Management of Sleep-Disordered Breathing in a Spinal Cord Injury Rehabilitation Center: Model of Care Adaptation and Implementation.

Background: Obstructive sleep apnea (OSA) is highly prevalent and poorly managed in spinal cord injury (SCI). Alternative management models are urgently needed to improve access to care. We previously described the unique models of three SCI rehabilitation centers that independently manage uncomplicated OSA. Objectives: The primary objective was to adapt and implement a similar rehabilitation-led model of managing OSA in an SCI rehabilitation center in Australia. Secondary objectives were to identify the local barriers to implementation and develop and deliver tailored interventions to address them. Methods: A clinical advisory group comprised of rehabilitation clinicians, external respiratory clinicians, and researchers adapted and developed the care model. A theory-informed needs analysis was performed to identify local barriers to implementation. Tailored behavior change interventions were developed to address the barriers and prepare the center for implementation. Results: Pathways for ambulatory assessments and treatments were developed, which included referral for specialist respiratory management of complicated cases. Roles were allocated to the team of rehabilitation doctors, physiotherapists, and nurses. The team initially lacked sufficient knowledge, skills, and confidence to deliver the OSA care model. To address this, comprehensive education and training were provided. Diagnostic and treatment equipment were acquired. The OSA care model was implemented in July 2022. Conclusion: This is the first time a rehabilitation-led model of managing OSA has been implemented in an SCI rehabilitation center in Australia. We describe a theory-informed method of adapting the model of care, assessing the barriers, and delivering interventions to overcome them. Results of the mixed-methods evaluation will be reported separately.

Dysautonomia after severe traumatic brain injury: evidence of persisting overresponsiveness to afferent stimuli.

OBJECTIVE: To differentiate between dysautonomic and nondysautonomic subjects with acquired brain injury by measuring sympathetic reactivity after a nociceptive clinical procedure and to determine the utility of heart rate variability as an indicator of sympathetic overresponsivity in dysautonomic subjects. DESIGN: This case-controlled study recruited subjects with acquired brain injury (mean, 5 yrs postinjury) attending a hospital-based outpatient clinic, comprising seven dysautonomic subjects with traumatic brain injury, eight nondysautonomic traumatic brain injury subjects, and 11 nondysautonomic subjects with nontraumatic acquired brain injury. Sympathetic reactivity after nociceptive stimuli (limb assessment and botulinum toxin injection for spasticity management) was compared among groups. RESULTS: Sympathetic overactivity in dysautonomic subjects was evident across all physiologic parameters, whereas nondysautonomic subjects demonstrated limited reactivity. Heart rate variability measures of the balance between sympathetic and parasympathetic cardiac control showed a significant elevation in response to nociceptive stimuli, a response not observed in either nondysautonomic group. This sympathetic overactivity showed a normalizing tendency with increasing time postinjury. CONCLUSIONS: This study found persistent sympathetic overactivity in response to nociceptive stimuli in dysautonomic subjects (mean, 5 yrs postinjury). This significantly extends the duration over which such sympathetic overactivity has been quantified in this group, contributing to the accumulating empirical evidence that dysautonomic paroxysms result from sympathetic overresponsiveness. Given that sympathetic overactivity has now been observed from day 7 through 5 yrs postinjury, quantitative evaluation of patients for overresponsiveness to stimuli should be added to current diagnostic procedures at all stages of recovery.

Diagnosing dysautonomia after acute traumatic brain injury: evidence for overresponsiveness to afferent stimuli.

OBJECTIVE: To differentiate between traumatic brain injury (TBI) subjects with normal and elevated autonomic activity by quantifying cardiac responsivity to nociceptive stimuli and to determine the utility of heart rate variability (HRV) and event-related heart rate changes in diagnosing dysautonomia. DESIGN: Prospective cohort study. SETTING: Intensive care unit in a tertiary metropolitan trauma center. PARTICIPANTS: Adults (N=27) with TBI recruited from 79 consecutive TBI admissions comprising 16 autonomically aroused and 11 control subjects matched by age, sex, and injury severity. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Immediate: pattern of autonomic changes indexed by HRV and event-related heart rate after nociceptive stimuli. Six months: length of stay, Glasgow Coma Scale, and Disability Rating Scale. RESULTS: Heart rate changes (for both HRV and event-related heart rate) were associated with the diagnostic group and 6-month outcome when evaluated pre- and poststimulus but not when evaluated at rest. When assessed on day 7 postinjury, the comparison of HRV and heart rate parameters suggested an overresponsivity to nociceptive stimuli in dysautonomic subjects. These subjects showed a 2-fold increase in mean heart rate relative to subjects with sympathetic arousal of short duration (16% vs 8%), and a 6-fold increase over nonaroused control subjects. Data suggest that post-TBI sympathetic arousal is a spectrum disorder comprising, at one end, a short-duration syndrome and, at the other end, a dramatic, severe sympathetic and motor overactivity syndrome that continued for many months postinjury and associated with a significantly worse 6-month outcome. These findings suggest that it is not the presence of reactivity per se but rather the failure of processes to control for overreactivity that contributes to dysautonomic storming. CONCLUSIONS: This study provides empirical evidence that dysautonomic subjects show overresponsiveness to afferent stimuli. Findings from this study suggest an evidence-driven revision of diagnostic criteria and a simple clinical algorithm for the improved identification of cases.

Diferencias según el sexo en la variabilidad de la frecuencia cardíaca luego de traumatismo craneoencefálico / Sex differences in heart rate variability following acute traumatic brain injury

Antecedentes: Se reconocen cada vez más diferencias según el sexo en el pronóstico luego del traumatismo craneoencefálico (TCE). Este artículo examina si dichas diferencias se observan en los valores de la variabilidad de la frecuencia cardíaca (VFC), medida de la cual se halló previamente que se correlacionaba con la gravedad de la lesión y su pronóstico. Materiales, métodos y resultados: Se obtuvieron datos de 16 sujetos que habían sufrido un TCE y de controles apareados por edad y sexo. Los datos incluyeron detalles del traumatismo, registro electrocardiográfico continuo y resultado de la rehabilitación. Se observaron pruebas de disfunción cardíaca en los datos del TCE comparados con sus controles sanos apareados. Además, hubo una sugerencia preliminar de diferencias según el sexo en los parámetros de la VFC del grupo con TCE. Conclusiones: Los hallazgos en este grupo concuerdan con la bibliografía sobre la VFC luego de un TCE. Es recomendable que este trabajo continúe con otros artículos en los que se realicen estudios con una muestra más grande de sujetos con TCE para examinar detalladamente las diferencias según el sexo en los parámetros de la VFC.

Background: Sex differences in outcome followingtraumatic brain injury (TBI) are becoming increasinglyrecognised. This paper examines whether suchdifferences are found on measures of heart rate variability(HRV), a measure previously found to correlate with injuryseverity and outcome. Materials, methods and results:Data was collected on 16 subjects with TBI and their ageand sex matched controls. Data included injury details,continuous electrocardiograph recordings andrehabilitation outcome. Evidence of cardiac dysfunctionwas found in the TBI data compared to their matchedhealthy controls. Furthermore, there was preliminarysuggestion of sex differences in the HRV parameters ofthe TBI group. Conclusions: These group findingsreplicate previous literature on HRV following TBI. Theneed to follow-up this paper with larger sample of TBIsubjects in order to thoroughly examine sex differencesin HRV parameters is recommended.

A critical review of the pathophysiology of dysautonomia following traumatic brain injury.

The management of Dysautonomia following severe traumatic brain injury (TBI) remains problematic, primarily due to an inadequate understanding of the pathophysiology of the condition. While the original theories inferred an epileptogenic source, there is greater support for disconnection theories in the literature. Disconnection theories suggest that Dysautonomia follows the release of one or more excitatory centres from higher centre control. Conventional disconnection theories suggest excitatory centre/s located in the upper brainstem and diencephalon drive paroxysms. Another disconnection theory, the Excitatory:Inhibitory Ratio (EIR) Model, suggests the causative brainstem/diencephalic centres are inhibitory in nature, with damage releasing excitatory spinal cord processes. Review of the available data suggests that Dysautonomia follows structural and/or functional (for example raised intracerebral pressure or neurotransmitter blockade) abnormalities, with the tendency to develop Dysautonomic paroxysms being more closely associated with mesencephalic rather than diencephalic damage. Many reports suggest that paroxysmal episodes can be triggered by environmental events and minimised by various but predictable neurotransmitter effects. This article presents a critical review of the competing theories against the available observational, clinical and neurotransmitter evidence. Following this process, it is suggested that the EIR Model more readily explains pathophysiological and treatment data compared to conventional disconnection models. In particular, the EIR Model provides an explanatory model that encompasses other acute autonomic emergency syndromes, accommodates 'triggering' of paroxysms and provides a rationale for all known medication effects.

The incidence of dysautonomia and its relationship with autonomic arousal following traumatic brain injury.

PRIMARY OBJECTIVE: To determine the incidence of autonomic arousal vs. Dysautonomia following traumatic brain injury (TBI) in an Intensive Care Unit (ICU) setting and to prospectively evaluate these groups against injury severity and outcome variables. RESEARCH DESIGN: Prospective observational group comparison (cohort) study of consecutive ICU admissions to a major trauma hospital over a 2-year period. MAIN OUTCOMES AND RESULTS: Eighty-nine of 113 subjects met inclusion and exclusion criteria, with consent gained for 79 subjects (61 male, 18 female: 89% of potential subjects). During the first 7 days post-injury, elevated autonomic parameters were almost universal in the sample (92%), predominantly hypertension and tachycardia. Nineteen of 79 subjects (24%) were autonomically aroused on day 7 (that is, had elevated heart rate, respiratory rate, blood pressure and temperature). Dysautonomia was diagnosed on day 14 post-injury in six of 79 subjects (8%) using previously published criteria. Autonomically aroused subjects had significantly more severe injuries, poorer outcomes and greater estimated costs than non-aroused subjects. Furthermore, Dysautonomic subjects within the autonomically aroused group had significantly worse outcome and, excluding early deaths, a greater period of hospitalization and higher estimated costs. CONCLUSIONS: The 8% incidence of Dysautonomia during ICU admission was in broad agreement with previous research. While day 7 autonomic arousal indicated a greater degree of injury, the diagnosis of Dysautonomia provided additional prognostic information. A coordinated multi-centre research effort into this condition appears appropriate.

Gabapentin in the management of dysautonomia following severe traumatic brain injury: a case series.

The pharmacological management of dysautonomia, otherwise known as autonomic storms, following acute neurological insults, is problematic and remains poorly researched. This paper presents six subjects with dysautonomia following extremely severe traumatic brain injury where gabapentin controlled paroxysmal autonomic changes and posturing in the early post-acute phase following limited success with conventional medication regimens. In two subjects, other medications were reduced or ceased without a recurrence of symptoms. It is proposed that medications that can block or minimise abnormal afferent stimuli may represent a better option for dysautonomia management than drugs which increase inhibition of efferent pathways. Potential mechanisms for these effects are discussed.

Dysautonomia and heart rate variability following severe traumatic brain injury.

PRIMARY OBJECTIVE: To investigate disconnection theories postulated as the cause of dysautonomia following severe traumatic brain injury (TBI) through analysis of heart rate variability (HRV). METHODS AND PROCEDURES: Data were collected on age-matched subjects with and without dysautonomia (eight subjects in each group) and 16 non-injured controls. Data included injury details, continuous electrocardiograph recordings and rehabilitation outcome. MAIN OUTCOMES AND RESULTS: The TBI group revealed significant differences in HRV parameters both compared to controls and between dysautonomic and non-dysautonomic subjects. Additionally, HRV parameters for dysautonomic subjects showed evidence of an uncoupling of the normal relationship between heart rate and sympathetic/parasympathetic balance. HRV changes persisted for the dysautonomia group for a mean of 14 months post-injury. CONCLUSIONS: Dysautonomic subjects revealed prolonged uncoupling of heart rate and HRV parameters compared to non-dysautonomic subjects and controls. These findings represent direct pathophysiological evidence supporting the disconnection theory postulated to produce dysautonomia following TBI.