18 results found
Farag S, Feeney C, Lee V, et al., 2019, Identifying risk factors for severity & activity of Graves Orbitopathy - a multi-centre analysis of the characteristics and treatment of patients with Thyroid Eye Disease, The 2019 European Association for Vision and Eye Research Conference, Publisher: European Association for Vision and Eye Research (EVER), Pages: 1-2, ISSN: 1395-3907
PurposeEarly diagnosis and treatment of Graves Orbitopathy (GO) is essential to prevent sight-threatening complications and long-term disability and therefore establishing a standard of care is highly desirable. Establishing predictors of a severe disease course are also vital to allow for early intervention.MethodsA retrospective patient-cohort study of 236 patients referred to three GO multidisciplinary (MDT) clinics between 2012–2019. Derived from this cohort, audit standards were compared against TEAMeD-5 guidelines, looking in particular at; (i) time between referral and specialist review (ii) offering of smoking cessation and selenium supplementation where appropriate (iii) time from referral to treatment for moderate-severe active disease. Patient characteristics were also analysed to investigate for any groupwise differences and correlations between variables collected at baseline to help predict subsequent disease activity.ResultsMedian patient age was 48.0 years, 77.5% female, 30.1% White Caucasian. Median initial clinical activity score (CAS) was 1 (range 0–7). Additionally, 80.5% had positive TSH antibody titre. The median time between referral and first MDT clinic was 50.0 days. Of the 254 patients, 80/236 received IVMP for active moderate-severe GO and the mean time to treatment was 9.3 days. All patients with sight-threatening GO were seen and treated within 2 weeks. There were 52/236 (22.0%) current smokers, all of whom received documented smoking cessation advice. A positive correlation was found between TSH antibody titre (R = −0.2902, p = 0.0545).ConclusionThe increasing recognition that an MDT approach is optimal for the management of GO requires a strong clinical governance framework. This work will further define the TEAMeD guidelines before the national implementation. Novel findings relating to the association of disease activtiy with biomarkers of diabetes and antibody titres are worth further investigation.
Feeney C, Buell K, 2018, A Case of Addison's Disease Nearly Mistaken for Anorexia Nervosa, AMERICAN JOURNAL OF MEDICINE, Vol: 131, Pages: E457-E458, ISSN: 0002-9343
- Author Web Link
- Citations: 3
Feeney C, Buell KG, Avari P, et al., 2018, Addisonian crisis: assessment and management, BRITISH JOURNAL OF HOSPITAL MEDICINE, Vol: 79, Pages: C34-C37, ISSN: 1750-8460
Scott GPT, Zetterberg H, Jolly A, et al., 2017, Minocycline reduces chronic microglial activation after brain trauma but increases neurodegeneration, Brain, Vol: 141, Pages: 459-471, ISSN: 1460-2156
Survivors of a traumatic brain injury can deteriorate years later, developing brain atrophy and dementia. Traumatic brain injury triggers chronic microglial activation, but it is unclear whether this is harmful or beneficial. A successful chronic-phase treatment for traumatic brain injury might be to target microglia. In experimental models, the antibiotic minocycline inhibits microglial activation. We investigated the effect of minocycline on microglial activation and neurodegeneration using PET, MRI, and measurement of the axonal protein neurofilament light in plasma. Microglial activation was assessed using 11C-PBR28 PET. The relationships of microglial activation to measures of brain injury, and the effects of minocycline on disease progression, were assessed using structural and diffusion MRI, plasma neurofilament light, and cognitive assessment. Fifteen patients at least 6 months after a moderate-to-severe traumatic brain injury received either minocycline 100 mg orally twice daily or no drug, for 12 weeks. At baseline, 11C-PBR28 binding in patients was increased compared to controls in cerebral white matter and thalamus, and plasma neurofilament light levels were elevated. MRI measures of white matter damage were highest in areas of greater 11C-PBR28 binding. Minocycline reduced 11C-PBR28 binding (mean Δwhite matter binding = −23.30%, 95% confidence interval −40.9 to −5.64%, P = 0.018), but increased plasma neurofilament light levels. Faster rates of brain atrophy were found in patients with higher baseline neurofilament light levels. In this experimental medicine study, minocycline after traumatic brain injury reduced chronic microglial activation while increasing a marker of neurodegeneration. These findings suggest that microglial activation has a reparative effect in the chronic phase of traumatic brain injury.
Tan CL, Alavi SA, Baldeweg SE, et al., 2017, The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance, JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Vol: 88, Pages: 971-981, ISSN: 0022-3050
Pituitary dysfunction is a recognised, but potentially underdiagnosed complication of traumatic brain injury (TBI). Post-traumatic hypopituitarism (PTHP) can have major consequences for patients physically, psychologically, emotionally and socially, leading to reduced quality of life, depression and poor rehabilitation outcome. However, studies on the incidence of PTHP have yielded highly variable findings. The risk factors and pathophysiology of this condition are also not yet fully understood. There is currently no national consensus for the screening and detection of PTHP in patients with TBI, with practice likely varying significantly between centres. In view of this, a guidance development group consisting of expert clinicians involved in the care of patients with TBI, including neurosurgeons, neurologists, neurointensivists and endocrinologists, was convened to formulate national guidance with the aim of facilitating consistency and uniformity in the care of patients with TBI, and ensuring timely detection or exclusion of PTHP where appropriate. This article summarises the current literature on PTHP, and sets out guidance for the screening and management of pituitary dysfunction in adult patients with TBI. It is hoped that future research will lead to more definitive recommendations in the form of guidelines.
Feeney C, Sharp DJ, Hellyer PJ, et al., 2017, Serum IGF-I levels are associated with improved white matter recovery after TBI., Annals of Neurology, Vol: 82, Pages: 30-43, ISSN: 0364-5134
OBJECTIVE: Traumatic brain injury (TBI) is a common disabling condition with limited treatment options. Diffusion tensor imaging (DTI) measures recovery of axonal injury in white matter (WM) tracts after TBI. Growth hormone deficiency (GHD) after TBI may impair axonal and neuropsychological recovery, and serum IGF-I may mediate this effect. We conducted a longitudinal study to determine the effects of baseline serum IGF-I concentrations on WM tract and neuropsychological recovery after TBI. METHODS: Thirty-nine adults after TBI (84.6% male; age median 30.5y; 87.2% moderate-severe; time since TBI median 16.3 months, n=4 with GHD) were scanned twice, 13.3 months (12.1-14.9) apart, and 35 healthy controls scanned once. Symptom and quality of life questionnaires and cognitive assessments were completed at both visits (n=33). Our main outcome measure was fractional anisotropy (FA), a measure of WM tract integrity, in a priori regions of interest: splenium of corpus callosum (SPCC), and posterior limb of internal capsule (PLIC). RESULTS: At baseline, FA was reduced in many WM tracts including SPCC and PLIC following TBI compared to controls, indicating axonal injury, with longitudinal increases indicating axonal recovery. There was a significantly greater increase in SPCC FA over time in patients with serum IGF-I above vs. below the median-for-age. Only the higher IGF-I group had significant improvements in immediate verbal memory recall over time. INTERPRETATION: WM recovery and memory improvements after TBI were greater in patients with higher serum IGF-I at baseline. These findings suggest that GH/IGF-I system may be a potential therapeutic target following TBI. This article is protected by copyright. All rights reserved.
Record C, De Simoni S, Feeney C, et al., 2016, Improved cerebral blood flow after natalizumab treatment in multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE Publications, Pages: 669-669, ISSN: 1352-4585
O'Shea T, Feeney C, Wise R, et al., 2016, Post-traumatic amnesia, but not acute CT findings is predictive of pituitary dysfunction following traumatic brain injury, IRISH JOURNAL OF MEDICAL SCIENCE, Vol: 185, Pages: 400-401, ISSN: 0021-1265
Feeney C, Scott GP, Cole JH, et al., 2016, Seeds of neuroendocrine doubt, Nature, Vol: 535, Pages: E1-E2, ISSN: 0028-0836
Feeney C, Scott G, Raffel J, et al., 2016, Kinetic analysis of the translocator protein positron emission tomography ligand [18F]GE-180 in the human brain, European Journal of Nuclear Medicine and Molecular Imaging, Vol: 43, Pages: 2201-2210, ISSN: 1619-7089
PURPOSE: PET can image neuroinflammation by targeting the translocator protein (TSPO), which is upregulated in activated microglia. The high nonspecific binding of the first-generation TSPO radioligand [(11)C]PK-11195 limits accurate quantification. [(18)F]GE-180, a novel TSPO ligand, displays superior binding to [(11)C]PK-11195 in vitro. Our objectives were to: (1) evaluate tracer characteristics of [(18)F]GE-180 in the brains of healthy human subjects; and (2) investigate whether the TSPO Ala147Thr polymorphism influences outcome measures. METHODS: Ten volunteers (five high-affinity binders, HABs, and five mixed-affinity binders, MABs) underwent a dynamic PET scan with arterial sampling after injection of [(18)F]GE-180. Kinetic modelling of time-activity curves with one-tissue and two-tissue compartment models and Logan graphical analysis was applied to the data. The primary outcome measure was the total volume of distribution (V T) across various regions of interest (ROIs). Secondary outcome measures were the standardized uptake values (SUV), the distribution volume and SUV ratios estimated using a pseudoreference region. RESULTS: The two-tissue compartment model was the best model. The average regional delivery rate constant (K 1) was 0.01 mL cm(-3) min(-1) indicating low extraction across the blood-brain barrier (1 %). The estimated median V T across all ROIs was also low, ranging from 0.16 mL cm(-3) in the striatum to 0.38 mL cm(-3) in the thalamus. There were no significant differences in V T between HABs and MABs across all ROIs. CONCLUSION: A reversible two-tissue compartment model fitted the data well and determined that the tracer has a low first-pass extraction (approximately 1 %) and low V T estimates in healthy individuals. There was no observable dependency on the rs6971 polymorphism as compared to other second-generation TSPO PET tracers. Investigation of [(18)F]GE-180 in populations with neuroinflammatory disease is nee
Zimmerman K, Scott G, Violante I, et al., 2016, Magnetic resonance spectroscopy of the thalamus in chronic traumatic brain injury, International Brain Injury Association’s Eleventh World Congress on Brain Injury, Publisher: Taylor &; Francis, Pages: 660-661, ISSN: 1362-301X
Ritchie AE, Lee V, Feeney C, et al., 2016, Using Nonechoplanar Diffusion-weighted MRI to Assess Treatment Response in Active Graves Orbitopathy: A Novel Approach with 2 Case Reports, OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY, Vol: 32, Pages: E67-E70, ISSN: 0740-9303
- Author Web Link
- Citations: 7
Jamall O, Feeney C, Zaw-Linn J, et al., 2016, Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury, Clinical Endocrinology, Vol: 85, Pages: 636-644, ISSN: 1365-2265
Objectives: Traumatic brain injury (TBI) is a major cause of long-term disability with variable recovery. Preclinicalstudies suggest that vitamin D status influences recovery after TBI. However, there is no publishedclinical data on links between vitamin D status and TBI outcomes. To determine the: (i) prevalence ofvitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors andTBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI.Design: Retrospective audit of patients seen between July 2009 and March 2015. Serum vitamin D (25-hydroxy-cholecalciferol) was categorised as deficient (<40nmol/L), insufficient (40-70nmol/L) or replete(>70nmol/L).Patients: 353 adults seen in tertiary hospital clinic (75.4% lighter-skinned, 74.8% male, age median 35.1y,range 26.6-48.3y), 0.3-56.5 months after TBI (74.5% moderate-severe).Measurements: Serum vitamin D concentrations; Addenbrooke’s Cognitive Examination (ACE-R), BeckDepression Inventory II (BDI-II), SF-36 Quality of Life, Pittsburgh Sleep Quality Index.Results: 46.5% of patients after TBI had vitamin D deficiency and 80.2% insufficiency/deficiency. Patientswith vitamin D deficiency had lower ACE-R scores than those vitamin D replete (mean effect size ± SEM 4.5± 2.1, P=0.034), and higher BDI-II scores than those vitamin D insufficient (4.5 ± 1.6, P=0.003), correcting forage, gender, time since TBI, TBI severity. There was no association between vitamin D status and markers ofTBI severity, sleep or quality of life.Conclusion: Vitamin D deficiency is common in patients after TBI and associated with impaired cognitivefunction and more severe depressive symptoms.
Gorgoraptis N, Zaw-Linn J, Feeney C, et al., 2015, THE IMPACT OF TRAUMATIC BRAIN INJURY ON PATIENT-REPORTED PHYSICAL AND MENTAL HEALTH, Annual Meeting of the Association-of-British-Neurologists (ABN), Publisher: BMJ PUBLISHING GROUP, ISSN: 0022-3050
Baxter D, Sharp DJ, Feeney C, et al., 2013, Pituitary Dysfunction after Blast Traumatic Brain Injury: The UK BIOSAP Study, ANNALS OF NEUROLOGY, Vol: 74, Pages: 527-536, ISSN: 0364-5134
- Author Web Link
- Citations: 55
Feeney CL, Meeran K, Hatfield E, et al., 2010, Complete Adrenal Failure Following Treatment of Cushing's Disease with Mitotane., 92nd Meeting and Expo of the Endocrine Society (ENDO 2010), Publisher: ENDOCRINE SOC, ISSN: 0163-769X
Feeney CL, Roberts NJ, Partridge MR, 2005, Do medical outpatients want 'out of hours' clinics?, BMC HEALTH SERVICES RESEARCH, Vol: 5, ISSN: 1472-6963
- Author Web Link
- Citations: 7
Feeney CL, Roberts NJ, Partridge MR, 2004, Do medical outpatients want "out of hours" clinics?, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: 87-88, ISSN: 0040-6376
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