Neurofeedback – learning to modulate brain function through real-time monitoring of current brain state – is both a powerful method to perturb and probe brain function and an exciting potential ...clinical tool. For neurofeedback effects to be useful clinically, they must persist. Here we examine the time course of symptom change following neurofeedback in two clinical populations, combining data from two ongoing neurofeedback studies. This analysis reveals a shared pattern of symptom change, in which symptoms continue to improve for weeks after neurofeedback. This time course has several implications for future neurofeedback studies. Most neurofeedback studies are not designed to test an intervention with this temporal pattern of response. We recommend that new studies incorporate regular follow-up of subjects for weeks or months after the intervention to ensure that the time point of greatest effect is sampled. Furthermore, this time course of continuing clinical change has implications for crossover designs, which may attribute long-term, ongoing effects of real neurofeedback to the control intervention that follows. Finally, interleaving neurofeedback sessions with assessments and examining when clinical improvement peaks may not be an appropriate approach to determine the optimal number of sessions for an application.
•Temporal pattern of symptom change following neurofeedback shared across studies.•Symptoms continued to improve for weeks after neurofeedback.•Neurofeedback studies should follow up subjects to maximize power.•Crossover designs may be contaminated by significant carryover effects.•Optimizing number of sessions by embedding assessments not recommended.
Highlights • Deficits in cognitive flexibility have been described in Obsessive-Compulsive Disorder (OCD). • These deficits may contribute to symptomatology. • Classical neuropsychological probes ...test multiple constructs simultaneously. • More specific behavioral tests, supplemented by neuroimaging, are needed.
Individuals with obsessive-compulsive disorder often identify psychosocial stress as a factor that exacerbates their symptoms, and many trace the onset of symptoms to a stressful period of life or a ...discrete traumatic incident. However, the pathophysiological relationship between stress and obsessive-compulsive disorder remains poorly characterized: it is unclear whether trauma or stress is an independent cause of obsessive-compulsive disorder symptoms, a triggering factor that interacts with a preexisting diathesis, or simply a nonspecific factor that can exacerbate obsessive-compulsive disorder along with other aspects of psychiatric symptomatology. Nonetheless, preclinical research has demonstrated that stress has conspicuous effects on corticostriatal and limbic circuitry. Specifically, stress can lead to neuronal atrophy in frontal cortices (particularly the medial prefrontal cortex), the dorsomedial striatum (caudate), and the hippocampus. Stress can also result in neuronal hypertrophy in the dorsolateral striatum (putamen) and amygdala. These neurobiological effects mirror reported neural abnormalities in obsessive-compulsive disorder and may contribute to an imbalance between goal-directed and habitual behavior, an imbalance that is implicated in the pathogenesis and expression of obsessive-compulsive disorder symptomatology. The modulation of corticostriatal and limbic circuits by stress and the resultant imbalance between habit and goal-directed learning and behavior offers a framework for investigating how stress may exacerbate or trigger obsessive-compulsive disorder symptomatology.
Background Brain white matter (WM) abnormalities have been hypothesized to play an important role in the neurobiology of bipolar disorder (BD). The nature of these abnormalities is not ...well-characterized, however, and it is unknown whether they occur after disease onset or represent potential markers of genetic risk. Methods We examined WM integrity (assessed via fractional anisotropy FA) with diffusion tensor imaging in patients with BD ( n =26), unaffected siblings of patients with BD ( n =15), and healthy volunteers ( n =27) to identify WM biomarkers of genetic risk. Results The FA differed significantly ( p <.05; corrected) among the three groups within the right temporal WM. Unaffected siblings had FA values that were intermediate to and significantly different from those of healthy volunteers and patients with BD (healthy control subjects>unaffected siblings>BD). Moreover, FA values in this region correlated negatively and significantly with trait impulsivity in unaffected siblings. Probabilistic tractography indicated that the regional abnormality lies along the inferior fronto-occipital fasciculus, a large intrahemispheric association pathway. Conclusions Our results suggest that lower WM integrity in the right temporal lobe might be a biomarker for genetic risk of BD. It is conceivable that the attenuated nature of these WM abnormalities present in unaffected siblings allows for some preservation of adaptive emotional regulation, whereas more pronounced alterations observed in patients is related to the marked emotional dysregulation characteristic of BD.
Tailoring treatments to the specific needs and biology of individual patients-personalized medicine-requires delineation of reliable predictors of response. Unfortunately, these have been slow to ...emerge, especially in neuropsychiatric disorders. We have recently described a real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback protocol that can reduce contamination-related anxiety, a prominent symptom of many cases of obsessive-compulsive disorder (OCD). Individual response to this intervention is variable. Here we used patterns of brain functional connectivity, as measured by baseline resting-state fMRI (rs-fMRI), to predict improvements in contamination anxiety after neurofeedback training. Activity of a region of the orbitofrontal cortex (OFC) and anterior prefrontal cortex, Brodmann area (BA) 10, associated with contamination anxiety in each subject was measured in real time and presented as a neurofeedback signal, permitting subjects to learn to modulate this target brain region. We have previously reported both enhanced OFC/BA 10 control and improved anxiety in a group of subclinically anxious subjects after neurofeedback. Five individuals with contamination-related OCD who underwent the same protocol also showed improved clinical symptomatology. In both groups, these behavioral improvements were strongly correlated with baseline whole-brain connectivity in the OFC/BA 10, computed from rs-fMRI collected several days prior to neurofeedback training. These pilot data suggest that rs-fMRI can be used to identify individuals likely to benefit from rt-fMRI neurofeedback training to control contamination anxiety.
Decision making in a complex world, characterized both by predictable regularities and by frequent departures from the norm, requires dynamic switching between rapid habit-like, automatic processes ...and slower, more flexible evaluative processes. These strategies, formalized as “model-free” and “model-based” reinforcement learning algorithms, respectively, can lead to divergent behavioral outcomes, requiring a mechanism to arbitrate between them in a context-appropriate manner. Recent data suggest that individuals with obsessive-compulsive disorder (OCD) rely excessively on inflexible habit-like decision making during reinforcement-driven learning. We propose that inflexible reliance on habit in OCD may reflect a functional weakness in the mechanism for context-appropriate dynamic arbitration between model-free and model-based decision making. Support for this hypothesis derives from emerging functional imaging findings. A deficit in arbitration in OCD may help reconcile evidence for excessive reliance on habit in rewarded learning tasks with an older literature suggesting inappropriate recruitment of circuitry associated with model-based decision making in unreinforced procedural learning. The hypothesized deficit and corresponding circuitry may be a particularly fruitful target for interventions, including cognitive remediation.
Background Age-related differences in white matter tract microstructure have been well established across the life span. In the present cross-sectional study, we examined whether these differences ...are associated with neurocognitive performance from childhood to late adulthood. Methods Diffusion tensor imaging was performed in 296 healthy subjects aged 8 to 68 years (mean = 29.6, SD = 14.6). The corpus callosum, two projection tracts, and five association tracts were traced using probabilistic tractography. A neurocognitive test battery was used to assess speed of processing, attention, spatial working memory, verbal functioning, visual learning, and executive functioning. Linear mediation models were used to examine whether differences in white matter tract fractional anisotropy (FA) were associated with neurocognitive performance, independent of the effect of age. Results From childhood to early adulthood, higher FA of the cingulum bundle and inferior frontooccipital fasciculus (IFOF) was associated with higher executive functioning and global cognitive functioning, respectively, independent of the effect of age. When adjusting for speed of processing, FA of the IFOF was no longer associated with performance in the other cognitive domains with the exception of visual learning. From early adulthood to late adulthood, white matter tract FA was not associated with cognitive performance independent of the age effect. Conclusions The cingulum bundle may play a critical role in protracted maturation of executive functioning. The IFOF may play a key role in maturation of visual learning and may act as a central “hub” in global cognitive maturation by subserving maturation of processing speed.
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