IntroductionTolosa Hunt syndrome (THS) is a disorder that is related to inflammation of cavernous sinus (CS) as well as superior orbital fissure although the exact etiology is unknown.1 THS affects any age group (10-80 yr.) and can present with headache, ophthalmoplegia, oculomotor nerve palsies or even loss of visual acuity. The duration of symptoms ranges from days to weeks and they can be ipsilateral or even contralateral. Moreover, recurrence of symptoms has been noted in some cases despite the initial remission.Currently, the neuroimaging modalities that are performed for the diagnosis of THS are MRI and high-resolution CT scans. However, the review of the literature shows that CT scan is less sensitive than MRI scan. 4 Other laboratory tests performed in cases of suspected THS are blood tests (complete blood count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)). THS seems to be associated with leukocytosis and raised erythrocytes sendimentation rate5. Usually the treatment for THS involves intravenous corticosteroid administration. However, some studies have reported the efficacy of immunosuppression therapy such as cyclosporin or methotrexate6 while even infliximab has been reported as a successful treatment to a patient with steroid resistant THS.7THS is a diagnosis of exclusion, as other causes can mimic this condition. The differential diagnosis includes neoplastic conditions such as meningioma or chordoma, vascular conditions such as intracavernous artery or posterior artery aneurysms, and finally inflammatory conditions such as sinusitis, or sarcoidosis5. Therefore, every patient should be evaluated thoroughly before the diagnosis is confirmed.Cavernous carotid aneurysm (CCA) accounts for 2-9% of all internal carotid aneurysms. The causes for CCA include trauma, inflammation or idiopathic. Usually patients are asymptomatic in the first stages of the aneurysm but as it is enlarged the patients manifest diplopia, ptosis, ophthalmoplegia. Finally, one must underline the possibility of aneurysm rupture, that requires prompt medical intervention and in the majority of cases can be fatal.In our study we present a patient suffering from an intracavernous aneurysm (ICA) mimicking Tolosa Hunt syndrome.

Dear Editor,We reviewed the article entitled: “Analysis of reflux as the etiology of laryngeal dysplasia progression through a matched case-control study ”.1 The authors did not find differences in the level of pepsin, enterokinase and bilirubin in laryngeal dysplasia (LD) of patients with malignant transformationversus those without transformation. The involvement of reflux in the development of LD and laryngeal cancers is an important topic and the realization of such a study is important. However, we wish to draw attention to many points.First, it is difficult to know if the included patients with tissue pepsin really suffered from reflux. The detection of pepsin into the tissue means that patients had some pharyngeal reflux events the day before the surgery but cannot confirm the diagnosis. The sensitivity of pepsin detection in laryngeal tissue depends on the technique and the material (antibodies), reaching 75 to 85% depending on the type of reflux (acid versus nonacid).2 Moreover, we have no detailed information about the immunostaining technique, limiting the reproducibility of the protocol. The presence of pepsin into the tissue does not ensure the reflux diagnosis. Thus, for example, it has been showed that the back flow of gastric content and the deposit of pepsin into the tissue are influenced by the meals preceding the sample collection, making the pepsin tissue a poorly reliable marker of reflux.3 To improve the sensitivity, authors1 could have performed hypopharyngeal-esophageal pH-impedance monitoring, which is the only way to confirm the diagnosis.4Second, the LD malignant transformation involves many factors such as tobacco history, environmental factors, genetic, or immune response.5 The authors did not provide information about the tobacco history (pack-year data) of groups, which is an important data to consider the risk of malignant transformation. Even many years after the tobacco cessation, it is conceivable that patients with long/more severe history of tobacco consumption may have more cell mucosa DNA impairments and a higher risk to develop cancer.Third, the focus on pepsin as the only enzyme associated with malignant transformation limits the understanding of transformation mechanisms. More than 50% of patients had mixed or nonacid reflux,4 in which the activity of pepsin is decreased regarding the alkaline pH of refluxate. To reliably investigate the involvement of reflux in the malignant transformation, authors have to consider the entire content of refluxate, including bile salts and trypsin.4 Furthermore, bile salts may be involved in laryngopharyngeal malignant transformation.6In future studies, reflux has to be diagnosed at the LD diagnosis time and physicians have to follow the reflux clinical course over the time. More than 50% of reflux patients had chronic course,4which leads to a potential higher risk to develop cell DNA damage and lesions. Thus, cross-sectional study design is probably not adequate to study a disease association involving chronic and repeated exposure.Acknowledgments: No.