Attention-deficit hyperactivity disorder other imaging findings: Difference between revisions

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{{ADHD}}
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==Overview==
==Overview==
Though the brains of ADHD patients follow a normal pattern of development, imaging findings indicative of ADHD may include delayed physical development of the brain. This may help explain why some adolescent ADHD patients do not experience symptoms into adulthood.
The diagnosis of ADHD is mostly clinical, based on a thorough history and physical exam. Imaging studies should not be routinely done, but rather be guided by pertinent findings in the history and physical exam.<ref name="pmid15322953">{{cite journal |vauthors=Taylor E, Döpfner M, Sergeant J, Asherson P, Banaschewski T, Buitelaar J, Coghill D, Danckaerts M, Rothenberger A, Sonuga-Barke E, Steinhausen HC, Zuddas A |title=European clinical guidelines for hyperkinetic disorder -- first upgrade |journal=Eur Child Adolesc Psychiatry |volume=13 Suppl 1 |issue= |pages=I7–30 |year=2004 |pmid=15322953 |doi=10.1007/s00787-004-1002-x |url=}}</ref>


==Key Findings in ADHD==
==Imaging Findings==
*Delays in the physical development of some brain structures have been observed in ADHD patients beginning in elementary school and through young adulthood, during the period when cortical thickening during childhood begins to change to thinning following [[puberty]]. The median value of the delay was three years.
===MRI===
*The delay was most prominent in the [[frontal cortex]] and [[temporal cortex]], which are believed responsible for the ability to control and focus thinking, suppress inappropriate actions and thoughts, remember things from moment to moment, and work for reward. These are all functions whose disturbance is associated with a diagnosis of ADHD.
High resolution [[MRI]] in ADHD shows:
*The region with the greatest average delay, the middle of the prefrontal cortex, lagged a full five years in development in ADHD patients. In contrast, the [[motor cortex]] in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the restlessness and fidgetiness that characterize an ADHD diagnosis.
*Decreased overall brain volume
*There appeared to be no significant difference in back-to-front development of brain maturation in ADHD patients as compared to healthy adolescents. This contrasts with the pattern of development seen in other disorders such as [[autism]], where the peak of cortical thickening occurs much earlier than normal.<ref>[http://www.nimh.nih.gov/science-news/2007/brain-matures-a-few-years-late-in-adhd-but-follows-normal-pattern.shtml Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern] NIMH Press Release, November 12, 2007 </ref>
*Decreased gray matter volume
*Decreased cortical thickness
*Increased white matter volume
These effects are most pronounced in the areas of the [[prefrontal]] cortex, [[caudate]] and [[cerebellum]].<ref name="pmid19730275">{{cite journal |vauthors=Narr KL, Woods RP, Lin J, Kim J, Phillips OR, Del'Homme M, Caplan R, Toga AW, McCracken JT, Levitt JG |title=Widespread cortical thinning is a robust anatomical marker for attention-deficit/hyperactivity disorder |journal=J Am Acad Child Adolesc Psychiatry |volume=48 |issue=10 |pages=1014–22 |year=2009 |pmid=19730275 |pmc=2891193 |doi=10.1097/CHI.0b013e3181b395c0 |url=}}</ref><ref name="pmid15949998">{{cite journal |vauthors=Seidman LJ, Valera EM, Makris N |title=Structural brain imaging of attention-deficit/hyperactivity disorder |journal=Biol. Psychiatry |volume=57 |issue=11 |pages=1263–72 |year=2005 |pmid=15949998 |doi=10.1016/j.biopsych.2004.11.019 |url=}}</ref><ref name="pmid24189200">{{cite journal |vauthors=Makris N, Liang L, Biederman J, Valera EM, Brown AB, Petty C, Spencer TJ, Faraone SV, Seidman LJ |title=Toward Defining the Neural Substrates of ADHD: A Controlled Structural MRI Study in Medication-Naïve Adults |journal=J Atten Disord |volume=19 |issue=11 |pages=944–53 |year=2015 |pmid=24189200 |doi=10.1177/1087054713506041 |url=}}</ref>
 
===SPECT===
*[[SPECT]] scans in patients with ADHD may reveal orbito-frontal and [[cerebellar]] hypoperfusion.<ref name="pmid26037855">{{cite journal |vauthors=Schneider H, Thornton JF, Freeman MA, McLean MK, van Lierop MJ, Schneider J |title=Conventional SPECT Versus 3D Thresholded SPECT Imaging in the Diagnosis of ADHD: A Retrospective Study |journal=J Neuropsychiatry Clin Neurosci |volume=26 |issue=4 |pages=335–43 |year=2014 |pmid=26037855 |doi=10.1176/appi.neuropsych.12110280 |url=}}</ref>
 
===PET===
*[[PET]] scan shows decreased activity in the front-straito-cerebellar and limbic networks.<ref name="pmid24163364">{{cite journal |vauthors=del Campo N, Fryer TD, Hong YT, Smith R, Brichard L, Acosta-Cabronero J, Chamberlain SR, Tait R, Izquierdo D, Regenthal R, Dowson J, Suckling J, Baron JC, Aigbirhio FI, Robbins TW, Sahakian BJ, Müller U |title=A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment |journal=Brain |volume=136 |issue=Pt 11 |pages=3252–70 |year=2013 |pmid=24163364 |pmc=4125626 |doi=10.1093/brain/awt263 |url=}}</ref>


==References==
==References==
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[[Category:Disease]]
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Latest revision as of 15:47, 14 January 2019

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Overview

The diagnosis of ADHD is mostly clinical, based on a thorough history and physical exam. Imaging studies should not be routinely done, but rather be guided by pertinent findings in the history and physical exam.[1]

Imaging Findings

MRI

High resolution MRI in ADHD shows:

  • Decreased overall brain volume
  • Decreased gray matter volume
  • Decreased cortical thickness
  • Increased white matter volume

These effects are most pronounced in the areas of the prefrontal cortex, caudate and cerebellum.[2][3][4]

SPECT

  • SPECT scans in patients with ADHD may reveal orbito-frontal and cerebellar hypoperfusion.[5]

PET

  • PET scan shows decreased activity in the front-straito-cerebellar and limbic networks.[6]

References

  1. ↑ Taylor E, Döpfner M, Sergeant J, Asherson P, Banaschewski T, Buitelaar J, Coghill D, Danckaerts M, Rothenberger A, Sonuga-Barke E, Steinhausen HC, Zuddas A (2004). "European clinical guidelines for hyperkinetic disorder -- first upgrade". Eur Child Adolesc Psychiatry. 13 Suppl 1: I7–30. doi:10.1007/s00787-004-1002-x. PMID 15322953.
  2. ↑ Narr KL, Woods RP, Lin J, Kim J, Phillips OR, Del'Homme M, Caplan R, Toga AW, McCracken JT, Levitt JG (2009). "Widespread cortical thinning is a robust anatomical marker for attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry. 48 (10): 1014–22. doi:10.1097/CHI.0b013e3181b395c0. PMC 2891193. PMID 19730275.
  3. ↑ Seidman LJ, Valera EM, Makris N (2005). "Structural brain imaging of attention-deficit/hyperactivity disorder". Biol. Psychiatry. 57 (11): 1263–72. doi:10.1016/j.biopsych.2004.11.019. PMID 15949998.
  4. ↑ Makris N, Liang L, Biederman J, Valera EM, Brown AB, Petty C, Spencer TJ, Faraone SV, Seidman LJ (2015). "Toward Defining the Neural Substrates of ADHD: A Controlled Structural MRI Study in Medication-Naïve Adults". J Atten Disord. 19 (11): 944–53. doi:10.1177/1087054713506041. PMID 24189200.
  5. ↑ Schneider H, Thornton JF, Freeman MA, McLean MK, van Lierop MJ, Schneider J (2014). "Conventional SPECT Versus 3D Thresholded SPECT Imaging in the Diagnosis of ADHD: A Retrospective Study". J Neuropsychiatry Clin Neurosci. 26 (4): 335–43. doi:10.1176/appi.neuropsych.12110280. PMID 26037855.
  6. ↑ del Campo N, Fryer TD, Hong YT, Smith R, Brichard L, Acosta-Cabronero J, Chamberlain SR, Tait R, Izquierdo D, Regenthal R, Dowson J, Suckling J, Baron JC, Aigbirhio FI, Robbins TW, Sahakian BJ, Müller U (2013). "A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment". Brain. 136 (Pt 11): 3252–70. doi:10.1093/brain/awt263. PMC 4125626. PMID 24163364.

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