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Attention deficit hyperactivity disorder secondary to lesion of the basal ganglia

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DOI: 10.4236/wjns.2012.21007    4,696 Downloads   9,121 Views  


Attention Deficit Hyperactivity Disorder (ADHD) is a childhood onset autoregulation disorder characterized by attention deficit, hyperactivity and/or impul- siveness, which results in social and academic functional impairment. ADHD has a complex aetiology: along with genetic factors, anomalies in several cere-bral districts have been reported. We describe the case of a 9 year old boy with glucose-6-phosphate dehydrogenase deficiency in association with memory, behavioural and attentive disabilities. The patient’s clinical history is characterized by cerebral stroke at 3 years of age during a febrile episode, resulted in slight hemiparesis. Neuroimaging revealed a cystic lesion in the anterior portion of the right lenticular nucleus. Neuropsychological and psychiatric assess- ment evidenced alterations of executive functions. Diagnosis of ADHD secondary to lesion of the basal ganglia was made. We report the patient’s clinical profile in the light of current evidence pointing towards dysfunction of the basal ganglia as a crucial aetiological factor in memory and executive function impairment.

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The authors declare no conflicts of interest.

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Mazzotta, G. , Lucia Cirulli, L. , Sposato, M. and Serino, D. (2012) Attention deficit hyperactivity disorder secondary to lesion of the basal ganglia. World Journal of Neuroscience, 2, 44-46. doi: 10.4236/wjns.2012.21007.


[1] Barkley, R.A. (1997) Behavioral inhibition, sustained attention and executive functions. Constructing a unifying theory of ADHD. Psychol Bull, 121, 65-94. doi:10.1037/0033-2909.121.1.65
[2] Tripp, G. and Wickens, J.R. (2009) Neurobiology of ADHD. Neuropharmacology, 57, 579-589. doi:10.1016/j.neuropharm.2009.07.026
[3] Adams, H.P., Butler, M.J., Biller, J. and Toffol, G.J. (1986) Non hemorragic cerebral infarction in young adults. Archives of Neurology, 43, 793-796. doi:10.1001/archneur.1986.00520080041017
[4] Vicari, S. (2007) Promea, prove di memoria e apprendimento per l’età evolutiva. Giunti OS Organizzazioni Speciali, Flo-rence.
[5] Biancardi, S. (1997) Test delle campanelle mod-ificato. Psichiatria dell’infanzia e dell’adolescenza, 64, 73-84.
[6] Marzocchi, G.M. Re, A. and Cornoldi, C. (2010) Batteria italiana per l’ADHD per la valutazione dei bambini con deficit di attenzione/iperattività. Edizioni Erickson, Tren-to.
[7] Kaufman, J., Birmaher, B., Brent, D., Rao, U. and Ryan, N. (2004) K-SADS-PL Intervista diagnostica per la va-lutazione dei disturbi psicopatologici in bambini ed adolescenti. Edizioni Erickson, Trento.
[8] Achenbach, T.M. and Rescorla, L.A. (2001) Manual for the ASEBA school-age forms and pro-files. University of Vermont, Burlington.
[9] Rother, R.P. and Bell, L. et al. (2005) The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin. The Journal of the American Medical Association, 293, 1653-1662.
[10] Gladwin, M.T. and Kato, G.J. (2008) Hemo-sis-associated hypercoagulability in sickle cell disease: the plot (and blood) thickens. Haematologica, 93, 1-3. doi:10.3324/haematol.12318
[11] Emond, V., Joyal, C. and Poissant, H. (2009) Structural and functional neuranatomy of attention-deficit hyperactivity disorder. Encephale, 35, 107-114.

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