Brain Structure and Function Abnormalities in Major Depression Disorder

Brain Structure and Function Abnormalities

in Major Depression Disorder

 

 

(1) Reduced Functioning of Preforntal Cortex (primarily dorsolateral prefrontal cortex and striatum).

The knowledge gained from imaging research and from the postmortem studies support a role for dysfunction within the prefrontal cortical and striatal systems that normally modulate limbic and brainstem structures involved in mediating emotional behavior in the pathogenesis of depressive symptoms. (Curr Opin Neurobiol. 2001 Apr;11(2):240-9)

(2) Amygdala Hyperactivity in Depression. 

Neuroimaging studies have demonstrated that adolescents with Major depression disorder without a concomitant psychiatric disorder have greater left amygdala and bilateral ACC (Anterior Cingulate Cortex) activity. (J Am Acad Child Adolesc Psychiatry. 2010 Jan;49(1):42-51)

Note:- Unaffected Children of Depressed Parents (at-risk group) showed:

  • Increased activation to fearful relative to neutral facial expressions in the amygdala and multiple cortical regions.
  • Decreased activation to happy relative to neutral facial expressions in the anterior cingulate cortex and supramarginal gyrus.
  • At-risk children also exhibited reduced amygdala volume.

 

This extensive hyperactivation to negative facial expressions and hypoactivation to positive facial expressions in at-risk children are consistent with behavioral evidence that risk for major depression involves a bias to attend to negative information. (Neuroimage Clin. 2015 May 21;8:398-407).

SO REDUCED PREFRONTAL FUNCTION LEADS TO DISINHIBITION OF AMYGDALA AND OTHER LIMBIC STRUCTURES.

(3) Abnormalities of Subgenual Cingulate Gyrus (Cg25) in Major Depression: Reduced Volume and Elevated Metabolic Activity.

Note: Cg25 is implicated in emotion regulation and processing, and amygdala is implicated in emotional memory formation and expression.

  • Cg25 is involved in the production of sad emotions and in antidepressant treatment response.
  • Cg25 is activated during transient sadness, and after recovery from depression its activity is decreased compared with baseline after recovery from depression.
  • Cg25 decreases in activity are seen in response to chronic fluoxetine treatment for MDD, as well as during recovery from depression related to Parkinson’s disease after chronic fluoxetine treatment. (Nat Neurosci. 2007 Sep;10(9):1116-24) and (CNS Spectr. 2008 Aug;13(8):663-81).

 

 

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Dr. Harvinder Singh, M.D. (Admin)


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