144 research outputs found

    Effects of intermittent fasting on experimental autoimune encephalomyelitis in C57BL/6 mice

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    Several religions recommend periods of fasting. One of the most frequently asked questions of MS patients before the holy month of Ramadan is weather fasting might have an unfavorable effect on their disease course. This debate became more challenging after the publication of experimental studies suggesting that calorie restriction prior to disease induction attenuates disease severity. We conducted this study to assess early and late effects of fasting on the animal model of MS, known as autoimmune encephalomyelitis. EAE was induced in the C57BL/6 mice, using Myelin Oligodendrocyte Glycopeptide (MOG) 35-55 and they fasted every other day either after the appearance of the first clinical sign or 30 days after disease induction for ten days. Thereafter, the mice were sacrificed for further histological and immunological evaluations. Intermittent fasting after the establishment of EAE did not have any unfavorable effect on the course of disease. Moreover, fasting at the early phase of disease alleviated EAE severity by ameliorating spinal cord demyelination. Fasting suppressed the secretion of IFN-γ, TNF-α and raised IL-10 production in splenocytes. Fasting was also associated with a lower percent of cytotoxicity. Intermittent fasting not only had no unfavorable effect on EAE but also reduced EAE severity if started at early phase of disease. © Summer 2016, Iran J Allergy Asthma Immunol. All rights reserved

    Alleviation of experimental allergic encephalomyelitis in C57BL/6 mice by Soy Daidzein

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    Experimental allergic encephalomyelitis (EAE) is considered as the murine model of multiple sclerosis. Daidzein a phytostrogenic compound of soy is known to impose immunomodulatory and antioxidative effects. We conducted this study to assess the potential protective and therapeutic effects of daidzein on allergic encephalomyelitis. C57BL/6 mice were induced with allergic encephalomyelitis using myelin oligodendrocyte glycoprotein (35-55) and received daidzein or dimethyl sulfoxide as the vehicle control. To assess the protective effect of daidzein, the mice were administered with 20 mg/kg of daidzein from 21 days prior to 21 days post EAE induction on a daily basis. To evaluate the therapeutic effect of daidzein, mice were fed with 300 mg/kg daidzein after the appearance of the first clinical signs for 10 days. One day after the last gavage, the mice were sacrificed. Spleen and brain were removed for further histological and immunological analysis. Feeding mice with low dose of daidzein prior to disease induction did not affect disease severity. However, treating with high dose of daidzein after the onset of the disease reduced interferon-3 and interleukin-12 secretion, enhanced interleukin-10 production, suppressed lymphocyte proliferation, and decreased cytotoxicity as judged by lactate dehydrogenase release. In conclusion, daidzein reduced the extent of demyelination and disease severity. Chronic oral therapy with low dose of daidzein did not prevent experimental autoimmune encephalomyelitis. However, high doses of daidzein could prohibit disease exacerbation. © Summer 2014, Iran J Allergy Asthma Immunol. All rights reserved

    Intravenous valproate versus subcutaneous sumatriptan in acute migraine attack

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    Migraine is a common and incapacitating neurologic disorder manifesting with episodic moderate to a severe headache and other symptoms such as photophobia, phonophobia, nausea, and vomiting. Triptans and ergot compounds have been used as treatment options for an acute migraine headache for many years. Triptans are considered the first line of treatment in patients with moderate to a severe migraine. Although the triptans are commonly used at any time during a migraine attack; they are more efficacious when used in the early stages of a migraine. Intravenous valproic acid has been shown to be well tolerated, safe, and with rapid onset of action in patients with acute moderate to severe and even refractory migraine. Sodium valproate is a Food and Drug Administration (FDA)�approved drug for prophylaxis of a migraine with and without aura. In this study, the main goal was to compare the effectiveness of sumatriptan versus valproate in an acute migraine. A randomized clinical trial including 37 patients with an acute migraine was considered to compare the effectiveness of sumatriptan versus valproate. The patients were divided into two groups. In first group, 6 mg subcutaneous of sumatriptan and in the second group 15 mg/Kg of valproate was administered. The outcomes including pain and drug adverse effects were compared across the groups. A total of 37 patients (7 male and 30 female) were evaluated in two groups. The difference between two groups regarding sex and age was not significant (P>0.05). The mean pain scores reduced from 8.3 to 4.7 and from 8.3 to 2.2 after one hour of treatment in sumatriptan and valproate groups, respectively. Response to treatment in valproate group was faster and more effective than sumatriptan group (P<0.05).The results indicated that valproate was more effective and with the faster response in patients with an acute migraine in comparison with sumatriptan without any recurrence and remarkable side effects. � 2015 Tehran University of Medical Sciences. All rights reserved

    Effect of oral genistein administration in early and late phases of allergic encephalomyelitis

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    Objective(s): Experimental allergic encephalomyelitis (EAE) is an autoimmune disease validated as animal model of multiple sclerosis (MS). Administration of genistein, a phytoestrogenic component of soy, to mice at the onset of EAE is known to attenuate the clinical signs of the disease. The potential effects of genistein on established EAE is less studied. In the current study, we aimed to compare the effects of genistein administration on EAE severity in early and late phases of the disease. Materials and Methods: The C57BL/6 mice were induced with EAE, using MOG 35-55 and gavaged with genistein (300 mg/kg) either after the appearance of the first clinical sign or 30 days post disease induction for ten days. 24 hr after the last gavage, mice were sacrificed. Brains and spleens were removed for assessing lymphocyte proliferation, cell cytotoxicity, and cytokine profile. Spinal cords were dissected to assess the amount of demyelination using Luxol fast blue/cresyl violet staining. Results: Administering mice with genistein, after the establishment of EAE, did not reverse the clinical signs of disease. However, treating with genistein at the onset of disease alleviated the clinical signs by reducing neuronal demyelination. Genistein suppressed the production of IFN-γ and enhanced IL-10 secretion in splenocyte and brain. Genistein also reduced IL-12 and TNF-α secretion in splenocytes, suppressed the proliferation of T-cells, and reduced the cell cytotoxicity. Conclusion: Genistein oral therapy might only reduce EAE severity if started in early phases of the disease

    Saphenous neuropathy in a patient with low back pain

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    Saphenous nerve, a pure sensory nerve, may compromise as a result or complication of a surgical procedure or secondary to trauma or insidiously. We present a male patient with low back pain concomitant with pain in medial portion of left thigh in addition to pain and numbness in medial part of leg and inferior part of patella after a strenuous activity. Preliminary diagnosis suggested that the patient had radiculopathy but electrodiagnostic tests revealed the absence of left saphenous response both in medial leg and infrapatellar region, while normal findings were recorded from right side. Needle electromyography in L4 innervated muscles were normal. The patient had saphenous nerve entrapment in left thigh. Two months later symptoms relieved with conservative therapy

    100 CHILDREN WITH ACUTE ATAXIA; A SURVEY IN MOFID CHILDREN'S HOSPITAL

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    Objective:The term "Ataxia" refers to disturbances of body posture and movement that are normally controlled by the cerebellum, frontal lobes and the posterior columns of the spinal cord. The primary symptom and the most prominent feature of ataxia is abnormal gait which is characterized by lurching and wide base walking. Ataxia was considered acute, if it had occurred within the two preceding weeks. Knowing how frightening acute-onset Ataxia is for the family is not surprising that the condition prompts an immediate visit to the physician.Material & Methods:In view of the lack of information in our country, on the etiology of sudden-onset Ataxia, the authors enrolled 100 children with the chief complaint of acute loss of equilibrium, who came to the attention of the Pediatric Neurology Department over a two year duration (Sept.2001-Sept 2003); they were admitted to the Mofid Childrens' Hospital and all necessary investigations were carried out.Results & Conclusion:The results revealed that Acute Cerebellar Ataxia was the most common cause of the problem, the second most frequent being drug intoxication, which most commonly occurred in patients, 2- 4years old. The remaining causative factors in order of descending frequency consisted of infectious polyneuropathy, migraine, opsoclonus-myoclonus, brain tumor, acute disseminated encephalomyelitis, multiple sclerosis, and epilepsy.Key words:Acute ataxia, Children, Acute cerebellar ataxi

    The Investigation of the effects of deep dry needling into trigger points of temporalis, sternocleidomastoid and upper trapezius on females with episodic tension type headache

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    Introduction: Tension type headache is the most common type of headache that is associated with myofascial pain syndrome and trigger points. The aim of this study was to evaluate the efficacy of deep dry needling into trigger points of temporalis, sternocleidomastoid and upper trapezius muscles of females with episodic tension type headache. Materials and Methods: The study was a clinical randomized, single-blind, parallel-group trial in which 24 participants were allocated into two groups. The first group received dry needling with passive stretching treatment and the second group (control group) received only passive stretching. Subjects were asked to record headache indices (headache intensity and frequency) for 4 weeks before treatment. Headache intensity and frequency and quality of life (SF-36) were measured at baseline and 4 weeks after the intervention. Results: In the dry needling group, the intensity and frequency of headache and physical functioning scores of quality of life questionnaire were significantly improved after treatment (p &lt;0.05). Conclusion: Due to the positive effects of deep dry needling and passive stretching in females with episodic tension type headache, the use of deep dry needling into trigger points of head and neck musculature is recommended in the presence of episodic tension type headache. &nbsp

    Cinnarizine versus Topiramate in Prophylaxis of Migraines among Children and Adolescents: A Randomized, Double-Blind Clinical Trial

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    How to Cite This Article: Ashrafi MR, Najafi Z, Shafiei M, Heidari K, Togha M. Cinnarizinev ersus Topiramate in Prophylaxis of Migraines among Children and Adolescents: A Randomized, Double-Blind Clinical Trial. Iran J Child Neurol. 2014 Autumn;8(4): 18-27. AbstractObjectiveMigraines, a common health problem in children and adolescents, still do not have an FDA approved preventive treatment for patients under the age of 18 years. This study compares and contrasts the efficacy and safety of cinnarizine and topiramate in preventing pediatric migraines.Materials &amp; MethodsIn this randomized, double-blind clinical trial 44 migrainous (from 4–15 years of age) were equally allocated to receive cinnarizine or topiramate. The primary efficacy measure was monthly migraine frequency. Secondary efficacy measures were monthly migraine intensity and ≥ 50% responder rate. Efficacy measures were recorded at the baseline and at 4, 8, and 12 weeks of treatment.ResultsDuring the double-blind phase of the study, monthly migraine frequency and intensity were significantly decreased in both the cinnarizine and topiramate groups when compared to the baseline. However, at the end of the study, the cinnarizine group exhibits a significant decrease from the baseline in the mean monthly migraine intensity when compared to the topiramate group (4.7 vs. 3, respectively; 95% CI = -0.8 to -3.2).ConclusionNo significant difference between cinnarizine and topiramate was found for the prevention of pediatric migraines. Both treatments were well tolerated.ReferencesHershey AD, Winner PK. Pediatric Migraine: Recognition and Treatment. J Am Osteopath Assoc. 2005;105:2S-8.Lewis DW, Yonker M, Winner P, Sowell M. The treatment of pediatric migraine. Pediatric Annals. 2005;34:448-460.Abu-Arefeh I, Russell G. Prevalence of headache and migraine in schoolchildren. BMJ. 1994;309:765-769.Linet MS, Stewart WF, Celentano DD, Ziegler D, Sprecher M. An Epidemiologic Study of Headache among Adolescents and Young Adults. JAMA: The Journal of the American Medical Association. 1989;261:2211-2216.Stewart WF, Linet MS, Celentano DD, Van Natta M, Ziegler D. Age- and sex-specific incidence rates of migraine with and without visual aura. Am J Epidemiol. 1991;134:1111-1120.Stewart WF, Lipton RB, Celentano DD, Reed ML. Prevalence of Migraine Headache in the United States. JAMA: The Journal of the American Medical Association. 1992;267:64-69.Split W, Neuman W. Epidemiology of Migraine among Students from Randomly Selected Secondary Schools in Lodz. Headache: The Journal of Head and Face Pain. 1999;39:494-501.Hershey AD, Kabbouche MA, Powers SW. Treatment of pediatric and adolescent migraine. Pediatr Ann. 2010;39:416-423.Hershey AD, Powers SW, Vockell AL, LeCates S, Kabbouche MA, Maynard MK. PedMIDAS: development of a questionnaire to assess disability of migraines in children. Neurology. 2001;57:2034-2039.Lewis D, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S. Practice Parameter: Pharmacological treatment of migraine headache in children and adolescents. Neurology. 2004;63:2215-2224.Brandes JL, Saper JR, Diamond M, et al. Topiramate for Migraine Prevention. JAMA: The Journal of the American Medical Association. 2004;291:965-973. Lakshmi CVS, Singhi P, Malhi P, Ray M. Topiramate in the Prophylaxis of Pediatric Migraine: A Double-Blind Placebo-Controlled Trial. Journal of Child Neurology. 2007;22:829-835.Lewis D, Winner P, Saper J, et al. Randomized, Double- Blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Topiramate for Migraine Prevention in Pediatric Subjects 12 to 17 Years of Age. Pediatrics. 2009;123:924-934.Winner P, Pearlman EM, Linder SL, et al. Topiramate for Migraine Prevention in Children: A Randomized, Double-Blind, Placebo-Controlled Trial. Headache: The Journal of Head and Face Pain. 2005;45:1304-1312.Winner P, Gendolla A, Stayer C, et al. Topiramate for Migraine Prevention in Adolescents: A Pooled Analysis of Efficacy and Safety. Headache: The Journal of Head and Face Pain. 2006;46:1503-1510.Campistol J, Campos J, Casas C, Herranz JL. Topiramate in the prophylactic treatment of migraine in children. Journal of Child Neurology. 2005;20:251-253.Hershey AD, Powers SW, Vockell A-LB, LeCates S, Kabbouche M. Effectiveness of Topiramate in the Prevention of Childhood Headaches. Headache: The Journal of Head and Face Pain. 2002;42:810-818.Unalp A, Uran N, Ozturk A. Comparison of the effectiveness of topiramate and sodium valproate in pediatric migraine. J Child Neurol. 2008;23:1377-1381. Younkin DP. Topiramate in the treatment of pediatric migraine. Headache: The Journal of Head and Face Pain. 2002;42:456.Rossi P, Fiermonte G, Pierelli F. Cinnarizine in migraine prophylaxis: efficacy, tolerability and predictive factors for therapeutic responsiveness. An open-label pilot trial. Funct Neurol. 2003;18:155-159.Togha M, Ashrafian H, Tajik P. Open-label trial of cinnarizine in migraine prophylaxis. Headache. 2006;46:498-502.Togha M, Rahmat Jirde M, Nilavari K, Ashrafian H, Razeghi S, Kohan L. Cinnarizine in refractory migraine prophylaxis: efficacy and tolerability. A comparison with sodium valproate. J Headache Pain. 2008;9:77-82.Headache Classification Committee of The International Headache Society. The International Classification of Headache Disorders, 2nd edn. Cephalalgia. 2004;24(Suppl. 1):1–160.Tonekaboni SH, Ghazavi A, Fayyazi A, Khajeh A, Taghdiri MM, AbdollahGorji F, Azargashb E. Prophylaxis of Childhood Migraine: Topiramate Versus Propranolol. Iran J Child Neurol. 2013 Winter; 7 (1):9-14.Fallah R, AkhavanKarbasi S, Shajari A, Fromandi M. The Efficacy and Safety of Topiramate for Prophylaxis of Migraine in Children. Iran J Child Neurol. 2013 Autumn; 7(4):7-11.Ferraro D, Di Trapani G. Topiramate in the prevention of pediatric migraine: literature review. J Headache Pain. 2008;9:147-150

    Is Herpes Simplex virus (HSV) a sign of Encephalitis in Iranian Newborns? Prevalence of HSV Infection in Pregnant Women in Iran: A Systematic Review and Meta-Analysis

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    How to Cite This Article: Arabsalmani M, Behzadifar M, Baradaran HR, Toghae M, Beyranvand Gh, Olyaeemanesh A, Behzadifar M. Is Herpes Simplex virus (HSV) a sign of Encephalitis in Iranian Newborns? Prevalence of HSV Infection in Pregnant Women in Iran: A Systematic Review and Meta-Analysis. Iran J Child Neurol.Spring 2017; 11(2):1-7. AbstractObjectiveHerpes Simplex virus (HSV) is one of the most common sexually transmitted diseases in the world. This study aimed to determine the prevalence of herpes simplex virus in pregnant women in Iran.Materials &amp; MethodsA systematic literature review was conducted to study the HSV subtypes in Persian and English papers through several databases. We searched Pub Med, Scopus, Ovid, Science Direct and national databases as Magiran, Iranmedex and Science Information Database (SID) up to October 2015. Random-effects model were applied to calculate the pooled prevalence of HSV subtypes.ResultsFive eligible studies were identified, including 1140 participants. The pooled prevalence of HSV infection in pregnant women was 0.64% (95% CI: 0.10- 1.18) in Iran. The pooled prevalence of studies on both HSV-1 and HSV-2 was 0.91% (CI: 0.81-1.02) and studies on only HSV-2 was 0.23% (CI: -0.61-0.63), respectively.ConclusionThe prevalence of HSV infection in pregnant women in Iran was higher. HSV infection of the central nervous system, especially with HSV-2, can also cause recurrent aseptic meningitis and monophasic, as well as radiuculitis or myelitis. The performance of screening to detect infection in pregnant women can play an important role in the prevention and treatment of patients and help to prevent the transmission of HSV infection to infants in Iran.References 1.Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA Neurol 2006; 296:964-73.2.Bochner AF, Madhivanan P, Niranjankumar B, Ravi K, Arun A, Krupp K, et al. The Epidemiology of Herpes Simplex Virus Type-2 Infection among Pregnant Women in Rural Mysore Taluk, India. J Sex Transm Dis 2013; 2013:1-6.3.Kulhanjian JA, Soroush V, Au DS, Bronzan RN, Yasukawa LL, Weylman LE, et al. Identification of women at unsuspected risk of primary infection with herpes simplex virus type 2 during pregnancy. N Engl J Med 1992; 326 :916–20.4.Whitley RJ, Corey L, Arvin A, Lakeman FD, Sumaya CV, Wright PF, et al. Changing presentation of herpes simplex virus infection in neonates. J Infect Dis 1988; 158:109–16.5.Cusini M, Ghislanzoni M. The importance of diagnosing genital herpes. J Antimicrob Chemother 2001; 47:9-16.6.Cherpes TL, Meyn LA, Krohn MA, Lurie JG, Hillier SL. Association between acquisition of herpes simplex virus type 2 in women and bacterial vaginosis. Clin Infect Dis 2003; 37:319-25.7.Gottlieb SL, Douglas JM, Schmid DS, Bolan G, Iatesta M, Malotte CK, et al. Seroprevalence and correlates of herpes simplex virus type 2 infection in five sexually transmitted–disease clinics. J Infect Dis 2002; 186:1381-9.8.Arvaja M, Lehtinen M, Koskela P, Lappalainen M, Paavonen J, Vesikari T. Serological evaluation of herpes simplex virus type 1 and type 2 infections in pregnancy. J Sex Transm Infect 1999;75:168-71.9.Brown ZA, Selke S, Zeh J, Kopelman J, Maslow A, Ashley RL, et al. The acquisition of herpes simplex virus during pregnancy. N Engl J Med 1997; 337:509-16.10.Anzivino E, Fioriti D, Mischitelli M, Bellizzi A, Barucca V, Chiarini F, et al. Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention. Virol J 2009; 6: 68-74.11.Weiss H. Epidemiology of herpes simplex virus type 2 infection in the developing world. Herpes 2004;11:24-35.12.Swetha G, Pinninti, David W, Kimberlin. Preventing HSV in the Newborn. Clin Perinatol 2014; 41:945–55.13.Sheffield JS, Hill JB, Hollier LM, Laibl VR, Roberts SW, Sanchez PJ. Valacyclovir prophylaxis to prevent recurrent herpes at delivery: a randomized clinical trial. Obstet Gynecol 2006; 108:141-7.14.Watts DH, Brown ZA, Money D, Selke S, Huang ML, Sacks SL. A double-blind, randomized, placebo-controlled trial of acyclovir in late pregnancy for the reduction of herpes simplex virus shedding and cesarean delivery. Am J Obstet Gynecol 2003; 188:836-43.15.Bulletin AP. Clinical management guidelines for obstetrician-gynecologists. Obstet Gynecol 2003; 45:102- 13.16.Curtis N, Finn A, Pollard A. Neonatal herpes simplex virus infections: where are we now? Hot Topics in Infection and Immunity in Children VII. 2nd ed. New York: Springer; 2011. P.146.17.Allen UD, Robinson JL. Prevention and management of neonatal herpes simplex virus infections. Pediatr Child Health 2014;19:19-31.18.Bernstein DI, Bellamy AR, Hook EW, Levin MJ, Wald A, Ewell MG, et al. Epidemiology, Clinical Presentation, and Antibody Response to Primary Infection With Herpes Simplex Virus Type 1 and Type 2 in Young Women. Clin Infect Dis 2013; 56:344-51.19.Whitley R, Arvin A, Prober C, Corey L, Burchett S, Plotkin S, et al. Predictors of morbidity and mortality in neonates with herpes simplex virus infections. N Engl J Med 1991; 324:450-4.20.Von Elm E, Altman DG, Egger M, Pocock SJ, Gotzsche PC, Vandenbroucke JP. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. Ann Intern Med 2007;147:573–7.21.Higgins JP, Green S. Cochrane Handbook for Systematic Reviews of Interventions. 5thed. London, UK: The Cochrane Collaboration; 2011.P.420.22.Danesh Shahraki A, Moghim S, Akbari P. Evaluation of the Serum Level of Herpes Simplex Type 2 Antibody among Pregnant Women in Shahid Beheshti Hospital, Isfahan. J Red Med Sci 2010;15:243.23.Bagheri Josheghani S, Moniri R, Baghbani Taheri F, Sadat S, Heidarzadeh Z. The Prevalence of Serum antibodies in TORCH Infections during the First Trimester of Pregnancy in Kashan, Iran. Iran J Neonatol 2015; 6:8-12.24.Ghasemi FS, Rasti S, Piroozmand A, Fakhrie-Kashan Z, Mousavi GA. Relationship between the prevalence of antibodies against cytomegalo, rubella, and herpes simplex viruses in women with spontaneous abortion compared to normal delivery. J Feyz 2015;19:86-92.25.Pourmand D, Janbakhsh A, Hamzehi K, Dinarvand F, Ahmadi D. Seroepide Miological Study of Herpes Simplex Virus in Pregnant Women Referring to Health and Care Center in Kermanshah. J Kermanshah Univ Med Sci 2008;11:462-9.26.Golalipour MJ, Khodabakhshi B, Ghaemi E. Possible role of TORCH agents in congenital malformations in Gorgan, northern Islamic Republic of Iran. East Mediterr Health J 2009;15:330-6.27.Chen KT, Segu M, Lumey LH, Kuhn L, Carter RJ, Bulterys M, et al. Genital herpes simplex virus infection and perinatal transmission of human immunodeficiency virus. Obstet Gynecol 2005; 106:1341-8.28.Ali S, Khan FA, Mian AA, Afzal MS. Seroprevalence of cytomegalovirus, herpes simplex virus and rubella virus among pregnant women in KPK province of Pakistan. J Infect Dev Ctries 2014;18:389-90.29.Hezarjaribi HZ, Fakhar M, Shokri A, Teshnizi SH, Sadough A, Taghavi M. Trichomonas vaginalis infection among Iranian general population of women: a systematic review and meta-analysis. Parasitol Res 2015;114:1291- 300.30.Sauerbrei A, Wutzler P. Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 1: herpes simplex virus infections. Med Microbiol Immunol 2007; 196:89–9431.Büchner S, Erni P, Garweg J, Gerber S, Kempf W, Lauper U, et al. Swiss recommendations for the management of genital herpes and herpes simplex virus infection of the neonate. Swiss Medi Wkly 2004; 134:205–21432.Meerbach A, Sauerbrei A, Meerbach W, Bittrich HJ, Wutzler P. Fatal outcome of herpes simplex virus type 1-induced necrotic hepatitis in a neonate. Med Microbiol Immunol 2006; 195:101–10533.Tyler KL. Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret’s. Herpes 2004. ; 11:57A-64A34.Corey L, Whitley RJ, Stone EF, Mohan K. Difference between herpes simplex virus type 1 and type 2 neonatal encephalitis in neurological outcome. Lancet 1988; 1:1-435.Berger JR, Houff S. Neurological complications of herpes simplex virus type 2 infection. Arch Neurol 2008.; 65:596-60036.Gallo MF, Warner L, Macaluso M, Stone KM, Brill I, Fleenor ME. Risk factors for incident herpes simplex type 2 virus infection among women attending a sexually transmitted disease clinic. 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