Depression

Depression

people can become depressed though several different routes, such as genetics, trauma, hormones, substance abuse and head injuries etc...
MAJOR DEPRESSIVE DISORDER
1. major depression more intense and pro-longed. DSM-IV (APA) sad and helpless everyday for weeks at a time, ABSENCE OF HAPPINESS more reliable symptom than sadness.
  1. ROTTENBERG ET AL. (2002) - examined films and individuals with depression acted normally to negative films but laughed less at comedies or smiled at happy pictures.
2. 5% of adults in the US are majorly depressed. 10% of people have it at some point in their life. no lab tests confirm such a diagnosis however.
  1. beyond age 14 there is a distinctive pattern that depression is more common in females.
3. It is more common to have episodes of depression separated by periods of a normal mood. the first episode in depression is likely to be triggered by an event but for later episodes it gets less and less likely to be triggered, it's as if brain learns to be depressed.
4. GENETICS
  1. twin and adoption studies indicate a moderate degree of heritability for depression, no one gene shows a strong link to depression.
    1. people with early onset depression (before 30) have a high probability of relatives with depression and anxiety disorders. whereas people with a late onset of depression have a high probability of relatives with circulatory problems. distinguishing between early and late onset may lead to progress in identifying genes and therapies.
  2. CAPSI et al. (2003) - the effect of a gene might interact with the environment. one gene controls the serotonin transporter, two short forms of this gene combined with increasing numbers of stressful experiences led to higher probability of depression than people with two long forms where the risk was only slight with increased events. HOWEVER this study has failed replications since
  3. OTHER BIOLOGICAL INFLUENCES
    1. a few cases of depression are linked to VIRAL INFECTIONS - such as BORNA disease in farm animals, 100% of people tested positive for BORNA disease were also depressed. viruses might PREDISPOSE depression.
    2. HORMONES might be another trigger for depression, stress increases release of cortisol. postpartum (after birth) depression, hormones are a contributing factor. In older men a decline in TESTOSTERONE was associated with increased probability of depression.
    3. LINKS TO HEMISPHERIC DOMINANCE - studies have found link between a happy mood and increased activity in the prefrontal cortex. Furthermore, most people with depression have DECREASED ACTIVITY in the LEFT and INCREASED IN THE RIGHT.
ANTIDEPRESSANT DRUGS
1. early antidepressants were discovered by accident. there are THREE TYPES OF ANTIDEPRESSANT, TRICYLICS, SELECTIVE SEROTONIN REUPTAKE INHIBITORS AND MONOAMINE OXIDASE INHIBITORS
  1. TRICYLICS - block the transporter proteins that reabsorb SEROTONIN, DOPAMINE AND NOREPINEPHRINE into the presynaptic neuron after their release. this PROLONGS the presence of neurotransmitters in the synaptic cleft, where they continue to stimulate the postsynaptic cell. HOWEVER TRICYLICS ALSO block histamine receptors (causes drowsiness), acetylcholine receptors (which causes dry mouth) and sodium channels (which causes heart irregularities)
  2. SSRIs - similar to TRICYCLICS but specific to the neurotransmitter serotonin. blocks reuptake of serotonin, milder side effects than tricyclics.
  3. MAOIs - MONOAMINE OXIDASE INHIBITORS - block the enzyme monoamine oxidase, which metabolizes serotonin into active forms.
  4. ATYPICAL ANTIDEPRESSANTS - e.g. ST. JOHN'S WORT - a herb, less expensive, not prescribed (+ or -) snd effectiveness is the same as an antidepressant drug. HOWEVER, the enzyme breaks down other medicines taken at the same time.
2. moat antidepressants increase the presence of serotonin so it would seem that the problem in depression is too little neurotransmitter. HOWEVER people with depression have a normal neurotransmitter release. There is no clear evidence that ANY ANTIDEPRESSANT DRUG PRODUCES ANY DIFFERENT EFFECTS from any other.
  1. TODAY research focuses on neurotrophins, which aid in the survival, growth and connections of neurons. most people with depression have lower than average levels of a neurotrophin called BNDF. people with LOW BDNF have a smaller than average hippocampus, impaired learning etc.. BDNF by itself does not automatically elevate / raise mood, but it helps facilitate new learning that builds new synapses.
3. HOW EFFECTIVE ARE ANTIDEPRESSANTS? depression occurs in episodes, giving someone medication produces expectation of improvement, enhancing probability of recovery, researchers compare the drug influence to a placebo. many people respond well to placebos.for patients with mild to moderate depression, results for placebos overlap with drugs, the only group where drugs produce an advantage is for severe depression.
AN ALTERNATIVE TO ANTIDEPRESSANTS and PSYCHOTHERAPY IS ELECTROCONVULSIVE THERAPY (ECT) - which is an ELECTRICALLY INDUCED SEIZURE. seizures WERE PREVIOUSLY induced with a large dose of insulin. HOWEVER NOWADAYS seizures are induced with an ELECTRIC SHOCK. ECT is quick and most people awaken calmly. it is used today mostly for people who haven't responded to therapy or drugs. A COMMON SIDE EFFECT OF ECT IS MEMORY LOSS and there is a HIGH RISK OF RELAPSING. not sure how ECT relieves depression.
1. a similar treatment is repetitive transcranial magnetic stimulation.
ALTERNATIVE TO DRUGS IS PSYCHOTHERAPY - drugs and psychotherapy are about equally effective. HOWEVER drugs work better for life-long unhappiness, secondly drugs are often of little use to people who have suffered childhood abuse. thirdly, psychotherapy is more likely to have long-term benefits
SLEEP PATTERNS - almost all people with depression have sleep problems, awaken early, unable to get back to sleep, sleep goes straight into REM sleep after 45 minutes. people who are depressed have more than average eye movements. ALTERED SLEEP is a life-long trait of people predisposed to depression.
1. SEASONAL AFFECTIVE DISORDER - DEPRESSION that recurs during a particular season. people with SAD have phase-delayed sleep and temperature rhythms. it is rarely as severe as normal depression. can cure SAD with very bright lights.
BIPOLAR DISORDER
1. UNIPOLAR DISORDER vary between depression and normality, people with BIPOLAR vary between depression and mania.was previously known as MANIC-DEPRESSIVE DISORDER. MANIA is characterised by restless activity, laughter, confidence, loss of inhibitions.
  1. BIPOLAR 1 MORE FULL-BLOWN EPISODES OF MANIA COMPARED TO BIPOLAR 2
  2. GENETICS IN BIPOLAR DISORDER - genetic predisposition for bipolar disorder, two genes increase the probability of it, some of the same genes that predispose major depression.
    1. TREATMENTS for bipolar disorder include LITHIUM SALTS. lithium stabilises mood. antidepressant drugs are risky for people with bipolar disorder as they sometimes provoke a switch from one end of the scale to the other.
      1. FURTHERMORE, getting people to maintain a constant sleep-wake cycle reduces the risk of intense mood swings

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	Created by becky.waine almost 11 years ago