To determine whether longitudinal progression of small vessel disease in chronic stroke survivors is associated with longitudinal worsening of chronic aphasia severity.
A longitudinal retrospective ...study. Severity of white matter hyperintensities (WMHs) as a marker for small vessel disease was assessed on fluid-attenuated inversion recovery (FLAIR) scans using the Fazekas scale, with ratings for deep WMHs (DWMHs) and periventricular WMHs (PVHs).
University research laboratories.
This study includes data from 49 chronic stroke survivors with aphasia (N=49; 15 women, 34 men, age range=32-81 years, >6 months post-stroke, stroke type: 46 ischemic, 3 hemorrhagic, community dwelling). All participants completed the Western Aphasia Battery-Revised (WAB) and had FLAIR scans at 2 timepoints (average years between timepoints: 1.87 years, SD=3.21 years).
Not applicable.
Change in white matter hyperintensity severity (calculated using the Fazekas scale) and change in aphasia severity (difference in WAB scores) were calculated between timepoints. Separate stepwise regression models were used to identify predictors of WMH severity change, with lesion volume, age, time between timepoints, body mass index (BMI), and presence of diabetes as independent variables. Additional stepwise regression models investigated predictors of change in aphasia severity, with PVH change, DWMH change, lesion volume, time between timepoints, and age as independent predictors.
22.5% of participants (11/49) had increased WMH severity. Increased BMI was associated with increases in PVH severity (P=.007), whereas the presence of diabetes was associated with increased DWMH severity (P=.002). Twenty-five percent of participants had increased aphasia severity which was significantly associated with increased severity of PVH (P<.001, 16.8% variance explained).
Increased small vessel disease burden is associated with contributing to chronic changes in aphasia severity. These findings support the idea that good cardiovascular risk factor control may play an important role in the prevention of long-term worsening of aphasic symptoms.
Abstract Premature brain aging is associated with poorer cognitive reserve and lower resilience to injury. When there are focal brain lesions, brain regions may age at different rates within the same ...individual. Therefore, we hypothesize that reduced gray matter volume within specific brain systems commonly associated with language recovery may be important for long-term aphasia severity. Here we show that individuals with stroke aphasia have a premature brain aging in intact regions of the lesioned hemisphere. In left domain-general regions, premature brain aging, gray matter volume, lesion volume and age were all significant predictors of aphasia severity. Increased brain age following a stroke is driven by the lesioned hemisphere. The relationship between brain age in left domain-general regions and aphasia severity suggests that degradation is possible to specific brain regions and isolated aging matters for behavior.
Knowledge regarding the neural origins of distinct upper extremity impairments may guide the choice of interventions to target neural structures responsible for specific impairments. This ...cross‐sectional pilot study investigated whether different brain networks explain distinct aspects of hand grip performance in stroke survivors. In 22 chronic stroke survivors, hand grip performance was characterized as grip strength, reaction, relaxation times, and control of grip force magnitude and direction. In addition, their brain structural connectomes were constructed from diffusion tensor MRI. Prominent networks were identified based on a two‐step factor analysis using the number of streamlines among brain regions relevant to sensorimotor function. We used regression models to estimate the predictive value of sensorimotor network connectivity for hand grip performance measures while controlling for stroke lesion volumes. Each hand grip performance measure correlated with the connectivity of distinct brain sensorimotor networks. These results suggest that different brain networks may be responsible for different aspects of hand grip performance, which leads to varying clinical presentations of upper extremity impairment following stroke. Understanding the brain network correlates for different hand grip performances may facilitate the development of personalized rehabilitation interventions to directly target the responsible brain network for specific impairments in individual patients, thus improving outcomes.
Different aspects of hand grip performance may be associated with the structural connectivity of distinct sensorimotor networks in chronic stroke survivors. This knowledge may facilitate the development of personalized rehabilitation interventions to target the responsible brain network for specific motor impairments in individual patients, thus improving outcomes.
Brain structure deteriorates with aging and predisposes an individual to more severe language impairments (aphasia) after a stroke. However, the underlying mechanisms of this relation are not well ...understood. Here we use an approach to model brain network properties outside the stroke lesion, network controllability, to investigate relations among individualized structural brain connections, brain age, and aphasia severity in 93 participants with chronic post-stroke aphasia. Controlling for the stroke lesion size, we observe that lower average controllability of the posterior superior temporal gyrus (STG) mediates the relation between advanced brain aging and aphasia severity. Lower controllability of the left posterior STG signifies that activity in the left posterior STG is less likely to yield a response in other brain regions due to the topological properties of the structural brain networks. These results indicate that advanced brain aging among individuals with post-stroke aphasia is associated with disruption of dynamic properties of a critical language-related area, the STG, which contributes to worse aphasic symptoms. Because brain aging is variable among individuals with aphasia, our results provide further insight into the mechanisms underlying the variance in clinical trajectories in post-stroke aphasia.
Background Cardiovascular risk factor burden in the absence of clinical or radiological "events" is associated with mild cognitive impairment. Magnetic resonance imaging techniques exploring the ...integrity of neuronal fiber connectivity within white matter networks supporting cognitive processing could be used to measure the impact of cardiovascular disease on brain health and be used beyond bedside neuropsychological tests to detect subclinical changes and select or stratify participants for entry into clinical trials. Methods and Results We assessed the relationship between verbal IQ and brain network integrity and the effect of cardiovascular risk factors on network integrity by constructing whole-brain structural connectomes from magnetic resonance imaging diffusion images (N=60) from people with various degrees of cardiovascular risk factor burden. We measured axonal integrity by calculating network density and determined the effect of fiber loss on network topology and efficiency, using graph theory. Multivariate analyses were used to evaluate the relationship between cardiovascular risk factor burden, physical activity, age, education, white matter integrity, and verbal IQ . Reduced network density, resulting from a disproportionate loss of long-range white matter fibers, was associated with white matter network fragmentation ( r=-0.52, P<10
), lower global efficiency ( r=0.91, P<10
), and decreased verbal IQ (adjusted R
=0.23, P<10
). Conclusions Cardiovascular risk factors may mediate negative effects on brain health via loss of energy-dependent long-range white matter fibers, which in turn leads to disruption of the topological organization of the white matter networks, lowered efficiency, and reduced cognitive function.
Mass flexion-extension co-excitation patterns during walking are often seen as a consequence of stroke, but there is limited understanding of the specific contributions of different descending motor ...pathways toward their control. The corticospinal tract is a major descending motor pathway influencing the production of normal sequential muscle coactivation patterns for skilled movements. However, control of walking is also influenced by non-corticospinal pathways such as the corticoreticulospinal pathway that possibly contribute toward mass flexion-extension co-excitation patterns during walking. The current study sought to investigate the associations between damage to corticospinal (CST) and corticoreticular (CRP) motor pathways following stroke and the presence of mass flexion-extension patterns during walking as evaluated using module analysis.
Seventeen healthy controls and 44 stroke survivors were included in the study. We used non-negative matrix factorization for module analysis of paretic leg electromyographic activity. We typically have observed four modules during walking in healthy individuals. Stroke survivors often have less independently timed modules, for example two-modules presented as mass flexion-extension pattern. We used diffusion tensor imaging-based analysis where streamlines connecting regions of interest between the cortex and brainstem were computed to evaluate CST and CRP integrity. We also used a coarse classification tree analysis to evaluate the relative CST and CRP contribution toward module control.
Interhemispheric CST asymmetry was associated with worse lower extremity Fugl-Meyer score (
= 0.023), propulsion symmetry (
= 0.016), and fewer modules (
= 0.028). Interhemispheric CRP asymmetry was associated with worse lower extremity Fugl-Meyer score (
= 0.009), Dynamic gait index (
= 0.035), Six-minute walk test (
= 0.020), Berg balance scale (
= 0.048), self-selected walking speed (
= 0.041), and propulsion symmetry (
= 0.001). The classification tree model reveled that substantial ipsilesional CRP or CST damage leads to a two-module pattern and poor walking ability with a trend toward increased compensatory contralesional CRP based control.
Both CST and CRP are involved with control of modules during walking and damage to both may lead to greater reliance on the contralesional CRP, which may contribute to a two-module pattern and be associated with worse walking performance.
Two primary areas of damage have been implicated in apraxia of speech (AOS) based on the time post-stroke: (1) the left inferior frontal gyrus (IFG) in acute patients, and (2) the left anterior ...insula (aIns) in chronic patients. While AOS is widely characterized as a disorder in motor speech planning, little is known about the specific contributions of each of these regions in speech. The purpose of this study was to investigate cortical activation during speech production with a specific focus on the aIns and the IFG in normal adults. While undergoing sparse fMRI, 30 normal adults completed a 30-minute speech-repetition task consisting of three-syllable nonwords that contained either (a) English (native) syllables or (b) non-English (novel) syllables. When the novel syllable productions were compared to the native syllable productions, greater neural activation was observed in the aIns and IFG, particularly during the first 10 min of the task when novelty was the greatest. Although activation in the aIns remained high throughout the task for novel productions, greater activation was clearly demonstrated when the initial 10 min was compared to the final 10 min of the task. These results suggest increased activity within an extensive neural network, including the aIns and IFG, when the motor speech system is taxed, such as during the production of novel speech. We speculate that the amount of left aIns recruitment during speech production may be related to the internal construction of the motor speech unit such that the degree of novelty/automaticity would result in more or less demands respectively. The role of the IFG as a storehouse and integrative processor for previously acquired routines is also discussed.
Summary
The assessment of neural networks in epilepsy has become increasingly relevant in the context of translational research, given that localized forms of epilepsy are more likely to be related ...to abnormal function within specific brain networks, as opposed to isolated focal brain pathology. It is notable that variability in clinical outcomes from epilepsy treatment may be a reflection of individual patterns of network abnormalities. As such, network endophenotypes may be important biomarkers for the diagnosis and treatment of epilepsy. Despite its exceptional potential, measuring abnormal networks in translational research has been thus far constrained by methodologic limitations. Fortunately, recent advancements in neuroscience, particularly in the field of connectomics, permit a detailed assessment of network organization, dynamics, and function at an individual level. Data from the personal connectome can be assessed using principled forms of network analyses based on graph theory, which may disclose patterns of organization that are prone to abnormal dynamics and epileptogenesis. Although the field of connectomics is relatively new, there is already a rapidly growing body of evidence to suggest that it can elucidate several important and fundamental aspects of abnormal networks to epilepsy. In this article, we provide a review of the emerging evidence from connectomics research regarding neural network architecture, dynamics, and function related to epilepsy. We discuss how connectomics may bring together pathophysiologic hypotheses from conceptual and basic models of epilepsy and in vivo biomarkers for clinical translational research. By providing neural network information unique to each individual, the field of connectomics may help to elucidate variability in clinical outcomes and open opportunities for personalized medicine approaches to epilepsy. Connectomics involves complex and rich data from each subject, thus collaborative efforts to enable the systematic and rigorous evaluation of this form of “big data” are paramount to leverage the full potential of this new approach.
Abstract
Serotonin syndrome is a life-threatening condition. Seizure is one of the complications of serotonin syndrome that may delay diagnosis and complicate management. We report a patient who had ...a focal seizure with abnormal electroencephalogram in the setting of serotonin syndrome with no prior history of epilepsy or seizure-provoking factors (fever, electrolyte abnormalities, specific medication combinations, and specific medication overdosing). Recognition of seizure as a symptom of serotonin syndrome is important for early treatment and avoidance of long-term consequences. Treatment of serotonin syndrome is mostly supportive. However, a short course of antiepileptics may be needed if these patients develop seizures.
Radiological identification of temporal lobe epilepsy (TLE) is crucial for diagnosis and treatment planning. TLE neuroimaging abnormalities are pervasive at the group level, but they can be subtle ...and difficult to identify by visual inspection of individual scans, prompting applications of artificial intelligence (AI) assisted technologies.
We assessed the ability of a convolutional neural network (CNN) algorithm to classify TLE vs. patients with AD vs. healthy controls using T1-weighted magnetic resonance imaging (MRI) scans. We used feature visualization techniques to identify regions the CNN employed to differentiate disease types.
We show the following classification results: healthy control accuracy = 81.54% (SD = 1.77%), precision = 0.81 (SD = 0.02), recall = 0.85 (SD = 0.03), and F1-score = 0.83 (SD = 0.02); TLE accuracy = 90.45% (SD = 1.59%), precision = 0.86 (SD = 0.03), recall = 0.86 (SD = 0.04), and F1-score = 0.85 (SD = 0.04); and AD accuracy = 88.52% (SD = 1.27%), precision = 0.64 (SD = 0.05), recall = 0.53 (SD = 0.07), and F1 score = 0.58 (0.05). The high accuracy in identification of TLE was remarkable, considering that only 47% of the cohort had deemed to be lesional based on MRI alone. Model predictions were also considerably better than random permutation classifications (p < 0.01) and were independent of age effects.
AI (CNN deep learning) can classify and distinguish TLE, underscoring its potential utility for future computer-aided radiological assessments of epilepsy, especially for patients who do not exhibit easily identifiable TLE associated MRI features (e.g., hippocampal sclerosis).
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