Relapse prevention through health technology program reduces hospitalization in schizophrenia

Homan, P.; Schooler, N. R.; Brunette, M. F.; Rotondi, A.; Ben-Zeev, D.; Gottlieb, J. D.; Mueser, K. T.; Achtyes, E. D.; Gingerich, S.; Marcy, P.; Meyer-Kalos, P.; Hauser, M.; John, M.; Robinson, D. G.; Kane, J. M.

doi:10.1101/626663

bioRxiv · 10.1101/626663

Relapse prevention through health technology program reduces hospitalization in schizophrenia

Homan, P.·Schooler, N. R.·Brunette, M. F.·Rotondi, A.·Ben-Zeev, D.·Gottlieb, J. D.·Mueser, K. T.·Achtyes, E. D.·Gingerich, S.·Marcy, P.·Meyer-Kalos, P.·Hauser, M.·John, M.·Robinson, D. G.·Kane, J. M.

View original source ↗Export metadata ↓

Abstract

ImportancePsychiatric hospitalization is a major driver of cost in the treatment of schizophrenia. Symptom relapses are a frequent cause of hospitalization and both are primary source of burden to patients and their supporters.\n\nObjectiveTo determine whether a novel, multicomponent, and technology-enhanced approach to relapse prevention in outpatients following a psychiatric hospitalization could reduce days spent in a hospital after discharge.\n\nDesignThe Improving Care and Reducing Cost (ICRC) study was a quasi-experimental clinical trial in outpatients with schizophrenia conducted between February 2013 and April 2015 at 10 different sites in the US. Data were obtained from 89 participants who received usual relapse prevention services, followed by a second cohort of 349 participants who received the technology-enhanced relapse prevention program. Both groups were followed for 6 months.\n\nSettingOutpatient setting.\n\nParticipantsPatients were between 18 and 60 years old; had a diagnosis of schizophrenia, schizoaffective disorder, or psychotic disorder not otherwise specified; and were currently hospitalized or had been hospitalized within the past 30 days.\n\nInterventionPatients received usual care or a technology-enhanced relapse prevention program during a 6-month period after discharge.\n\nMain Outcome(s) and Measure(s)Days spent in a psychiatric hospital during 6 months after discharge.\n\nResultsThe study included 438 patients. Control participants (N = 89; 37 females) were enrolled first and received usual care for relapse prevention, and followed by 349 participants (128 females) who received technology-enhanced relapse prevention. Days of hospitalization were reduced by 4 days (Mean days: b = -4.25, 95% CI: -8.29; -0.21, P = 0.039) during follow-up in the intervention condition compared to control.\n\nConclusions and RelevanceThe reduction in days spent in the hospital for participants in the technology-informed relapse prevention program compared to those who received usual care, and the previously reported high satisfaction and usability suggest that technology-enhanced relapse prevention is an effective and feasible way to reduce rehospitalization days among patients with schizophrenia.\n\nKey pointsO_ST_ABSQuestionC_ST_ABSCan rehospitalizations in schizophrenia be prevented at reduced cost by innovative mobile technology-delivered interventions?\n\nFindingsIn this clinical trial with 438 patients, a technology-enhanced relapse prevention program compared to usual services reduced an average of four days of hospitalization per patient during the first 6 months following an index hospitalization.\n\nMeaningRelapse prevention through a health technology may improve care while reducing costs associated with hospitalization.

Source connections

Published article ↗

Explore related subjects

neuroscience Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Homan, P., Schooler, N. R., Brunette, M. F., Rotondi, A., Ben-Zeev, D., Gottlieb, J. D., Mueser, K. T., Achtyes, E. D., Gingerich, S., Marcy, P., Meyer-Kalos, P., Hauser, M., John, M., Robinson, D. G., Kane, J. M.. 2019-05-03. Relapse prevention through health technology program reduces hospitalization in schizophrenia. https://doi.org/10.1101/626663

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Epidermal Langerhans Cells Act as Neuroimmune Regulators of Pain and Itch

Neuroimmune interactions in the skin coordinate immune defense and somatosensory perception, yet how immune cells shape sensory signaling remains poorly defined. Here, we show that Langerhans cells (LCs), epidermal antigen-presenting cells, function as local immune-derived amplifiers of cutaneous sensory signaling. Anatomical and transcriptomic analyses reveal preferential LC association with non-peptidergic sensory neurons. LC activation increases neuronal and behavioral responses to thermal, mechanical, and pruritic stimuli without directly exciting sensory neurons, whereas LC inhibition or ablation selectively reduces pruritogen-evoked itch. We identified semaphorin 7A as a candidate LC-expressed mediator. Semaphorin 7A sensitized cultured sensory neurons to chloroquine and histamine, and neutralizing semaphorin 7A abolished the increase in chloroquine-evoked scratching produced by LC activation. Its receptor PlexinC1 was expressed by most MrgprA3 pruriceptors and blocking PlexinC1 reduced semaphorin 7A-evoked neuronal responses. Together, these findings identify epidermal LCs as local immune-derived amplifiers that regulate the responsiveness of cutaneous sensory circuits and identify semaphorin 7A as a mediator of LC-induced itch potentiation.

neuroscience↗

bioRxiv2026

Feasible closed-loop stimulation for neural latent dynamics control

Modern neuroscience benefits from powerful computational and experimental methods for studying neural populations, including latent dynamics models that predict behavior with few dimensions. But despite their explanatory utility, latent factors are seldom targeted explicitly with experimental perturbations, leaving causal relationships to behavior and inferred dynamical landscapes untested. A promising solution is closed-loop, multi-channel optogenetic control, which, when paired with model predictions, could steer neural trajectories in real time--a feat impossible for traditional, hand-designed stimulation. However, because closed-loop latent control has not been demonstrated in vivo, the hardware and software requirements remain unclear--particularly the necessary stimulation dimensionality and how limited resources such as implant volume and bandwidth should be allocated between stimulation and recording capabilities. Preliminary experiments would thus help guide ongoing technological development. As large-scale exploration of these design spaces in vivo is prohibitively expensive, we conducted a high-throughput simulation survey using biophysically grounded spiking neural networks. We found that low-dimensional actuation is sufficient: in the reference configuration, ~20% of the stimulation channels achieved ~85% of peak control performance, far fewer than the number of neurons. Furthermore, allocating channels roughly equally between stimulation and recording optimized behavioral control, whereas pairing many electrodes with a single light source--the prevailing practice in experimental labs--performed poorly. Even without heavily optimizing modeling or control, we obtained >60% tracking error reduction and >90% evoked behavior accuracy on average for optimal channel counts. These results held across extensive parameter variations, suggesting that closed-loop latent control is feasible with accessible channel counts and establishing design principles for future tool development and in vivo experiments.

neuroscience↗

bioRxiv2026

Identification of Kinome Biomarkers and Therapeutic Rescue in cGMP-Linked Retinal Degeneration

Inherited retinal degenerations, such as Retinitis Pigmentosa (RP) and Leber's congenital amaurosis (LCA), are major causes of progressive and irreversible vision loss. The large number of genes associated with these disorders makes their clinical and molecular characterization difficult, while systemic biomarkers for disease progression or treatment response remain limited. These challenges were addressed by targeting cGMP-associated mechanisms shared by RP and LCA and integrating systemic biomarker profiling with retinal outcomes. Kinase activity analysis (kinome analysis) in peripheral blood mononuclear cells distinguished healthy and diseased states and captured therapy-associated signatures in rd10 mice treated with LP-CN03, a liposomal formulation of the cGMP analog CN03. This first systemic analysis in a therapeutically responsive animal model highlights kinome analysis as a potential translational readout. Given shared cGMP signaling in RP and AIPL1-associated LCA, LP-CN03's therapeutic potential was further evaluated in a new CRISPR-Cas9-generated Aipl1-/- mouse model. Treatment with LP-CN03 preserved retinal structure and function, as shown by electroretinography, longitudinal optical coherence tomography, fundus imaging, optomotor testing, and photoreceptor-specific gene expression. Together, these findings provide independent in vivo evidence for the neuroprotective effect of LP-CN03 in both cGMP-related RP and LCA, also highlighting the translational value of kinome profiling.

neuroscience↗