摘要
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.
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.
