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Background and purpose There is a lack of comparative safety data on the risk of pseudotumor cerebri syndrome (PTCS) associated with different hormonal contraceptives. We sought to quantify the risk of PTCS associated with eight different types of hormonal contraceptives compared with oral levonorgestrel. Methods We conducted a retrospective cohort study, with a case-control analysis of 4 871 504 women aged 15-45 years in the period 2008-2015, using IQVIA Ambulatory Electronic Medical Records data in the USA. Patients who used nine different contraceptive agents including intrauterine levonorgestrel, medroxyprogesterone injection, etonogestrel/ethinyl estradiol vaginal ring and combination oral contraceptives (COCs) that contained ethinyl estradiol and the progestins levonorgestrel, norgestimate, desogestrel, norethindrone and drospirenone, were included. Diagnosis of PTCS was defined using the first International Classification of Diseases, 9th or 10th revision, code for intracranial hypertension in patients who had also received an imaging code in the 30 days prior to the index date. Results A total of 3323 PTCS cases and 13 292 matched controls were identified. No increase in risk was found when analysing intrauterine levonorgestrel or COCs containing desogestrel, norethindrone, drospirenone, norgestimate or norgestrel versus COC levonorgestrel. The adjusted incidence rate ratio for etonogestrel/etonogestrel/ethinyl estradiol vaginal ring and medroxyprogesterone suspension compared with levonorgestrel COC was 4.45 [95% confidence interval (CI) 1.98-9.96] and 2.20 (95% CI 1.33-3.64), respectively. Conclusions This study found an elevated risk for PTCS among users of etonogestrel vaginal ring and medroxyprogesterone suspension when compared with oral levonorgestrel. Future studies are needed to confirm these findings.

Purpose To develop and validate neural network (NN) vs logistic regression (LR) diagnostic prediction models in patients with suspected giant cell arteritis (GCA). Design: Multicenter retrospective chart review. Methods An audit of consecutive patients undergoing temporal artery biopsy (TABx) for suspected GCA was conducted at 14 international medical centers. The outcome variable was biopsy-proven GCA. The predictor variables were age, gender, headache, clinical temporal artery abnormality, jaw claudication, vision loss, diplopia, erythrocyte sedimentation rate, C-reactive protein, and platelet level. The data were divided into three groups to train, validate, and test the models. The NN model with the lowest false-negative rate was chosen. Internal and external validations were performed. Results Of 1,833 patients who underwent TABx, there was complete information on 1,201 patients, 300 (25%) of whom had a positive TABx. On multivariable LR age, platelets, jaw claudication, vision loss, log C-reactive protein, log erythrocyte sedimentation rate, headache, and clinical temporal artery abnormality were statistically significant predictors of a positive TABx (P≤0.05). The area under the receiver operating characteristic curve/Hosmer-Lemeshow P for LR was 0.867 (95% CI, 0.794, 0.917)/0.119 vs NN 0.860 (95% CI, 0.786, 0.911)/0.805, with no statistically significant difference of the area under the curves (P=0.316). The misclassification rate/false-negative rate of LR was 20.6%/47.5% vs 18.1%/30.5% for NN. Missing data analysis did not change the results. Conclusion Statistical models can aid in the triage of patients with suspected GCA. Misclassification remains a concern, but cutoff values for 95% and 99% sensitivities are provided (https://goo.gl/THCnuU).

An infant presented with bilateral disk edema and an acute left sixth cranial nerve (CN VI) palsy because of pseudotumor cerebri (PTC). PTC is rare in infants where it is often associated with endocrine abnormalities, medications, viral infections, systemic conditions, and nutritional etiologies such as vitamin A toxicity. We report a case of PTC in an infant associated with hypervitaminosis A with an unlikely source-a common prenatal vitamin.

Objectives The objectives of the present study were: (i) to examine the leading clinical indications and pathologic diagnoses of penetrating keratoplasties in Vancouver, BC; and (ii) to evaluate the correlation between the clinical and pathologic diagnoses. Design Retrospective chart review of all pathologic records of corneal tissue submitted to the Department of Pathology & Laboratory Medicine, Vancouver General Hospital, during an 11-year period. Methods For each penetrating keratoplasty, information regarding the clinical indication and pathologic features identified on histopathologic analysis was compiled. Results The top 5 clinical indications for transplant were failed graft (21%); bullous keratopathy (20%); keratoconus (17%); scarring, with or without inflammation (14%); and Fuchs dystrophy (11%). The top 5 pathologic diagnoses corresponded to these clinical diagnoses. In the majority of cases, there was agreement between clinical and pathologic diagnoses; however, in 6% of records, the clinical and pathologic diagnoses did not correlate. This situation occurred most often when considering grafts with clinical diagnoses of bullous keratopathy, Fuchs dystrophy, or keratoconus. A review of the grafts with infectious keratitis illustrated the potential for histopathologic evaluation of corneal buttons to identify unsuspected infectious agents. Conclusion Routine histopathologic evaluation of penetrating keratoplasty clarifies the clinical diagnosis in a proportion of cases and aids in identifying infectious agents.

Purpose: Vitamin A deficiency is a very rare condition in the developed world and can lead to a variety of ocular changes from xerosis and xerophthalmia to corneal ulcer and perforation. The treatment of this devastating disease is simple and inexpensive. It is therefore important to recognize and treat accordingly, especially in the event of ulcers unresponsive to treatment or in the presence of severe malnutrition/malabsorption syndromes. The purpose of this case report is to remind physicians of the potentially devastating effects of vitamin A deficiency on the eyes and to demonstrate outcomes after vitamin A treatment. Methods: Single observational case report. Results: A 29-year-old male with known eosinophilic gastroenteropathy was treated with oral steroids for peripheral ulcerative keratitis. Two weeks after resolution, the patient suffered from peripheral ulcerative keratitis in his other eye, with a self-sealing perforation. Vitamin A deficiency was confirmed and successfully treated, leading to subsequent resolution of signs and symptoms. Conclusions: Vitamin A deficiency can be present in patients with malabsorption and malnutrition syndromes and should be considered as cause of corneal ulceration.

The reading of text is predominantly a left hemisphere function. However, it is also possible to process text for attributes other than word or letter identity, such as style of font or handwriting. Anecdotal observations have suggested that processing the latter may involve the right hemisphere. We devised a test that, using the identical stimuli, required subjects first to match on the basis of word identity and second to match on the basis of script style. We presented two versions, one using various computer fonts, and the other using the handwriting of different individuals. We tested four subjects with unilateral lesions who had been well characterized by neuropsychological testing and structural and/or functional MRI. We found that two prosopagnosic subjects with right lateral fusiform damage eliminating the fusiform face area and likely the right visual word form area were impaired in completion times and/or accuracy when sorting for script style, but performed better when sorting for word identity. In contrast, one alexic subject with left fusiform damage showed normal accuracy for sorting by script style and normal or mildly elevated completion times for sorting by style, but markedly prolonged reading times for sorting by word identity. A prosopagnosic subject with right medial occipitotemporal damage sparing areas in the lateral fusiform gyrus performed well on both tasks. The contrast in the performance of patients with right versus left fusiform damage suggests an important distinction in hemispheric processing that reflects not the type of stimulus but the nature of processing required.

A case of giant cell arteritis was diagnosed in a woman who presented with bilateral loss of vision that did not improve with intravenous corticosteroid therapy. Preceding her vision loss, the patient had other symptoms consistent with this diagnosis, notably significant jaw pain and arthralgias. The diverse symptoms of giant cell arteritis are discussed, along with the features that can be used to distinguish jaw pain associated with this condition from the pain of temporomandibular joint pathology. An increased awareness of giant cell arteritis should lead to earlier diagnosis and treatment and avoidance of the devastating consequences of this condition.

The effects of anoxia on intracellular pH (pHi) were examined in acutely isolated adult rat hippocampal CA1 neurons loaded with the H+-sensitive fluorophore, 2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein. During perfusion with HCO[Formula: see text]/CO2- or HEPES-buffered media (pH 7.35) at 37°C, 5- or 10-min anoxic insults were typified by an intracellular acidification on the induction of anoxia, a subsequent rise in pHiin the continued absence of O2, and a further internal alkalinization on the return to normoxia. The steady-state pHichanges were not consequent on changes in [Ca2+]iand, examined in the presence of HCO[Formula: see text], were not significantly affected by (DIDS). In the absence of HCO[Formula: see text], the magnitude of the postanoxic alkalinization was attenuated when external Na+was reduced by substitution with N-methyl-d-glucamine (NMDG+), but not Li+, suggesting that increased Na+/H+exchange activity contributes to this phase of the pHiresponse. In contrast, 100–500 μM Zn2+, a known blocker of H+-conductive pathways, reduced the magnitudes of the internal alkalinizations that occurred both during and following anoxia. The effects of NMDG+-substituted medium and Zn2+to reduce the increase in pHithat occurred after anoxia were additive. Consistent with the steady-state pHichanges, rates of pHirecovery from internal acid loads imposed immediately after anoxia were increased, and the application of Zn2+and/or perfusion with NMDG+-substituted medium slowed pHirecovery. Reducing extracellular pH from 7.35 to 6.60, or reducing ambient temperature from 37°C to room temperature, also attenuated the increases in steady-state pHiobserved during and after anoxia and reduced rates of pHirecovery from acid loads imposed in the immediate postanoxic period. Finally, inhibition of the cAMP/protein kinase A second-messenger system reduced the magnitude of the rise in pHiafter anoxia in a manner that was dependent on external Na+; conversely, activation of the system with isoproterenol increased the postanoxic alkalinization, an effect that was attenuated by pretreatment with propranolol, Rp-cAMPS, or when NMDG+(but not Li+) was employed as an external Na+substitute. The results suggest that a Zn2+-sensitive acid efflux mechanism, possibly a H+-conductive pathway activated by membrane depolarization, contributes to the internal alkalinization observed during anoxia in adult rat CA1 neurons. The rise in pHiafter anoxia reflects acid extrusion via the H+-conductive pathway and also Na+/H+exchange, activation of the latter being mediated, at least in part, through a cAMP-dependent signaling pathway.