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11 Cards in this Set
- Front
- Back
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Endogenous (natural/biological) Symptoms |
- Biological - Early morning wakening - Depressed in morning - Psychomotor Retardation - Weight Loss more likely - No memory of specific triggering event - increase in ventricle area |
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Non-Endogenous (environmental/reactive) |
- initial insomnia - ok in morning but feels worse at night - gains weight - can identify a triggering event |
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Endogenous vs. Non Endogenous Debate |
- in the past, a differential diagnosis was made between the two types - currently not the case - it is argued that we should still be making differential diagnosis because there are differences between the 2, and different treatment implications |
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Endogenous Studies |
- Harness & Monroe: ED is associated with severe abuse - Young: Related to 5HT transporter that is linked to enlargement in thalamus Developmental Trauma exacerbates enlargement of thalamus through the effects of 5HT transporter - Implications: Is related to neurological etiology due to a genetic predisposition that can be triggered by environmental factors (abuse, trauma) - Treatment: Prophylactic treatment suggested depression is often recurrent |
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Kindling Effect/State (Depression: Chronic and Recurrent) |
- depression results from sensitization process to a depressed state - subsequent episodes = increased susceptibility - related to the fact that cells adapt to environmental and neurochemical changes - # of prior episodes, and presence of stressful events, and genetic risk all play a role - there is no hippocampal volume reduction in the first episode of depression but more episodes leads to reduction Treatment: treatment should continue until full remission - if not treated until all symptoms are gone there is a greater risk of recurrence - 50% who end treatment early relapse - residual symptoms strongly predict early relapse (76%) - Treatment should last 6-12 months and should be tapered off |
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Why has research began to focus on Neuroendicrine Abnormalities?
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1. To understand the neuroendocrine abnormalities in depression 2. Their relationship to endogenous depression 3. as a predictor to antidepressant response |
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TRH Challenge Test |
TRH: a hormone that stimulates the release of TSH from pituitary gland TSH: stimulates the production of Thyroid Hormones - Depressed patients show a blunted response in this process (not enough TSH) - research suggests that the defect is in the hypothalamus - individuals with this defect would respond better to anti-depressants because they target those neurotransmitters - this is consistent with the monoamine Theory of Depression |
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DST Suppression Test |
DST: synthetic hormone similar to cortisol Cortisol: a steroid hormone made in the adrenal glands that secretes more in response to stress It is controlled by the HPA axis: hypothal. - (CRH) - Pituitary - (ACTH) - Adrenal = increased cortisol - when cortisol gets too high negative feedback occurs and the system regulates itself (normal suppression) - individuals with endogenous depression don't show this suppression - cortisol levels remain high - cortisol is high and resistant to suppression |
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Failure to Suppress (Cortisol) |
Failure to suppress = no change in increased cortisol levels - this is not found in all studies Vreeburg: higher cortisol levels in the morning is related to an increased biological vulnerability to depression, but not failure to suppress Owens: Elevated cortisol levels I'm the morning is a marker for endogenous depression in adolescent boys |
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Problems with Prolonged exposure to elevated cortisol |
- neurotoxic - atrophy of hippocampus, amygdala, prefrontal cortex - reduction in hippocampal volume with the length of untreated depressive episodes - recurrent depressive episodes may be producing cumulative brain damage due to recurrent increased levels of cortisol - related to idea of prophylactic treatment: if there is a family history should we just treat them? Major Depression: associated with enlargement of the thalamus (may be due to an adaptation to atrophy) |
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REM Latency (theoretical view) |
- the time it takes to get into REM sleep - in depressed patients: low sleep continuity, slow wave sleep deficits, low time to get into REM sleep, high REM density, and time spent in REM - Decreased REM latency found in 65% of endogenous and 34% non endogenous - Most significant predictor of severity of depression = early morning wakening - related to hypothalamus and REM latency |
