Brodmann area 25

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Brain: Brodmann area 25
Brodmann Cytoarchitectonics 25.png
Brodmann area 25 is shown in orange.
Gray727-Brodman.png
Medial surface of the brain with Brodmann's areas numbered.
Latin Area subgenualis
NeuroLex ID birnlex_1726
Sagittal MRI slice with highlighting indicating location of the subgenual anterior cingulate cortex.
Sagittal MRI slice with highlighting indicating location of the subgenual anterior cingulate cortex.

Brodmann area 25 (BA25) is an area in the cerebral cortex of the brain and delineated based on its cytoarchitectonic characteristics. It is also called the subgenual area, area subgenualis or subgenual cingulate. It is the 25th "Brodmann area" defined by Korbinian Brodmann (thus its name). BA25 is located in the cingulate region as a narrow band in the caudal portion of the subcallosal area adjacent to the paraterminal gyrus. The posterior parolfactory sulcus separates the paraterminal gyrus from BA25. Rostrally it is bound by the prefrontal area 11 of Brodmann.[1]

History[edit]

Brodmann described this area as it is labeled now in 1909. Originally in 1905, Brodmann labeled the area as part of area 24. In 1909, he divided the area into area 24 and 25.[2]

Function[edit]

This region is extremely rich in serotonin transporters and is considered as a governor for a vast network involving areas like hypothalamus and brain stem, which influences changes in appetite and sleep; the amygdala and insula, which affect the mood and anxiety; the hippocampus, which plays an important role in memory formation; and some parts of the frontal cortex responsible for self-esteem.[3] This region is particularly implicated in the normal processing of sadness.[4][5]

Involvement in depression[edit]

The subcallosal cingulate gyrus which consists of BA25 as well as parts of BA24 and BA32 has been implicated as playing an important role in major depression and has been the target of deep brain stimulation to treat that disease.[6]

One study found that BA25 is metabolically overactive in treatment-resistant depression.[7] A different study found that metabolic hyperactivity in this area is associated with poor therapeutic response of persons with Major Depressive Disorder to cognitive-behavioral therapy and venlafaxine.[8]

In 2005 Helen S. Mayberg and collaborators described how they successfully treated a number of depressed people — individuals virtually catatonic with depression despite years of talk therapy, drugs, even shock therapy — with pacemaker-like electrodes (deep brain stimulation) in area 25.[9]

A decade earlier, Mayberg had identified area 25 as a key conduit of neural traffic between the "thinking" frontal cortex and the phylogenetically older central limbic region that gives rise to emotion. She subsequently found that area 25 appeared overactive in these depressed people — "like a gate left open," as she puts it — allowing negative emotions to overwhelm thinking and mood. Inserting the electrodes closed this gate and rapidly alleviated the depression of two-thirds of the trial's patients.[10]

A recent study found that Transcranial magnetic stimulation is more clinically effective treating depression when targeted specifically to Brodmann area 46, because this area has intrinsic functional connectivity (negative correlation) with area 25.[11]

Another recent study has found that the responses of area 25 to viewing sad stimuli are affected by cortisol.[12] This suggests that depression related changes in the activity in area 25 could be due to Hypothalamic–pituitary–adrenal axis dysregulation.

Image[edit]

See also[edit]

Notes and references[edit]

  1. ^ subgenual area 25. braininfo.rprc.washington.edu, retrieved November 18, 2006.
  2. ^ area 25 of Brodmann-1909. braininfo.rprc.washington.edu, retrieved November 19, 2006.
  3. ^ "Faulty Circuits", Scientific American, April 2010
  4. ^ Mayberg, HS; Liotti M; Brannan SK; McGinnis S; Mahurin RK; Jerabek PA; et al. (May 1999). "Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness.". Am J Psychiatry 156 (5): 675–82. 
  5. ^ Phan, KL; Wager T; Taylor SF; Liberzon I (June 2002). "Functional neuroanatomy of emotion: a meta-analysis of emotion activation studies in PET and fMRI.". NeuroImage 16 (2): 331–48. 
  6. ^ Hamani C, Mayberg H, Stone S, Laxton A, Haber S, Lozano AM. (15 February 2011). "The subcallosal cingulate gyrus in the context of major depression". Biological Psychiatry 69 (4): 301–309. doi:10.1016/j.biopsych.2010.09.034. PMID 21145043. 
  7. ^ Deep Brain Stimulation for Treatment-Resistant Depression neuron.org, March 3, 2005. Retrieved November 18, 2006.
  8. ^ Predictors of nonresponse to cognitive behavioural therapy or venlafaxine using glucose metabolism in major depressive disorder cma.ca, May 2009. Retrieved May 23, 2009.
  9. ^ Lozano, Andres M; Peter Giacobbe, Clement Hamani, Sakina J Rizvi, Sidney H Kennedy, Theodore T Kolivakis, Guy Debonnel, Abbas F Sadikot, Raymond W Lam, Andrew K Howard, Magda Ilcewicz-Klimek, Christopher R Honey, Helen S Mayberg (2011-11-18). "A multicenter pilot study of subcallosal cingulate area deep brain stimulation for treatment-resistant depression". Journal of Neurosurgery 116 (2): 315–22. doi:10.3171/2011.10.JNS102122. PMID 22098195. 
  10. ^ Mayberg HS, Lozano AM, Voon V, et al. (March 2005). "Deep brain stimulation for treatment-resistant depression". Neuron 45 (5): 651–60. doi:10.1016/j.neuron.2005.02.014. PMID 15748841. 
  11. ^ Fox, MD; Buckner, RL; White, MP; Greicius, MD; Pascual-Leone, A (2012). "Efficacy of transcranial magnetic stimulation targets for depression is related to intrinsic functional connectivity with the subgenual cingulate". Biological psychiatry 72 (7): 595–603. doi:10.1016/j.biopsych.2012.04.028. PMID 22658708.  edit
  12. ^ Sudheimer, KD; Abelson JL; Taylor SF; Martis B; Welsh RC; Warner C; et al (April 2013). "Exogenous glucocorticoids decrease subgenual cingulate activity evoked by sadness". Neuropsychopharmacology 38 (5): 826–45. PMID 23303057.