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Institutional deprivation in early childhood is associated with neuropsychological deficits in adolescence. Using 20-year follow-up data from a unique natural experiment – the large-scale adoption of children exposed to extreme deprivation in Romanian institutions in the 1980s –we examined, for the first time, whether such deficits are still present in adulthood and whether they are associated with deprivation-related symptoms of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).
Adult neuropsychological functioning was assessed across five domains (inhibitory control, emotion recognition, decision-making, prospective memory and IQ) in 70 previously institutionalized adoptees (mean age = 25.3, 50% female) and 22 non-deprived UK adoptees (comparison group, mean age = 24.6, 41% female). ADHD and ASD symptoms were assessed using parent-completed questionnaires.
Early institutionalization was associated with impaired performance on all tasks in adulthood. Prospective memory deficits persisted after controlling for IQ. ADHD and ASD symptoms were positively correlated. After controlling for ASD symptoms, ADHD symptoms remained associated with deficits in IQ, prospective memory, proactive inhibition, decision-making quality and emotion recognition. ASD symptoms were not independently associated with neuropsychological deficits when accounting for their overlap with ADHD symptoms. Multiple regression analysis revealed that the link between childhood deprivation and adult ADHD symptoms was statistically explained by deprivation-related differences in adult IQ and prospective memory.
These results represent some of the most compelling evidence to date of the enduring power of early, time-limited childhood adversity to impair long-term neuropsychological functioning across the lifespan – effects that are linked specifically to deprivation-related adult ADHD symptoms.
Postpartum psychosis (PP) is a severe postpartum disorder. While working memory and emotional processing-related brain function are consistently impaired in psychoses unrelated to the puerperium, no studies have investigated them in PP.
Twenty-four women at risk of developing PP (11 developed an episode – PE; 13 remained well – NPE) and 20 healthy postpartum women completed two functional magnetic resonance imaging tasks within a year of delivery: working memory (n-back) and emotional face recognition (fearful faces). We compared women at-risk of PP to controls, as well as NPE, PE, and controls to test for potential effects of a PP episode occurrence.
Women at-risk of PP and PE showed hyperactivation of lateral visual areas, precuneus, and posterior cingulate during the n-back task. The at-risk group as a whole, as well as the PE and NPE groups, showed hyperconnectivity of the right dorsolateral prefrontal cortex (DLPFC) with various parieto-occipito-temporo-cerebellar regions compared to controls during several n-back conditions. Increases in connectivity between the right DLPFC and ipsilateral middle temporal gyrus were observed in the PE group compared to NPE during 2-back. During the fearful faces task, at-risk women as a group showed hyperactivation of fronto-cingulo-subcortical regions, and hypoconnectivity between the left amygdala and ipsilateral occipito-parietal regions compared to controls. No significant performance differences were observed.
These results present preliminary evidence of a differential nature of functional brain abnormalities in PP compared to the typically observed reduced connectivity with the DLPFC in psychoses unrelated to puerperium, such as bipolar disorder.
Aberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2 antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression.
We recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0–43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest.
Lurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high- v. low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF.
Lurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.
Ethnic minority individuals have an increased risk of developing a psychotic disorder, particularly if they live in areas of ethnic segregation, or low own group ethnic density. The neurobiological mechanisms underlying this ethnic minority associated risk are unknown. We used functional MRI to investigate neural responses to faces of different ethnicity, in individuals of black ethnicity, and a control group of white British ethnicity individuals.
In total 20 individuals of black ethnicity, and 22 individuals of white British ethnicity underwent a 3T MRI scan while viewing faces of black and white ethnicity. Own group ethnic density was calculated from the 2011 census. Neighbourhood segregation was quantified using the Index of Dissimilarity method.
At the within-group level, both groups showed greater right amygdala activation to outgroup faces. Between groups, the black ethnicity group showed greater right amygdala activation to white faces, compared to the white ethnicity group. Within the black ethnicity group, individuals living in areas of lower own group ethnic density showed greater right amygdala reactivity to white faces (r = −0.61, p = 0.01).
This is the first time an increased amygdala response to white faces has been demonstrated in individuals of black ethnicity. In the black ethnicity group, correlations were observed between amygdala response and neighbourhood variables associated with increased psychosis risk. These results may have relevance for our understanding of the increased rates of paranoia and psychotic disorders in ethnic minority individuals.
Neurotransmitters are the means by which one neuron influences the action of another. Abnormalities in neurotransmitter function are implicated in a variety of neurological and neuropsychiatric disorders and drugs that influence the neurotransmitter systems are often used in treating the symptoms of such disorders. The effects of these drugs can be paradoxical. A small dose of a pharmacological agent might have entirely the opposite effect to a large dose, a drug may improve one ability whilst impairing another, a drug may have opposite effects in different populations or opposite effects in the same individual at different times. In this chapter, we illustrate these effects using clinical data and data from healthy volunteers in experimental studies. With one of the best studied neuromodulators – dopamine – as our focus, we introduce key principles that can help to explain these apparent paradoxes. First, the effect of a drug depends on baseline levels of the neurotransmitter already in the system. When baseline levels are low, a given pharmacological dose can increase function closer to an optimal level. When baseline levels are high, the same dose can over-stimulate the system and trigger compensatory mechanisms that reduce performance on a given task. Second, a drug could have quite different effects in different brain regions. Accordingly, a function that is predominantly influenced by one region may be enhanced, whilst another function, more dependent on another region, may be impaired. In the final section of the chapter, we turn to attention deficit hyperactivity disorder (ADHD).
This chapter reviews emission tomography studies in attention-deficit hyperactivity disorder (ADHD) that address the neurobiology of this disorder and treatment effects. It examines the potential for these imaging techniques to help undercover possible mechanisms underlying the behavioral and cognitive changes that follow treatment. Single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies of cerebral perfusion and dopamine synthesis, release, and receptors have shown clear sensitivity to ADHD, with differential measurements across all modalities. Striatal markers of perfusion and functional activation in adults are proving important in understanding functional deficits in ADHD. In addition, striatal dopamine markers potentially relevant in mediating differences in cognition and personality differ in both children and adults with ADHD. The most recent studies have confirmed that dopaminergic markers are indeed valuable targets for understanding the neurobiology of ADHD.
The adequacy of pharmacotherapy received in practice by patients after an acute episode of depression has been little studied.
To describe and assess adequacy of drug continuation and maintenance in patients with depression.
Patients with depression were interviewed 18 months after discharge from hospital. Quantitative assessments of drug treatment doses and compliance were made monthly over this period, and qualitative ratings in continuation and maintenance phases.
About 20% of patients were prescribed low drug doses after discharge and 10% were prescribed no drugs at all. Reported compliance was around 70%. About 30% failed to receive adequate longer-term treatment, mostly due to the continuation phase being too short. Deficiencies of dosage and compliance were greater in patients who never achieved full recovery. Patient refusal was the most common reason for not using antidepressants. Further episodes of depression were not particularly associated with inadequate treatment.
There were deficiencies in drug treatment that did not appear to be the principal cause of further episodes but may be important in non-recovery. Patient fears require discussion.
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