1136 Trauma-Associated Sleep Disorder in Young Service Members: Evaluating Synucleinopathy Biomarkers to Assess Neurodegeneration Risk

Abstract Introduction Trauma-associated sleep disorder (TSD) is an emerging parasomnia increasingly recognized in young service members who present with loud vocalizations, complex dream enactment, and autonomic arousal during disturbing dreams following a trauma. Clinically, TSD appears distinct from nightmare disorder and PTSD-related sleep disturbance, exhibiting behaviors suggestive of impaired REM-atonia regulation. This phenotype has notable overlap with isolated REM sleep behavior disorder (iRBD), in which dysfunction of pontine and medullary circuits responsible for REM muscle atonia leads to motor dream enactment and is strongly linked to underlying synucleinopathy. The parallels between TSD and iRBD raise the mechanistic question of whether TSD may similarly reflect disruption of REM-atonia pathways or early prodromal neuronal injury. This study evaluates phosphorylated α-synuclein (p-α-syn) via a validated skin biopsy to determine whether individuals with TSD exhibit biomarker evidence associated with neurodegeneration risk. Methods Participants aged 18–50 with clinically suspected TSD were referred from our academic military Sleep Disorder Center. After informed consent was obtained, eligibility was confirmed through comprehensive chart review. Enrolled participants completed a structured neurologic evaluation, validated sleep and neurobehavioral questionnaires, and a skin biopsy performed at the Department of Neurology. Three 2–3 mm punch biopsies (posterior cervical region, proximal leg, distal leg) were processed using a standardized protocol to assess p-α-syn status, intraepidermal nerve fiber density, and additional cutaneous biomarkers. Clinical data collected included sleep history, autonomic features, neurologic symptoms, MDS-UPDRS findings, and results from validated instruments assessing sleep quality, insomnia severity, daytime sleepiness, and dream enactment behaviors. Results Data collection is ongoing. This abstract describes study design, biomarker acquisition procedures, clinical and military-related history, physical examination, and planned analyses to evaluate the prevalence and pattern of p-α-syn positivity in TSD. Conclusion We present a prospective biomarker study evaluating whether trauma-associated sleep disorder may represent a prodromal marker of synucleinopathy in a young service member population. Identifying p-α-syn deposition in TSD will support a novel neurodegeneration-risk signal, providing a potential early detection pathway for long-term neurological monitoring and intervention. Findings from this study will help clarify whether TSD reflects downstream neurodegenerative processes, post-traumatic neural injury, or a distinct parasomnia phenotype. Support (if any)

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SLEEP
Published
2026-05-01
DOI
https://doi.org/10.1093/sleep/zsag091.1135
Primary Topic
Sleep and Wakefulness Research
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article
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article

1136 Trauma-Associated Sleep Disorder in Young Service Members: Evaluating Synucleinopathy Biomarkers to Assess Neurodegeneration Risk

Jessie Jacobson, Elijah Miranda, William Hoffman, Matthew Brock et al.
SLEEP
Sleep and Wakefulness Research
article

1136 Trauma-Associated Sleep Disorder in Young Service Members: Evaluating Synucleinopathy Biomarkers to Assess Neurodegeneration Risk

Jessie Jacobson, Elijah Miranda, William Hoffman, Matthew Brock, Victoria Nguyen, Zahari Tchopev, Margaux Salas
article en

Abstract

Abstract Introduction Trauma-associated sleep disorder (TSD) is an emerging parasomnia increasingly recognized in young service members who present with loud vocalizations, complex dream enactment, and autonomic arousal during disturbing dreams following a trauma. Clinically, TSD appears distinct from nightmare disorder and PTSD-related sleep disturbance, exhibiting behaviors suggestive of impaired REM-atonia regulation. This phenotype has notable overlap with isolated REM sleep behavior disorder (iRBD), in which dysfunction of pontine and medullary circuits responsible for REM muscle atonia leads to motor dream enactment and is strongly linked to underlying synucleinopathy. The parallels between TSD and iRBD raise the mechanistic question of whether TSD may similarly reflect disruption of REM-atonia pathways or early prodromal neuronal injury. This study evaluates phosphorylated α-synuclein (p-α-syn) via a validated skin biopsy to determine whether individuals with TSD exhibit biomarker evidence associated with neurodegeneration risk. Methods Participants aged 18–50 with clinically suspected TSD were referred from our academic military Sleep Disorder Center. After informed consent was obtained, eligibility was confirmed through comprehensive chart review. Enrolled participants completed a structured neurologic evaluation, validated sleep and neurobehavioral questionnaires, and a skin biopsy performed at the Department of Neurology. Three 2–3 mm punch biopsies (posterior cervical region, proximal leg, distal leg) were processed using a standardized protocol to assess p-α-syn status, intraepidermal nerve fiber density, and additional cutaneous biomarkers. Clinical data collected included sleep history, autonomic features, neurologic symptoms, MDS-UPDRS findings, and results from validated instruments assessing sleep quality, insomnia severity, daytime sleepiness, and dream enactment behaviors. Results Data collection is ongoing. This abstract describes study design, biomarker acquisition procedures, clinical and military-related history, physical examination, and planned analyses to evaluate the prevalence and pattern of p-α-syn positivity in TSD. Conclusion We present a prospective biomarker study evaluating whether trauma-associated sleep disorder may represent a prodromal marker of synucleinopathy in a young service member population. Identifying p-α-syn deposition in TSD will support a novel neurodegeneration-risk signal, providing a potential early detection pathway for long-term neurological monitoring and intervention. Findings from this study will help clarify whether TSD reflects downstream neurodegenerative processes, post-traumatic neural injury, or a distinct parasomnia phenotype. Support (if any)

SLEEPVol. 49(Supplement_1)
Brooke Army Medical Center (US), Wilford Hall Ambulatory Surgical Center (US), 59th Medical Wing (US), The Geneva Foundation (US)
Good health and well-being
Openalex Percentile: Top 8%
Sleep and Wakefulness Research
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