Reversible Anorgasmia with Acetazolamide Treatment for Idiopathic Intracranial Hypertension

Dear Editor, Idiopathic intracranial hypertension (IHH) is a clinical disorder characterized by symptoms and signs of increased intracranial pressure without abnormal cerebrospinal fluid composition and structural parenchymal abnormalities (1,2). There is no related systemic disorder and its etiology is unknown yet. Patients usually present with headache, vomiting, visual loss, and diplopia. Bilateral papilledema is found in most cases as a neurological sign and acetazolamide is an effective drug for the treatment of IIH. Acetazolamide is a carbonic anhydrase inhibitor and has been used for many relatively common disorders such as congestive heart failure, some forms of epilepsy, glaucoma, IHH, and also for some rare diseases such as acute mountain sickness. Paresthesia, fatigue, taste alterations, vomiting, and polyuria are common side effects of the treatment with acetazolamide. Usually acetazolamide is well tolerated, and sometimes this treatment may be associated with anorgasmia and this effect is thought to be dose related. Organic impotence has been reported in glaucoma patient therapy with acetazolamide. In this paper, we report a case admitted to our hospital that developed anorgasmia during treatment with acetazolamide. The patient, a 25-year-old female was admitted to the neurology department of our university hospital due to presence of anorgasmia. Previously, the patient had applied to a center for headache, nausea and vomiting, and visual loss, which had persisted for the past three months. The patient was evaluated with brain magnetic resonance imaging, in addition to examination of the cerebrospinal fluid and the other possible reasons of headache. Other possible causes of bilateral papilledema were ruled out; therefore, she was diagnosed with IIH and was started with appropriate treatment at our center. The patient reported that she was taking acetazolamide for IIH treatment orally during the last 15 days with an onset dosage of 750 mg/day, increased to 1500 mg/day after the 7 th day of usage. She was not using antidepressants, antipsychotics, or any other medications. The patient reported that the anorgasmia appeared during the last 5 days of acetazolamide treatment (three days after the onset of 1500 mg/days dosage). Except for the bilateral papilledema and light visual loss, the physical, psychiatric, gynecological, and neurological examinations as well as the brain magnetic resonance imaging were normal. Routine blood and hormonal tests were also normal. When the acetazolamide was decreased to 1000 mg/day, the anorgasmia resolved within 7 days. Female orgasmic disorder is characterized by the persistent or recurrent delay in, or absence of orgasm following a normal sexual excitement phase. Anorgasmia is defined as failure to achieve orgasm (climax) during sexual intercourse. Anorgasmia has many causes, it is believed that approximately 90% of anorgasmia problems are related to psychological issues, and some cases may result from the use of certain drugs such as serotoninergic drugs including antidepressants (particularly selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors), antiepileptic, and antipsychotic drugs (3,4). The new onset of the patient' s complaints, the lack of any additional drug use, and the absence of previous similar complaints suggested that the present anorgasmia was due to acetazolamide. We believe that acetazolamide treatment produced a dose-related anorgasmia in our patient. To the best of our knowledge, no other case of acetazolamide induced reversible anorgasmia has been reported previously for a female patient. It is difficult to present the precise mechanism between acetazolamide and anorgasmia. Acetazolamide is an enzyme inhibitor that acts on carbonic anhydrase specifically and catalyzes the reversible reaction of hydration of carbon dioxide and dehydration of carbonic acid. Although the underlying neurochemical changes of anorgasmia are not fully understood, orgasm, in both sexes, is particularly controlled by noradrenergic activity. Serotonin and dopamine are also essentia

Delirium in patients with acute ischemic stroke admitted to the non-intensive stroke unit: Incidence and association between clinical features and inflammatory markers

Background Stroke patients with development of delirium have unfavorable outcomes, higher mortality, longer hospitalizations, and a greater degree of dependence after discharge. Studies suggest that delirium is associated with abnormal immunological responses and a resultant increase in inflammatory markers. Objective Our aim was to determine whether there is an entity relationship between delirium, inflammation and acute ischemic stroke (AIS). Methods Sixty AIS patients admitted to the hospital were consecutively recruited. Delirium was diagnosed with the clinical assessment according to the Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) criteria. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of Interleukin-1 beta (IL-1 beta), Interleukin 18 (IL-18), Tumor Necrosis Factor-alpha (TNF-alpha), Brain-Derived Neurotrophic Factor (BDNF), and Neuron Specific Enolase (NSE) at admission. Results Eleven (18.3%) of 60 patients were diagnosed with delirium, and the majority (n=8, 72.7%) was the hypoactive type. Delirious and non-delirious patients had similar demographic and clinical features. Delirious patients had significantly higher lengths of hospital stay, National Institutes of Health Stroke Scale (NIHSS) at admission and discharge compared to non-delirious patients. In addition, there was no significant statistical difference between delirious and non-delirious patients with AIS in respect of levels of TNF-alpha, IL-1 beta, IL-18, BDNF and NSE. This study suggests that delirium is not scarce in patients with AIS admitted to the non-intensive stroke unit, and that delirium developing after AIS seems not to be associated with serum TNF-alpha, IL-1 beta, IL-18, BDNF and NSE but is associated with length of hospital stay and stroke severity

Kronik böbrek yetmezliğinde göz kırpma refleksi değişiklikleri

Supraorbital sinirin tek taraflı olarak yüzeyel bipolar elektrotlar ile uyartılmasıve yüzeyel elektrotlar ile orbikülaris oküli kaslarından iki taraflı kayıtlanmasısonrasında elde edilebilen polisinaptik refleks Göz Kırpma Refleksi (GKR) olarakbilinir. SOS'un uyartılması ile orbikülaris oküli kaslarından elde edilen yanıtlar erkenipsilateral R1, geç bilateral R2 yanıtlarıdır. GKR'nin afferent arkını trigeminal sinirinduysal lifleri, efferent arkını ise fasiyal sinirin motor lifleri oluşturur. Klinik vepatolojik çalışmalar da, R1'in ponsta V. kranial sinirin ana duyusal çekirdeğiüzerinden, R2'nin medulla oblangatada spinal çekirdek ve V. sinir üzerindenyayıldığını ileri sürmüştür. Bu yüzden beyin sapı fonksiyonunu değerlendirmede gözkırpma refleks çalışmaları uzun yıllardır kullanılmaktadır.Kronik böbrek yetmezliği, periferik ve santral sinir sistemini, hastalığın diğersistemler üzerindeki olumsuz etkisinden, daha sık olarak etkilemektedir. KBY'deperiferik nöropati prevalansı, böbrek yetersizliğinin şiddet ve süresine bağlı olarak %10 ile % 80 arasında değişmektedir. Üreminin, toksik etkileri bilinen metabolikkomponentlerinin ve de dializ ile ilişkili metabolik değişikliklerin beyin ve beyinsapında bazı bölgelerde değişiklikler yaptığı bilinmektedir. Göz kırpma refleksçalışmaları kronik böbrek yetmezliğinde 1987'den beri santral sinir sistemifonksiyonunu değerlendirmede kullanılagelmektedir.Bu çalışmada otuzbeş hemodiyaliz otuzbeş periton diyalizi hastasında; kronikböbrek yetmezliği, hemodiyaliz ve periton diyalizinin periferik ve santral sinir sistemiüzerine etkilerini araştırmak amacıyla polinöropati ve göz kırpma refleks ölçümleriyapılarak kontrol grubu ile karşılaştırıldı.KBY olan olgular kontrol grubu ile karşılaştırıldığında R2i ve R2k yanıtlarındaanlamlı derecede uzama bulunmuştur. Ayrıca, polinöropati tespit edilen hemodiyaliz53hastalarında R2 yanıtları, polinöropati tespit edilen periton diyaliz hastalarına göre anlamlıderecede uzun bulunmuştur. R1 yanıtları etkilenmemiştir. Ekstra-aksiyal lezyonlarda R2,R1'e göre daha az duyarlıdır, fakat intra-aksiyal lezyonlarda R2 anormalliği kısa latanslıcevaplar kadar sıktır, R2 daha komplekstir ve medullanın kaudaline kadar yayılır.Dolayısıyla kronik böbrek yetmezliği olan tüm hastalarda R1'in korunmuş olup R2'lerinuzamış bulunması kronik böbrek yetmezliğinde subklinik düzeyde ekstra-aksiyaletkilenmeden çok, intra-aksiyal etkilenmenin olduğunu gösterir. Polinöropatisi olanhemodiyaliz ve periton diyalizi hastalarında R1 komponenti R2 değerleri ilekarşılaştırıldığında daha yüksek oranda elde edilememiştir. Bu bulgular göz kırpmarefleksinin R1 komponentinin eksteroseptif, orta çaplı myelinli A-beta lifleri iletaşındığını; R2 komponentinin ise nosiseptif, ince myelinli A-delta lifleri ile taşındığınıdestekler. Periton diyalizine giren polinöropatisi olan hastalar kontrol grubu ilekarşılaştırıldığında R1 , R2i, R2k değerleri açısından anlamlı bir fark bulunamamıştır.Hemodiyalize giren polinöropatisi olan hastalar kontrol grubu ile karşılaştırıldığında R1değerleri korunmuş, buna karşın R2i, R2k değerlerinde anlamlı uzama bulunmuştur. Bu dahemodiyalize giren hastalarda intra-aksiyal subklinik etkilenmenin periton diyalizine göredaha yüksek oranda olduğunu gösterir.Sonuç olarak, göz kırpma refleksi, kronik böbrek yetmezliğinde klinik olaraksessiz intra-aksiyal beyin sapı fonksiyonel anormalliklerini veya ekstra-aksiyal lezyonlarıdeğerlendirmede önemli bir yöntemdir.The blink reflex is a polysynapthic reflex recorded bilaterally from orbicularisoculi muscles after stimulation of the supraorbital nerve unilaterally with surfaceelectrodes. The reflex consists of two components; an early ipsilateral component R1 andthe late component R2. The reflex arc of the blink reflex includes the afferents of thetrigeminal nerve sensory branches and the efferents of the facial nerve motor branches. Inclinical and pathological studies it was demonstrated that R1 is mediated via the mainsensory nucleus of the trigeminal nerve in pons, while the R2 is mediated via the spinaltrigeminal nucleus in medulla oblongata. For this reason, blink reflex has been widely usedin the evaluation of brainstem functioning.Peripheral and central nervous system is more frequently affected by chronicrenal failure than other body systems. The prevalance of peripheral neuropathy in chronicrenal failure ranges between 10-80 % correlated with the duration and degree of the renalpathology. The toxic metabolic components of uremia and metabolic changes resultedfrom dialysis are known to cause structural changes in same of the brain and brainstemregions. The blink reflex has been used to evaluate the central nervous system functioningin chronic renal failure since 1987.In order to search possible central nervous system changes that may be resultedfrom periton dialysis, hemodialysis and chronic renal failure, blink reflex and nerveconduction studies were evaluated in 35 hemodialysis and 35 periton dialysis patients.R2i and R2k responses were found to be significantly prolonged in chronicrenal failure patients as compared to these of the control group. Also, R2 responses fromhemodialysis patients in whom polyneuropathy was detected were significantly longer thanthose of the periton dialysis patients, while R1 responses were unaffected. For extraaxiallesions, R2 is less sensitive than R1 but in intraaxial lesions abnormality of R2 is as55frequent as short latency responses, the R2 being more complex and spreads to the caudalmedulla. Hence, in chronic renal failure patients sparing of the R1 and prolongation of theR2 indicates a subclinical intraaxial involvement. In a higher percent of dialysis patientswith polyneuropathy, the R1 component could not be elicited when compared with the R2results. Results indicate that R1 component of the blink reflex is conveyed by extroceptive,middle myelinated A beta fibers , while the R2 component is conveyed by nociceptive,small myelinated A delta fibers. Periton dialysis patients with polyneuropathy did notshow any significant difference from controls with regard to the R1, R2i and R2k values.R1 values of the hemodialysis patients with polyneuropathy were found to be withinnormal range while R2i and R2k values of these patients were significantly prolongedwhen compared to controls; suggesting that intraaxial subclinical involvement is morefrequently seen in this patient group.In conclusion, the blink reflex appears to be a useful laboratory investigationtool to determine subtle intra and extra-axial brainstem involvement in patients withchronic renal failure

İdiyopatik İntrakraniyal Hipertansiyon Tedavisinde Asetazolamid Kullanımına BağlıGeri Dönüşlü Anorgazm

WOS:000356420100023PubMed ID: 28360710

Cortical Blindness

Lateral genikülat cismin başlangıcı ile oksipital korteks arasındaki herhangi bir yerde oluşan bilateral retrokiazmal lezyonların yol açtığı tabloya kortikal körlük denir.When bilateral retrochiasmal lesions from the beginning of the lateral geniculate body to the occipital cortex are present, there is a cortical blindness

The Alice in Wonderland Syndrome: A Case of Aura Accompanying Cluster Headache

Background: Cluster headache (CH) is a primary headache which has highly specific and sensitive criteria, and notpresence of an aura. It has been recently reported that CH may not presence with aura more than ever and this condition will be identified by headache specialists as a new form of CH. Case Report: As there is no report to our knowledge on Alice in Wonderland syndrome (AIWS) manifest- ed as CH aura in the literature, we present a case of a 35-year-old man having AIWS as CH aura. Conclusion: Clinically, AIWS is not uncommon and is likely to be underestimated as a diagnostic entity. Val- proate may be preferred for treatment in CH patients with AIWS aura