Examining the Central and Peripheral Processes of Written Word Production Through Meta-Analysis

Producing written words requires “central” cognitive processes (such as orthographic long-term and working memory) as well as more peripheral processes responsible for generating the motor actions needed for producing written words in a variety of formats (handwriting, typing, etc.). In recent years, various functional neuroimaging studies have examined the neural substrates underlying the central and peripheral processes of written word production. This study provides the first quantitative meta-analysis of these studies by applying activation likelihood estimation (ALE) methods (Turkeltaub et al., 2002). For alphabet languages, we identified 11 studies (with a total of 17 experimental contrasts) that had been designed to isolate central and/or peripheral processes of word spelling (total number of participants = 146). Three ALE meta-analyses were carried out. One involved the complete set of 17 contrasts; two others were applied to subsets of contrasts to distinguish the neural substrates of central from peripheral processes. These analyses identified a network of brain regions reliably associated with the central and peripheral processes of word spelling. Among the many significant results, is the finding that the regions with the greatest correspondence across studies were in the left inferior temporal/fusiform gyri and left inferior frontal gyrus. Furthermore, although the angular gyrus (AG) has traditionally been identified as a key site within the written word production network, none of the meta-analyses found it to be a consistent site of activation, identifying instead a region just superior/medial to the left AG in the left posterior intraparietal sulcus. These meta-analyses and the discussion of results provide a valuable foundation upon which future studies that examine the neural basis of written word production can build

Sequence learning in the human brain: a functional neuroanatomical meta-analysis of serial reaction time studies

Sequence learning underlies numerous motor, cognitive, and social skills. Previous models and empirical investigations of sequence learning in humans and non-human animals have implicated cortico-basal ganglia-cerebellar circuitry as well as other structures. To systematically examine the functional neuroanatomy of sequence learning in humans, we conducted a series of neuroanatomical meta-analyses. We focused on the serial reaction time (SRT) task. This task, which is the most widely used paradigm for probing sequence learning in humans, allows for the rigorous control of visual, motor, and other factors. Controlling for these factors (in sequence-random block contrasts), sequence learning yielded consistent activation only in the basal ganglia, across the striatum (anterior/mid caudate nucleus and putamen) and the globus pallidus. In contrast, when visual, motor, and other factors were not controlled for (in a global analysis with all sequence-baseline contrasts, not just sequence-random contrasts), premotor cortical and cerebellar activation were additionally observed. The study provides solid evidence that, at least as tested with the visuo-motor SRT task, sequence learning in humans relies on the basal ganglia, whereas cerebellar and premotor regions appear to contribute to aspects of the task not related to sequence learning itself. The findings have both basic research and translational implications

The BrainMap strategy for standardization, sharing, and meta-analysis of neuroimaging data

<p>Abstract</p> <p>Background</p> <p>Neuroimaging researchers have developed rigorous community data and metadata standards that encourage meta-analysis as a method for establishing robust and meaningful convergence of knowledge of human brain structure and function. Capitalizing on these standards, the BrainMap project offers databases, software applications, and other associated tools for supporting and promoting quantitative coordinate-based meta-analysis of the structural and functional neuroimaging literature.</p> <p>Findings</p> <p>In this report, we describe recent technical updates to the project and provide an educational description for performing meta-analyses in the BrainMap environment.</p> <p>Conclusions</p> <p>The BrainMap project will continue to evolve in response to the meta-analytic needs of biomedical researchers in the structural and functional neuroimaging communities. Future work on the BrainMap project regarding software and hardware advances are also discussed.</p

Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema

<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p

Integrating Lesion-Symptom Mapping with Other Methods to Investigate Language Networks and Aphasia Recovery

Voxel-based lesion-symptom mapping (VLSM) has provided valuable insights into the neural underpinnings of various language functions. Integrating lesion mapping methods with other neuroscience techniques may provide new opportunities to investigate questions related both to the neurobiology of language and to plasticity after brain injury. For example, recent diffusion tensor imaging studies have explored relationships between aphasia symptomology and damage in specific white matter tracts (Forkel et al., 2014) or disruption of the white matter connectome (Bonilha, Rorden, & Fridriksson, 2014). VLSM has also recently been used to assess correlations between lesion location and response to transcranial direct current stimulation aphasia treatment (Campana, Caltagirone, & Marangolo, 2015). We have recently undertaken studies integrating VLSM with other techniques, including voxel-based morphometry (VBM) and functional MRI, in order to investigate how parts of the brain spared by stroke contribute to recovery. VLSM can be used in this context to map lesions associated with particular patterns of plasticity in brain structure, function, or connectivity. We have also used VLSM to estimate the variance in behavior due to the stroke itself so that this lesion-symptom relationship can be controlled for when examining the contributions of the rest of the brain. Using this approach in combination with VBM, we have identified areas of the right temporoparietal cortex that appear to undergo hypertrophy after stroke and compensate for speech production deficits. In this talk, I will review recent advances in integrating lesion-symptom mapping with other imaging and brain stimulation techniques in order to better understand the brain basis of language and of aphasia recovery