Telerehab at Home: Mobile Tablet Technology for Patients With Poststroke Communication Deficits-A Pilot Feasibility Randomized Control Trial.

PURPOSE: Poststroke communication deficits (PSCD) are common following stroke. Early and intensive speech and language therapy is recommended to maximize outcomes. We wanted to test the feasibility of providing telerehabilitation for patients with PSCD using mobile tablet-based technology to bridge the gap between acute stroke care and outpatient speech-language therapy (SLT) services. METHOD: This was a prospective, randomized, open-label, blinded end-point design. Patients were randomized to either the treatment arm (mobile tablet) or the control arm (standard of care). The study duration was either 8 weeks or when the patient was called to start outpatient SLT services, whichever occurred first. The primary outcome was feasibility, while secondary objective was to assess patient engagement and to explore improvement in communication ability. RESULTS: We had a 38% recruitment rate, with a 100% retention rate for the treatment arm and a 50% retention rate for the control arm. Fifty percent of patients in the treatment arm adhered to the recommended 1 hr per day, whereas none of the control arm did. Patients were engaged in using the mobile tablet and feedback on the protocol was positive. CONCLUSIONS: SLT using telerehabilitation via mobile technology is feasible in the very early stages of acute stroke recovery. It is potentially an effective means of bridging the gap between discharge from the acute care setting to the start of outpatient SLT services. Our study supported proceeding to a clinical trial to assess efficacy of the intervention. SUPPLEMENTAL MATERIAL: https://doi.org/10.23641/asha.21844569.

Time-dependent changes in CRH concentrations and release in discrete brain regions following global ischemia: effects of MK-801 pretreatment.

The excitatory actions of corticotropin-releasing hormone (CRH) in the brain and the neuroprotective effects of CRH antagonists in models of ischemia suggest a role for this peptide in the cascade of events leading to cellular damage. The present study aimed to characterize endogenous activation of CRH in discrete brain regions following global ischemia. Time-dependent changes in CRH concentrations were assessed in 10 brain regions including hippocampal, parahippocampal, and hypothalamic regions as well as the amygdala and the frontal cortex at three post-ischemic intervals: 4, 24, and 72 h (Experiment 1). The impact of pretreatment with a neuroprotective dose of the NMDA antagonist (5R,10S)-(+)-5-Methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801; hydrogen maleate) on 24-h ischemia-induced CRH concentrations in the 10 brain regions was also determined (Experiment 2). In vivo microdialysis was used to assess dynamic fluctuations in CRH release at the dorsal hippocampus (CA1 pyramidal layer) and central nucleus of the amygdala (CeA; Experiment 3). Our findings revealed a rapid elevation of CRH concentrations at the piriform cortex (Pir) and hypothalamic nuclei following global ischemia. This was followed by decreased CRH concentrations at the amygdala, the frontal cortex (FC), the CA3, and the hypothalamus 24-h post-ischemia. MK-801 reversed the decreases in the hypothalamic nuclei but not in the other brain regions. Seventy-two hours post-ischemia, CRH levels returned to control values in all regions except the dentate gyrus (DG) where elevated CRH levels were observed. In vivo, a significant increase in CRH release in response to global ischemia was found at the CeA with no alterations at the CA1. These findings support brain region-specific ischemia-induced CRH alterations and suggest that CRH actions to mediate neuronal damage at the hippocampal CA1 layer may be indirect.