Serdar Tasdemir

The factors causing bad sleep.

Dear Sir, We have read Aric A. Prather et al.’s study entitled ‘Tired telomeres: Poor global sleep quality, perceived stress, and telomere length in immune cell subsets in obese men and women’ with great interest. In this study, they aimed to investigate the associations between self-reported sleep duration, measured via daily diary reports, and subjective global sleep quality, assessed using the Pittsburgh Sleep Quality Index, with telomere length in granulocytes, PBMCs and sorted cells (CD4+ and CD8+ T lympho-cytes, and B lymphocytes) in a sample of obese men and women (Prather et al., 2015). When we inspected the article, in the model of the study, the exclusion criteria were as follows: untreated hypothyroidism, use of immunomodulatory medications in the past 6 months (e.g., corticosteroids), being pregnant or planning to become pregnant in the next 12 months, presence of a psychiatric or medical condition that would preclude participation in the group intervention, current bulimia and/or weight loss of 15 lbs or more in the past 3 months, and participation in mindfulness-based therapies in the past 2 months prior to enrollment. The study evaluating the prevalence of sleep continuity disorders in women during menopausal transition reported that difficulties in falling asleep, difficulties in maintaining sleep and waking up too early had been found in 57.8%, 70%, 60.7% of women, respectively (Słopień et al., 2015). However, another study evaluating the sleep quality in different menopause status groups showed more deep and longer total sleep time in postmenopausal age (Young et al., 2003). Caffeine is another factor deteriorating the sleep hygiene. It was shown that caffeine taken before bedtime had increased the sleep onset latency and decreased the total sleep time (Drake and et al., 2013). In a review about the about the sleep hygiene, Leah A. Irish et al. stated that nicotine and alcohol disturbed the sleep and these matters were avoided to have a good sleep (Irish et al., 2015). When we consider these factors, the results in Aric A. Prather et al.’s study may be controversial without considering those factors. We believe that the authors took care of such factors, possibly a typing error occurred during writing the article. Authors should declare these issues and readers should keep in mind that these factors might have effects on sleep quality.

Vitamin B12 and cognitive decline.

They reported significantly decreased concentration of 25(OH) D and increased concentration of homocysteine in the serum of patients with dementia when compared to age-matched controls and patients with mild cognitive impairment (MCI) and also reported that an association of serum levels of vitamin D with markers of cognitive decline as well as serum homocysteine levels was observed in patients with dementia and MCI when compared to controls.[1]

Decreased cerebral vasomotor reactivity in patients with obstructive sleep apnea syndrome

OBJECTIVE In obstructive sleep apnea syndrome (OSAS), any of the activated neural, vascular, hemodynamic, metabolic, inflammatory, and thrombotic mechanisms may be related to increased cerebrovascular disease and risk of death; however, the possible pathophysiological process between obstructive sleep apnea syndrome and stroke has not been clearly explained. We hypothesize that alterations in vasomotor reactivity in patients may be responsible for their altered cerebral blood flow, and may contribute to the increased risk of ischemic stroke. METHODS A total of 30 untreated patients with severe obstructive sleep apnea and 26 control subjects were included in the study. The mean blood flow velocity and breath holding index were measured in middle cerebral artery bilaterally in both patient and control groups by using transcranial Doppler ultrasound. We compared the values between two groups. RESULTS The mean blood flow velocity and breath holding indexes were significantly decreased in the patient group when compared with the control group. There were no correlations between cerebral hemodynamic parameters and polysomnographic findings in patients. CONCLUSION Our findings suggest that there was a deteriorated vasodilator response to hypercapnia in patients with OSAS. This deterioration may stem from chemoreceptors or endothelial damages that lead to vascular relaxation and vasodilatation in cerebrovascular circulation. This impaired cerebral vascular regulation may contribute to the increased risk of stroke in patients with OSAS.

The causes of worsening sleep quality

Dear Sir, We have read the study entitled ‘Sleep status of cervical cancer patients and predictors of poor sleep quality during adjuvant therapy’ written by Tian J. et al. with great interest. In this study, they aimed to detect the prevalence of poor sleep quality in cervical cancer patients prior to and after adjuvant therapy and whether the prevalence of poor sleep quality in cervical cancer patients is higher than that in the general population. They reported that the prevalence of poor sleep quality in stages I and II cervical cancer patients had been approximately twice that of women in the communities, and they concluded that cancer treatment was responsible for sleep problems [1]. According to the model the authors describe, they included individuals with 20 to 70 years of age and literate, without cancer and without mental or psychological disease as controls. The patient arm included people who were more than 20 days post-operative, without mental or psychological disease history, aged 20 to 70 years and literate. Only patients receiving adjuvant chemotherapy or adjuvant chemotherapy + radiotherapy were included. They excluded patients with a history of sleep disorders prior to cancer diagnosis [1]. Studies of other health conditions have also demonstrated a number of different factors that influence sleep quality. The studies about diabetes mellitus (DM) indicate that sleep disorders are more common in the patient with DM compared to without DM [2, 3]. In a study evaluating 10,000 participants aged 35 to 74 years of a population, it was reported that cardiovascular risk factors and diseases had an effect on the severity of complaints in sleep disturbances [4]. Menopause is another factor influencing the sleep. Women in midlife have increased sleep complaints compared to men in these ages [5–7]. In a clinical review about sleep hygiene, Leah A. Irish stated that alcohol, caffeine, nicotine, and daytime nap might influence sleep quality [8]. Unfortunately, the authors failed to consider those factors as exclusion criteria. The results in Tian J.’s study may be controversial without considering those factors. Perhaps the authors at the time of preparing their manuscript failed to include these other relevant factors. It is important to acknowledge there are many factors that can influence sleep quality to ensure readers have a full appreciation of the causes of sleep problems.

Cortical excitability in restless legs syndrome

To the Editor: We have read with great interest the study of Lanza et al. about cortical excitability in obstructive sleep apnea syndrome (OSAS) and restless legs syndrome (RLS) [1]. In their study, they aimed to detect any changes in the electrocortical excitability of patients with OSAS and RLS. Lanza et al. reported that resting motor threshold was higher in OSAS than in RLS and controls and cortical silent period (CSP) was shorter in RLS only when compared apneic patients, whereas it was similar between OSAS and controls [1]. They also reported that OSAS subjects exhibited slightly longer central motor conductivity, whereas motor evoked potential (MEP) amplitude was smaller in both patient groups and the intracortical inhibition ratio at interstimulus interval of 3 ms was decreased in RLS patients only [1]. On the other hand, Oz et al. evaluated 25 patients with RLS and 25 healthy volunteers by examining cutaneous silent period (CuSP) latency and duration in the upper and lower extremities; in patients with RLS, the variables were examined before and after pramipexole treatment [2]. In this study, Oz et al. reported that lowerextremity CuSP latency was longer and CuSP duration was shorter in RLS patients compared with controls [2]. In the patient group, CuSP durations in the upper and lower extremities were prolonged after treatment compared with pre-treatment values. The authors concluded that short CuSP durations in the lower extremities may occur due to decreased inhibitory spinal reflexes in the CuSP and decreased inhibition of the inhibitory anterior-horn interneurons following cortical hyperexcitability and cortical inhibitory mechanism dysfunction and recovery after treatment. However, Lanza et al. did not state the study of Oz et al. in the conclusion, although they tried to explain the studies about cortical excitability. The discussion by Lanza et al. [1] would be strengthened if they take into consideration the findings of Oz et al. [2].

Asymmetric Dimethylarginine as a Vascular Risk Factor in Antiepileptic Drug Treated Individuals

We have read the recent article by El-Farahaty et al with great interest. They studied metabolic and atherogenic effects of longterm antiepileptic drugs in a group of 69 Egyptian epileptic patients on antiepileptic drug monotherapy for at least 2 years. Patients were divided into 5 subgroups according to antiepileptic drugs used (valproate, carbamazepine, lamotrigine, topiramate, and levetiracetam). They recruited 34 controls for their study. The authors have measured fasting lipid profile (total cholesterol, triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol), lipoprotein(a), homocysteine, free thyroxine, thyroid-stimulating hormone, and common carotid artery intima-media thickness in patient and control groups. They demonstrated significantly higher mean values of low-density lipoprotein cholesterol, low-density lipoprotein/high-density lipoprotein ratio, lipoprotein(a), homocysteine, significantly lower mean value of high-density lipoprotein cholesterol, and also significantly larger diameter of common carotid artery intima-media thickness in each drug treated group versus control group. The authors concluded that their study supported that long-term monotherapy treatment with valproate, carbamazepine, lamotrigine, and topiramate had altered markers of vascular risk that might enhance atherosclerosis, whereas levetiracetam exerted minimal effect. They have discussed atherosclerotic markers together with lipid profile, subclinical hypothyroidism, and carotid artery intima-media thickness and assessed their individual longterm metabolic and vascular effects. However, the authors failed to note the role of asymmetric dimethylarginine on the vascular system. It is an endogenous inhibitor of nitric oxide synthase and may cause endothelial dysfunction. A high level of asymmetric dimethylarginine is associated with many of cardiovascular risk factors. Available prospective studies suggest associations between circulating asymmetric dimethylarginine concentration and cardiovascular disease outcomes. Oz et al first demonstrated elevated asymmetric dimethylarginine levels in epileptic patients treated with antiepileptic drugs. They studied asymmetric dimethylarginine levels in 35 newly diagnosed epilepsy patients before and after valproic acid (n 1⁄4 17) and carbamazepine (n1⁄4 18) monotherapies. They found that asymmetric dimethylarginine levels significantly increased after (3rd month) valproic acid (P 1⁄4 .002) and carbamazepine (P 1⁄4 .024) groups. They concluded that elevated asymmetric dimethylarginine levels may be responsible for the increased cardiovascular risk in patients with epilepsy who are receiving antiepileptic drug therapy. This issue has been discussed previously. Ozdemir et al investigated serum asymmetric dimethylarginine, homocysteine, lipid, folate, and vitamin B12 levels in 44 epileptic children under valproic acid monotherapy and 28 healthy children aged between 4 and 16 years. Serum Hcy, asymmetric dimethylarginine, and vitamin B12 levels were higher in patients than in controls (P < .001 for tHcy and asymmetric dimethylarginine levels; P < .05 for vitamin B12 levels). On the other hand Emeksiz et al found no significant differences in homocysteine, asymmetric dimethylarginine, nitric oxide, vitamin B12 and folate levels between children treated with valproic acid, oxcarbazepine, and control groups. We think that the role of asymmetric dimethylarginine should be considered in children treated with antiepileptic drugs. It appears to be another important factor that may increase the long-term risk of atherosclerotic disease in children with epilepsy.

The factors influencing sleep quality.

1. Duman T, Dede ÖH, Uluduz D, Seydaoğlu G, Okuyucu E, Melek İ. Sleep changes during prophylactic treatment of migraine. Ann Indian Acad Neurol 2015;18:298‐302. 2. Sridhar GR, Madhu K. Prevalence of sleep disturbances in diabetes mellitus. Diabetes Res Clin Pract 1994;23:183‐6. 3. Buysse DJ, Reynolds CF 3rd, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: A new instrument for psychiatric practice and research. Psychiatry Res 1989;28: 193‐213. 4. Michal M, Wiltink J, Kirschner Y, Schneider A, Wild PS, Münzel T, et al. Complaints of sleep disturbances are associated with cardiovascular disease: Results from the Gutenberg Health Study. PloS One 2014;9:e104324. 5. Kravitz HM, Ganz PA, Bromberger J, Powell LH, Sutton‐Tyrrell K, Meyer PM. Sleep difficulty in women at midlife: A community survey of sleep and the menopausal transition. Menopause 2003;10:19‐28. 6. Young T, Rabago D, Zgierska A, Austin D, Laurel F. Objective and subjective sleep quality in premenopausal, perimenopausal, and postmenopausal women in the Wisconsin Sleep Cohort Study. Sleep 2003;26:667‐72. 7. Cirignotta F, Mondini S, Zucconi M, Lenzi PL, Lugaresi E. Insomnia: An epidemiological survey. Clin Neuropharmacol 1985;8(Suppl 1):S49‐54. 8. Irish LA, Kline CE, Gunn HE, Buysse DJ, Hall MH. The role of sleep hygiene in promoting public health: A review of empiric al evidence. Sleep Med Rev 2015;22:23‐36. Sir, We have read the study of Duman et al. entitled “Sleep changes during prophylactic treatment of migraine” with great interest. In this study, they aimed to assess sleep quality in patients with primary headaches before and after prophylactic treatment using a validated sleep-screening instrument. They evaluated a total of 147 patients including 63 tension type headache (TTH) patients and 84 migraine patients.[1] They reported that poor quality of sleep prior to prophylactic treatment was observed in 61.4% of the migraine patients and in 77.7% of the TTH patients. Comparison of sleep quality scores before and 3 months following treatment showed a significantly improved quality of sleep in all the treatment groups; the greatest significance was detected in migraine patients treated with amitriptyline.[1]

Meralgia paresthetica after the fragmentation of renal stone using extracorporeal shock wave lithotripsy: a case report

Meralgia paresthetica (MP) is painful mononeuropathy of the lateral femoral cutaneous nerve (LFCN). The LFCN originates from the roots of the second and third lumbar nerves and innervates the skin on the anterolateral part of the thigh. MP presents with a burning sensation, pain, numbness, and tingling on this part of the thigh. Many different factors are reported as etiologies. The most common are positional mechanical compression, anterior hip surgery, thigh injury, disk herniation, and the use of tight corsets or tight belts. We report a case of MP due to extracorporeal shock wave lithotripsy (ESWL).