Kapitel 18: Biopsykologien bag psykiatriske sygdomme

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Chapter 18: Biopsychology of Psychiatric Disorders - Overview

• This chapter covers the biopsychology of five types of psychiatric disorders: schizophrenia, depressive disorders, bipolar disorder, anxiety disorders, and Tourette's disorder.
• It discusses the diagnosis, symptoms, theories, treatments, genetic and epigenetic factors, and neural bases of each disorder.
• The chapter also outlines the process of developing new psychotherapeutic drugs using clinical trials.
• A key difficulty in studying psychiatric disorders is the difficulty in diagnosing them and distinguishing them from normal human variation. Diagnosis relies on patient symptom profiles, using the DSM-5.

Schizophrenia

• LO18.1: Positive symptoms (excess of typical function) include delusions (e.g., being controlled, persecution, grandeur), hallucinations (imaginary voices), inappropriate affect (inappropriate emotional responses), disorganized speech or thought (illogical thinking), and odd behaviors (difficulty with everyday tasks, unusual beliefs). Negative symptoms (loss of typical function) include affective flattening (lack of emotional expression), avolition (lack of motivation), and catatonia (immobility).
• LO18.2: The first widely prescribed antipsychotic drugs, chlorpromazine and reserpine, were discovered accidentally. Chlorpromazine was developed as an antihistamine.
• LO18.3: The dopamine theory of schizophrenia proposes that schizophrenia is caused by excessive dopamine activity in the brain. Research on Parkinson's disease and the effects of antipsychotic drugs influenced this theory. Subsequent research refined the theory, suggesting that the issue lies with D2 dopamine receptors rather than dopamine levels themselves.
• LO18.4: Current research into schizophrenia includes the role of atypical antipsychotics (acting on dopamine and serotonin receptors) and hallucinogenic drugs. Psychedelic drugs are being studied as a model for symptoms (like illusions), or as tools in treatment.
• The dopamine theory of schizophrenia proposes that schizophrenia is caused by excessive activity in the mesocorticolimbic pathway but research has suggested that the neuropathological changes occur in the nigrostriatal dopamine pathway rather than in the mesocorticolimbic pathway.
• Recent research studies the functional connectivity in the brains of individuals with schizophrenia with modern functional brain imaging techniques.
• When participants with schizophrenia are hallucinating there are changes in the pattern of functional connectivity as compared to when the participants are not.
• Intrinsic functional connectivity might be used to predict treatment response to antipsychotic medications

Depressive Disorders

• LO18.7: Clinical depression (major depressive disorder) is a prolonged period of deep sadness and loss of pleasure. It can impair cognition and daily life.

• LO18.8: Antidepressant medications, including five major classes, were discovered through various early research, beginning with monoamine oxidase inhibitors (MAOIs). Fluoxetine's structure is a slight variation of that of imipramine and other tricyclic antidepressants and act against a wide range of psychological disorders in addition to depression. Specific examples for each class are given in the text.

• LO18.9: Two forms of treatment for depression utilizing brain stimulation are repetitive transcranial magnetic stimulation (rTMS) and deep brain stimulation (DBS) for individuals who are not helped by other treatments. High-frequency rTMS and low-frequency rTMS are believed to stimulate and inhibit respectively, activity within those brain regions to which they are applied.

• LO18.10: One prominent theory of of clinical depression is the monoamine theory, where depression is associated with underactivity at serotonergic and noradrenergic synapses.

• Three lines of evidence have challenged the monoamine theory of depression relating to evidence with monoamine agonists such as drugs that other neurotransmitters play a role in development.

• The neuroplasticity theory of depression purposes that depression results from a decrease of neuroplastic processes in various brain structures, and general support comes from research showing stress and depression.

• LO18.11: Studies have reliably identified many genes as contributors to depression since 2015. Depression is considered a complex trait that involved interactions through epigenetic mechanisms with environmental factors.

• Changes to genes of an individual might one day predict a future clinical depression.

• LO18.12: Structural neuroimaging shows a strong correlation with reductions in gray matter volumes in the prefrontal cortex, hippocampus, and amygdala. Functional neuroimaging studies show atypical function in the amygdala,thalamus, striatium, and insula.

• Studies show that functional connectivity in depressed individuals and the neural networks are markedly different from healthy participants.

Bipolar Disorder

• LO18.13: Bipolar disorder type I is characterized by mania and possible episodes of depression, while bipolar disorder type II involves hypomania and periods of depression.
• LO18.14: Lithium carbonate was discovered to be a mood stabilizer, and its effects were initially noticed in treating manic patients. This discovery is an example of accidentally discovering a treatment.
• LO18.15: Several factors may contribute to bipolar disorder, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation, circadian rhythm disruptions, and alterations in GABA, glutamate, and dopamine neurotransmission. The reward hypersensitivity theory suggests that reactions to rewards and lack thereof in the brain can cause Bipolar disorder.
• LO18.16: Many genes contribute to bipolar disorder; researchers are now looking at how epigenetic mechanisms may affect the expression of those genes to reveal mechanisms.
• LO18.17: MRI studies have shown reduced gray matter volume in some brain structures of those with bipolar disorder and changes in brain function related to cognition. Reduction in gray matter in frontal and limbic areas is correlated with clinical outcome and reports of specific brain structures.

Anxiety Disorders

• LO18.18: Four anxiety disorders are generalized anxiety disorder, specific phobias, agoraphobia, and panic disorder.

• LO18.19: Three sorts of drugs used to treat anxiety disorders include benzodiazepines (e.g., chlordiazepoxide, diazepam), antidepressants, and pregabalin.

• LO18.20: Animal models of anxiety disorders include the elevated plus-maze, defensive burying, and risk assessment. Elevated-plus-maze, defensive-burying, and risk-assessment tests of anxiety have been all validated towards benzodiazepines.

• LO18.21: Genes associated with anxiety disorders are not clear. Research has shifted towards understanding environmental and epigenetic mechanisms.

• LO18.22: Anxiolytic drugs affect the body's neurotransmitters (e.g. GABAergic) or (serotoninergic), also, a substantial overlap with structures in major depressive disorders and anxiety disorders (e.g. hippocampus, amygdala.)

Tourette's Disorder

• LO18.23: Tourette's disorder is a disorder of involuntary, repetitive movements or vocalizations (tics). These can vary in complexity and occur in different body parts.
• LO18.24: Treatment for Tourette's disorder often starts by educating patients, family members, and teachers. Medication (antipsychotics) can help with symptoms, while alternative treatments (behavioral interventions) are also helpful.
• LO18.25: The genetic and epigenetic mechanisms of Tourette's disorder are being studied. Specific genes that are methylated have been found in individuals with the disorder. and those that are related to potassium channels.
• LO18.26: Research has focused on the striatum (caudate plus putamen). Smaller striatal volumes and changes in functional connectivity (between prefrontal, striatum) have been observed. The thinning of gray matter is prominent in the areas that controlled the face, mouth, and larynx (voice box).

Clinical Trials

• LO18.27, LO18.28, LO18.29: The chapter details the phases of clinical trials (screening for safety, establishing protocols, final testing). Ethical, financial issues, and the length of the process are some controversies within clinical trials. These factors and the importance of diverse subject groups are also discussed. The effectiveness of clinical trials and the role of financial conflicts remain significant aspects influencing results. Active placebos (drugs that have no effect on the body) have been recorded being more effective than inert placebos (drugs).

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