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Amaç: Tipik antipsikotikler ve klozapin EEG anormalliklerine ve epileptik nöbetlere neden olabilir. Yeni kuşak antipsikotiklerin EEG üzerindeki etkileri çok fazla bilinmemektedir. Yapılan bu çalış- mada klozapin, ketiapin, risperidon ve olanzapin gibi atipik antipsikotikler, amisülpirid, aripiprazol, paliperidon gibi yeni diğer atipik antipsikotikler ve klorpromazin, haloperidol, zuklopentiksol, pimozid gibi tipik antipsikotiklerin EEG anormallikleri üzerine etkileri araştırılmıştır.Gereç ve Yöntemler: Şizofreni veya şizoaffektif bozukluk tanılı 102 hasta prospektif olarak de- ğerlendirilerek EEG’leri çekildi. Bunların 82’si atipik [klozapin (n:16), risperidon (n:20), ketiapin (n:10), olanzapin (n:14), diğer yeni atipik antipsikotikler (n:10)] ve tipik [haloperidol (n:5), klorpromazin (n:2), zuklopentiksol (n:3), pimozid (n:2)] antipsikotik kullanıyordu, 20’si ise ilaç kullanmıyordu. Bu üç alt grup; cinsiyet ve yaş uyumlu sağlıklı kontrol grubunun (n=29) EEG’leri ile karşılaştırıldı.Bulgular: Gruplar arasında demografik özellikler bakımından istatiksel olarak anlamlı fark saptanmadı. Hem ilaç kullanmayan hastaların hem de sağlıklı kontrollerin EEG’leri normaldi. Klozapin kullanan hastaların % 31,3’ünde (p < 0,05), ketiapin kullananların da %10’unda (p > 0,05) epileptik aktivite gözlendi. Epileptik aktivite dışındaki EEG anormallikleri tipik antipsikotik kullananların %58,3’ünde (p < 0,01), risperidon kullananlarında %35’inde (p < 0,01) saptandı. EEG ketiapin ve yeni atipik antipsikotik kullananların %80’inde normalken, tipik antipsikotik kullananların %33,3’ünde normaldi (p=0,012).Tartışma ve Sonuç: Burada klozapinin en epileptojen antipsikotik olduğunu ve tipik antipsikotiklerin EEG’yi en fazla bozduğunu bulduk. Ancak klozapin tedavisi alan psikotik hastalarda EEG bir gerekliliktir. Epilepsinin eklendiği psikotik hastalara yeni atipik antipsikotikler verilebilir, çünkü EEG üzerine en az istenmeyen etkiler bu ilaçlarla gözlenmiştir. Buna ilaveten antipsikotik ilaçlar ve epilepsi eşiği arasındaki kompleks ilişkileri açığa çıkarmak için daha fazla bilimsel araştırmaya ihtiyaç olduğunu da vurgulanmamız lazımdır., Aim: Typical antipsychotics and clozapine could cause EEG abnormalities and risk of epileptic seizures. Little is known about the effects of newer antipsychotics on EEG. The present study therefore examined the risk of EEG abnormalities associated with the use of atypical antipsychotics [clozapine, quetiapine, risperidone, olanzapine and new atypical antipsychotics (amisulpride, aripiprazole, paliperidone)] and of the typical antipsychotics (chlorpromazine, haloperidol, zuclopenthixol, pimozide).Materials and Methods: EEG patterns were prospectively investigated in 102 patients with schizophrenia or schizoaffective disorders. While 82 out of the 102 patients were under atypical [clozapine (n=16), risperidone (n=20), quetiapine (n=10), olanzapine (n=14), and new atypical antipsychotics (n=10)] and typical [haloperidol (n=5), chlorpromazine (n=2), zuclopenthixol (n=3), pimozide (n=2)] antipsychotic treatment, 20 of them were not under any treatment. These three groups were compared with a sex- and aged- matched control group of healthy volunteers(n=29).Results: No statistically significant difference regarding demographic characteristics was found between the groups. Both the patients who were not on any medication and the healthy volunteers had normal EEG’s. Epileptic activity was observed in 31.3% of the patients under clozapine treatment (p0.05). EEG abnormalities other than epileptic activity were observed in 58.3% of the patients under typical antipsychotics (p

WOS: 000294350400019, PubMed: 21935841, Soccer, one of the most popular sports worldwide among young men, can result in a wide range of orthopedic injuries. Although vascular injuries such as dissection occur rarely, they can cause significant mortality if left undiagnosed. We report herein a 31-year-old male who suffered a large middle cerebral artery infarction due to traumatic internal carotid artery dissection after a ball struck his head and neck. He recovered with mild neurologic deficit after decompressive surgery.

Carotid cavernous fistula (CCF) is an abnormal communication between cavernous sinus and carotid arterial system. Diagnosis depends on clinical manifestations and MRI findings and angiography. Clinical presentation of CCFs is characterized with chemosis, orbital bruit and pulsatile proptosis. Cranial nerve dysfunction and orbital pain might accompany these symptoms. Although spontaneous remission might occur, sometimes CCF might develop life threatening complications. Here in this case we presented a patient with CCF who afterwards developed bilateral thalamic infarct. Cerebral ischemia in CCF is a rare complication and CCF together with bilateral thalamic infarct has not been reported before.

Homocysteine, a sulfur-containing amino acid, is an intermediate during the conversion of methionine to cysteine. Homocysteine can cause vascular injury and atherosclerotic plaque instability. In addition, homocysteine may be directly correlated with hyperlipidemia and lipoprotein(a) and inversely with high-density lipoprotein cholesterol. However, the results regarding the association of homocysteine level with subtypes of stroke and traditional risk factors for stroke have been inconsistent, perhaps due to ethnic differences. The aim of this study was to evaluate the role of serum homocysteine levels in Turkish patients diagnosed with atherosclerotic stroke and those with cardioembolic stroke. We measured homocysteine levels, traditional risk factors for stroke (hypertension, diabetes mellitus, and smoking) and lipoprotein(a) levels in 103 patients with large-vessel atherosclerotic stroke, 37 patients with cardioembolic stroke, and 37 controls with normal cranial magnetic resonance imaging. Only hypertension was found to be a risk factor in all patient groups (p = 0.001). Hyperhomocysteinemia (homocysteine level ? 15.90 µmol/L) was more common in patients with large-vessel atherosclerotic stroke and cardioembolic stroke (p = 0.0435 and p = 0.007, respectively); nevertheless, it was found to be a risk factor only in patients with cardioembolic stroke (p = 0.023; odds ratio (OR): 5.745). Furthermore, in the patients with large-vessel atherosclerotic stroke, hyperhomocysteinemia was positively correlated with the lipoprotein(a) level (r = 0.227, p = 0.035). In conclusion, hyperhomocysteinemia is common in patients with large-vessel atherosclerotic stroke and cardioembolic stroke. More importantly, hyperhomocysteinemia is an independent risk factor only for cardioembolic stroke in the Turkish population. © 2009 Tohoku University Medical Press.

Background and purpose: Stroke is a heterogeneous multifactorial disease. Hence, a large number of candidate genes are involved in stroke pathophysiology, such as blood pressure regulation and atherosclerosis. Although angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism is considered to have a role in hypertension, coronary artery disease, and myocardial infarction, its relationship with cerebrovascular disease and hypertension in stroke in different ethnic populations is still inconsistent. Methods: ACE I/D polymorphism, detected by polymerase chain reaction (PCR), was studied in 97 patients with large-vessel and 60 patients with small-vessel atherosclerotic stroke (44 asymptomatic, 16 symptomatic lacunes) and 85 healthy subjects with normal brain imaging. The demographic data, lipid profile and risk factors of patients and controls were obtained retrospectively. Results: ACE genotypes were in Hardy-Weinberg equilibrium in both patients and controls. Prevalences of DD, ID and II genotype were 41%, 40%, and 19%, respectively, in the stroke group. Differences in ACE I/D polymorphism distribution were statistically insignificant between the groups. This lack of association between stroke and ACE I/D polymorphism did not change in the presence of traditional risk factors (hypertension, diabetes mellitus, smoking, and dyslipidemia). Although hypertension was significantly more common in the patient groups, ACE I/D polymorphism showed no effect on hypertension risk. This lack of association also did not change according to groups or in the presence of diabetes mellitus, male gender or smoking. Conclusion: ACE I/D polymorphism did not predict the risk of stroke or hypertension in our population living in the western Black Sea region of Turkey. © 2009 Elsevier B.V. All rights reserved., 106S235-SBAG-HD-158, Most of the controls were taken from another study sponsored by the Scientific and Technological Research Council of Turkey (STRCT) (no. 106S235-SBAG-HD-158). Hence, we wish to thank STRCT.

Background and purpose: Apolipoprotein E (apoE) polymorphism is suggested to be a risk factor in stroke in some populations, either by affecting lipid parameters or independently. Its effect on lipoprotein(a) [Lp(a)] is not known. The roles of apoE polymorphism and of high Lp(a) levels in atherosclerotic stroke (AS) in the Turkish population are unclear. Our aim was to investigate the relationship of apoE alleles and Lp(a) level with AS and the relationship of apoE alleles with Lp(a) and other lipid parameters. Methods: ApoE polymorphisms and lipid parameters were prospectively evaluated in 85 patients and 77 controls with normal brain imaging. Results: Only hypertension, diabetes mellitus, associated vascular diseases and decreased high-density lipoprotein cholesterol levels were found to be independent risk factors for stroke. However, in the presence of apoE/E4 allele, increased low-density lipoprotein cholesterol (LDL-chol), apolipoprotein B (apoB) and Lp(a) levels and in the presence of apo E/E3 allele, only Lp(a) levels were determined as risk factors. Conclusion: This study showed that while apoE polymorphism was not a risk factor itself, high Lp(a), LDL-chol and apoB were determined to be risk factors in E3 or E4 carriers. © 2008 Elsevier B.V. All rights reserved.