Mood Disorders (PS2008- Week 5) PDF

[Mood Disorders] A diagram of a person\'s mood Description automatically generated **Bipolar disorders** are marked by **depression and mania**, while **Unipolar** disorders are only marked by **depression**. [MDD:] In order to be **diagnosed** with **Major Depressive Disorder** an individual mu...

[Mood Disorders] A diagram of a person\'s mood Description automatically generated **Bipolar disorders** are marked by **depression and mania**, while **Unipolar** disorders are only marked by **depression**. [MDD:] In order to be **diagnosed** with **Major Depressive Disorder** an individual must experience a **major depressive episode** that lasted for at least **2 consecutive weeks**. This is **characterized by 5 of the following**: (**must** have either) **Depressed mood** or **Diminished interest** in activities **most of the day**, significant **weight loss**, **in/hypersomnia**, psychomotor **agitation/retardation**, **fatigue**, feeling of **worthlessness/guilt/concentration/indecisiveness**, **recurrent** **thoughts of** **death** (includes ideations or attempts). These symptoms **cannot be attributed to "expected" reactions** (grief) and must **cause** significant **distress/social or occupational dysfunction**. It must not be caused by **substances or medical conditions or another disorder**. For diagnosis, they **cannot** ever have experienced a **manic** episode. **Psychosis** can be perceptual (see), tactile (touch) or olfactory experiences (smell). Depression can include **delusions and hallucinations**, where the **content** of the psychosis (delusions and hallucinations) is **syntonic** **with depression**. [PDD:] **Persistent Depressive Disorder** is where people have a **depressed mood** for most of the day, across the span of **2 years**. They must also experience **2 of the following**: **poor** **appetite/overeating**, **sleep** disturbances, **fatigue**, **poor self-esteem**, trouble **concentrating/indecisiveness**, feeling of **hopelessness**.  A diagram of a diagram Description automatically generated **Remission** is where the patient **returns** to their **baseline** original state. **Recurrence** of symptoms within **6-9 months** of remission, is defined as a **relapse**. Ater this time period, the symptoms would be considered a **new episode** of major depression. **MDD** is often **triggered by life events** (usually centering around **loss**). This disorder has a **high relapse and recurrence** rate (**50-85**%) and after the **2^nd^/3^rd^ episode**, the risk rises to **70-90**%. **60**% recover after **2 years**, **40**% at **4** and **30**% after **6** years, suggesting there is an element of **chronicity** making recovery more difficult. **50**% of people with this disorder have **1** episode, **70**% of them have a **2^nd^** and **90**% have a **3^rd^** and **20**% are **chronic** with no signs of permanent improvement. Studies found the **prognosis** was **worse** in **early** and **old** age onset. [Biological Theories for Unipolar depression:] **Heritability** was estimated to be around **40**% and **twin** **concordance** studies found **MZ** twins had **31-42% risk** and **DZ** twins had **20%**. The risk was 2-3% for anyone with 1^st^ degree relatives with MDD. **Heritability** of MD is **higher in** **women** than men. Most research focuses on the genetic and environmental **interaction** (d**iathesis-stress model**). For example, **experiencing** **maltreatment** **in childhood** while having **a genetic vulnerability increases the risk of developing depression** more than either factor alone. A drug meant to lower blood pressure (50s) led to symptoms of **depression** due to the medicine **depleting the level of serotonin** in the brain. Therefore, medication was developed to **increase serotonin levels to treat depression**. For example, **SSRIs blocks** the **reuptake** and the reabsorption of **serotonin**. The **monoamine** hypothesis is that **low levels of serotonin, dopamine and norepinephrine** are involved in the development of depression. **Antidepressants** like **tricyclics** and **monoamine oxidase inhibitors** cause **short term increase in serotonin and norepinephrine**. Research consistently found that people with depression have **hyperactivity** in their Prefrontal **Cortex and Anterior Cingulate Cortex**, which is used to **anticipate rewards and manage emotions**. Also, they find the **hippocampus** has a **reduced volume** of activity, this may lead to **inappropriate emotional responses** retrieved for a certain **context**. Those who **remit** often had **larger** **hippocampus volumes before treatment** and those with **smaller** ones, were prone to **relapse**. The **Amygdala** was found to be **hyperactive**, perhaps due to the **lack of downregulation** of emotions from the **PFC**. These studies do **not establish a precise causal relationship** between biology and MDD. [Behavioural theories:] One theory is that depression develops when individuals **lack rewarding experiences** and **insufficient positive reinforcement** in their environment, this coincides with the idea that **losses and failures can be a trigger** for depression. One way depression may be **maintained** is through its effect on **social interactions**, studies found people interact **less positively** **with depressed people**, leading to **further reduction in positive reinforcement**. Another way to **maintain** it is through **negative reinforcement**, this is where **depressive behaviours** like **avoidance coping** reinforces symptoms. Similarly, symptoms are reinforced through the **punishment of healthy behaviours** (going outside) VIA stress. [Cognitive theories:] This is the idea that our **beliefs** lead to the development of depression. These theories suggest that the **thoughts** trigger the **emotion** which triggers the **behaviour**. **Beck's theory of Cognitive depression** was extremely influential and has been adapted to treat anxiety, PTSD, etc. He argues depression forms due to **negative schemas**, which are **dysfunctional** sets of broad **beliefs** and **assumptions** about **the negative triad (beliefs about the self, the world and the future)**. These **negative view** are learnt from **early experiences**. When these **schemas** are activated, it leads to **bias in selecting, processing, categorising and evaluating stimuli** in negative ways. Studies found they are linked to **adverse childhood events**: **25-60%** of **MDD** patients experienced **sexual/emotional abuse or neglect** (**50**% of **BD**). He believed that these schemas turn into **negative automatic** **thoughts** that were characterized by **information processing errors by biases**. These are often the **target** of **treatment** in CBT or other cognitive therapies.  information processing errors  Beck also speaks how **self-fulfilling prophecies**, where **predictions/beliefs** are **confirmed** by **consequences** of expectations and behaviours, **reinforces negative thoughts**. Another theory is **Learned helplessness**, where an individual experiences an **unavoidable negative life event (Seligman, 1975)** and learns to be **helpless**, **lethargic** and **depressed** as a result. Since there is a belief that there is **no control** and the situation **cannot change,** the individual **lacks initiative and motivation**. This may explain the development of depression in **victims of prolonged abuse**, but it doesn't explain why sufferers **self-blame** or why **only some** people that experience the event are depressed. **Causal attribution theory** is the idea that people with **depression** **attribute negative events to internal factors** which likely **reduces self-esteem**. They can also blame **stable factors** (things that **cannot change**) and **global factors** (**fail** in other paths of life too). **This casual attribution** has been shown to **predict suicide** and experimental manipulations **cause depression** due to the absence of a solution. However, evidence found this remits in between relapse, so the **causal relationship is unclear**. **Rumination** is a **repetitive thinking style**, focused on the **causes, meanings, experiences and consequences of events of depression**. This is often framed as **open-ended questions driven by meta-cognitive beliefs** that this process is **useful** and lead to **solutions** but is often **automatic and continuous**. Empirical evidence found **excessive rumination** is experiments led to an **exacerbation of negative mood and cognition**. It also **predicts anxiety, onset, duration, symptom severity** and **effectiveness of therapy (less).** [BD:] This disorder is characterized by **pathological mood swings**, from **mania to depression**. There are **several types**, depending on the **pattern and intensity** of the **mood swings**. **Episodes** can consist of symptoms of **both mania and depression**, called "**mixed state**". **DSM-5** defines **manic episodes** as having a **distinctly elevated or irritable mood**, as well as **3** of the following: increase in **goal-oriented activity/psychomotor agitation**, unusual **rapid speech**, **racing thoughts**, **decreased** need for **sleep**, **increased self-esteem, distractibility,** and **risk-taking** behaviour. These symptoms cause significant functional distress and should be **present most of the day, nearly every day**. They **last 1 week,** if not they must require **hospitalization** or include **psychosis**. This **same criteria** is consistent with **Hypomanic episodes** but there is **less impaired social/occupational functioning**. They **do not require hospitalization** or display **psychotic symptoms**. Symptoms only need to be present for **4 days**. To **qualify** as having a **manic and hypomanic episode** with **mixed features** (mixed state), individuals must have **3** of the following during the **majority of the days** of the **recent episode**: prominent dysphoria/**depressed mood**, **diminished interest** in activities, **psychomotor retardation, fatigue, worthlessness/excessive guilt** and **recurrent thoughts of death** (including ideation, attempts and plans). A diagram of different colored lines Description automatically generated The **onset** of BD is early **20s**, if the 1^st^ episode is after 40 years of age, it suggests substance use or another general medical condition. Ther **earlier** the onset, the **worse** the **prognosis** (childhood). **Lifetime prevalence** depend on the **type of disorder** (BD **1** is **1**% and BD **2** is **0.4**%). There are **no gender differences** found in bipolar disorder, but it is **higher among minority groups** (UK). The **course of illness** can either be **episodic or unstable**. **Episodic** is where people experience **discrete** episodes, and their **functionality is restored between episodes**. **Unstable** illness is where individuals are **unstable throughout** the process, even in between episodes (worse prognosis).  A white background with black text Description automatically generated **15**% of people with BD **commit suicide**, with **50**% **attempting** at least **once**. These **rates drop significantly** when the individual is **adequately treated**. The **attempt** itself is often **more lethal** in BD than in unipolar states. **Suicide ideation** and **behaviours** occur mostly **in episodes of major depression** but are **less likely** in people affected by **unipolar depression** as people with BD **experience more depressive episodes** while those in a **consistent depressive state** experience a **cumulative effect**. [Aetiology of BD:] **Heritability** estimates up to **85**% and the chances of **inheriting the disorder** from a **1st** **degree relative is 5-10**%. Twin studies placed **concordance rates at** **40-70 % in MZ** twins. Genetic studies have found features of **BD overlapping with SZ and unipolar depression** but the **exact gene** that causes these cycle of episodes is **unknown**. Some research found **suicide may run in some families with BD**, this suggests some form of **genetic vulnerability**. **Increased dopamine** had been suggested to **explain manic phases** in people with BD, this suggests DA may play a **role in the cyclical mood shifts** through **high levels** of dopamine **during a depressive state**. Some **fMRI** data suggested that the **frontal cortex** was **underactive** during cognitive and emotional processing which may account for **impulsivity, distractibility and emotional dysregulation**. This was **only in manic, not depressive states**. The **Limbic areas** (Parahippocampal gyrus, hippocampus, amygdala & basal ganglia) tend to be **overactive** during emotional processing which can be linked to **emotional reactivity**.  [BD & Immune dysfunction:] People with BD have **high rates of inflammatory medical conditions** (autoimmune, chronic infections, cardiovascular disease, metabolic). The immune system has a **direct impact on the functioning of the brain**. Measuring **Cytokine** levels, which is measuring **molecules of the immune system** that **increase/decrease** inflammatory responses, has shown **elevated levels of pro-inflammatory cytokines** in BD. This suggests **chronic low-grade inflammation**. One observation found variability I how cytokine fires depending on the mood state. **Gut microbiota** may have a large impact on **Cytokines** produced by the **Gastrointestinal system**. The GI system may **induce the production of pro-inflammatory cytokines** on an acute or chronic basis, which directly affect functioning. Evidence suggests those with **BD have worse gut microbiota**. [Treatment:] In terms of **psychopharmacotherapy**, **lithium** carbonate is used to treat BD. **1/3** of people do **not remit**, so it is not always effective. There is a **high intolerance, drop-out (40%), relapse and recurrence rate**. It takes at least **2-8 weeks** for the medication to take effect and may **induce depression** at the beginning. Many **side effects** that affect the heart, liver, etc. Researchers are using **drugs like Ketamine and LSD for quicker effects**. Ketamine was found to be effective within **4 hours**, however, it is **expensive** as **monitoring** is required with illegal drugs. **Electroconvulsive therapy** induces **small seizures to correct brain activity** for 6-8 sessions, 2 times a week. Its used **for severe treatment-restraint depression, mania or catatonia**. It has an **efficacy** of **70-80**% with **12,00 participants** (Uk) per year. **71**% are **women**, **46**% are **above 65** years old and **16**% of participants did **not provide consent**. **TMS** and **deep brain stimulation** can also be beneficial treatment options but are more **invasive**. **Behavioural activation** includes daily **monitoring** of un/pleasant events, **assessing** the **function** of depressed behaviour, **identifying** behavioural **goals** within major life areas, **social skills**, **time management**, goals/schedule, fostering **cognitive change**. It **increases access to pleasant event/reward and decreases experiences of aversive events**. It is **cheap** and as **effective** as CBT. A white text on a black background Description automatically generated