EMPOWERING PHYSICIANS WITH EVIDENCE-BASED CONTENT
 

Home > Browse Topics

<< The Depressed Patient And Suicidal Patient In The Emergency Department: Evidence-Based Management And Treatment Strategies

Pathophysiology

While there is no current universally accepted model for the etiology of depression or suicide, there has been a recent explosion of interest in attempting to better understand the etiology of major depression. Current work on the etiology and pathophysiology of depression draws upon a multidisciplinary, multifactorial model and includes neurochemical, neuroanatomical, environmental, and social/cultural components.

Biological Perspectives

Current models have conceptualized depression as a complex interplay between neurochemical and neural circuitry lesions. Evidence supports the presence of decreased dopaminergic activity/transmission in the striatal cortex of individuals with depressive symptoms as well as deficits in gamma-aminobutyric acid (GABA) uptake in the prefrontal cortex.33-35 Other research has documented the presence of serotonergic uptake abnormalities along the hippocampus.36 Neuroanatomical models making use of functional magnetic resonance imaging (fMRI) and other imaging modalities have noted the presence of prefrontal cortex, hippocampal, and striatum hypoactivation in depressed individuals compared to controls.37

One model attempting to integrate neuroanatomical and neurochemical processes in depression has theorized that decreased affect is a complex interplay of hypodopaminergic activity preferentially in the left prefrontal region.38,39 Initial interest in this theory came about from case reports noting that post-trauma patients with left-frontal-cortex damage often manifested depressive-like symptoms,40 and subsequent studies have found samples of clinically depressed subjects who had associated decreased left-frontal activity compared to matched nondepressed controls.41 Many current pharmaceutical interventions for depression capitalize on the concept of a neurochemical imbalance. For example, selective serotonin reuptake inhibitors (SSRIs) prevent the reuptake of serotonin between synapses, functionally raising the amount of serotonin available.

While there have been several forays into understanding possible neurochemical correlates of suicide, most work has been mixed. Earlier studies have investigated the possibility of a relationship between serotonin levels and suicidal behavior, noting that decreased levels of serotonin or receptor modulators were associated with suicidal behavior.42,43 However, the evidence regarding the specific serotonergic receptors and gene loci have been mixed and inconclusive.44

There also appears to be some genetic component associated with depression. A study of nearly 15,000 monozygotic and heterozygotic twin pairs found a concordance rate of 38%.45 However, there has been little consistent work towards documenting a reliable and specific chromosomal pattern, single gene, or multiple gene loci.46-48 A meta-analysis carried out by Roy and Segal examined existing published twin case reports for suicide from 1967-2001 and noted an increased concordance rate for monozygotic twins compared to dizygotic twins (23% vs 0.7%).49

Cognitive Perspectives

Cognitive theories of the etiology of depression focus on the development of maladaptive thinking patterns or “schema,” or ways of processing information about the world.50 Depressed individuals may develop a pattern of thinking/cognitive processing that interprets and frames social interactions and beliefs about themselves in a negative light such that they may have a predominance of thoughts resulting in helplessness, hopelessness, self-blame, and decreased self-worth.50,51 These maladaptive cognitive patterns may perpetuate a negatively biased framework on viewing the world. One concept in the literature – the theory of learned helplessness – was based on early animal studies in which animals given a noxious stimuli in a setting in which they could not escape would eventually cease attempts to avoid the noxious stimuli, even when their initial restrictions were lifted.52 This idea of learned helplessness has been extrapolated to the realm of clinical depression, with the idea that clinical depression may represent a cognitive state of inertia and resignation by patients that their negative affect is a state/condition with which there is no escape, and as such, little benefit would come from attempting to reframe or adjust their current depressed status.53,54 The notion of the creation and perpetuation of negative schema and attributional style has been a cornerstone of cognitive perspectives on depression and a foundation upon which cognitive therapies are directed towards helping patients to structure and organize their depressive symptomatology.55

Social Perspectives

Multiple social factors have been documented to play a role in the development of major depression. Incidents such as social isolation,56 early social trauma,57 and persistent criticism from family members58 have all been associated with higher rates of depression. Taken together with the cognitive and biological studies on depression, it appears that major depression is a multilevel, multifactorial disease with varied modulators and driving factors.

Related Links:

Emergency Stroke Care, Advances and Controversies

 

About EB Medicine:

Products:

Accredited By:

ACCME ACCME
AMA AMA
ACEP ACEP
AAFP AAFP
AOA AOA
AAP AAP

Endorsed By:

AEMAA AEMAA
HONcode HONcode
STM STM

 

Last Modified: 12/11/2017
© EB Medicine