Please enable JavaScript.
Coggle requires JavaScript to display documents.
Biopsychology of Psychiatric Disorders - Coggle Diagram
Biopsychology of Psychiatric Disorders
Diagnosis of Mental Disorders
2 main references used
Diagnostic and Statistical Manual of Mental Disorders - Fifth Edition (DSM-5)
APA 2013
Mental disorders
International Classification of Disorders (ICD-11)
WHO 2018
Diseases, disorders, injuries and other related health conditions
DSM-5-TR
APA 2022 (March)
new diagnosis
Biopsychology of Mental Disorders
difficulty in diagnosis
same disorder, different presentation of symptoms
Major Depressive Disorder
A: low mood, anhedonia, appetite loss, insomnia, fatigue
B: low mood, weight gain, feelings of worthlessness, insomnia, suicidal ideation
different disorder, same presentation of symptoms
A: increase heart rate, heart palpitations, heavy breathing (Anxiety disorder)
B: Increased heart rate, heart palpitations, heavy breathing (Heart disease)
subjectivity of interpretation by clinician making diagnosis
Schizophrenia
2 or more symptoms present for at least 6 months, with 1 month of active symptoms
delusions
hallucinations
disorganised speech
grossly disorganised or catatonic behaviour
negative symptoms (diminished emotional expression or avolition)
significant impairment in work, interpersonal relations, self-care
rule out schizoaffective disorder, depressive or bipolar disorder with psychotic features, psychological effects of substance or medical condition
approx 1% prevalence
strong genetic component
Dopamine theory of Schizophrenia
disruption on dopaminergic transmission
Parkinson's disease
antipsychotic effects (similar to chlorpromazine and reserpine)
evidence for dopamine theory
initially thought brain has too much dopamine
antipsychotic drugs
Chropromazine
levels of dopamine remain unchanged, binds to dopamine receptors without activating them (receptor blocker)
alleviate schizophrenic symptoms (not cure)
Reserpine
lower dopamine levels by breaking down synaptic vesicles storing NT, depletes dopamine levels
antischizophrenic action
side effect: dangerously reduce blood pressure, no longer used
drugs that increase dopamine levels
cocaine and amphetamines trigger similar episodes that resemble symptoms of schizophrenia
Dopamine receptors
5 dopamine receptors
different antipsychotics have different affinity to different receptors
some binds to D1 and D2 receptors (e.g. chlorpromazine)
some binds to only D2 receptors (e.g. haloperidol)
discovery of selective binding led to
revision of dopamine theory
schizophrenia caused by
hyperactivity
specifically at
D2 receptors
effectiveness of antipsychotics depends on its affinity to binding to D2 receptors
haloperidol
effective in selective binding at D2 receptors -
antischizophrenic drugs: neuroleptics
Depressive disorders
triggers for depression
reactive
depression
negative expression (e.g. death, divorce, exam failure)
endogenous
depression
no apparent cause
Depressive symptoms
depressed mood
anhedonia (markedly diminished interest//pleasure in almost all activities)
significant weight loss/weight gain/decrease appetite
insomnia or hypersomnia
psychomotor agitation or retardation
fatigue
feelings of worthlessness or excessive guilt
poor concentration, difficulty making decisions
recurrent thoughts of death
treatment
pharmacological
antidepressants take effect by increasing reuptake, inhibiting receptors/enzymes
monoamine oxidase inhibitors (MAO inhibitors)
Iproniazid
increase monoamines
tricyclic antidepressants
Imipramine
block reuptake of serotonin and norepinephrine, increasing levels in the brain
selective monoamine-reuptake inhibitors (SSRIs)
atypical antidepressants
NMDA-receptors antagonist
psychological
psychotherapy
counselling
medical
repetitive transcrania magnetic stimulation (rTMS)
electroconvulsive therapy (ECT)
deep brain stimulation
Theories of depression
often based on effective therapies
Monoamine Theory of Depression
underactivity of erotogenic and noradrenergic synapse
Neuroplasticity Theory of Depression
decrease of neuroplastic processes in various brain structures (e.g. hippocampus)
leads to neuron loss and other neural pathology (e.g. loss of gray and white matter resulting in atypical activity in different parts of the brain)
Mania
overconfidence, impulsivity, distractibility, high energy
bipolar affective disorder (depressive + mania)
unipolar affective disorder (depressive no mania)
Lithium
calming effect on manic patients
mood stabiliser the blocks rapid transition between depression and mania
seasonal affective disorder (SAD)
Bipolar disorder
maniac symptoms
inflated self-esteem/grandiosity
decreased need for sleep
more talkative than usually, pressured to keep talking
flight of ideas
distractibility
increased in goal-directed activitye
excessive involvement in activities that have high potential for painful consequence
hypomania vs mania
bipolar 1: mania + major depressive episode (can precede with hypomania episode as well)
bipolar 2: hypomania + major depressive episode
treatment
pharmacological: mood stabilisers (e.g. lithium), SSRIs
psychological: psychotherapy
Theories
HPA-axis dysregulation
GABA, monoamine NT, lower BDNF levels
overall reduction in grey matter
neural basis/correlates
smaller medial prefrontal cortex, left anterior cingulate, left superior temporal gyrus, certain prefrontal regions, and hippocampus
atypical activation in the frontal cortex, medial temporal lobe structures, and basal ganglia
Anxiety disorders
generalised disorders
stress response and extreme feelings in absence of obvious precipitating stimuli
phobic disorder
triggered by exposure to particular object/situation
panic disorder
rapid onset of extreme fear and sever symptoms of stress
post-traumatic stress disorder
psychological distress after exposure to actual/threatened death
obsessive-compulsive disorder
frequently recurring and uncontrollable anxiety-provoking thoughts/impulses
treatment
pharmacological
anxiolytics such as Benzodiapines (e.g. diazepam)
usually prescribed for short-term used due to side-effects
mechanism of action through GABA receptors
psychological
psychotherapy (e.g. exposure therapy)
neural basis/correlates
prefrontal cortex, hippocampus, and amygdala
no atrophy unlike in depression but atypical activity
Tourette syndrome
Main symptoms: tics - involuntary, repetitive, stereotyped movements, or vocalisation
major genetic component to this disorder
may comorbid with ADHD, OCD, or both
symptoms tend to subside with age
neural basis/correlates
smaller caudate nuclei, fMRI activity I both prefrontal cortex and caudate nuclei
thinning in sensorimotor cortex gray matter
treatment
pharmacological
neuroleptics (e.g. haloperidol), reduces tics by up to 70%
D2 blockers
psychological
psychotherapy for individual and family