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Neuroscience - own questions > Mental Illness > Flashcards

Mental Illness Flashcards

1
Q

brain is the

product of two interacting factors

A

heredity and environment;own experiences->plasticity

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2
Q

Psychoanalysis

A

1) Much of mental life is unconscious 2)past experiences, particularly in childhood, shape how a person will feel and respond throughout life.
- >mental disorder from hidden secrets(physical mental or sexual abuse) during childhood and were suppressed from consciousness.

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3
Q

Behaviorism

A

observable behaviors and their control by the environment. Probability of type of behavior increases when it satisfies a craving or produces a pleasurable sensation.

->mental disorders represent learned maladaptive (huonosti sopeutuva) behaviors.

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4
Q

molecular medicine

A

Approach using genetic information to develop a treatment

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5
Q

pathophysiology

A

discovery of an abnormal physiological condition->If drug candidates succeed in human clinical trials then new therapeutics can be introduced to treat the disease

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6
Q

Challenges of molecular medicine

A
  1. diagnoses done by the description of symptoms, not by knowledge of underlying case
    - >No single treatment is likely to succeed in all patients
  2. Not all mental illness have a clear genetic basis-> numerous mutations in different genes
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7
Q

Approaches to overcome these challenges in molecular medicine:

A
  • pathophysiology of neurons: skin cells->treated with chemicals->transformed to induced pluripotent stem cells (iPSCs)-> treatment of other chemicals->differentiate to neurons and keep alive in culture dish->compare with healthy ones to determine their pathophysiology
    (problem: brain is far more than single neuron)
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8
Q

How is anxiety disorders determined? Examples of these.

A

most common disorder, inappropriate expression of fear

Panic disorder, agoraphobia, generalized anxiety disorder, specific phobias, social phobia

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9
Q

Agoraphobia

A

Anxiety about places or situations where it is hard to escape

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10
Q

Panic disorder

A

sudden onset of intense apprehension (pidättäytyminen), fearfulness or terror associated with feeling of impending doom (uhkaava tuho)

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11
Q

Generalized anxiety disorder

A

At least 6 months of persistent anxiety

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12
Q

Specific phobias ans social phobia

A

anxiety provoked by exposure to a specific feared object or situation->avoidance

Social phobia: anxiety provoked by exposure to certain types of social or performance situations

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13
Q

Other disorders characterized by increased anxiety:

A
  • Post-traumatic stress disorder (PTSD): wounds cost by shocking event(s), intrusive memories, dreams and flashbacks, irritability, emotional numbness
  • Obsessive-Compulsive Disorder (OCD): obsessions, which are recurrent, intensive thoughts, ideas or impulses that person perceives as being inappropriate, grotesque(irvokas) or forbidden
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14
Q

Biological bases of anxiety disorders

A
  • genetic predisposition (alttius) for many anxiety disorders
  • occurrence of inappropriate stress response, even though stressor is not present of it is not immediately threatening
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15
Q

Stress response:

A
  • Avoidance behavior
  • increased vigilance(valppaus) and arousal
  • Activation of the sympathetic division of the ANS
  • Release of cortisol from the adrenal ANS
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16
Q

Control of the stress response by the amygdala:

A

receives ascending sensory information from the thalamus as well as descending inputs from neocortex. This information is integrated by the basolateral nuclei and is relayed to the central nucleus. Activation of central nucleus (hypothalamus, gray matter, diffuse modulatory system) leads to the stress response.

Amygdala and hippocampus regulate the HPA axis and stress response in pull-push fashion.

17
Q

Treatments for anxiety Disorders

A
  • Psychotherapy->no more stress response evoked by the stimuli causing it
  • Anxiolytic Medication->altering synaptic transmission in the brain (benzodiazepines (bind to GABA_A receptors) and serotonin-selective reuptake inhibitors (SSRIs))

selitystä:
-Alcohol and valium also stimulate GABA actions and release anxiety

  • Reduced benzodiazepine binding sites reduces in anxiety disorder
  • SSRI is not immediate, and the extracellular serotonin is not responsible for the anxiolytic effect, the effect seems to be due adaption of NS to chronically elevated brains serotonin (might act on enchaning the feedback regulation of CRH)

(kun serotonin takaisin ottoa estetään, glukokortikoidi reseptorit hippokampuksella lisääntyy jolloin CRH:ta eritetään vähemmän hypotalamuksesta ja stressi vähenee)

18
Q

How would you describe affective disorders?

A

disorders of mood

19
Q

Major depression

A 
Most common mood disorder affecting 6% population every year 
Symptoms: 
-lowered mood 
-decreased interest in all activities 
-insomnia or hypersomnia 
-Fatigue 
-feeling of wothless 
-hard to concentrate 
-recurrent thoughts of death 
-loss of appetite

If not treated it will recur in 50% of cases and odds increase after every episode

20
Q

Bipolar Disorder, manic-depressive disorder

A

-recurrent mood disorder

Symptoms:

  • mixed episodes of mania and dipression
  • Inflated selfesteem or grandiosity(mahtipontisuus)
  • A decreased need of sleep
  • Increased talkativeness ot feelings of pressure to keep talking
  • Flight of ideas, thoughts are racing
  • Distractibility
  • Increased goal-directed activity
  • other reckless behavior

Two types:

  1. with or without major depression, 1% of population
  2. Affecting 0.6% of population, hypomania, not associated with marked impairment of judgement or performance but always associated with episodes of major depression.
21
Q

Biological bases of Affective disorders

A

The monoamine hypothesis, The Diathesis-stress hypothesis

22
Q

The Diathesis-stress hypothesis

A

early childhood abuse or neglect(laiminlyönti) and other stresses of life are important risk factors in the development of mood disorders in adults. HPA is the main site where genetic and environmental influences converge to cause mood disorders.

Diathesis: predisposition for a certain disease

23
Q

The monoamine hypothesis

A

Mood is closely tied into levels of released monoamine neurotransmitters (NE or serotonin)-> depression is a consequence of a deficit in one of these diffuse modulatory systems.

Problem in this: Action of all these drugs take several weeks to develop even though they have immediate effects on transmission at the modulatory synapses

->new hypothesis: drugs promote long-term adaptive changes in the brain

24
Q

What regulates glucocorticoid receptor number in hippocampus?

A

genes, monoamines, and early childhood experience.

-The maternal influence can be replaced by increasing the tactile stimulation of the pups-> activates the ascending serotonergic inputs to the hippocampus->more glucocorticoid receptors

25
Q

What has anterior cingulate cortex to do with depression?

A

The hypothesis that anterior cingulate cortex dysfunction contributes to the symptoms of major depression is supported by a number of findings.

  • increased resting-state metabolic activity in the anterior cingulate cortex of depressed patients
26
Q

Treatments for Affective Disorders

A
  • Electroconvulsive therapy (ECT): inducing seizure activity in the temporal lobes (maybe affecting hippocampus which is involved regulating CRH and HPA axis)->adverse effect is memory loss
  • Psychotherapy
  • Antidepressant drugs: several ways to block reuptake of serotonin or NE and MAO inhibitors that degrative NE or 5-HT
  • Subsequent studies showed that lithium is highly effective in stabilizing the mood of patients with bipolar disorder, by preventing not only the recurrence of mania but also the episodes of depression
  • prevent normal turnover of PIP2
  • interferes with the actions of adenylyl cyclase
  • Deep brain stimulation: electrode is implanted deep in the brain->modulates activity
27
Q

A Description of Schizophrenia

A
  • loss of contact with reality and a disruption of though, perception, mood and movement.
  • oscillate between normal and abnormal state
28
Q

symptoms?

A

positive symptoms:

  • delusions(harhaluulo)
  • hallucinations
  • disorganized speech
  • crossly disorganized or catatonic behavior

Negative symptoms:

  • reduced expression of emotion
  • poverity of speech
  • difficulty in initiating goal-directed behavior
  • memory impairment
29
Q

Biological bases of schizophrenia

A

Genes and environment

  • runs in families
  • genes have important roles in synaptic transmission, its plasticity or the growth of synapses
  • The risk of developing schizophrenia increases with the number of shared genes

->enviromental factors infect of developing it

30
Q

Changes in brain in schizophrenia

A
  • schizophrenics often have defects in the myelin sheaths surrounding axons in their cerebral cortex, although it is not clear whether this is a cause or consequence of the disease.
  • reduced cortical thickness and abnormal neuronal lamination
  • Changes in synapses and several neurotransmitter systems
31
Q

Dopamine hypothesis of schizophrenia

A

psychosis is somehow related to too much catecholamine in the brain.

Reasons: symptoms of overdose of amphetamine are indistinguishable of those of schizophrenia

Drugs that help it are dopamine bloggers, also effective in the treatment of amphetamine and cocaine psychosis.

32
Q

Glutamate hypothesis of schizophrenia

A

-Ketamine and PCP have same symptoms as schizophrenia but affect synapses that use glutamate as neurotransmitter

(inhibite NMDA receptors)

33
Q

Treatments for schizophrenia

A

drug therapy and psychosocial support

34
Q

conclusion of disorders:

A
  • we don’t know why the drugs affect as they do

- we don’t know the cause of most mental disorders

Neuroscience - own questions (10 decks)

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