Neurodivergence and radiology: How medical professionals can optimise the standard of care provided to autistic paediatric patients.

INTRODUCTION: Several studies have been published regarding patients with various neurodevelopmental diagnoses attending hospital appointments, however, few focus on autism and the radiology department. This paper aims to identify how implementing patient-centred strategies and protocols for autistic paediatric patients will benefit the patient pathway and provide a more comfortable experience for those undergoing different scans and procedures within the radiology department. METHODS: Using several electronic databases, articles were collected using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and analysed with the Critical Appraisals Skills Programme (CASP). DISCUSSION: A total of 8 articles are discussed and analysed in this review, focussing specifically on patient-centred procedures and practice, costs of healthcare services and how multidisciplinary teamwork compares to applied behavioural analysis. RESULTS: The articles concluded that the current practice of multidisciplinary working is the most beneficial for patients. Furthermore, implementing autism awareness programmes and patient-specific protocols will help reduce anxiety surrounding scans within the radiology department. CONCLUSION AND IMPLICATIONS FOR PRACTICE: Implementing mandatory autism awareness programmes and continuing with the multidisciplinary approach for autistic paediatric patients would provide the best possible patient-centred care.

Solid-phase synthesis of Rhodamine-110 fluorogenic substrates and their application in forensic analysis.

A novel synthetic route for the rapid and efficient preparation of fluorogenic substrates utilizing Rhodamine-110 or similar fluorophores is reported. Applicability of the synthesized peptide substrate within a forensic casework context is also presented.

Assessment of animal impacts on bacterial water quality in a South Carolina, USA tidal creek system.

Fecal pollution may adversely impact water quality in coastal ecosystems. The goal of this study was to determine whether cattle were a source of fecal pollution in a South Carolina watershed. Surface water samples were collected in June 2002 and February through March 2003 in closed shellfish harvesting waters of Toogoodoo Creek in Charleston County, SC. Fecal coliform concentrations in 70 % of the water samples taken for this study exceeded shellfish harvesting water standards. Ribotyping was performed in order to identify animal sources contributing to elevated fecal coliform levels. Escherichia coli isolates (n = 253) from surface water samples were ribotyped and compared to a ribotype library developed from known sources of fecal material. Ribotypes from water samples that matched library ribotypes with 90 % maximum similarity or better were assigned to that source. Less than half of the unknown isolates (38 %) matched with library isolates. About half (53 %) of the matched ribotypes were assigned to cattle isolates and 43 % to raccoon. Ribotyping almost exclusively identified animal sources. While these results indicate that runoff from cattle farms was a likely source of fecal pollution in the watershed, wildlife also contributed. Given the small size of the library, ribotyping was moderately useful for determining the impact of adjacent cattle farms on Toogoodoo Creek. Increasing the number and diversity of the wildlife sources from the area would likely increase the usefulness of the method.

A real-time qPCR assay for the detection of the nifH gene of Methanobrevibacter smithii, a potential indicator of sewage pollution.

AIMS: To develop a quantitative, real-time PCR assay to detect the nifH gene of Methanobrevibacter smithii. Methanobrevibacter smithii is a methanogenic archaea found in the intestinal tract of humans that may be a useful indicator of sewage pollution in water. METHODS AND RESULTS: Quantification standards were prepared from Meth. smithii genomic DNA dilutions, and a standard curve was used to quantify the target gene and calculate estimated genome equivalency units. A competitive internal positive control was designed and incorporated into the assay to assess inhibition in environmental extracts. Testing the assay against a panel of 23 closely related methanogen species demonstrated specificity of the assay for Meth. smithii. A set of 36 blind water samples was then used as a field test of the assay. The internal control identified varying levels of inhibition in 29 of 36 (81%) samples, and the Meth. smithii target was detected in all water samples with known sewage input. CONCLUSIONS: The quantitative PCR assay developed in this study is a sensitive and rapid method for the detection of the Meth. smithii nifH gene that includes an internal control to assess inhibition. Further research is required both to better evaluate host specificity of this assay and the correlation with human health risks. SIGNIFICANCE AND IMPACT OF THE STUDY: This research is the first description of the development of a rapid and sensitive quantitative assay for a methanogenic archaeal indicator of sewage pollution.

Growth and survival of Vibrio parahaemolyticus in postharvest American oysters.

Oysters at the retail stage of distribution generally contain greater densities of Vibrio parahaemolyticus than do oysters at harvest. The objective of this study was to determine the effects of postharvest storage at 26 and 3 degrees C on the growth and survival of naturally occurring V. parahaemolyticus in shellstock American oysters (Crassostrea virginica). Oysters were collected monthly from May 1998 through April 1999 from Mobile Bay, Alabama, and their V. parahaemolyticus densities were determined after 0, 5, 10, and 24 h of postharvest storage at 26 degrees C. After 24 h of storage at 26 degrees C, oysters were transferred to a refrigerator at 3 degrees C and analyzed 14 to 17 days later. V. parahaemolyticus numbers were determined by a direct plating method involving an alkaline-phosphatase-labeled DNA probe that targets the species-specific thermolabile hemolysin gene (tlh-AP) to identify suspect isolates. From April to December, when water temperatures at harvest were >20 degrees C, the geometric mean harvest density of V. parahaemolyticus was 130 CFU/g. When water temperatures were <20 degrees C, the geometric mean harvest density was 15 CFU/g. After harvest, V. parahaemolyticus multiplied rapidly in live oysters held at 26 degrees C, showing a 50-fold increase (1.7 log CFU/g) at 10 h and a 790-fold increase (2.9 log CFU/g) at 24 h (April through December). Average V. parahaemolyticus numbers showed a sixfold decrease (0.8 log CFU/g) after approximately 14 days of refrigeration. These results indicate that V. parahaemolyticus can grow rapidly in unrefrigerated oysters.

Heterogeneity of environmental, retail, and clinical isolates of Vibrio vulnificus as determined by lipopolysaccharide-specific monoclonal antibodies.

The opportunistic pathogen Vibrio vulnificus expresses lipopolysaccharide (LPS) antigens on its outer membrane surface. A serological typing system was developed for these antigens, utilizing the discriminatory recognition of monoclonal antibodies (MAb) by ELISA. MAb were used to recognize five unique types of LPS-associated antigens for examination of clinical. environmental, and retail isolates of V. vulnificus. The overall serotype profile of the clinical isolates was significantly different (P < 0.05) from that of the environmental and retail isolates. A higher percentage of clinical isolates were typable (61%) compared to the environmental isolates (41%) and retail isolates (44%). In particular, the percentage of serotype 1/5 among clinical isolates (33%), compared to that of environmental (9%) and retail (4%), was highly significant (P < 0.0001). Among the environmental Gulf Coast isolates, there were differences in the prevalence of serotypes 2 and 3 (P < 0.05), depending on whether isolates were obtained from Louisiana or Alabama harvest sites. There were no statistically significant differences between the serotype profiles of Gulf and Atlantic Coast retail isolates despite the absence of serotype 1/5 from the Atlantic Coast. While some serotype diversity was detected in V. vulnificus isolated during different seasons, from different geographic locations, and at retail versus at harvest, there was no apparent concordance between any of the serotype distributions obtained from oysters versus that isolated clinically. The heterogeneity of environmental isolates and relative homogeneity among clinical isolates suggest that human risk may not be predicted on quantitative exposure alone.

Insulin-like growth factor-I induces renal cell hypertrophy via a calcineurin-dependent mechanism.

Insulin-like growth factor-I (IGF-I) may play an important role in the development of renal hypertrophy. In this study we determined the effect of IGF-I on cultured mesangial cells (MCs) and examined activation of key signaling pathways. IGF-I induced hypertrophy as determined by an increase in cell size and an increase in protein to DNA ratio and increased accumulation of extracellular matrix (ECM) proteins. IGF-I also activated both Erk1/Erk2 MAPK and phosphatidylinositol 3-kinase (PI3K) in MCs. Inhibition of either MAPK or PI3K, however, had no effect on IGF-I-induced hypertrophy or ECM production. Next, we examined the effect of IGF-I on activation of the calcium-dependent phosphatase calcineurin. IGF-I treatment stimulated calcineurin activity and increased the protein levels of calcineurin and the calcineurin binding protein, calmodulin. Cyclosporin A, an inhibitor of calcineurin, blocked both IGF-I-mediated hypertrophy and up-regulation of ECM. In addition, calcineurin resulted in sustained Akt activation, indicating possible cross-talk with other signaling pathways. Finally, IGF-I treatment resulted in the calcineurindependent nuclear localization of NFATc1. Therefore, IGF-I induces hypertrophy and increases ECM accumulation in MCs. IGF-I-mediated hypertrophy is associated with activation of Erk1/Erk2 MAPK and PI3K but does not require either of these pathways. Instead, IGF-I mediates hypertrophy via a calcineurin-dependent pathway.

Reliability of listener transcriptions of compensatory articulations.

OBJECTIVE: This study examined the ability of speech-language pathologists to transcribe compensatory articulation errors. DESIGN: Speech-language pathologists phonetically transcribed audiorecordings of 130 monosyllabic words, 70 of which contained compensatory articulations. PARTICIPANTS: The participants for this study were two groups of 10 speech-language pathologists. Group I included speech-language pathologists who were experienced in evaluating children with cleft palate, and group II speech-language pathologists were not. RESULTS: Marked variability was evident across listeners, with percentages of agreement ranging from 19 to 71 (mean agreement = 41%). The experienced listeners performed significantly better on the transcription task than the inexperienced listeners, but poor interjudge agreement was evident across both groups. CONCLUSIONS: The results of this study suggest that speech-language pathologists may differ in their understanding of the auditory perceptual characteristics of compensatory articulations. The results underscore the need for increased training and standardization of transcription procedures.

Evaluation of two direct plating methods using nonradioactive probes for enumeration of Vibrio parahaemolyticus in oysters.

Oysters (Crassostrea virginica) were collected monthly from May 1998 to April 1999 from Mobile Bay, Ala., and analyzed to determine Vibrio parahaemolyticus densities at zero time and after 5, 10, and 24 h of postharvest storage at 26 degrees C. After 24 h of storage at 26 degrees C, oysters were transferred to a refrigerator at 3 degrees C and then analyzed 14 to 17 days later. The V. parahaemolyticus numbers were determined by the most-probable-number procedure using alkaline phosphatase-labeled DNA probe VPAP, which targets the species-specific thermolabile hemolysin gene (tlh), to identify suspect isolates (MPN-VPAP procedure). Two direct plating methods, one using a VPAP probe (Direct-VPAP) and one using a digoxigenin-labeled probe (Direct-VPDig) to identify suspect colonies, were compared to the MPN-VPAP procedure. The results of the Direct-VPAP and Direct-VPDig techniques were highly correlated (r = 0.91), as were the results of the Direct-VPAP and MPN-VPAP procedures (r = 0.91). The correlation between the Direct-VPDig and MPN-VPAP results was 0.85. The two direct plating methods in which nonradioactive DNA probes were used were equivalent to the MPN-VPAP procedure for identification of total V. parahaemolyticus, and they were more rapid and less labor-intensive.

Intrathecal baclofen withdrawal simulating neuroleptic malignant syndrome in a child with cerebral palsy.

Intrathecal baclofen infusion (IBI) is being used with increasing frequency in children to treat spasticity and dystonia. In this report, we summarize the clinical course of a 9-year-old boy with quadriplegic cerebral palsy with mixed tonal abnormalities (spasticity and dystonia) experiencing withdrawal from intrathecal baclofen. His clinical course is compared to that of adults experiencing withdrawal from IBI and to neuroleptic malignant syndrome. If unrecognized, this disorder may have significant potential for morbidity and mortality. Clues to diagnosis, appropriate evaluation, and potential treatments are discussed. When a child treated with IBI presents with unexplained multiorgan system dysfunction, particularly if accompanied by evidence of rhabdomyolysis, the integrity of the IBI system must be evaluated. In some cases, evaluation might necessitate surgical exploration. Caregivers most commonly seek urgent evaluation and treatment from their primary care provider when their child experiences fever or acute illness. Primary care providers of children treated with IBI should be made aware of this clinical scenario to prevent delays in diagnosis.

Transcriptional repression by nuclear receptors: mechanisms and role in disease.

Co-repressor proteins mediate transcriptional repression by nuclear receptors in the absence of ligand. The identification of a co-repressor-receptor interaction motif, and the finding that co-repressors and co-activators compete for the same site on the receptor, suggests a simple mechanism for the switch from repression to activation upon ligand binding. Defects in this mechanism result in dominant-negative receptors that repress transcription. Such receptors have been implicated in several clinically important diseases, including thyroid hormone resistance and diabetes mellitus.

The role of p21 in interferon gamma-mediated growth inhibition of human breast cancer cells.

IFN-gamma-mediated growth inhibition requires signal transducers and activators of transcription (STAT)-1 activation and may require induction of the cyclin-dependent kinase inhibitor p21. Using an electrophoretic mobility shift assay, we identified STAT1 activation after IFN-gamma treatment in breast cancer cell lines. Accordingly, IFN-gamma inhibited proliferation of monolayer cultured MCF-7 and MDA-MB-231 breast cancer cells. Interestingly, IFN-gamma inhibited anchorage-independent growth of MCF-7 cells but had no effect on MDA-MB-231 colony formation. Because p21 has been shown to play a role in anchorage-independent growth and is a transcriptional target of STAT1, we examined the effect of IFN-gamma on p21 mRNA. We found that IFN-gamma induced p21 mRNA in MCF-7 cells but not in MDA-MB-231 cells. Furthermore, IFN-gamma induced activation of a p21 promoter-luciferase reporter construct that contained the STAT1-inducible element in MCF-7 cells, but not in MDA-MB-231 cells. IFN-gamma treatment resulted in increased p21 protein in MCF-7 cells, whereas MDA-MB-231 cells did not appear to express detectable p21, even after IFN-gamma treatment. However, in MDA-MB-231 cells, p21 protein was detected only after proteosome inhibition, suggesting that degradation may be responsible for the undetectable level of p21 in these cells, despite the abundant mRNA levels. Finally, focus formation of MDA-MB-231 cells was inhibited by overexpression of p21. In conclusion, STAT1 activation does not appear to be sufficient for IFN-gamma-mediated growth inhibition. Furthermore, the role of p21 appears to be complex because monolayer growth inhibition occurs in the absence of p21, but anchorage-independent growth inhibition may require p21. Breast cancer cells may provide a unique model for further study of IFN-gamma signaling.

Insulin-like growth factor I-induced degradation of insulin receptor substrate 1 is mediated by the 26S proteasome and blocked by phosphatidylinositol 3'-kinase inhibition.

Insulin receptor substrate 1 (IRS-1) is a critical adapter protein involved in both insulin and insulin-like growth factor (IGF) signaling. Due to the fact that alteration of IRS-1 levels can affect the sensitivity and response to both insulin and IGF-I, we examined the ability of each of these ligands to affect IRS-1 expression. IGF-I (10 nM) stimulation of MCF-7 breast cancer cells caused a transient tyrosine phosphorylation of IRS-1 that was maximal at 15 min and decreased thereafter. The decrease in tyrosine phosphorylation of IRS-1 was paralleled by an apparent decrease in IRS-1 levels. The IGF-mediated decrease in IRS-1 expression was posttranscriptional and due to a decrease in the half-life of the IRS-1 protein. Insulin (10 nM) caused tyrosine phosphorylation of IRS-1 but not degradation, whereas high concentrations of insulin (10 microM) resulted in degradation of IRS-1. IGF-I (10 nM) stimulation resulted in transient IRS-1 phosphorylation and extracellular signal-related kinase (ERK) activation. In contrast, insulin (10 nM) caused sustained IRS-1 phosphorylation and ERK activation. Inhibition of 26S proteasome activity by the use of lactacystin or MG132 completely blocked IGF-mediated degradation of IRS-1. Furthermore, coimmunoprecipitation experiments showed an association between ubiquitin and IRS-1 that was increased by treatment of cells with IGF-I. Finally, IGF-mediated degradation of IRS-1 was blocked by inhibition of phosphatidylinositol 3'-kinase activity but was not affected by inhibition of ERK, suggesting that this may represent a direct negative-feedback mechanism resulting from downstream IRS-1 signaling. We conclude that IGF-I can cause ligand-mediated degradation of IRS-1 via the ubiquitin-mediated 26S proteasome and a phosphatidylinositol 3'-kinase-dependent mechanism and that control of degradation may have profound effects on downstream activation of signaling pathways.

Insulin-like growth factor (IGF)-I rescues breast cancer cells from chemotherapy-induced cell death--proliferative and anti-apoptotic effects.

Insulin-like growth factor (IGF)-I protects many cell types from apoptosis. As a result, it is possible that IGF-I-responsive cancer cells may be resistant to apoptosis-inducing chemotherapies. Therefore, we examined the effects of IGF-I on paclitaxel and doxorubicin-induced apoptosis in the IGF-I-responsive breast cancer cell line MCF-7. Both drugs caused DNA laddering in a dose-dependent fashion, and IGF-I reduced the formation of ladders. We next examined the effects of IGF-I and estradiol on cell survival following drug treatment in monolayer culture. IGF-I, but not estradiol, increased survival of MCF-7 cells in the presence of either drug. Cell cycle progression and counting of trypan-blue stained cells showed that IGF-I was inducing proliferation in paclitaxel-treated but not doxorubicin-treated cells. However, IGF-I decreased the fraction of apoptotic cells in doxorubicin- but not paclitaxel-treated cells. Recent work has shown that mitogen-activated protein kinase (MAPK) and phosphotidylinositol-3 (PI-3) kinase are activated by IGF-I in these cells. PI-3 kinase activation has been linked to anti-apoptotic functions while MAPK activation is associated with proliferation. We found that IGF-I rescue of doxorubicin-induced apoptosis required PI-3 kinase but not MAPK function, suggesting that IGF-I inhibited apoptosis. In contrast, IGF-I rescue of paclitaxel-induced apoptosis required both PI-3 kinase and MAPK, suggesting that IGF-I-mediated protection was due to enhancement of proliferation. Therefore, IGF-I attenuated the response of breast cancer cells to doxorubicin and paclitaxel by at least two mechanisms: induction of proliferation and inhibition of apoptosis. Thus, inhibition of IGF-I action could be a useful adjuvant to cytotoxic chemotherapy in breast cancer.

Strain-specific differences in formation of apoptotic DNA ladders in MCF-7 breast cancer cells.

We tested the ability of seven MCF-7 strains to undergo DNA fragmentation, as measured by DNA laddering, following doxorubicin-induced apoptosis. Four strains were found to undergo DNA laddering while three were not. All strains were inhibited by doxorubicin, although sensitivity differed. Finally, we show by detection of sub-G1 DNA that doxorubicin induced the same fold increase in apoptosis in MCF-7-ATCC, which did not ladder, and MCF-7-MG, which did ladder. Therefore, detection of DNA ladders is not an accurate indicator of apoptosis in MCF-7 cells as fragmentation of DNA appears to vary between strains.

Enhancement of insulin-like growth factor signaling in human breast cancer: estrogen regulation of insulin receptor substrate-1 expression in vitro and in vivo.

Cross-talk between insulin-like growth factor (IGF)- and estrogen receptor (ER)-signaling pathways results in synergistic growth. We show here that estrogen enhances IGF signaling by inducing expression of three key IGF-regulatory molecules, the type 1 IGF receptor (IGFR1) and its downstream signaling molecules, insulin receptor substrate (IRS)-1 and IRS-2. Estrogen induction of IGFR1 and IRS expression resulted in enhanced tyrosine phosphorylation of IRS-1 after IGF-I stimulation, followed by enhanced mitogen-activated protein kinase activation. To examine whether these pathways were similarly activated in vivo, we examined MCF-7 cells grown as xenografts in athymic mice. IRS-1 was expressed at high levels in estrogen-dependent growth of MCF-7 xenografts, but withdrawal of estrogen, which decreased tumor growth, resulted in a dramatic decrease in IRS-1 expression. Finally, we have shown that high IRS-1 expression is an indicator of early disease recurrence in ER-positive human primary breast tumors. Taken together, these data not only reinforce the concept of cross-talk between IGF- and ER-signaling pathways, but indicate that IGF molecules may be critical regulators of estrogen-mediated growth and breast cancer pathogenesis.

Mechanism of corepressor binding and release from nuclear hormone receptors.

The association of transcription corepressors SMRT and N-CoR with retinoid and thyroid receptors results in suppression of basal transcriptional activity. A key event in nuclear receptor signaling is the hormone-dependent release of corepressor and the recruitment of coactivator. Biochemical and structural studies have identified a universal motif in coactivator proteins that mediates association with receptor LBDs. We report here the identity of complementary acting signature motifs in SMRT and N-CoR that are sufficient for receptor binding and ligand-induced release. Interestingly, the motif contains a hydrophobic core (PhixxPhiPhi) similar to that found in NR coactivators. Surprisingly, mutations in the amino acids that directly participate in coactivator binding disrupt the corepressor association. These results indicate a direct mechanistic link between activation and repression via competition for a common or at least partially overlapping binding site.

Conversational skills of preschool and school-age children with cleft lip and palate.

OBJECTIVE: The purpose of this study was to examine the conversational skills of preschool and school-age children with cleft lip and palate. DESIGN: The children were audio- and videotaped during interactions with an unfamiliar adult. In addition, standardized measures of speech and language were administered, and ratings of resonance were obtained. Comparisons were made between the children with cleft lip and palate and their same-age peers on measures of conversational participation and a standardized test of pragmatic skills. PARTICIPANTS: Participants were 20 children with unilateral cleft lip and palate (10 preschoolers and 10 school-age children) recruited from the Craniofacial Team at Rainbow Babies and Children's Hospital, Cleveland (OH) and 20 noncleft peers matched for gender, age, and socioeconomic status. MAIN OUTCOME MEASURES: Separate comparisons were made for the preschool children with cleft lip and palate and their noncleft peers, and the school-age children with cleft lip and palate and their noncleft peers on eight measures of conversational assertiveness/responsiveness and the standardized tests of pragmatics. Next, each child with cleft lip and palate was classified for level of conversational participation. RESULTS: Paired t tests revealed no significant differences between the preschool and school-age children with cleft lip and palate and their noncleft peers in level of conversational participation. However, individual child comparisons revealed less assertive profiles of conversational participation for 50% of the preschool and 20% of the school-age children with cleft lip and palate. CONCLUSIONS: Children with cleft lip and palate may show a less assertive style of conversational participation, at least during the preschool years. Therefore, craniofacial team evaluations should include examination of conversational competency, particularly for children who are demonstrating difficulty with other aspects of speech, language, or social development.

Interleukin 4 inhibits growth and induces apoptosis in human breast cancer cells.

Interleukin-4 (IL-4) is a pleiotropic cytokine produced by mast cells and T lymphocytes that promotes proliferation and immunoglobulin class-switching in B cells. IL-4 receptors (IL-4Rs) are also expressed by nonhematopoietic cells as well as some tumor cells. Unlike its mitogenic effect on B cells, IL-4 inhibits the growth of some cancer cells in vitro. In this study, we show that IL-4R is expressed by breast and ovarian cancer cell lines. Furthermore, anchorage-dependent and -independent growth of breast cancer cell lines MCF-7 and MDA-MB-231 is inhibited by IL-4 treatment, and this effect requires IL-4R. Interestingly, IL-4 only inhibited proliferating breast cancer cells and had no effect on basal, unstimulated growth. We therefore characterized the effect of IL-4 on breast cancer cell growth stimulated by either estradiol or insulin-like growth factor I (IGF-I). In both anchorage-dependent and -independent growth assays, IL-4 inhibited estradiol-stimulated growth. The antiestrogen effect of IL-4 was not due to IL-4 interference with the estrogen receptor, because IL-4 did not interfere with estrogen receptor-mediated reporter gene transactivation. In contrast, IL-4 had no effect on IGF-I-stimulated proliferation. Because IGF-I is known to inhibit programmed cell death, we examined apoptosis as a possible mechanism of IL-4 action. We established that IL-4 induced apoptosis in breast cancer cells by five independent criteria: (a) morphological indicators including pyknotic nuclei and cytoplasmic condensation; (b) DNA fragmentation; (c) the formation of DNA laddering; (d) the cleavage of poly(ADP-ribose) polymerase; and (e) the presence of cells with sub-G1 DNA content. IL-4 increased the percentage of apoptotic cells in MCF-7 and MDA-MB-231 cells 6.0- and 6.7-fold over that of the control, respectively. Finally, the addition of IGF-I reversed IL-4-induced apoptosis, suggesting that the mechanism of IL-4-induced growth inhibition in human breast cancer cells is the induction of programmed cell death.

Primary idiopathic optic neuritis in U.S. Air Force Aviators.

The records of 31 male aviators seen at the Ophthalmology Branch of the USAF Aeromedical Consultation Service (formerly the USAF School of Aerospace Medicine) for a diagnosis of primary idiopathic optic neuritis (PION) were reviewed. Each subject received comprehensive ophthalmologic and neurologic examinations. The long-term follow-up data were collected through repeat examinations and by survey. Despite 39% of aviators being grounded due to complications of their PION or multiple sclerosis (MS), many aviators diagnosed with PION may be safely returned to flying duties. However, any aviator diagnosed with PION has a risk of recurrence or a potential to develop systemic MS and must be carefully reevaluated and followed to ensure they remain a viable asset and do not compromise flight safety or mission completion.