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        Percutaneous Radiofrequency Thermocoagulation in Trigeminal Neuralgia : Analysis of Early and Late Outcomes of 156 Cases and 209 Interventions

        Gunduz, Hasan Burak,Cevik, Orhun Mete,Asilturk, Murad,Gunes, Muslum,Uysal, Mustafa Levent,Sofuoglu, Ozden Erhan,Emel, Erhan The Korean Neurosurgical Society 2021 Journal of Korean neurosurgical society Vol.64 No.5

        Objective : Trigeminal neuralgia is one of the most common causes of facial pain. Our aim is to investigate the efficacy and borders of percutaneous radiofrequency thermocoagulation in the treatment of trigeminal neuralgia. Methods : Between May 2007 and April 2017, 156 patients with trigeminal neuralgia were treated with radiofrequency thermocoagulation. These 156 patients underwent 209 procedures. In our study, we investigated the early and late results of percutaneous radiofrequency thermocoagulation under guiding fluoroscopic imaging in the treatment of trigeminal neuralgia. Barrow Neurological Institute (BNI) pain scale was used for grading the early results. In addition, Kaplan-Meier survival analysis was used to assess long-term outcomes. Of the 156 patients who underwent radiofrequency thermocoagulation for trigeminal neuralgia, 45 had additional disease. Patients with this condition were evaluated with their comorbidities. Early and late results were compared with those without comorbidity. Results : In 193 of 209 interventions BNI pain scale I to III results were obtained. Out of the 193 successful operation 136 patients (65.07%) were discharged as BNI I, 14 (6.70%) as BNI II, 43 (20.58%) as BNI III. Sixteen patients (7.65%) remained uncontrolled (BNI IV and V). While the treatment results of trigeminal neuralgia patients with comorbidity seem more successful in the early period, this difference was not observed in follow-up examinations. Conclusion : Finally, we concluded that percutaneous radiofrequency thermocoagulation of the Gasserian ganglion is a safe and effective method in the treatment of trigeminal neuralgia. However, over time, the effectiveness of the treatment decreases. Neverthless, the reapprability of this intervention gives it a distinct advantage.

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        The Effects of Galantamine Hydrobromide Treatment on Dehydroepiandrosterone Sulfate and Cortisol Levels in Patients with Chronic Fatigue Syndrome

        Tayfun Turan,Hasan Basri Izgi,Saliha Ozsoy,Fatih Tanrıverdi,Mustafa Basturk,Akif Asdemir,Aslı Beşirli,Ertugrul Esel,Seher Sofuoglu 대한신경정신의학회 2009 PSYCHIATRY INVESTIGATION Vol.6 No.3

        Objective: Mental fatigue, cognitive disorders, and sleep disturbances seen in chronic fatigue syndrome (CFS) may be attributed to cholinergic deficit. A functional deficiency of cholinergic neurotransmission may cause the hypothalamic-pituitary-adrenal axis hypoactivity seen in CFS. Therefore, we investigated the alterations in stress hormones such as cortisol and dehydroepiandrosterone sulfate (DHEAS) in CFS patients before and after 4- week administration of galantamine hydrobromide, a selective cetylcholinesterase inhibitor, and aimed to investigate whether there are any relationships between the probable hormonal changes and cholinergic treatment. Methods: Basal levels of cortisol and DHEAS were measured in 29 untreated CFS patients who were diagnosed according to Centers for Disease Control (CDC) criteria and in 20 healthy controls. In the patient group, four weeks after 8 ㎎/d galantamine hydrobromide treatment, cortisol and DHEAS levels were measured again. After the treatment 22 patients who stayed in study were divided into two subgroups as responders and nonresponders according to the reduction in their Newcastle Research Group ME/CFS Score Card (NRG) scores. Results: Important findings of this study are lower pre-and post-treatment cortisol levels and in all CFS patients compared to controls (F=4.129, p=0.049; F=4.803, p=0.035, respectively); higher basal DHEAS values and higher DHEAS/cortisol molar ratios which were normalized following four weeks’ treatment with 8 ㎎/d galantamine hydrobromide in the treatment-respondent group (F=5.382, p=0.029; F=5.722, p=0.025, respectively). Conclusion: The findings of the decrease in basal DHEAS levels and DHEAS/cortisol molar ratios normalizing with galantamine treatment may give some support to the cholinergic deficit hypothesis in CFS. Objective: Mental fatigue, cognitive disorders, and sleep disturbances seen in chronic fatigue syndrome (CFS) may be attributed to cholinergic deficit. A functional deficiency of cholinergic neurotransmission may cause the hypothalamic-pituitary-adrenal axis hypoactivity seen in CFS. Therefore, we investigated the alterations in stress hormones such as cortisol and dehydroepiandrosterone sulfate (DHEAS) in CFS patients before and after 4- week administration of galantamine hydrobromide, a selective cetylcholinesterase inhibitor, and aimed to investigate whether there are any relationships between the probable hormonal changes and cholinergic treatment. Methods: Basal levels of cortisol and DHEAS were measured in 29 untreated CFS patients who were diagnosed according to Centers for Disease Control (CDC) criteria and in 20 healthy controls. In the patient group, four weeks after 8 ㎎/d galantamine hydrobromide treatment, cortisol and DHEAS levels were measured again. After the treatment 22 patients who stayed in study were divided into two subgroups as responders and nonresponders according to the reduction in their Newcastle Research Group ME/CFS Score Card (NRG) scores. Results: Important findings of this study are lower pre-and post-treatment cortisol levels and in all CFS patients compared to controls (F=4.129, p=0.049; F=4.803, p=0.035, respectively); higher basal DHEAS values and higher DHEAS/cortisol molar ratios which were normalized following four weeks’ treatment with 8 ㎎/d galantamine hydrobromide in the treatment-respondent group (F=5.382, p=0.029; F=5.722, p=0.025, respectively). Conclusion: The findings of the decrease in basal DHEAS levels and DHEAS/cortisol molar ratios normalizing with galantamine treatment may give some support to the cholinergic deficit hypothesis in CFS.

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