Association Between Carpal Tunnel Syndrome and Abdominal Obesity

OBJECTIVE: Obesity has been suggested as a risk factor for carpal tunnel syndrome (CTS). Previous studies on the association of CTS and obesity have generally considered body mass index (BMI). However, the relationships between CTS and waist circumference or waist-to-hip ratio (WHR), which are known as more sensitive measures for abdominal obesity, have not been studied previously. In this study, it was aimed to evaluate the role of BMI and abdominal obesity in patients with CTS. METHODS: Female patients who applied to the neurology outpatient clinics with pain, numbness, paresthesia, or dysesthesia in the hands were included. The patients were divided into two groups, according to the clinical evaluation, as CTS or non-CTS. CTS diagnosis was electrophysiologically confirmed in 44 patients. Thirty-one subjects who were not diagnosed as CTS electrophysiologically were recruited as the control group. Clinical findings, nerve conduction studies and anthropometric measurements (height, weight, BMI, hip circumference, waist circumference and WHR) of CTS patients were compared with those of the control group. RESULTS: The CTS group had significantly higher BMI, waist circumference and WHR values compared to the control group (for each parameter, p< 0.0001). The rates of obesity in the CTS group were 55.8%, 47.7% and 34.9%, respectively, according to waist circumference, BMI and WHR measurements. In the CTS group, 16% of the patients, who were defined as non-obese according to BMI, were determined as obese according to waist circumference. In the CTS group, significant positive correlations were found between BMI and WHR and median-ulnar sensory interpeak latency of the fourth digit (r= 0.26, p< 0.05; r= 0.25, p< 0.05, respectively). CONCLUSION: In this study, it was found that abdominal obesity is an important risk factor for CTS, and nerve conduction may be affected by waist circumference, BMI and WHR. In addition to general obesity, abdominal obesity may be an important risk factor for CTS

Post-Cough Dissection of Carotid Artery: Case with Fibromuscular Dysplasia

Dissection of the internal carotid artery due to fibromuscular dysplasia is a rare cause of transient ischemic attack in young patients. Usually, the diagnosis of fibromuscular dysplasia is usually based on conventional and/or magnetic resonance angiography. A 44- years-old female patient presented with transient ischemic attack after severe cough caused by acute laryngitis. Magnetic resonance imaging disclosed subacute left temporal infarction and dissection of the internal carotid artery. Carotid angiography demonstrated the dissection of the internal carotid artery and a “string of beads” appearance confirming fibromuscular dysplasia. The case was is reported because of the unique feature

Cryptogenic Isolated Cortical Venous Infarct: A Report of Three Cases

Cortical vein infarction without dural sinus involvement is extremely rare. Herein, we present three patients with headache, partial seizure and right-sided numbness. On neurological examination, focal neurologic deficit was not observed in our patients. Magnetic resonance imaging revealed cerebral ischemia which showed as hypointense on T1-weighted images and hyperintense on T2-weighted images that do not follow the boundary of arterial territories, indicating cortical venous infarct. Cortical venous infarct should be suspected in patients who present with sudden onset headache and/or focal epileptic seizures even if there is no neurologic deficit. The diagnosis and treatment of cortical venous infarct should be considered as an emergency because of the high potential for full recovery with anticoagulant treatment

L-Name ile hipertansiyon oluşturulan sıçanların beyin dokularındaki oksidatif stres üzerine lisinoprilin etkisi

Amaç: Arteriyel hipertansiyon sıklıkla oksidatif stresle bağlantılı patolojilerle ilişkilidir. Anjiotensin Dönüştürücü Enzim (ADE) inhibitörleri hipertansiyon ve koroner kalp hastalıkları tedavisinde etkili ve güvenilir bir şekilde kullanılmaktadır. Ancak hipertansiyonla ilişkili serebrovasküler ve nörodejeneratif hastalıklardaki ADE inhibitörleri kullanımının önemi henüz netlik kazanmamıştır. Bu çalışmada, bir ADE inhibitörü olan lisinoprilin L-NAME (N? -nitro-L-Arjinin Metil Ester hidroklorid) ile hipertansiyon oluşturulan sıçanların beyin dokularındaki oksidatif stres ve antioksidan enzim aktiviteleri üzerine olan etkisini araştırmayı amaçladık. Yöntem: 32 adet Sprague-Dawley cinsi sıçan 4 gruba bölündü: Kontrol, L-Name, L-Name ve lisinopril, sadece lisinopril. Hipertansiyon, sıçanların içme sularına 75mg/kg L-Name katılıp, ağız yoluyla 6 hafta verilerek oluşturuldu. Sıçanlar 6 hafta süreyle 10mg/kg dozunda lisinopril ile tedavi edildi. Tail cuff metoduyla birinci, üçüncü ve altıncı haftalarda sistolik kan basınçları ölçüldü. Malondialdehid (MDA), süperoksit dismutaz (SOD), katalaz (CAT) ve glutatyon peroksidaz (GSH-Px) enzim aktiviteleri beyin dokusundan ölçüldü. Nitrik oksit (NO) seviyeleri ise plazmadan ölçüldü. Bulgular: Bizim sonuçlar L-NAME'nin hayvanların sistolik kan basıncında artışa yol açtığını göstermiştir. Lisinoprilin antihipertansif etkisi gözlendi. L-Name verilen grupta malondialdehid seviyeleri önemli oranda arttı ve antioksidan enzim aktiviteleri azaldı (p0.05). Sonuçlar: Çalışmamızda, hipertansiyon beyin dokusunda oksidatif hasara yol açmıştır. Lisinopril hipertansiyon nedenli oksidatif hasarı önlemesine rağmen, doğrudan antioksidan etkilere sahip değildi. Lisinoprilin beyin dokusundaki etkisinin kesinleşmesi için ileri çalışmalara ihtiyaç vardırObjective: Arterial hypertension is often associated with pathologies related with oxidative stress. Angiotensin converting enzyme (ACE) inhibitors have been used as a safe and effective treatment of hypertension and coronary heart disease. However, the significance of ACE inhibitor usage in hypertension-induced cerebrovascular and neurodegenerative diseases is still unknown. In this study, we aimed to investigate the effects of lisinopril, an ACE inhibitor, on oxidative stress and antioxidant enzyme activities in brain tissues of rats with L-NAME (N?-Nitro-L-Arginine Methyl Ester hydrochloride) induced hypertension. Methods: Thirty-two Sprague-Dawley rats were divided into four groups: Control, L-NAME, L-NAME plus lisinopril, and only lisinopril. Hypertension was induced by oral administration of the L-NAME (75 mg/kg/day) in drinking water for 6 weeks. Rats were treated with Lisinopril (10 mg/kg/day) for six weeks. Systolic blood pressures were measured at the first, third and sixth weeks by using tail cuff method. Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GSH-Px) activity were measured from the brain tissue. Nitric oxide (NO) levels were measured from plasma. Results: Our results showed that L-NAME leads to an increase in systolic blood pressure of animals. The antihypertensive effect of lisinopril was observed. MDA level was significantly increased, and antioxidant enzymes activities were decreased in L-NAME given group (p0.05). Conclusion: In our study, hypertension led to oxidative damage in brain tissues. Although lisinopril prevents the hypertension induced oxidative damage, direct antioxidant effect was not observed. Further studies are needed in order to gain certainty effect of lisinopril in brain tissue

Effect of Caffeic Acid Phenethyl Ester on Cerebellar Tissue Damage Secondary to Methanol Intoxication: Experimental Study

OBJECTIVE: Previous studies have shown the role of oxidative stress in methanol neurotoxicity. CAPE is noted to have an antioxidant property by many experimental studies. In this study, we aim to investigate whether CAPE has a protective effect against oxidative stress observed in the cerebellar tissue in methanol intoxication METHODS: In this study, a total of 40 rats were split into 5 groups: Control group (n=8), MTX-alone group (n=8), MTX+Methanol group (n=8), MTX+Methanol+Ethanol group (ie., ethanol group) (n=8), and MTX+Metanol+CAPE group (ie.,CAPE group) (n=8). All the rats except the control group were delivered methotrexate (MTX) therapy (0.3 mg/kg/day, via i.p. route) for 7 days in order to induce methanol toxicity. The control group received no drug therapy. Seven days later, 3 g/kg (i.p.) methanol was delivered in the ethanol and CAPE groups. Four hours after the delivery of methanol, ethanol group received 0.5 g/kg ethanol (i.p.) and CAPE group received 10 µmol/kg CAPE (i.p.), while the other groups were delivered only saline (i.p.). The rats were decapitated at 8 hours and the cerebellar tissues were removed. PON-1, TAS, and MDA levels were measured in the tissues. RESULTS: MTX-alone group demonstrated decreased TAS and PON-1 levels (p=0.001 and p=0.004, respectively) and increased MDA level (p=0.001), as compared to the Control group. When MTX+Methanol group was compared with the MTX-alone group, MTX+Methanol group was found to have decreased TAS and PON-1 activities (p=0.037 and p=0.046, respectively) and increased MDA level (p=0.022). The Ethanol group was found to show a significant decrease in MDA level (p=0.001), as compared with the MTX+Methanol group. The CAPE group exhibited increased TAS and PON-1 levels (p=0.001 and p=0.001, respectively) and decreased MDA level, as compared with the MTX+Methanol group. CONCLUSION: Cerebellum demonstrates oxidative stress secondary to methanol intoxication. CAPE therapy is more effective against cerebellar oxidative stress than ethanol therap

Investigation of Mean Platelet Volume in Patients with Multiple Sclerosis

OBJECTIVE: Alterations in platelet function have been observed in patient with multıple sclerosis (MS). Mean platelet volume (MPV) is a marker of the platelet activity and is reported to increase in vascular diseases. The aim of this retrospective study was to investigate the correlation between MPV and MS. METHODS: The patient group consisted of 46 MS patients who were presented to MS attacks (males/females: 10/36, mean age: 34.3±9.4). In the MS patients, during the attack MPV value compared with the value of MPV after attack. Also, their MPV values were compared with those of 38 age/sex-matched healthy individuals (males/females: 14/24, mean age: 36.4±10.4). RESULTS: No difference was found in terms of MPV values between during the attack of MS (8.0±1.2) and after MS attack (7.9±1.2), and no relation was found between MPV and EDSS parameters (p>0.05). No difference was found in terms of MPV values between the MS group (8.1±1.3) and control group (8.1±1.1) (p>0.05). CONCLUSION: As a result, no significant change in MPV was seen between the during the MS attack and after the MS attack. This finding support that platelet activation not an important role pathogenesis in MS. But, relation between MS and MPV should investigated with prospectively

The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

OBJECTIVE: The mean platelet volume (MPV) is a biomarker of platelet function and activity. The influence of platelet function disorders on the aetiology of intracerebral haemorrhages (ICH) and mortality is not clear yet. The purpose of this study is to investigate the change in the MPV values in patients with ICH and to observe its influence on mortality in a retrospective manner. METHODS: Sixty-six patients with intracerebral haemorrhage (32 males, 34 females; mean age: 61.9± 16.9) were enrolled in the study. Patients with ICH were divided into two groups as those who died within the first 10 days and those who survived. The MPV values and the haematoma volumes were compared between the groups. Also, the MPV values and platelet counts of the patients with ICH were compared with the values of healthy volunteers from similar age and sex groups (27 males, 17 females; mean age: 59.9 ±3.2). RESULTS: The MPV values of the patients with ICH measured within 24 hours following the intracerebral haemorrhage (8.33 ± 1.27 fl/mL) were statistically significantly higher than the MPV values of the control group (7.76 ± 1.14 fl/mL) (p=0.018). The platelet counts of the patients with ICH also measured within the first 24 hours (235.8±94.9 x103/mL) were statistically significantly lower than the platelet counts of the control group (279.1 ± 94.9 x103/mL) (p=0.022). No statistically significant difference in terms of the MPV values and platelet counts was observed between the patients with ICH who died within the first 10 days and those who survived (p>0.05). However, the difference observed in the haematoma volume between the patients with ICH who died within the first 10 days (31.1 ±33.7 ml) and those who survived (8.7± 13.4 ml) was statistically significant (p<0.001). No correlation was found between the haematoma volume and the MPV value in the patients with ICH. CONCLUSION: The increase observed in the mean platelet volume in patients with ICH may point to a disorder in the platelet function. No relationship was found between the increase in the MPV and the mortality rates