The prevalence of carpal tunnel syndrome in patients with epilepsy.

Objective: Carpal tunnel syndrome (CTS) is the most common type of entrapment neuropathy caused by compression of the median nerve in the carpal tunnel. Epilepsy is characterised by recurrent seizures caused by abnormal neuronal discharges in the brain.This study aimed to investigate whether there is a link between epilepsy and carpal tunnel and, if so, the underlying factors. Materials and methods: Two hundred patients with epilepsy were included in this study. The patients' history of epilepsy, seizure type, and seizure frequency were assessed. The Tinel, Phalen, and Flick physical examination tests were performed on patients with complaints that matched those of median nerve neuropathy. Patients with epilepsy and clinically diagnosed carpal tunnel syndrome completed the Boston Carpal Tunnel Syndrome Questionnaire, and nerve conduction studies were performed. The relationship between seizure type and frequency in patients with carpal tunnel syndrome was compared. Results: Compared to focal-aware motor-onset seizures, the risk of detecting carpal tunnel syndrome was 88.7 times higher in focal-onset bilateral tonic-clonic seizures. Patients with a seizure frequency of one per month or more had a 0.704 times lower risk of CTS than those with a frequency of one per week or more (p = 0.026). Discussion: Patients with epilepsy, especially those experiencing frequent seizures or specific seizure types, may be more susceptible to repetitive wrist flexion-extension postures. Therefore, during clinical follow-up, it is important to inquire about the presence of carpal tunnel syndrome in patients with epilepsy.

Could NCOA5 a novel candidate gene for multiple sclerosis susceptibility?

BACKGROUND: Multiple sclerosis (MS) is an inflammatory immune-mediated demyelinating disease that causes a challenging and disabling condition. Environmental and genetic factors play a role in appearing the state of the disease. Recent studies have shown that nuclear cofactor genes may play a role in the pathogenesis of MS. NCOA5 is a nuclear receptor coactivator independent of AF2 that modulates ERa-mediated transcription. This gene is involved in the pathogenesis of diseases such as psoriasis, Behcet's disease, and cancer. METHODS AND RESULTS: We investigated the relationship between the rs2903908 polymorphism of the NCOA5 gene and MS among 157 unrelated MS patients and 160 healthy controls by RT-PCR. The frequencies of the CC, CT, and TT genotypes were 19.87%, 37.82%, and 42.31%, respectively, for the MS group and 5.63%, 43.75%, and 50.62%, respectively, for the control group. The CC genotype and the C allele were found to be significantly higher in the patient group (the p values were 0.0002 and 0.003, respectively). CONCLUSIONS: The fact that the CC genotype was found to be significantly higher in the patient group compared to the control group (p = 0.0002) and that it had a statistically significantly higher OR value (OR, 95% CI = 4.16, 1.91-9.05) suggests that the C allele may recessively predispose to MS for this polymorphism. These results suggest for the first time that the NCOA5 gene may have an effect on the occurrence of MS through different molecular pathways, which are discussed in the manuscript.

Clinical and Molecular Findings in a Turkish Family Who Had a (c.869- 1G>A) Splicing Variant in PSEN1 Gene with A Rare Condition: The Variant Alzheimer's Disease with Spastic Paraparesis.

BACKGROUND: Early-onset Alzheimer's disease (EOAD) is commonly diagnosed with an onset age of earlier than 65 years and accounts for 5-10% of all Alzheimer's disease (AD) cases. To date, although only 10-15% of familial EOAD cases have been explained, the genetic cause of the vast proportion of cases has not been explained. The variant Alzheimer's disease with spastic paraparesis (var- AD) is defined as a rare clinical entity characterized by early-onset dementia, spasticity of the lower extremities, and gait disturbance. Although the disease was first associated with variants in exon 9 of the PSEN1 gene, it was later shown that variations in other exons were also responsible for the disease. OBJECTIVE: The current study aims to raise awareness of varAD, which occurs as a rare phenotype due to pathogenic variants in PSEN1. In addition, we aimed to evaluate the spectrum of mutations in varAD patients identified to date. METHODS: Detailed family histories and clinical data were recorded. Whole exome sequencing was performed and co-segregation analysis of the family was done by Sanger sequencing. Also, a review of the molecularly confirmed patients with (varAD) from the literature was evaluated. RESULTS: We identified a heterozygous splicing variant (c.869-1G>A) in the PSEN1 gene, in a family with two affected individuals who present with varAD. We reported the clinical and genetic findings from the affected individuals. CONCLUSION: We present the detailed clinical and genetic profiles of a Turkish patient with the diagnosis of varAD together with subjects from the literature. Together, we think that the clinical characteristics and the effect of the (c.869-1G>A) variant will facilitate our understanding of the PSEN1 gene in AD pathogenesis.

The prevalence of restless legs syndrome in patients undergoing coronary angiography and its relationship with the severity of coronary artery stenosis.

PURPOSE: Results from studies on the relationship between restless legs syndrome (RLS) and coronary artery disease (CAD) are conflicting. Some studies associate RLS with CAD by heart rate variability, blood pressure variability, and other autonomic, neuronal reasons, while other studies do not support these observations. The aim of this study was to investigate the prevalence of RLS in patients undergoing coronary angiography for CAD and to assess RLS prevalence with severity of CAD. METHODS: After inclusion and exclusion criteria were applied, enrolled patients with less than 50% coronary artery stenosis by angiography (0-49%) were assigned to group 1, and patients with 50% or more coronary artery stenosis were assigned to group 2. Patients were diagnosed with RLS if they met all five essential criteria of the International RLS study group. RLS prevalence and other comorbidities were compared between the two groups. RESULTS: Of 126 patients, 74 men (59%), mean age 64.0 ± 8.7 years, mean BMI 29.6 kg/m2, 47 (37%) were assigned to group 1 (no or nonobstructive CAD) and 79 (63%) were assigned to group 2 (obstructive CAD). No significant differences were found between the groups in terms of mean age, BMI, gender, or prevalence of hypertension, hypercholesterolemia, and DM. The prevalence of RLS in group 2 (29%) was significantly higher than in group 1 (15%), p = 0.013. CONCLUSION: These results suggest that prevalence of RLS is associated with CAD and with CAD severity. We conjecture that RLS may be related to vascular endothelial dysfunction in cardiovascular disease.

Evaluation of different ulegyria patterns with magnetic resonance imaging.

Ulegyria is a parenchymal sequel of hypoxic ischemic encephalopathy causing mushroom-like appearance in gyri. Aim of the present study was to evaluate clinico-radiological findings of patients who applied with different clinical features, predominantly epilepsy, and who were found to have ulegyria formations in MRI examinations. The study included a total of 30 patients (12 female and 18 male) who applied with different types of seizures in February 2011-August 2016 period and had brain MRI examinations using 1.5T MRI scanner. Mushroom-shaped gyri accompanied by gliosis and atrophy in subcortical white matter were considered ulegyria. Locations, MRI features and accompanying pathologies of ulegyria formations were studied. Age of the patients ranged from 4 to 62 (mean 26.0 ±â€¯13.8). Both cerebral lobes were involved in 18 patients. In terms of involved area, symmetrical or asymmetrical involvements were observed in occipital lobes in 26 patients, parietal lobes in 19, frontal lobes in 12 and temporal lobes in 4. The most common involvement type was bilateral occipital and bilateral parieto-occipital lobe involvements with five patients each. Lesions were symmetrical in 11 patients. Six patients had cingulate gyrus atrophy. Nineteen patients had different levels of symmetrical or asymmetrical ventricular dilatation. Cranial asymmetry was observed in six patients with unilateral involvement and in one patient with generalized involvement. Although ulegyria predominantly involves parasagittal watershed areas in MRI examinations of patients applying with epilepsy, clinical manifestations and appearance of lesions could vary depending upon the size of involved area and level of injury.

Characteristics of headache and its relationship with disease severity in patients with Crimean-Congo hemorrhagic fever.

OBJECTIVES: Crimean-Congo Hemorrhagic Fever (CCHF) is a fatal, tick-borne disease. The classic clinical presentation of CCHF is characterized by sudden onset of high fever, chills, and severe headache. There are no previous reports on the characteristics of headaches caused by CCHF. Therefore, we investigated the relationship between CCHF-induced headache and the clinical course of the disease. METHODS: We included 60 patients with headache diagnosed with CCHF; they were divided into two groups: group 1 included patients with hospital stay <7 days and group 2 included patients with hospital stay >7 days. The control group included 43 viral pneumonia patients with headache. Patients described the characteristics of headaches and also self-rated the severity with a numeric pain scale that classified headache as either mild or severe. RESULTS: In the group with CCHF, 66.7% of the reported headaches met criteria for diagnosis of migraine. This ratio was significantly higher than that in the control group (37.5%). The headache severity scores in group 1 were lower than those in group 2. The hospitalization length was shorter (p=0.004) and the platelet levels were higher in CCHF patients with mild headache compared with CCHF patients with severe headache (p=0.005). CONCLUSION: CCHF patients had more often and severe headaches than the controls. The severity of headache may be associated with the severity of vascular endothelial damage, vasodilatation, and abnormal release of inflammatory cytokines in CCHF similar in migraine. Most CCHF patients experienced migraine-like headaches, suggesting that cerebral vessel involvement might be important in both CCHF and migraine.

ERLIN1 mutations cause teenage-onset slowly progressive ALS in a large Turkish pedigree.

Amyotrophic lateral sclerosis (ALS) is a late-onset motor neuron disease with mostly dominant inheritance and a life expectancy of 2-5 years; however, a quite common occurrence of atypical forms of the disease, due to recessive inheritance, has become evident with the use of NGS technologies. In this paper, we describe a family with close consanguinity for at least four generations, suffering from a slowly progressive form of ALS. Spastic walking is observed since teenage years, while bulbar symptoms start much later, at the fifth or sixth decade of life. Patients usually die because of respiratory failure. Using whole-exome sequencing, we identified a novel homozygous p.(Val94Ala) (c.281T>C) (NG_052910.1) (NM_006459) variation in the endoplasmic reticulum lipid raft associated protein 1 (ERLIN1) gene, which segregates with the disease in the family. Here we suggest that ERLIN1 variants, previously shown in juvenile hereditary spastic paraplegia cases, may also be the cause of a slowly progressive early-onset ALS, starting with upper motor neuron features and developing into classical ALS with the addition of lower motor neuron dysfunction. We also demonstrate that ATP-binding cassette subfamily C member 2 (ABCC2) gene, responsible for hyperbilirubinemia, is linked to ERLIN1.

The investigation of association between IL-1Ra and ACE I/D polymorphisms in carpal tunnel syndrome.

BACKGROUND: Carpal tunnel syndrome (CTS) is a common neurologic impairment caused by injury on the median nerve in the wrist, characterized by pain and loss of sensory. CTS usually occurs through three factors, such as a mechanical pressure on median nerve, immunologic changes, and oxidative stress. The aim of this study was to evaluate the influence of interleukin-1 receptor antagonist (IL-1Ra) and angiotensin-converting enzyme (ACE) I/D polymorphisms on the susceptibility of patients to the CTS. METHODS: One hundred fifty-eight patients with CTS and 151 healthy controls were enrolled in this study. Each patient was analyzed according to diseases symptoms, such as gender, a positive Tinel's sign, a positive Phalen maneuver, disease sides, EMG findings, and clinical stage. We applied the polymerase chain reaction (PCR) to determine the polymorphisms of IL-1Ra and ACE I/D. RESULTS: The statistically significant relation was not found between IL-1Ra, ACE I/D polymorphisms and CTS (respectively, P>.05; P>.05, OR: 1.51, CI: 0.82-1.61). Additionally, in the result of the statistical analysis compared with gene polymorphisms and clinical characteristics, we did not find any correlation (P>.05). CONCLUSIONS: Our findings showed that there are no associations of IL-1Ra and ACE I/D polymorphisms with susceptibility of a person for the development of CTS. So, it means that these polymorphisms do not create a risk for the development of CTS. Further studies with larger populations will be required to confirm these findings in different study populations.

Neuroprotective effects of erythropoietin on Alzheimer's dementia model in rats.

BACKGROUND: Although Alzheimer's disease (AD) is the most common age-related neurodegenerative disease and characterized by memory impairment, only symptomatic treatments are available. OBJECTIVES: Because recombinant human erythropoietin (rhEPO) has various neuroprotective effects and improves cognitive function in animal models of neurodegenerative disorders, we investigated the therapeutic effects of rhEPO in an intracerebroventricular (ICV)-streptozotocin (STZ) animal model of sporadic-AD. MATERIAL AND METHODS: A total of 24 Sprague-Dawley adult rats were divided into 4 groups of naive control (n = 6), sham-operated (n = 6), ICV-STZ + saline (n = 6) and ICV-STZ + rhEPO (n = 6). Twelve rats with Alzheimer's disease, induced by STZ injection (3 mg/kg) into both lateral ventricles using a stereotaxic frame (bilaterally ICV-STZ), were divided into 2 groups 5 days after the STZ injection: one treated with rhEPO 5000 (IU/kg/day, i.p.) and the other with 0.9% NaCl (1 mL/kg/day, i.p.) for 2 weeks. The sham-operated rats received bilaterally ICV-0.9% NaCl. No surgical operation or treatment was given to the naive-control animals. On day 20, a passive avoidance learning (PAL) test was used followed by sacrification and removal of the brain tissue in all animals. Brain TNF-α and ChAT levels were determined, and neurons in the hippocampal CA1 and CA3 regions were counted by Cresyl violet staining. RESULTS: ICV-STZ was found to significantly shorten the latency time on the PAL, increase brain TNF-α level, and decrease brain ChAT activity and the number of neurons in the hippocampal CA1 and CA3 regions. On the other hand, rhEPO significantly attenuated all these detrimental effects induced by STZ. CONCLUSIONS: RhEPO treatment significantly prevented the ICV-STZ-induced memory deficit by attenuating the hippocampal neuronal loss, neuroinflammation and cholinergic deficit in rats. This result suggests that rhEPO may be beneficial for treating AD.

Atypical Features in a Large Turkish Family Affected with Friedreich Ataxia.

Here, we describe the clinical features of several members of the same family diagnosed with Friedreich ataxia (FRDA) and cerebral lesions, demyelinating neuropathy, and late-age onset without a significant cardiac involvement and presenting with similar symptoms, although genetic testing was negative for the GAA repeat expansion in one patient of the family. The GAA repeat expansion in the frataxin gene was shown in all of the family members except in a young female patient. MRI revealed arachnoid cysts in two patients; MRI was consistent with both cavum septum pellucidum-cavum vergae and nodular signal intensity increase in one patient. EMG showed demyelinating sensorimotor polyneuropathy in another patient. The GAA expansion-negative 11-year-old female patient had mental-motor retardation, epilepsy, and ataxia. None of the patients had significant cardiac symptoms. Description of FRDA families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease. Furthermore, the genetic heterogeneity observed in this family draws attention to the difficulty of genetic counseling in an inbred population and to the need for genotyping all affected members before delivering comprehensive genetic counseling.

Analysis of MMP2-1306C/T and TIMP2G-418C polymorphisms with relapsing remitting multiple sclerosis.

AIMS: Multiple sclerosis (MS) is an autoimmune, inflammatory disease characterized by loss of myelin forming oligodendrocytes and changes in the blood-brain barrier. Matrix metalloproteinase (MMP) -2 and -9 are known to cause disruption of the blood-brain barrier, remodeling of the basal lamina, regeneration of axons, and remyelination in MS. The imbalance between MMPs and tissue inhibitor metalloproteinases (TIMPs) may lead to the emergence of pathological processes such as MS. The roles of MMP2-1306 C/T and TIMP2-418 G/C genetic variants in MS have not been studied before. We aimed to investigate whether MMP2-1306C/T and TIMP2-418 G/C gene variants are risk factors for patients with relapsing remitting multiple sclerosis (RRMS). METHODS: The study included 102 RRMS and 102 healthy controls. Genomic DNA was extracted from peripheral leukocytes from ethylenediaminetetraacetic acid anticoagulated blood. Genotyping of the MMP2-1306C/T and TIMP2G-418C polymorphisms was performed using real-time PCR. RESULTS: There were significant differences in terms of distribution of genotype (MMP2-1306- CT, TT) and T allele frequency between the patients with RRMS and the control group (p<0.0001; p<0.0001). The groups were not different in terms of TIMP2G-418C polymorphisms. CONCLUSIONS: In the RRMS group, the genotype and allele frequencies of MMP2-1306C/T polymorphism showed significant differences from the controls. These results indicate that MMP2 might play a role in the pathogenesis of MS even during the inflammation stage.

The Effect of Autologous Fat Graft with Different Surgical Repair Methods on Nerve Regeneration in a Rat Sciatic Nerve Defect Model.

BACKGROUND: The aim of this study was to evaluate the efficacy of autologous fat graft with different surgical repair methods on reconstruction of a 10-mm-long rat sciatic nerve defect model. METHODS: One hundred forty-four sciatic nerves were operated on in 72 Wistar rats. The right limbs were assigned as group A (n = 72) and the left limbs as group B (n = 72). In group B, autologous fat graft was added to the surgical area so as to stay in contact with the coaptation site. Nerve regeneration was evaluated by walking track analysis, Sciatic Functional Index, pin-prick, and electrophysiologic and histologic tests at commencement and at 4 and 12 weeks after the operation. RESULTS: The rats receiving fat graft showed better regeneration, but the difference was only significant according to Sciatic Functional Index and pin-prick test (p < 0.05). Primary repair, autogenous nerve graft, acellularized nerve graft, vein filled with fresh and denatured muscle graft subgroups in group B showed significantly better regeneration than those in group A according to the Sciatic Functional Index (p < 0.05). In terms of latency and amplitude, all subgroups in groups A and B were found significantly different from the commencement of the study, but there was no difference between groups A and B (p < 0.05). CONCLUSIONS: Although there was no significant difference between the groups, rats receiving autologous fat graft showed better regeneration. Combined use of autologous fat graft with surgical repair methods induced significantly better regeneration. It was concluded that autologous fat grafting may have a beneficial effect on nerve regeneration when it is present in the coaptation site during healing.

Montelukast inhibits pentylenetetrazol-induced seizures in rats.

BACKGROUND: Montelukast is an antiinflammatory drug with an antioxidant property. In this study, we aimed to reveal whether montelukast has a preventive effect against seizures and post-seizure oxidative stress in pentylenetetrazol (PTZ)-induced seizures in rats. MATERIAL AND METHODS: Of the 48 male Sprague-Dawley rats used in the study, 24 were assigned to EEG recordings (group A) and 24 were assigned to behavioral studies (group B). In group A, the electrodes were implanted on dura over the left frontal cortex for EEG recording. After 10 days, in group A, i.p. saline, 25, 50, or 100 mg/kg montelukast+35 mg/kg PTZ was administered to the rats. EEG was recorded and spike percentage was evaluated. In group B, i.p. saline, 25, 50, or 100 mg/kg montelukast+70 mg/kg PTZ was administered to the rats. Racine's Convulsion Scale (RCS) and onset times of first myoclonic jerk (FMJ) was used to evaluate the seizures. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined in the brain tissue of animals. RESULTS: Animals treated with 50 or 100 mg/kg montelukast had significantly lower RCS and significantly increased FMJ onset time compared to the saline-treated animals. Moreover, groups given 25, 50, or 100 mg/kg montelukast had significantly lower MDA and higher SOD levels compared to the saline-treated group. The differences were more pronounced in the 100 mg/kg montelukast-pretreated group (p<0.001). CONCLUSIONS: Montelukast showed anticonvulsant action and led to amelioration of oxidative stress markers in PTZ-induced seizures in rats.

Lack of association between MIF gene -173G>C polymorphism with multiple sclerosis.

AIM: The aim of the present study was to investigate a possible association between the MIF -173G>C polymorphism and MS in Turkish patients. MATERIALS AND METHODS: The study included 153 MS-patients and 210 controls. Genomic DNA was isolated and genotyped using PCR-RFLP assay for the MIF -173G>C promoter polymorphism (rs755622). RESULTS: There was no statistically significant difference in allele and genotype frequencies between MS-patients and controls (p=0.227 and p=0.157, respectively). Accordingly, no association was observed when the patients were compared against controls in terms of GG versus GC+CC genotypes and GG+GC versus CC genotypes (p=0.324 and p=0.179, respectively). Also, there was no statistically significant association between MIF-173G>C polymorphism and clinical and demographic characteristics of MS-patients. Conlusion: The results of the present study suggest no relation between MS susceptibility and MIF gene - 173G>C polymorphism in the examined Turkish population.

Association of methylenetetrahydrofolate reductase gene C677T polymorphism with multiple sclerosis in Turkish patients.

BACKGROUND AND AIM: Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease of the central nervous system. Genetic risk factors are known to contribute to the etiology of MS. Methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism has been associated with susceptibility to various autoimmune diseases. The aim of this study was to investigate a possible association between the MTHFR gene C677T polymorphism and MS in Turkish patients. METHODS: The study included 130 MS patients and 150 group-matched controls. Genomic DNA was isolated and genotyped using polymerase chain reaction-based restriction fragment length polymorphism assay for the MTHFR gene exon C677T polymorphism. RESULTS: The genotype and allele frequencies of C677T polymorphism showed statistically significant differences between MS patients and controls (P = 0.002 and P = 0.002; odds ratio, 1.79; 95% confidence interval, 1.23-2.63, respectively). A significant association was observed when the patients were compared with the controls according to CC genotype versus CT + TT genotypes (P = 0.0005; odds ratio, 2.35; 95% confidence interval, 1.45-3.82). There were no statistically significant association between MTHFR gene C677T polymorphism and baseline clinical and demographical characteristics of MS patients. CONCLUSIONS: These results showed that T allele of C677T polymorphism was associated with MS susceptibility in Turkish population.

Protein S Deficiency and an Adult Case with Moyamoya Syndrome that Presented with Primary Intraventricular Haemorrhage.

BACKGROUND: Moyamoya syndrome associated with protein S deficiency is rarely encountered and is usually reported in paediatric cases with cerebral ischaemia. CASE REPORT: A 32-year-old woman had symptoms of sudden-onset severe headache, projectile vomiting, impaired consciousness, and slight neck stiffness. The computed tomography scan of her brain showed primary intraventricular haemorrhage, and the subsequent four vessel cerebral angiographies revealed stage 3 to 4 Moyamoya disease according to Suzuki and Takaku's angiographic classification. The coagulation profile showed the presence of protein S deficiency. The patient was treated with external ventricular drainage and conservative management until blood clot resolution. The patient was discharged with normal neurological examination findings after her initial impaired consciousness and orientation defect gradually recovered. CONCLUSION: This case report would alert physicians to the possible coexistence of Moyamoya syndrome and protein S deficiency, even in adult cases presenting with primary intraventricular haemorrhage.

Hypokalemia and hypomagnesaemia related to levetiracetam use.

Levetiracetam (LEV), used for both partial and generalized seizures, is a frequently preferred antiepileptic because of its few side effects. We present a 23-year-old man who developed hypokalemia after switching from valproate to LEV. The patient was sent to our clinic due to hypokalemia 1 month after initiation of LEV, and his neurological examination was normal. Further examinations revealed hypokalemia (3.1 mmol/L) and hypomagnesaemia (0.56 mmol/L). His hemogram, blood urea nitrogen, creatinine, total cortisol, thyroid function tests, creatinine clearance, and renal Doppler ultrasound were normal. LEV was tapered off and treatment with 200mg/day lamotrigine begun. Potassium and magnesium levels returned to normal ranges in subsequent tests. While hypokalemia and hypomagnesaemia have not been reported before to our knowledge, interstitial nephritis and renal failure after the use of LEV have been. Hypokalemia, found in the early period in this case, may be an indicator of a recently developed renal tubular disorder. This experience indicates that unpredictable side effects of increasingly used new antiepileptic drugs should be taken into consideration.

Central corneal thickness and its relationship to Parkinson's disease severity.

OBJECTIVE: To investigate the effect of Parkinson's disease (PD) on blink rate (BR), tear breakup time test (TBUT), Schirmer's test, and corneal thickness, and the relationship of these effects with disease severity. DESIGN: Prospective controlled study. PARTICIPANTS: Fifty-five eyes from 55 patients with PD and 40 eyes from 40 healthy subjects were analyzed in the study. METHODS: The patients were divided into 2 groups according to their Hoehn-Yahr (H-Y) scores; patients classified as H-Y 1-2 were designated as the mild group, and those classified as H-Y 3-5 were designated as the moderate group. Subjects were screened for BR, TBUT, and Schirmer's test, and the central corneal thickness (CCT) was measured. RESULTS: The BR, Schirmer's test, TBUT, and CCT values of the patient group were significantly lower than those of the control group. The BR and TBUT of the mild group were significantly lower than those of the control group, but the decreases in the Schirmer's test values and CCT were not statistically significant. In addition, significant decreases in the BR, TBUT, Schirmer's test scores, and CCT were observed in the patient group as the H-Y score increased. CONCLUSIONS: A reduced BR and poor tear quality in the early stages of PD, as well as decreased tear production as the disease progresses, can result in reduced CCT. The possibility of a thin cornea should be taken into consideration while measuring the intraocular pressure in patients with severe PD.

Clinical, demographic and prognostic features of sporadic amyotrophic lateral sclerosis in Northern Turkey.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease for which progression cannot be prevented. In this study, we evaluated 37 patients diagnosed with sporadic definitive-probable ALS who were monitored in our neurology clinic between 2002 and 2012 in terms of age, gender, profession, onset, and clinical course within the disease process. The hospital ethics committee approved the study. Nineteen female and 18 male patients diagnosed with sporadic definitive or probable ALS were evaluated for age, gender, level of education, residence, onset of disease, the time between the first symptom and diagnosis, and average lifetime after diagnosis. Twenty-eight of the patients had graduated from primary-secondary school, six were illiterate, and three of them were college graduates. Eighteen patients were living in city center, 19 were living in the country. Fourteen patients were farmers, 11 were housewives, and the remaining was working in various different occupations. The age of onset was 62.13. The men and women were diagnosed 10.27 months and 17.91 months after the first symptom, respectively (p = 0.001). The average survival time after diagnosis was 36.70 months for males and 49.80 months for females (p < 0.05). This difference was particularly evident among patients from rural areas. In addition, our female patients required interventions such as ventilation at a later period than did males. In conclusion, female gender seems to be one of the good prognostic factors for our ALS patients. This may be due to the protection by hormonal mechanisms in women or differences in their responses to exogenous toxins.