Attention deficit disorder (ADD) could be considered as an early onset, clinically heterogeneous condition that involves three sets of symptoms: inattention, impulsive behaviors, hyperactivity or a combination of them ^(1,2). ADD is the most commonly diagnostic behavior disorder of childhood, estimated to affect 3 to 5 percent of school-age children. Some authors reported male-female ratios between 4:1 to 6:1⁽³⁾. The diagnosis of this condition seems easy, but on contrary is quite difficult due to the low particular organic signs or neurologic indicators that definitely indicate the presence of ADD. The most common features associated with ADD include emotional immaturity, distractibility, impulsivity, social alienation, low self-esteem, mood liability, temper outbursts, irregular academic performance and low frustration tolerance among others.

From the biochemistry point of view, there are little evidences that suggest metabolic implications associated with ADD. Some studies suggest a correlation between cerebral hypoxia or anoxia and greater frequency of attention deficits and hyperactivity ^(4,5). ADD characteristics have been observed in children with epilepsy and seizure disorders ⁽⁶⁾.

Previous imaging studies have tried to indicate which brain regions might miss or overfunction in ADD. Magnetic Resonance Imaging (MRI) has demonstrated that the size of the posterior vermis of the cerebellum was significant decreased in males with ADD ⁽⁷⁾ as well as significant loss of normal right/left symmetry in the caudate, smaller right globus pallidus, smaller right anterior frontal region and reversal of normal lateral ventricular asymmetry ⁽⁸⁾. Swanson et al. ⁽⁹⁾ report a 10% decrease in the basal ganglia size (caudate nucleus and globus pallidus) in ADD. Volumetric studies report localized hemispheric structural anomalies, which are concordant with models of abnormal frontal-striatum and parietal function ⁽¹⁰⁾. However the most relevant information comes from the frontal regions. Previous studies from Functional Magnetic Resonance Imaging (fMRI) suggest an inability of the basal ganglia in the right frontal-striatum circuitry in suppressing outgoing stimulus ⁽¹¹⁾ or subnormal activation of the prefrontal systems responsible for higher-order motor control ⁽¹²⁾. The executive functions and working memory observed in ADD children show similar patterns to those observed in patients with some kind of mistake in the function of the frontal lobe or in the neuroanatomic regions there projected. Positron Emission Tomography (PET) realized at the premotor and superior prefrontal cortex show decreased glucose metabolism in adults with ADD ⁽¹³⁾. On the other hand, many studies report differences in the Electroencephalogram (EEG) patterns in ADD. Thus, adolescents were found to have increased anterior EEG absolute theta activity and reduced posterior relative beta activity compared with controls. These support the continuation of a maturational lag and reduced cortical arousal in adolescent ADD ⁽¹⁴⁾. Concepts from Niedermeyer and Naidu have relationated EEG patterns in ADHD with, not a damaged but, a lazy frontal lobe, which results in uninhibited motor activity and disturbed attention ⁽¹⁵⁾.

The purpose of our work was to determine 1H Magnetic Resonance Spectroscopy (1H-MRS) profile in children with ADD and compare them with Healthy Children (HC) and to correlate the findings with EEG patterns on the frontal lobe of ADD children.