Neurorecovery and Neuroplasticity*
Date/Time: Sunday, September 10, 2023 - 3:30 PM – 5:00 PM
Track: Cross-Cutting Special Interest Group (SIG)
Room: Franklin Hall 4 (4th Floor)
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Session Evaluation Form: https://myana.org/form/ana2023-session-evaluation-nan
Chair: S. Thomas Carmichael, MD, PhD, FANA
Co-Chair: Steven Cramer, MD, MMSc, FAAN, FAHA, FANA
This session will develop a consensus of what neurorecovery is across neurological diseases, how this is studied, emerging principles, and directions forward. Topics covered will include mechanisms of recovery in the setting of stroke, multiple sclerosis, and spinal cord injury, spanning domains including motor and cognitive function.
- Following this session, learners will be better prepared to discover or understand the mechanisms of nervous system repair, develop valid outcome measures and clinical trials for emerging therapies, integrate the protocols in clinical trials and the understanding of nervous repair biology with the activity patterns of patients with these diseases and in the rehabilitation of these diseases.
Brain-Computer Interfaces in Neurorecovery
Speaker: Leigh R. Hochberg, MD, PhD, FANA
An update on the BrainGate clinical trials and other brain-computer interfaces for the restoration of communication and mobility.
New systems of care for neurorehabilitation and recovery
Speaker: Preeti Raghavan, MBBS
The current model of stroke care delivery in the United States and in many parts of the world is fragmented, resulting in lack of continuity of care, inability to track recovery meaningfully across the continuum, and lack of access to the frequency, intensity, and duration of high-quality rehabilitation necessary to optimally harness recovery processes. The process of recovery itself has been overshadowed by a focus on length of stay and the movement of patients across levels of care. This talk will describe the rationale behind the recent efforts at the Johns Hopkins Sheikh Khalifa Stroke Institute to define and coordinate an intensive, strategic effort to develop effective stroke systems of care across the continuum through the development of a unified Sheikh Khalifa Stroke Institute model of recovery and rehabilitation.
Biomarkers to guide restorative therapies after stroke
The majority of patients with a new stroke do not receive acute reperfusion therapies, resulting in substantial disability. Restorative therapies have promise to improve outcomes. Stroke is a very heterogeneous disease, however, and it becomes essential to connect the right patients with the right restorative therapy. Doing so requires a biological model as to how the therapy works as well as a biomarker that probes the nervous along that model. This talk will consider several classes of biomarker, including those capturing neural structure, neural function and connectivity, and genetics.
Potential Effects of Untreated Moderate-to-Severe Sleep-Related Breathing Disorders on the Number of Silent Episodes of Autonomic Dysreflexia during Sleep in People with Spinal Cord Injury
Oral Abstract Presenter: Julio Furlan, MD, LLB, MBA, PhD, MSc, FRCPC
Background: Sleep-related breathing disorders (SRBDs) are common but under-recognized medical conditions among individuals with spinal cord injury (SCI). However, the effect of SRBDs on cardiovascular function in individuals with SCI is still unclear. Individuals with SCI commonly experience cardiovascular dysfunction, including low baseline blood pressure (BP), orthostatic hypotension and episodes of autonomic dysreflexia (AD) and, hence, any impact of SRBDs on cardiovascular function after SCI is important to characterize. This ongoing cross-sectional study examined on the potential association between moderate-to-severe SRBDs and more severe cardiovascular dysfunction post-SCI. Methods: This cross-sectional study included adults with subacute or chronic (≥1 month after SCI onset), cervical or high-thoracic (T6 or above) SCI, who reported clinical symptoms and/or signs suggestive of SRBD. The diagnosis of SRBD was established using a home-based/hospital unattended sleep screening test that quantifies the apnea-hypopnea index (AHI). Moderate-to-severe SRBD was defined as an AHI ≥15 events/hour. Episodes of AD were defined as a sudden increase in systolic BP of at least 20 mmHg. For the purpose of this study, we did not count episodes of AD during sleep that were caused by triggers other than hypopnea or apnea. Results: This study included 45 individuals (14 females, 31 males; mean age: 57.0 years; age range: 20-84 years) with motor complete (n=22) or incomplete SCI at cervical (n=38), or high thoracic levels, who reported symptoms and signs suggestive of SRBDs. Time from SCI onset varied from 1.5 months to 52 years (mean time: 49.4 months). Their mean apnea-hypopnea index (AHI) was 16.0 events/ hour (AHI range: 0.8 to 51.7 events/hour). The AHI was not associated with systolic BP (mean +/- SEM: 122.0+/-2.2 mmHg; p=0.903), diastolic BP (72.6+/-3.0 mmHg; p=0.639), mean arterial pressure (90.1+/-2.4 mmHg; p=0.714), and heart rate (70.6+/-1.4 bpm; p=0.669) during sleep. However, the AHI was significantly and positively correlated with the number of silent episodes of AD (mean +/- SEM: 3.6+/-0.4; Rsqr=0.220, p=0.001) during sleep. Conclusions: The results of this cross-sectional study suggest, for the first time, that more severe SRBD is associated with frequent silent episodes of AD during sleep among individuals living with a cervical or high-thoracic SCI. Future research is needed to assess the effects of continuous positive airway pressure (CPAP) therapy on cardiovascular dysfunction following SCI. Funding: 2018-RHI-SLEEP-1056, Ministry of Health Grant #719.
Neural Correlates of Phantom Motor Execution: A Systematic Review and Functional Neuroimaging Meta-Analysis
Oral Abstract Presenter: Kevin Pacheco-Barrios MD, MSc, MPH
Background: The current understanding of the neural correlates of phantom motor execution (PME) and their ability to reduce post-amputation pain is limited and will therefore be further investigated in this multimodal neuroimaging meta-analysis. Methods: We systematically searched PubMed and Embase until February 28, 2023. We included studies that used multimodal neuroimaging techniques (fMRI, PET, and EEG). We performed a coordinate-based meta-analysis testing two contrasts: a) PME versus rest (within group comparison), and b) PME versus motor execution (ME) in healthy controls (between group comparison). We generated voxel-wise (random effects) activation effect size maps using seed-based d-mapping (SDM) software. we utilized the I-squared index to assess the between-study heterogeneity. Statistical significance was evaluated using a randomization test and SDM default thresholds (voxel-level P < 0.005 uncorrected). Finally, we assessed the risk of bias and evidence certainty by applying the GRADE approach. Results: We included 17 studies (n=327, 181 amputees, and 146 controls). The average age ranged from 36 to 50 years old, and most of the participants were males. Fifteen studies targeted upper limb amputees, and only two studies lower limb amputees. Most studies were fMRI paradigms (12/17), two used PET, and three used EEG. Due to heterogeneity, only seven studies were included in the meta-analyses. We found that during PME, there is a differential activation of the supplementary motor area BA6 (SDM-Z=2.692, p<0.0001), post-central gyrus (SDM-Z=1.876, p<0.0001), and dorsolateral superior frontal gyrus (SDM-Z=1.943, p<0.0001) compared to resting state (5 studies). Interestingly, when comparing PME and ME (two studies), the right insula anterior cingulate (SDM-Z=6.433, p<0.0001), left insula amygdala (SDM-Z=2.388, p<0.0001), and right striatum (SDM-Z=1.960, p<0.0001) were activated differentially. The I-squared index ranged from 10 to 25%. From the integrative synthesis, we found that the degree of BOLD signal of the PME-related areas correlated positively with the intensity of PLP (r=0.60, p=0.017). However, the risk of bias and the certainty level was graded as moderate. Conclusions: Our results suggest that the PME neural correlates represent a distinct type of motor network activation with partial overlap with ME and motor imagery activations (sensorimotor and premotor cortices) but with a differential engagement of the insular cortex, suggesting a maladaptive activation due to disrupted body awareness and motor control. The association of PME with PLP intensity requires further causal exploration and opens the possibility of modulatory PME interventions to revert PLP.