No open-access location is known for this record yet.
No open-access location is known for this record yet.
Many take it for granted that learning and behaviour problems are caused by brain dysfunction (1). Others tend to view academic failure and psychological adjustment difficulties as reflections of deficient education and/or psychosocial disadvantage (including parental failure) (2). Some try to find middle ground in referring to the combined effects of nature and nurture, but may vary in the extent to which they emphasize additive, interactive or transactional effects (3). Most people, including those who are not at all experts in the field, have a point of view on these matters (4). This may be based on sound knowledge, but, more often, it is not rooted in empirical research. That is why the paper by Batstra et al. in this issue of the journal (5) makes for refreshing reading. A carefully designed prospective controlled study of a fairly representative sample of children is presented in a dispassionate way such that new light is shed on the vexed questions of whether and how the brain is involved in learning and behaviour problems in childhood. Mijna Hadders-Algra and her Groningen group (including her tutors Prechtl, Touwen and Kalverboer) now have a long tradition of studying the relationship of neurological status and academic and psychological problems, both longitudinally and cross-sectionally. They have previously demonstrated that 5–11 years after showing clear signs of neurological abnormality in the newborn period, children still show learning and behaviour problems – in addition to those associated with mental retardation and cerebral palsy. In their new study, they go on to show that, quite regardless of the contribution of newborn problems, independently rated minor neurological dysfunction (MND) at the time of follow-up predicted parent and teacher reported scholastic, attention and behavioural problems, albeit in a differential fashion. Academic failure was predicted by any combination of several indices of MND, suggesting that learning and attentional problems may result from brain dysfunction affecting many different parts of the brain. Behaviour problems on the other hand were predicted rather more specifically by fine manipulative dysfunction (internalizing problems), and choreiform movements and coordination problems (externalizing problems), suggesting that such problems may be associated with more localized brain dysfunction. The Groningen group have previously shown that the presence of a high number of MNDs (found in those with learning/attention problems but not in those with behaviour problems) is strongly related to pre- and perinatal adversity (6). They argue that pre- and perinatal adversity may be an important background factor in the attention deficit part of so-called attention-deficit/hyperactivity disorder (A-D/HD) (7), but may have less impact in the externalizing part (hyperactive-impulsive) of the condition. These findings are in line with recent hypotheses that the A-D and HD constructs may represent different disorders that are quite often comorbid but not more so than ADHD with developmental coordination disorder (DCD) or ADHD with oppositional defiant disorder (ODD) (8, 9). They are also in accord with the studies of our own group on children with so-called deficits in attention, motor control, and perception (DAMP) showing pre- and perinatal factors to be an important predictor of A-D and DCD (equivalent to DAMP) but not necessarily of some of the comorbid externalizing psychiatric problems (such as ODD and conduct disorder), which tended to be more strongly associated with psychosocial adversity including non-optimal rearing conditions (10, 11). Now, the Groningen study was not specifically geared at studying the syndrome of ADHD. However, the fact that strong effects were found even when studying only rather loosely defined ‘attention defict’, suggests that more marked correlations would have been found had the research included clinically impaired children with ADHD instead. Another very interesting finding was the failure of gender to have any effect on neurobehavioural and neurocognitive relationships. The authors suggest that this would point in the direction of the high rate of psychiatric morbidity among prepubescent boys compared to girls being especially attributable to a higher vulnerability of the neural hardware and not to psychosocial effects in boys. From the clinical point of view, the authors cautiously conclude that ‘evaluation of the neurological condition of the child with learning and behavioural problems offers insight into the aetiology and pathogenesis of these problems’. This sounds almost like a truism, but is, in effect, a bold statement in the real world of child psychiatry (and to some extent behavioural paediatrics). Children with the kinds of learning and behavioural problems referred to in the present context often receive no neurological evaluation whatsoever. In fact, it is not uncommon for the affected child not to be medically examined at all. It is high time that the failure to examine physically/neurologically/neurodevelopmentally any child presenting with learning and/or behavioural problems come to be regarded as a severe breech of the code of good medical practice. Having said that, we do believe, contrary to the assertion of Batstra et al., that the field is in need of a clinically slightly less cumbersome tool for neurological examination than the one they used in their study. The Touwen manual is excellent for research purposes, but in clinical practice, there will never be time for all children to be examined with this instrument. We must not forget that several per cent of the whole population of school age children are affected by clinically impairing ADHD and associated learning and behavioural problems (12). They are all in need of our medical attention!
Loading…
Stored only when both papers are in the corpus — 5 citations exist upstream.
Papers that cite the same references — the relational fallback while embeddings are still backfilling.
Imported from OpenAlex (CC0) — nothing here is generated.