Short-lived effect, time-consuming, memory loss.
Tricyclic Antidepressants (TCAs)
- Mechanism: Block the reuptake of serotonin and norepinephrine.
- Pros: Effective for treating MDD.
- Cons: Block other receptors (Ach, histamine, epinephrine), leading to undesirable side effects like confusion, memory impairment, sedation, and cardiotoxicity (especially in overdose).
- Metabolism: Long duration of active metabolites in the body, specifically longer in older individuals.
Monoamine Oxidase Inhibitors (MAOIs)
- Mechanism: Inhibit the activity of Monoamine Oxidase (MAO), either permanently or temporarily.
- Pros: Effective, particularly in treatment-resistant patients.
- Cons: Tyramine in food interacts with MAOIs, requiring dietary restrictions. Also, potential for cardiotoxicity if combined with adrenaline-like drugs.
Selective Serotonin Reuptake Inhibitors (SSRIs)
- Mechanism: Primarily block serotonin reuptake.
- Pros: Relatively safe mechanism.
- Cons: Potential for "serotonin syndrome" with cognitive disturbances, autonomic nervous system issues, neuromuscular impairments, and sexual dysfunction. Also discontinuation syndrome upon cessation.
Dual-Action Antidepressants
- Mechanism: Target serotonin and norepinephrine reuptake to address multiple symptoms.
- Examples: Venlafaxine (Effexor), desvenlafaxine (Pristiq), duloxetine (Cymbalta).
- Pros: Potentially fewer side effects than TCAs.
- Cons: Potential sexual side effects and elevated blood pressure.
Monoamine Hypothesis and Beyond
- Mechanism: Antidepressants primarily alter monoamine neurotransmitter levels (serotonin and norepinephrine), but beyond this, they may increase BDNF, decrease oxidative stress, increase allopregnanolone, and increase hippocampal neurogenesis to enhance neuroplasticity.
Future Treatments
- Needs: Faster therapeutic onset, improved efficacy, and reduced side effects.
- Potential Approaches: NMDA receptor antagonists to stimulate synaptic plasticity. Also anti-inflammatory drug treatment.
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