Neurodevelopmental View Research Articles

Functioning and neurocognition in very early and early-life onset bipolar disorders: the moderating role of bipolar disorder type.

Defining homogeneous subgroups of bipolar disorder (BD) is a major goal in personalized psychiatry and research. According to the neurodevelopmental theory, age at onset may be a key variable. As potential trait markers of neurodevelopment, cognitive and functional impairment should be greater in the early form of the disease, particularly type 1 BD (BD I). The age at onset was assessed in a multicenter, observational sample of 4190 outpatients with BD. We used a battery of neuropsychological tests to assess six domains of cognition. Functioning was measured using the Functioning Assessment Short Test (FAST). We studied the potential moderation of the type of BD on the associations between the age at onset and cognitive and functioning in a subsample of 2072 euthymic participants, controlling for potential clinical and socio-demographic covariates. Multivariable analyses showed cognition to not be impaired in individuals with early (21-30years) and very early-life (before 14years) onset of BD. Functioning was equivalent between individuals with early and midlife-onset of BD II and NOS but better for individuals with early onset of BD I. In contrast, functioning was not worse in individuals with very early-onset BD I but worse in those with very early-onset BD II and NOS. Early-life onset BDs were not characterized by poorer cognition and functioning. Our results do not support the neurodevelopmental view that a worse cognitive prognosis characterizes early-life onset BD. This study suggests that functional remediation may be prioritized for individuals with midlife-onset BD I and very early life onset BD 2 and NOS.

Intellectual outcome after a cortical lesion with versus without epilepsy: A life span neurodevelopmental view

In patients with cortical lesions, the structure of intelligence has never been studied as a function of age at lesion onset and presence vs absence of lesional epilepsy over the life span. MethodTwo thousand one hundred eighty-six cases were assembled bearing unilateral cortical lesions occurring at all ages (1301 with seizures) with postlesion verbal intelligence quotient (IQ) (VIQ) and performance IQ (PIQ). ResultsGlobal IQ significantly and constantly decreased as a function of age at lesion onset in the cases without epilepsy, and increased in the cases with epilepsy. Beyond the lesion onset age of 12 years, VIQ was significantly higher than PIQ in the cases without epilepsy, and lower in the cases with epilepsy. The VIQ/PIQ × lesion-side interaction indicative of hemispheric specialization increased significantly linearly with age at lesion onset in the patients without epilepsy but ceased to progress at the lesion-onset age of 30 years and beyond in the cases with epilepsy. ConclusionPostlesion global IQ, the difference between VIQ and PIQ, and the laterality index all vary significantly as a function of age at lesion onset. In addition, these changes over the life span are all quite different between cases with and without epilepsy.

Early Verb-Action and Noun-Object Mapping Across Sensory Modalities: A Neuro-Developmental View

ABSTRACTThe authors provide an alternative to the traditional view that verbs are harder to learn than nouns by reviewing three lines of behavioral and neurophysiological evidence in word-mapping development across cultures. First, preverbal infants tune into word-action and word-object pairings using domain-general mechanisms. Second, while post-verbal infants from noun-friendly language environments experience verb-action mapping difficulty, infants from verb-friendly language environments do not. Third, children use language-specific conventions to learn all types of words, although still strongly influenced by their language environment. Additionally, the authors suggest neurophysiological research to advance these lines of evidence beyond traditional views of word learning.

Evidence for alterations of cortical folding in anorexia nervosa.

Anorexia nervosa (AN) is highly heritable, and the perspective on the etiology of AN has changed from a behavioral to a neurobiological and neurodevelopmental view. However, cortical folding as an important marker for deviations in brain development has yet rarely been explored in AN. Hence, in order to determine potential cortical folding alterations, we investigated fine-grained cortical folding in a cohort of 26 patients with AN, of whom 6 patients were recovered regarding their weight at the time point of MRI measurement. MRI-derived cortical folding was computed and compared between patients and healthy controls at about 150,000 points per hemisphere using a surface-based technique (FreeSurfer). Patients with AN exhibited highly significant increased cortical folding in a right dorsolateral prefrontal cortex region (DLPFC). Furthermore, a statistical trend in the same direction was found in the right visual cortex. We did not find a correlation of local cortical folding and current symptoms of the disease. In conclusion, our analyses provide first evidence that altered DLPFC cortical folding plays a role in the etiology of AN. The absence of correlations with clinical parameters implicates a relatively independence of cortical folding alterations from the current symptomatology and might thus be regarded as a trait characteristic of the disease potentially related to other neurobiological features of AN.

Prenatal maternal influenza and schizophrenia in offspring: What does this tell us about fetal programming of chronic disease?

Accumulating evidence suggests that chronic diseases, physical as well as neuropsychiatric, may have their origins in early life. Alterations in fetal development have been reported to be associated with an increased risk of subsequent cardiovas- cular and metabolic disorders. This has been formulated as the fetal or developmental programming hypothesis. Schizophrenia is a severe and chronic neuropsychiatric illness of teenage and adult life. Birth cohort studies have reported low birth weight, delays in attaining motor milestones, and deficits in premorbid cognitive and social functioning as factors associated with, and possible risk factors for future schizophrenia. These provide empirical support for the currently widely accepted neurodevelopmental hypothesis of schizophrenia, where abnormalities in early brain development contribute to the evolution of the disorder. Inter- ference with brain development from infections in early life is in line with a neurodevelopmental view of schizophrenia. Prenatal maternal infections such as influenza have been linked with increased risk of both childhood sub-clinical psychotic symptoms and adult schizophrenia. Prenatal maternal infections can increase fetal exposure to excessive maternal glucocorticoids. This can reprogram the hypothalamic-pituitary-adrenal axis leading to increased risk of several chronic diseases including schizophrenia. In this review we focus on epidemiological and preclinical studies concerning prenatal maternal influenza and risk of both childhood psychotic symptoms and later development of schizophrenia in the offspring. We discuss these findings in light of the fetal programming hypothesis, which points towards common links, in early life, between chronic diseases, physical (such as hypertension and type-two diabetes) and neuropsychiatric (such as schizophrenia).

Longitudinal Evaluation of the Psychomotor Syndrome in Schizophrenia

Little is known about the longitudinal course of psychomotor signs and symptoms after illness onset in schizophrenia. Therefore, a 1-year follow-up study was conducted in which patients with schizophrenia were assessed three times with an extensive battery of psychomotor rating scales and tests. The syndromic structure of psychomotor symptoms was also studied. In accordance with a neurodevelopmental view on schizophrenia, psychomotor functioning was found to remain stable or improve slightly. Prospective studies with longer follow-up periods are needed to rule out the possibility of neurodegeneration in subgroups of patients and to evaluate possible covariation in the course of psychomotor symptoms.

A neurodevelopmental approach for helping gifted learners with diagnosed dyslexia and attention deficit/hyperactivity disorder (AD/HD)

Many intellectually and creatively gifted learners experience barriers to learning and development. These may be incorrectly diagnosed as distinct mental disorders, such as Attention Deficit Disorder, hyperactivity, dyslexia and so on. Medication, behaviour and remedial therapy are among the most frequently cited treatments. Emerging approaches to therapy, based on applied neuroscience and the importance of movement in structuring the brain, are finding that it is possible to ‘heal’ interactive links of dysfunctional behaviours and ensuing learning difficulties. This article presents a neurodevelopmental view of learning and attentional problems that are not uncommon in some gifted learners. By means of two case studies, a neurodevelopmental approach will be illustrated whereby such learners have been helped to overcome their learning barriers.

IQ decline during childhood and adult psychotic symptoms in a community sample: a 19-year longitudinal study.

The goal of this study was to examine cognitive antecedents of psychosis by determining whether variability in IQ during childhood was predictive of psychotic symptoms in adulthood. Deviant responder analyses were used to examine prospectively the relationship of IQ at ages 4 and 7 to psychotic symptoms at age 23 in 547 offspring from a community sample (National Collaborative Perinatal Project) that was unselected for psychiatric illness. The authors compared three hypotheses: that 1) low IQ, 2) large IQ fluctuations regardless of direction, or 3) large IQ declines would predict the presence of adult psychotic symptoms. The 10% of individuals with substantially larger than expected IQ declines from age 4 to 7 had a rate of psychotic, but not other psychiatric, symptoms at age 23 that was nearly seven times as high as the rate for other persons. Parental socioeconomic status and IQ at age 7 also predicted adult psychotic symptoms. However, when IQ at age 7, IQ decline between ages 4 and 7, and socioeconomic status were all included in a logistic regression analysis, only IQ decline remained significant. There is an increased likelihood of developing psychotic symptoms in adulthood for a subgroup of individuals with substantially greater than expected IQ declines during childhood. IQ decline is specific for psychotic symptoms, but follow-up assessment when the study participants are further into the age of risk will be necessary to determine specificity for schizophrenia. The authors discuss the implications of this early cognitive downturn for a neurodevelopmental view of schizophrenia.

Homeostasis, Stress, Trauma, and Adaptation: A Neurodevelopmental View of Childhood Trauma

All experiences change the brain, but not all experiences affect the brain equally. Because the brain is developing and organizing at such an explosive rate in the first years of life, experiences during this period have more potential to influence the brain in positive and negative ways. Traumatic events disrupt homeostasis in multiple areas of the brain that are recruited to respond to the threat. Use-dependent internalization of elements of the traumatic experience can result in the persistence of fear-related neurophysiologic patterns affecting emotional, behavioral, cognitive, and social functioning. A neurodevelopmental view of childhood trauma can help future clinical and research efforts to define and use child-specific and developmentally informed models to guide assessment, intervention, education, therapeutics, and policy.

Schizophrenia: a disorder of neurodevelopment?

For the first time, there is a pathogenic hypothesis of schizophrenia based upon reasonable empirical data. The hypothesis is that schizophrenia is a disorder arising from aberrant brain development. The neurodevelopmental view of schizophrenia is supported by neuropathological, epidemiological and clinical findings. Here, the evidence in favour of the model is summarized, together with a consideration of its weaknesses.

Support for a neurodevelopmental view of schizophrenia

Support for a neurodevelopmental view of schizophrenia

Eye-movement dysfunctions and the neurodevelopmental view of schizophrenia

Background: Eye tracking dysfunction (ETD) has been put forward as a trait marker for biological susceptibility to schizophrenia with the hope of identifying a link to specific cerebral lesions.Methods: Eye movements were recorded using infrared oculography in 8 families (67 members) showing multiple occurrence of schizophrenia and in 9 nonpsychotic families (80 members). Triangle wave stimuli at 15°/s and 30°/s were used and gains (eye velocity/target velocity), rates and amplitudes of different saccade categories (catch-up, back-up, anticipatory saccades, and square-wave-jerks) were determined.Results: In the relatives, the same deficit in maintenance of smooth pursuit performance was found as was seen in the schizophrenic patients. This deficit, which was not observed in the nonpsychotic families, consisted of lower gains for leftward as compared to rightward pursuit. This was emphasized most clearly at 30°/s and was associated with an excess of catch-up saccades in the schizophrenic patients, whereas in the relatives a tendency to exhibit more and larger anticipatory saccades was observed.Conclusions: The results confirm the hypothesis that eye-tracking dysfunction is a phenotypic marker for genetic liability to schizophrenia. Neurophysiologically, a cerebral dysfunction which includes one or more of the oculomotor centers can be assumed in subjects who carry a genetic susceptibility to schizophrenia.