RESUMEN
OBJECTIVE: To examine the merits of using microRNAs (miRNAs) as biomarkers of disorders of consciousness (DoC) due to traumatic brain injury (TBI). SETTINGS: Acute and subacute beds. PARTICIPANTS: Patients remaining in vegetative and minimally conscious states (VS, MCS), an average of 1.5 years after TBI, and enrolled in a randomized clinical trial ( n = 6). Persons without a diagnosed central nervous system disorder, neurotypical controls ( n = 5). DESIGN: Comparison of whole blood miRNA profiles between patients and age/gender-matched controls. For patients, correlational analyses between miRNA profiles and measures of neurobehavioral function. MAIN MEASURES: Baseline measures of whole blood miRNAs isolated from the cellular and fluid components of blood and measured using miRNA-seq and real-time polymerase chain reaction (RT-PCR). Baseline neurobehavioral measures derived from 7 tests. RESULTS: For patients, relative to controls, 48 miRNA were significantly ( P < .05)/differentially expressed. Cluster analysis showed that neurotypical controls were most similar to each other and with 2 patients (VS: n = 1; and MCS: n = 1). Three patients, all in MCS, clustered separately. The only female in the sample, also in MCS, formed an independent group. For the 48 miRNAs, the enriched pathways identified are implicated in secondary brain damage and 26 miRNAs were significantly ( P < .05) correlated with measures of neurobehavioral function. CONCLUSIONS: Patients remaining in states of DoC an average of 1.5 years after TBI showed a different and reproducible pattern of miRNA expression relative to age/gender-matched neurotypical controls. The phenotypes, defined by miRNA profiles relative to persisting neurobehavioral impairments, provide the basis for future research to determine the miRNA profiles differentiating states of DoC and the basis for future research using miRNA to detect treatment effects, predict treatment responsiveness, and developing targeted interventions. If future research confirms and advances reported findings, then miRNA profiles will provide the foundation for patient-centric DoC neurorehabilitation.
Asunto(s)
Lesiones Traumáticas del Encéfalo , Lesiones Encefálicas , MicroARNs , Humanos , Femenino , Estado de Conciencia , Lesiones Traumáticas del Encéfalo/complicaciones , Lesiones Traumáticas del Encéfalo/diagnóstico , Lesiones Traumáticas del Encéfalo/genética , Lesiones Encefálicas/rehabilitación , MicroARNs/genética , Estado Vegetativo Persistente , Trastornos de la Conciencia/complicacionesRESUMEN
BACKGROUND: Spinal cord injury (SCI) has been found to affect the physiology of the gastrointestinal tract. Changes in gastric motility occur in tetraplegia because of dissociation of antral and duodenal motility. Among individuals with high-level tetraplegia, antral quiescence has been hypothesized as a manifestation of autonomic dysreflexia after surgery. This case series shows the issues with gastric hypomotility after gastrointestinal surgery in tetraplegic patients with tetraplegia, including management strategies. OBJECTIVE: To report 3 patients with complete high cervical SCI who developed gastroparesis after abdominal surgery and discuss the effect of autonomic dysfunction on gastric motility. METHODS: Retrospective chart review of 3 cases. RESULTS: Gastroparesis occurred after abdominal surgery in 3 patients with C4 American Spinal Injury Association (ASIA) A tetraplegia and seemed to be a sign of autonomic hyperreflexia caused by postoperative pain. Management was challenging because it consisted of balancing of appropriate pain medication and dealing with absorption issues and dysmotility. Often gastric motility agents were not effective in improving gastric emptying. However, increased use of pain medication improved gastric emptying, which supports the hypothesis that this issue represents gastric dysfunction from autonomic hyperreflexia. CONCLUSIONS: In persons with complete cervical SCI who have undergone abdominal surgery, postoperative gastroparesis can be a manifestation of pain. This may occur as the excessive sympathetic response from autonomic hyperreflexia inhibits distal antral activity. Thus, treatment of postoperative gastroparesis should focus on improved pain control to decrease excessive splanchnic sympathetic output and circulating norepinephrine.