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.
The Diagnostic and Statistical Manual for Mental Disorders (DSM-IV-TR) defines ADHD as an autoregulation disorder with onset before 6 years of age, characterized by the following symptoms: attentional deficits (low levels of sustained attention, poor ability in inhibiting distracting stimuli), hyperactivity (poor motor inhibition, avoidance of sedentary activities), and impulsiveness (rash behaviour, poor pulsional inhibition) [
Current scientific evidence suggests a neurobiological origin of the disorder related in particular to functional anomalies of two specific brain regions, the orbitofrontal cortex and the basal ganglia [
The patient, affected by glucose-6-phosphate dehydrogenase (G6PD) deficiency, was sent to our institute for behavioural and attentional difficulties. His clinical history was characterized by cerebral stroke at 36 months of age during a febrile episode. The patient’s parents reported the appearance of high levels of hyperactivity and impulsiveness following the ictal event, which became even more evident when the patient began attending school, due to difficulties in focusing on school work and maintaining adequate attention levels both in school and at home.
Neurological assessment showed hyposthenia of the left inferior limb at the Mingazzini manoeuvre, asymmetry of osteotendinous reflexes with left hypoexcitability, dysmetria of the left superior limb with adiadochokinesis, athetosic movements of the fingers of the left hand when extended, spastic gait pattern.
MRI scan of the brain showed a cystic lesion in correspondence with the anterior portion of the right lenticular nucleus (see
Cognitive level was determined through the administra-
tion of the Wechsler Intelligence Scale for Chidren— Third Edition (WISC-III), from which the following scores were obtained: Verbal I.Q. 105, Performance I.Q. 85, Total I.Q. 95. Different tests were used to assess the patient’s attentive, mnesic and learning abilities. The Childhood Memory and Learning Abilities Battery (PRO-MEA) [
Psychiatric assessment was undertaken through administration of semi-structured interviews and psychiatric questionnaires. The DSM-IV oriented Kiddie-Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version (K-SADS-PL) [
Clinical evaluation of our patient revealed the presence of ADHD. We know that ADHD is related to a dysfunction of the fronto-striatal network which includes the lateral prefrontal cortex (PCF), the anterior dorsal cingulate gyrus, the caudate nucleus, the putamen and the cerebellum. In particular, the PCF has a key role in learning and in executive functions, as in behavioural strategy programming; its hypofunctionality would entail the alteration of such functions. This circuitry receives stimuli from different associative areas which project towards the dorso-lateral PCF. In turn, the latter projects towards the basal ganglia and consequently to the thalamic nuclei which provide a feedback for the regulation of behaviour and problem-solving strategies [
Neuropsychological assessment revealed a dysfunction in executive functions. The patient had a poor performance in tasks involving sustained attention, problemsolving and regulation of inhibition. Both semantic memory and explicit long term memory were compromised, with pitfalls in logical memory. The resulting neuropsychological profile, in relation to the underlying anatomical lesion, can be superimposed to what is reported in literature regarding ADHD not associated with evident morphological alterations [
In conclusion, we believe that data obtained from the present case represents further evidence of the close relationship between ADHD and dysfunctionality of the executive function network [1-11]. Such close relation is not often easisly highlighted, given the low incidence of ischemic stroke during childhood and the rare occurrence of such a direct time-related appearance of ADHD symptomatology after a lesion of one of the cerebral structures involved in the executive function network [