Penn State equation versus indirect calorimetry for nutritional assessment in patients with traumatic brain injury.

BACKGROUND: Nutritional assessment can be challenging in patients with traumatic brain injury (TBI), and indirect calorimetry may be a more suitable method than predictive equations. We compared the Penn State equation versus the gold standard of indirect calorimetry for the nutritional assessment of patients with TBI, and quantified the difference between nutritional requirements and actual patient intake. METHODS: This single-centre, prospective cohort study included patients with moderate (Glasgow Coma Scale score 9-12) and severe (Glasgow Coma Scale score 3-8) TBI admitted to the Montreal General Hospital intensive care unit (ICU) between June 2018 and March 2019. Penn State equation estimates and indirect calorimetry measurements were collected, and actual intake was drawn from medical records. We compared the 2 assessment methods using a Spearman correlation coefficient. RESULTS: Twenty-three patients with TBI (moderate in 7 and severe in 16) were included in the study. Overall, there was a moderate positive correlation between the Penn State equation estimate and indirect calorimetry readings (correlation coefficient 0.457, p = 0.03); however, the correlation was weaker in severe TBI (correlation coefficient 0.174, p = 0.5) than in moderate TBI (correlation coefficient 0.929, p = 0.003). When compared to indirect calorimetry assessment, patients received 5.4% (p = 0.5) of required intake on the first day and 43.9% (p = 0.8) of required daily intake throughout their ICU stay. CONCLUSION: Patients with moderate or severe TBI in the ICU received less than 50% of their nutritional requirements. The difference between the Penn State equation and indirect calorimetry assessments was most noticeable for patients with severe TBI, which indicates that indirect calorimetry may be a more suitable tool for assessment of nutritional needs in this population.

Effector/memory CD8+ T cells synergize with co-stimulation competent macrophages to trigger autoimmune peripheral neuropathy.

Autoimmune peripheral neuropathy (APN) such as Guillain Barre Syndrome (GBS) is a debilitating illness and sometimes life threatening. The molecular and cellular mechanisms remain elusive but exposure to environmental factors including viral/bacterial infection and injury is highly associated with disease incidence. We demonstrated previously that both male and female B7.2 (CD86) transgenic L31 and L31/CD4KO mice develop spontaneous APN. Here we further reveal that CD8+ T cells in these mice exhibit an effector/memory phenotype, which bears a resemblance to the CD8+ T cell response following persistent cytomegalovirus (CMV) infection in humans and mice, whilst CMV has been considered as one of the most relevant pathogens in APN development. These activated, peripheral myelin Ag specific CD8+ T cells are required for the disease initiation. While an injury to a peripheral nerve results in Wallerian degeneration in control littermates, the same injury accelerates the development of APN in other non-injured nerves of L31 mice which have a predisposed inflammatory background consisting of effector/memory CD8+ T (CD8+ TEM) cells. However, CD8+ TEM cells alone are not sufficient. A certain threshold of B7.2 expression on nerve macrophages is an additional requisite. Our findings reveal that indeed, the synergism between CD8+ TEM cells and co-stimulation competent macrophages is crucial in inducing autoimmune-mediated peripheral neuropathy. The identification of decisive molecular/cellular players connecting environmental triggers and the occurrence of APN provides opportunities to prevent disease onset, reduce relapses and develop new therapeutic strategies.

Evidence from Human and Animal Studies: Pathological Roles of CD8(+) T Cells in Autoimmune Peripheral Neuropathies.

Autoimmune peripheral neuropathies such as Guillain-Barre Syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) affect millions of people worldwide. Despite significant advances in understanding the pathology, the molecular and cellular mechanisms of immune-mediated neuropathies remain elusive. T lymphocytes definitely play an important role in disease pathogenesis and CD4(+) T cells have been the main area of research for decades. This is partly due to the fact that the most frequent animal model to study autoimmune peripheral neuropathy is experimental allergic neuritis (EAN). As it is induced commonly by immunization with peripheral nerve proteins, EAN is driven mainly by CD4(+) T cells. However, similarly to what has been reported for patients suffering from multiple sclerosis, a significant body of evidence indicates that CD8(+) T cells may play a pathogenic role in GBS and CIDP disease development and/or progression. Here, we summarize clinical studies pertaining to the presence and potential role of CD8(+) T cells in autoimmune peripheral neuropathies. We also discuss the findings from our most recent studies using a transgenic mouse line (L31 mice) in which the T cell co-stimulator molecule B7.2 (CD86) is constitutively expressed in antigen presenting cells of the nervous tissues. L31 mice spontaneously develop peripheral neuropathy, and CD8(+) T cells are found accumulating in peripheral nerves of symptomatic animals. Interestingly, depletion of CD4(+) T cells accelerates disease onset and increases disease prevalence. Finally, we point out some unanswered questions for future research to dissect the critical roles of CD8(+) T cells in autoimmune peripheral neuropathies.

Children's preference of benzocaine gel versus the lidocaine patch.

PURPOSE: This study compared pain, acceptance, and preference associated with 2 topical anesthetics: benzocaine gel and lidocaine patch (DentiPatch). METHODS: Thirty patients aged 3 to 10 years participated in this within-subjects study. All children required identical or similar dental work bilaterally (restorations, extractions, endodontic procedures, or sealants). Subjects chose either DentiPatch or benzocaine gel at the first visit. The anesthetic the child did not choose was used at the second visit. The Whali-Wong scale was used to measure comfort before and after application of topical anesthetic and after injection, and the Sounds, Eyes, Motor (SEM) scale measured pain upon injection. RESULTS: At the first visit, 80% of subjects selected DentiPatch; 60% of subjects made their choice based on appearance. Younger children more than older children were influenced by appearance in their selection. After trying both topical anesthetics, 77% preferred DentiPatch; final preference and either age or gender were not significantly related. The gel had greater scores than the patch for the Sounds pain value and for the SEM scale composite score. CONCLUSIONS: The lidocaine patch was associated with some objective evidence of reduced pain compared to the gel and was preferred by most children.