Search

Ajitasyon, pek cok psikiyatrik ve tibbi durumun seyri sirasinda ortaya cikabilen yasami tehdit edebilen bir durumdur. Ajitasyon, bir kisinin, kendisi ya da yakin cevresinin guvenligini tehlikeye sokan her turlu sesli, sozlu ve/veya motor davranislar kumesidir. Saldirgan davranislarin gelisiminde biyolojik, sosyal, cevresel etkenler gibi bircok etmen rol oynar. Oncesinde psikiyatrik hastalik oykusu olmayan aniden ortaya cikan ajitasyon, saldirgan davranis ve durtusellik gosteren hastalarda, psikiyatri disi tibbi durumlarin mutlaka dislanmasi gerekir. Klinisyenler acisindan da tani ve tedavi yontemleri konusunda bazi gucluklere yol acabilen ajitasyonun izlemi onemlidir. Bu nedenle klinisyenlerin ajitasyonu olan olgulara yaklasimi, risk faktorlerini konusunda bilgi sahibi olmalari yasam kurtarici olabilir. Bu derlemede ajite davranis acisindan riskli bireylere yaklasim ve tedavi surecleri konusunda mevcut literatur bilgilerinin gozden gecirilmesi amaclanmistir. Calisma icin PubMed, Google Scholar, Turk Psikiyatri Dizini gibi arama motorlari taranmis ve konu ile ilgili Ingilizce, Turkce dillerinde yazilmis tam metin olarak ulasilabilen yayinlar calismaya dahil edilmistir. Saglik calisanlarinin ajitasyonu olan hastanin yonetimi konusunda egitilmesi, bilgilendirilmesi gereklidir. Saglik calisanlarina ve hasta yakinlarina zor anlar yasatan saldirgan davranis nedeni ile basvuran olgular icin oncelikle guvenlik tedbirleri alinmalidir. Saldirgan hastalarin tedavisinde cevresel duzenleme, yatistirma, bedensel tespit veya tecrit ve farmakolojik yaklasim uygulanir.

Ajitasyon, pek çok psikiyatrik ve tıbbi durumun seyri sırasında ortaya çıkabilen yaşamı tehdit edebilen bir durumdur. Ajitasyon, bir kişinin, kendisi ya da yakın çevresinin güvenliğini tehlikeye sokan her türlü sesli, sözlü ve/veya motor davranışlar kümesidir. Saldırgan davranışların gelişiminde biyolojik, sosyal, çevresel etkenler gibi birçok etmen rol oynar. Öncesinde psikiyatrik hastalık öyküsü olmayan aniden ortaya çıkan ajitasyon, saldırgan davranış ve dürtüsellik gösteren hastalarda, psikiyatri dışı tıbbi durumların mutlaka dışlanması gerekir. Klinisyenler açısından da tanı ve tedavi yöntemleri konusunda bazı güçlüklere yol açabilen ajitasyonun izlemi önemlidir. Bu nedenle klinisyenlerin ajitasyonu olan olgulara yaklaşımı, risk faktörlerini konusunda bilgi sahibi olmaları yaşam kurtarıcı olabilir. Bu derlemede ajite davranış açısından riskli bireylere yaklaşım ve tedavi süreçleri konusunda mevcut literatür bilgilerinin gözden geçirilmesi amaçlanmıştır. Çalışma için PubMed, Google Scholar, Türk Psikiyatri Dizini gibi arama motorları taranmış ve konu ile ilgili İngilizce, Türkçe dillerinde yazılmış tam metin olarak ulaşılabilen yayınlar çalışmaya dahil edilmiştir. Sağlık çalışanlarının ajitasyonu olan hastanın yönetimi konusunda eğitilmesi, bilgilendirilmesi gereklidir. Sağlık çalışanlarına ve hasta yakınlarına zor anlar yaşatan saldırgan davranış nedeni ile başvuran olgular için öncelikle güvenlik tedbirleri alınmalıdır. Saldırgan hastaların tedavisinde çevresel düzenleme, yatıştırma, bedensel tespit veya tecrit ve farmakolojik yaklaşım uygulanır.

Objective: Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) are neuro-trophins and they are critical regulators of the survival, differentiation, growth and plasticity of neuronal networks. There is plenty of evidence suggesting the involvement of altered levels of expression of neurotrophic factors in the pathophysiology of neuropsychiatric disorders. However, the relationship between neurotrophins and majör depres-sion (MD) remains unclear. In this study, we assessed the relationship between the BDNF, NT-3, NT-4 gene ex-pression levels in blood cells and MD. Methods: In a case-control study, total RNA was obtained from blood cells, 51 MD patients (diagnosed according to the DSM-5 criteria) and 75 healthy controls. Detected with quantitative Real Time PCR, expression levels of BDNF, NT-3, NT-4 genes were compared between the groups. Results: In this study, BDNF expression levels of the patients with MD were significantly higher than the control group but no statistically significant difference between NT-3 and NT-4 expression levels. There was no differences in expression levels of BDNF, NT-3 and NT-4 genes in MD patients with family history. There was no statistically significant differ-ence in the BDNF, NTF-3 and NTF-4 expression levels among the sex groups for the patient group and no statis-tically significant difference between MD patients according to antidepressant usage time. Discussion: Not only in understanding the pathogenesis of MD but also in the follow-up of treatment, expression level changes of BDNF gene in blood cells of MD patients must be considered because of the bidirectional movement of BDNF between the periphery and the brain and effect of changing serum BDNF levels. © 2019, (publisher name). All Rights Reserved.

Objective: Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) are neurotrophins and they are critical regulators of the survival, differentiation, growth and plasticity of neuronal networks. There is plenty of evidence suggesting the involvement of altered levels of expression of neurotrophic factors in the pathophysiology of neuropsychiatric disorders. However, the relationship between neurotrophins and major depression (MD) remains unclear. In this study, we assessed the relationship between the BDNF, NT-3, NT-4 gene expression levels in blood cells and MD. Methods: In a case-control study, total RNA was obtained from blood cells, 51 MD patients (diagnosed according to the DSM-5 criteria) and 75 healthy controls. Detected with quantitative Real Time PCR, expression levels of BDNF, NT-3, NT-4 genes were compared between the groups. Results: In this study, BDNF expression levels of the patients with MD were significantly higher than the control group but no statistically significant difference between NT-3 and NT-4 expression levels. There was no differences in expression levels of BDNF, NT-3 and NT-4 genes in MD patients with family history. There was no statistically significant difference in the BDNF, NTF-3 and NTF-4 expression levels among the sex groups for the patient group and no statistically significant difference between MD patients according to antidepressant usage time. Discussion: Not only in understanding the pathogenesis of MD but also in the follow-up of treatment, expression level changes of BDNF gene in blood cells of MD patients must be considered because of the bidirectional movement of BDNF between the periphery and the brain and effect of changing serum BDNF levels. C1 [Yuksel Balim, Damla; Izci Ay, Ozlem; Ay, Mustafa Ertan; Karakas, Umit; Erdal, Mehmet Emin] Mersin Univ, Tip Fak, Tibbi Biyol ABD, Mersin, Turkey. [Inci Kenar, Aysenur] Pamukkale Univ, Tip Fak, Psikiyatri ABD, Denizli, Turkey.

Amaç: Beyin kökenli nörotrofik faktör (BDNF), nörotrofin-3 (NT-3) ve nörotrofin-4 (NT-4); nöronal sağlıklı kalımın,farklılaşmanın, büyümenin ve nöronal plastisitenin düzenlenmesinde önemli rolleri olan nörotrofinlerdir. Nöropsiki-yatrik hastalıkların patofizyolojisi ile nörotrofik faktörlerin ifade düzeyleri arasındaki ilişki bilinmekle birlikte, majördepresyon (MD) patogenezi ve nörotrofinler arasındaki ilişki henüz tam olarak aydınlatılamamıştır. Bu çalışmada,kan hücrelerindeki BDNF, NT-3, NT-4 gen ekspresyonları ile MD arasındaki ilişkiyi araştırdık. Yöntem: Bu olgu-kontrol çalışmasında, DSM-5 ölçütlerine göre MD’li 51 hasta ve 75 sağlıklı kontrole ait kanlardan total RNA eldeedildi. Kantitatif Real-Time PCR yöntemi ile saptanan, MD ve kontrol gruplarındaki BDNF, NT-3, NT-4 genlerine aitekspresyon düzeyleri karşılaştırıldı. Bulgular: Çalışma sonucunda, MD hastalarının BDNF gen ekspresyon düzey-lerinin, kontrol grubuna göre anlamlı derecede yüksek olduğu; NT-3 ve NT-4 değerleri bakımından ise gruplar ara-sında istatistiksel olarak anlamlı bir farklılık olmadığı belirlendi. Aile öyküsü olan MD hastalarının BDNF, NT-3 veNT-4 ekspresyon düzeylerinde farklılık saptanmadı. Hasta grubu içinde cinsiyetler arasında ve antidepresan kulla-nım sürelerine göre, BDNF, NT-3 ve NT-4 ekspresyon düzeyleri bakımından istatistiksel olarak anlamlı bir farklılıkbulunmadı. Tartışma: MD hastalarının kan hücrelerindeki BDNF geni ekspresyon düzeyi değişiklikleri, sadeceMD'nin patogenezini anlamada değil, tedavinin izlenmesinde de, BDNF'nin perifer ile beyin arasındaki çift yönlühareketi ve serum BDNF düzeyini değiştirme etkisinden dolayı göz önünde bulundurulmalıdır. (Anadolu PsikiyatriDerg 2019; 20(6):581-588)

Hyperprolactinemia is an important but often a neglected side effect of antipsychotic treatment. Aripiprazole is one of the new atypical antipsychotics that has partial agonist effects on dopamine D2 receptors and has a low possibility of hyperprolactinemia. In the present case report, we discuss a female patient who was diagnosed as suffering from depression with psychotic symptoms. Her prolactin levels were elevated while on treatment with aripiprazole. Clinicians should consider that aripiprazole may result in moderate elevation of prolactin levels although it is reported that it has a lower risk of elevation of prolactin levels. © 2014, Cukurova Univ Tip Fakultesi Psikiyatri Anabilim Dali. All rights reserved.

OBJECTIVE: This study investigated the relationship between the use of methylphenidate (MPH) and changes in creatine, choline, and N-acetyl-aspartate (NAA) in the dorsolateral prefrontal cortex (DLPFC), striatum, cerebellum, and anterior cingulate cortex (ACC) in adults with attention-deficit hyperactivity disorder (ADHD). PATIENTS AND METHODS: The study enrolled 60 patients 18-60 years of age who met the criteria in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) for ADHD. The amounts of NAA, creatine, and choline in the ACC, cerebellum, striatum, and DLPFC were measured using magnetic resonance spectroscopy. After the first measurement, the patients were given 10 mg oral MPH, and the same metabolite levels were measured 30 minutes later. RESULTS: No significant differences were observed in the NAA and choline levels in the DLPFC, ACC, cerebellum, and striatum after MPH. Although there were no significant differences in the creatine levels in the DLPFC, ACC, and striatum after MPH, the creatine level in the cerebellum increased significantly. CONCLUSIONS: Our results suggest that MPH affects the cerebellum in adult ADHD. Therefore, we suggest that, due to its effects on the cerebellum, MPH can be used in adult ADHD not only for attention deficit symptoms but also for hyperactivity symptoms.

OBJECTIVE: This study investigated the relationship between the use of methylphenidate (MPH) and changes in creatine, choline, and N-acetyl-aspartate (NAA) in the dorsolateral prefrontal cortex (DLPFC), striatum, cerebellum, and anterior cingulate cortex (ACC) in adults with attention-deficit hyperactivity disorder (ADHD)., PATIENTS AND METHODS: The study enrolled 60 patients 18-60 years of age who met the criteria in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) for ADHD. The amounts of NAA, creatine, and choline in the ACC, cerebellum, striatum, and DLPFC were measured using magnetic resonance spectroscopy. After the first measurement, the patients were given 10 mg oral MPH, and the same metabolite levels were measured 30 minutes later., RESULTS: No significant differences were observed in the NAA and choline levels in the DLPFC, ACC, cerebellum, and striatum after MPH. Although there were no significant differences in the creatine levels in the DLPFC, ACC, and striatum after MPH, the creatine level in the cerebellum increased significantly., CONCLUSIONS: Our results suggest that MPH affects the cerebellum in adult ADHD. Therefore, we suggest that, due to its effects on the cerebellum, MPH can be used in adult ADHD not only for attention deficit symptoms but also for hyperactivity symptoms.

The effects of certain genetic alterations in the brain function of patients with attention deficit hyperactivity disorder (ADHD) remain unclear and, in fact, there is a limited amount of data in this field. For example, the relationship between the SNAP-25 polymorphism and brain metabolites in response to methylphenidate (MPH) has yet to be investigated. Thus, the present study aimed to determine the relationship between changes in creatine (Cr), choline (Cho), and N-acetyl aspartate (NAA) levels in the prefrontal cortex (PFC) and anterior cingulate cortex (ACC) of adults with ADHD and the SNAP-25 gene polymorphism following the use of MPH.The present study assessed 60 patients between 18 and 60 years of age who were diagnosed with ADHD according to criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV). Genetic analyses were carried out using blood samples obtained from the ADHD patients and included a detailed clinical evaluation for the SNAP-25 gene polymorphism. The NAA, Cr, and Cho levels in the ACC and PFC were measured using magnetic resonance spectroscopy (MRS). Following the evaluation, 10 mg of oral MPH was given to the patients, and the same metabolite levels were measured after 30 minutes.The levels of NAA, Cr, and Cho in the PFC and ACC of patients with the SNAP-25 Ddel and Mnll polymorphism genotypes did not significantly differ before and after the administration of MPH. However, in patients with the SNAP-25 Ddel polymorphism T/T genotype and the Mnll polymorphism G/G genotype, there was a significant increase in NAA levels in the ACC after MPH treatment compared with before MPH treatment.The present results suggest that the SNAP-25 Ddel and Mnll polymorphisms might be associated with MPH-related changes in NAA levels in the ACC.

OBJECTIVE: This study investigated the relationship between DAT1 gene polymorphisms and the effects of methylphenidate (MPH) administration on N-acetyl aspartate (NAA), creatine (Cr), and choline (Cho) levels in the anterior cingulate cortex, prefrontal cortex, striatum, and cerebellum in adult patients with attention deficit hyperactivity disorder (ADHD). This was the first study to investigate the relationship between DAT gene variable number tandem repeat (VNTR) polymorphisms and the responses of brain metabolites to MPH. PATIENTS AND METHODS: Samples in this study were collected from 60 patients aged between 18 and 60 years with ADHD according to DSM-IV criteria. Genetic analysis of DAT1 gene polymorphisms was carried out using blood samples obtained after a detailed clinical evaluation. Levels of NAA, Cr, and Cho were measured in the anterior cingulate cortex, prefrontal cortex, striatum, and cerebellum by magnetic resonance spectroscopy. After this evaluation, 10 mg of MPH was given orally to patients, and the levels of the same metabolites were measured 30 min later. RESULTS: No marked difference in NAA, Cr, or Cho levels was detected before and after MPH administration with respect to the DAT1 gene VNTR polymorphisms. A considerable increase in Cr levels in the cerebellum was identified after MPH administration in individuals with the 10/10 repeat genotype as the DAT1 VNTR polymorphism (p=0.008). CONCLUSIONS: An increase in the previously decreased blood flow after MPH therapy may induce an increase in creatine levels in patients with the 10/10 repeat genotype. Our results thus suggest that the 10R allele as the DAT1 gene VNTR polymorphism might be associated with MPH-related changes in brain metabolites in adults with ADHD.

Objective: Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) are neuro-trophins and they are critical regulators of the survival, differentiation, growth and plasticity of neuronal networks. There is plenty of evidence suggesting the involvement of altered levels of expression of neurotrophic factors in the pathophysiology of neuropsychiatric disorders. However, the relationship between neurotrophins and major depression (MD) remains unclear. In this study, we assessed the relationship between the BDNF, NT-3, NT-4 gene expression levels in blood cells and MD. Methods: In a case-control study, total RNA was obtained from blood cells, 51 MD patients (diagnosed according to the DSM-5 criteria) and 75 healthy controls. Detected with quantitative Real Time PCR, expression levels of BDNF, NT-3, NT-4 genes were compared between the groups. Results: In this study, BDNF expression levels of the patients with MD were significantly higher than the control group but no statistically significant difference between NT-3 and NT-4 expression levels. There was no differences in expression levels of BDNF, NT-3 and NT-4 genes in MD patients with family history. There was no statistically significant difference in the BDNF, NTF-3 and NTF-4 expression levels among the sex groups for the patient group and no statistically significant difference between MD patients according to antidepressant usage time. Discussion: Not only in understanding the pathogenesis of MD but also in the follow-up of treatment, expression level changes of BDNF gene in blood cells of MD patients must be considered because of the bidirectional movement of BDNF between the periphery and the brain and effect of changing serum BDNF levels.

Wilson's disease (WD) is a rarely seen autosomal recessive inherited genetic disease of copper metabolism, which leads to various hepatic, orbital and neuropsychiatric disorders. Neuropsychiatric symptoms are due to degeneration that results from the acccumulation of copper in the neurons of the brain, especially in the basal ganglia. Clinicians should consider that toxicity of copper might trigger the episode in a patient with WD, who displays a manic episode. When persistent manic symptoms are encountered in WD, treatment of copper toxicity should be checked and necessary consultation should be performed. In this case report, a patient with WD who developed a manic episode as a result of stopping d-penicillamine treatment is presented, and improvement of clinical symptoms when d-penicillamine was added to the psychiatric treatment is emphasized.

Objective: Electroconvulsive therapy (ECT) can be given as the form of acute, continuation or maintenance ECT according to the process of administration. We report our 7 years' observation with acute and maintenance ECT in a university hospital in Turkey. Methods: The medical records of the hospitalized patients treated with acute or maintenance ECT between the years 2007 and 2013 was retrospectively analyzed. The sociodemographic characteristics, diagnosis, data of ECT and the co-administered psychotropic drugs were recorded. The frequency of ECT was calculated by identifying the total number of the hospitalized patients during the study period from the hospital records. Results: A total number of 1,432 female and 1,141 male patients hospitalized in a period of 7 years, with a total number of 111 patients treated with ECT. The ratio of ECT was 4%, maintenance/acute ECT 11%. For acute ECT, affective disorders (65.3%) and psychotic disorders (21.6%) were among the leading diagnoses. Maintenance ECT, the diagnosis was; 6 affective disorders, 4 psychotic disorders and 1 obsessive compulsive disorder. There was a significant difference between the patients receiving acute and maintenance ECT in terms of age, duration of illness, and number of previous hospitalizations and ECTs. Conclusion: The percentage of patients treated with acute ECT is lower in our institution than that in many other institutions from our country. Acute and maintenance ECT should be considered as an important treatment option particularly for patients with long disease duration, a high number of hospitalizations and a history of benefiting from previous ECTs. Copyright © 2016, Korean College of Neuropsychopharmacology.

The effects of methylphenidate (MPH) treatment on N-acetyl aspartate (NAA), choline and creatine are being examined in individuals with different subtypes of attention deficit hyperactivity disorder (ADHD). Sixty ADHD subjects were included into the study aging between 18 and 60 years. Levels of NAA, creatine and choline in anterior cingulate cortex, cerebellum, striatum and dorsolateral prefrontal cortex were measured with magnetic resonance spectroscopy. Then, 10 mg oral MPH was given to the subjects and the same metabolite levels were measured after an interval of 30 min. Distribution of the patients according to the ADHD subtypes was as follows: 21 of them (35.0%) were in the inattentive type, 11 of them (18.3%) were in the hyperactive type and 28 of them were (46.7%) in the combined type. Changes of brain metabolite levels after MPH were found not to be statistically significantly different between the subtypes. The increase of choline levels after MPH compared to the levels of choline before MPH in striatum in the combined type patients were statistically significant. No clear association was found between ADHD subtypes and changes of brain metabolites with use of MPH in adult ADHD. © 2015 Elsevier Ireland Ltd.

Objective The synaptosomal-associated protein of 25 kDa (SNAP-25) gene is a presynaptic plasma membrane protein and an integral component of the vesicle docking and fusion machinery mediating secretion of neurotransmitters. Previously, several studies reported association between SNAP-25 and attention deficit hyperactivity disorder (ADHD). We investigated whether these SNAP-25 polymorphisms (MnlI T/G and DdelI T/C) were also associated with ADHD in the Turkish population. Methods: Our study comprised unrelated 139 subjects who met DSM-IV criteria for ADHD and 73 controls and all were of Turkish origin. Genetic analyses were performed and patients were evaluated with Wender-Utah Rating Scale and Adult ADD/ADHD DSM IV-Based Diagnostic Screening and Rating Scale. Results: SNAP-25 DdelI polymorphism was not associated with ADHD but there was a statistically significant difference between ADHD patients and controls for SNAP-25 MnlI polymorphism. For SNAP-25 MnlI polymorphism patients with G/G genotype of the SNAP-25 gene MnlI polymorphism had higher Wender-Utah scores and higher scores in the 1st and 3rd parts of adult ADD/ADHD Scale. Conclusion: We detected a significant association of the MnlI polymorphism in our ADHD sample which was similar to previous findings. Our study also revealed that SNAP-25 MnlI polymorphism was also associated with symptom severity of ADHD. This study is also, the first report on the association of SNAP-25 with ADHD in the Turkish population. © 2014 Korean Neuropsychiatric Association.

Objective The etiology of attention deficit hyperactivity disorder (ADHD) has not been entirely clarified yet. Structural and metabolic differences at the prefrontal striatal cerebellary system and the interaction of gene and environment are the main factors that thought to play roles in the etiology. Genetic investigations are performed especially about the dopamine pathways and receptors. In this study; it was aimed to investigate the association of the synaptobrevin-2 (VAMP-2) gene Ins/Del polymorphism and syntaxin 1A gene intron 7 polymorphism, which take place in encoding presynaptic protein, with adult ADHD. Methods One hundred thirty-nine patients, having ADHD aging between 18 and 60 years and 106 healthy people as controls were included into the study. DNA samples were extracted from whole blood and genetic analysis were performed. Results A significant difference was determined between ADHD and VAMP-2 Ins/Del polymorphism and syntaxin 1A intron 7 polymorphism according to the control group. These polymorphisms were found not to be associated with subtypes of ADHD. Conclusion It is supposed that synaptic protein genes together with dopaminergic genes might have roles in the etiology of ADHD. © 2014 Korean Neuropsychiatric Association.

It was aimed to investigate the association of the synapsin III gene -196 G> A and -631 C>G polymorphisms that takes place in an encoding presynaptic protein, with adult attention deficit hyperactivity disorder (ADHD). One hundred thirty-nine patients having adult ADHD and 106 controls were included in the study. DNA samples were extracted from whole blood and genetic analyses were performed. A significant difference was determined between ADHD and synapsin III gene -631 C>G polymorphism compared to the control group. No significant difference was determined between ADHD and synapsin III gene -196 G>A polymorphism. These polymorphisms were found not to be associated with subtypes of ADHD. It is supposed that synaptic protein genes together with dopaminergic genes might have roles in the etiology of ADHD. © Copyright 2013, Mary Ann Liebert, Inc. 2013.

Dikkat eksikliği hiperaktivite bozukluğu çocukluk döneminde başlayan ve temel belirtileri dikkatsizlik, aşırı hareketlilik ve dürtüsellik olan bir bozukluktur. DEHB'nin etiyolojisi henüz tam olarak aydınlatılamamıştır. Etiyolojide özellikle gen?çevre etkileşiminin ve prefrontal striatal serebellar dizgenin yapısal ve metabolik farklılığının rol oynadığı düşünülmektedir. Genetik araştırmalar daha çok dopaminerjik yolaklar ve dopamin reseptörleri üzerinedir. Bu çalışmada, erişkin DEHB ile presinaptik proteinleri kodlayan genlerden olan sinaptobrevin-2 (VAMP2), sinapsin III ve sintaksin 1A genlerinin ilişkisi ve bu genlerin nöropsikolojik test performansları üzerine etkisinin araştırılması hedeflenmiştir.Çalışmaya DEHB tanısı almış olan 18-60 yaş arası 139 olgu ve 106 sağlıklı kontrol alındı. Katılımcılardan kan örneği alınarak genetik analizler yapıldı. Her iki gruba Nörolojik Değerlendirme Ölçeği ve nöropsikolojik testler (Sayı dizleri, sözel bellek, stroop ve Wisconsin kart eşleme testi) uygulandı.DEHB ile VAMP2 geni İns/Del polimorfizmi, sinapsin III geni -631 C>G polimorfizmi ve sintaksin 1A geni intron 7 polimorfizmi arasında kontrol grubuna göre anlamlı bir ilişki bulundu. DEHB ile sinapsin III geni -196 G>A polimorfizmi arasında ise anlamlı bir ilişki bulunmadı.Erişkin DEHB grubunda sayı dizileri, sözel bellek ve stroop testlerinde kontrol grubuna göre anlamlı düzeyde düşük performans saptandı. WKET'de erişkin DEHB grubu ile kontrol grubu arasında farklılık bulunmadı. Erişkin DEHB grubunda silik nörolojik belirtilerde kontrol grubuna göre düşük performans saptandı.VAMP2 geni İns/Del polimorfizmi İns/İns genotipi sayı dizileri ve sözel bellek testlerinde kötü performans, stroop testinde daha iyi performans ile ilişkili bulundu. Sinapsin III geni -196 G>A polimorfizmi G/G genotipi sayı dizileri testinde düşük performans, sinapsin III geni -631 C>G polimorfizmi C/G genotipi sayı dizileri ve stroop testlerinde daha iyi performans ile ilişkili bulundu. Sintaksin 1A intron 7 polimorfizmi T/T genotipi sayı dizileri testinde daha iyi performans ile ilişkili bulundu. WKET performansı ile herhangi bir gen arasında ilişki bulunmadı.DEHB'nin etiyolojisinde dopamin genlerinin yanı sıra sinaptik protein genlerinin de rol aldığı, parietal korteks ve frontostriatal yolaklarda işlev bozukluğu olduğu düşünüldü. Riskli genler ile nöropsikolojik bulguların paralellik göstermediği düşünüldü. Attention deficit hyperactivity disorder (ADHD) is a disorder that begins in childhood and has main symptoms of inattention, overactivity and impulsivity. The etiology of ADHD has not been entirely clarified yet. Structural and metabolic differences at the prefrontal striatal cerebellary system and the interaction of gene and environment are the main factors thought to play a role in the etiology. Genetic investigations are performed especially about the dopamine pathways and receptors. In this study; it was aimed to investigate the association of the synaptobrevin-2 (VAMP2), synapsin III and syntaxin 1A genes, which take place in encoding presynaptic proteins, with adult attention deficit hyperactivity disorder and the effects of these genes on the neuropsychological test performances.One hundred thirty-nine patients, having ADHD aging between 18 and 60 years and 106 healthy people as controls were included into the study. Blood samples were taken from the participants and genetic analysis were performed. Neurological Grading Scale and neuropsychological tests (Digit span, verbal memory, stroop test and Wisconsin Card Sorting Test (WCST)) were performed to both groups.A significant difference was determined between ADHD and VAMP2Ins/Del polymorphism, synapsin III-631 C>G polymorphism and syntaxin 1A intron 7 polymorphism according to the control group. No significant difference was determined between ADHD and synapsin III-196 G>A polymorphism.Significantly low performance was determined on the digit span, verbal memory and stroop tests in the adult ADHD group according to the control group. No significant difference was determined between the adult ADHD group and the control group on the WCST. Low performance was determined at the neurological soft signs in the adult ADHD group according to the control group.While Ins/Ins genotype of VAMP2 Ins/Del polymorphism was found to be related to worse performance on the digit span and verbal memory tests, it was found to be related to better performance on stroop test. G/G genotype of synapsin III-196 G>A polymorphism was found to be associated with worse performance on the digit span test. C/G genotype of synapsin III-631 C>G polymorphism was found to be associated with better performance on the digit span and stroop tests. T/T genotype of syntaxin 1A intron 7 polymorphism was found to be associated with better performance on the digit span test. No association was found between WSCT performance and any genes.It is believed that dopaminergic genes together with synaptic protein genes might have roles in the etiology of ADHD and functional defects at the parietal cortex and frontostriatal pathways might interfere in this disorder. It was also believed that risky genes do not show any parallelism with neuropsychological signs. 123

Objective To investigate the effects sex and age on the methylphenidate HCl treatment in adult ADHD. Methods Sixty ADHD subjects were included into the study aging between 18 and 60 years. Levels of N-acetyl aspartate (NAA), creatine and choline in anterior cingulate cortex, cerebellum, striatum and dorsolateral prefrontal cortex were measured with magnetic resonance spectroscopy. Then, 10 mg oral methylphenidate HCl was given to the subjects and the same metabolite levels were measured after an interval of 30 minutes. Results Twelve (20%) of the subjects were women and 48 (80%) of them were men. Age distribution of subjects is as follows: 15 were between 18–24 years, 26 were between 25–30 years, 19 were older than 30 years. No difference was determined between NAA levels before and after methylphenidate in both sexes. Creatine levels were determined higher after methylphenidate in women in prefrontal cortex and in men in cerebellum. Choline levels were determined higher after methylphenidate in women in striatum. NAA levels were determined higher after methylphenidate in prefrontal cortex of 18–24 years old age group and in striatum and cerebellum of 25–30 years old age group. Creatine levels in striatum after methylphenidate were determined higher in 18–24 years old age group than 25–30 years old age group. No difference was determined between choline levels before and after methylphenidate in each age groups. Conclusion It is thought that pharmacotherapy can be effective on brain metabolites and this effect can vary upon sex and age.