Ufuk Can

Validation of Montreal Cognitive Assessment and Discriminant Power of Montreal Cognitive Assessment Subtests in Patients With Mild Cognitive Impairment and Alzheimer Dementia in Turkish Population

Montreal Cognitive Assessment (MoCA) is a new cognitive tool developed for screening mild cognitive impairment (MCI). The authors examined validity of MoCA and discriminating power of subtests in a Turkish population comprising of 474 participants (246 healthy controls, 114 subjects with MCI and 114 subjects with dementia). The ANCOVAs showed that age and education had a main effect on MoCA scores. Cut scores were computed according to different education levels. The overall cut-off values for MCI and dementia were found to be lower compared to western studies. MoCA was found to have good internal consistency. The subtests most useful in discriminating MCI from healthy controls were recall, visuospatial and language, while in discriminating dementia from MCI were visuospatial, orientation and attention subtests. The results demonstrated that MoCA is a valid and reliable instrument in screening MCI, and compared with the MMSE, MoCA was proved to have superior sensitivity and specificity in detecting MCI.

Prevalence of Thrombophilic Mutations and ACE I/D Polymorphism in Turkish Ischemic Stroke Patients

The aim of this study was to evaluate the prevalence of factor V Leiden (FVL), prothrombin G20210A, methylenetetrahydrofolate reductase (MTHFR) C677T gene mutations, and angiotensin-converting enzyme (ACE) I/D polymorphism in ischemic stroke (IS) patients. A total of 162 Turkish IS patients were included and analyzed according to stroke subtype by the TOAST classification. Their genotype data were compared with those of the control group, representing the healthy population, using the χ2 test. The frequency of FVL heterozygocity was 12.3% in this series—higher than that in the normal population (9.8%; statistically insignificant, P = .478). The frequency of the ACE D/D genotype in all stroke patients and those with stroke of undetermined etiology was higher than that in our population (52.5% and 59.2%, respectively, vs 39.3%; statistically significant, P = .034, P = .020). Our results may suggest that ACE D/D genotype is a risk factor for IS, particularly in those with stroke of undetermined etiology in the Turkish population.

Rare Presentation of Midbrain Infarction: Isolated Medial Rectus Palsy.

A 69-year-old woman presented with sudden onset of diplopia. In neurologic examination left medial rectus palsy without abduction nystagmus was detected. Brain magnetic resonance imaging revealed acute ischemic lesion in mesencephalon on diffusion-weighted images. Sponteneous resolution was observed after 1 month. Medial rectus palsy is a rare presention of acute ischemic stroke and early neuroimaging is important to establish such lesions.

Can subdural hematoma be a trigger for Guillain-Barré syndrome?

Guillain–Barré syndrome (GBS) is an acute inflammatory polyneuropathy which follows a precipitating event in approximately two thirds of cases. Although its pathogenesis is unclear, it is likely to be a consequence of an immune-mediated process. In the literature there are three case reports of GBS following subarachnoid hemorrhage, subdural hematoma, and facial bone fracture after head trauma.The unique feature of our case with GBS after subdural hematoma is the presence of cerebellar symptoms. We believe that GBS results from an aberrant immune response following trauma that somehow mistakenly attacks the nerve tissue of its host, and we discuss the effects of the trauma of head injury on cellular and humoral immunities and the absence of antiganglioside antibody (anti-GD1b IgG, which is accused of ataxia and cerebellar symptoms) in this case report.

Intrathecal Methotrexate-Induced Posterior Reversible Encephalopathy Syndrome (PRES).

Posterior reversible encephalopathy syndrome (PRES) is an acute neuroradiological diagnosis presenting with headache, vomiting, seizure, abnormalities of the mental status, and visual disturbances associated with a breakdown in cerebral vasculature regulation. It has a unique neuroradiological pattern of symmetrical parietooccipital vasogenic edema [1]. The most common causes of this syndrome are sudden arterial hypertension, preeclampsia, eclampsia, uremia, immunosuppressive drugs, and cancer chemotherapies such as cyclosporine, tacrolimus, L-asparaginase, vincristine, gemcitabine, cytarabine, and cisplatin, typically used in cases of hematopoietic malignancies [2,3,4,5,6,7]. Intrathecal methotrexate-induced PRES in an adult is exceedingly rare [8].A 43-year-old woman was admitted to gynecology with metrorrhagia. Cervical cancer was diagnosed and radical hysterectomy with lymph node dissection was performed. Final pathology and immunohistochemical analyses revealed B-cell phenotype malign lymphoma, which is consistent with Burkitt lymphoma. A chemotherapy treatment protocol with R-Hyper CVAD, consisting of rituximab, cyclophosphamide, vincristine, adriamycin, and dexamethasone plus 12 mg of intrathecal methotrexate without preservative, was then started. Twelve days after chemotherapy she had severe analgesic-irresponsive headache, nausea, motor agitation, and cooperation failure. Her vital signs and laboratory findings were normal. Cranial computed tomography revealed hypodense areas due to edema in the bilateral cerebral hemispheres, predominantly in the posterior regions. Magnetic resonance imaging (MRI) of the brain showed

Clinical results of carotid artery stenting versus carotid endarterectomy

Objective: To review our results of carotid artery stenting (CAS) and carotid endarterectomy (CEA). Methods: We evaluated the medical records of patients undergoing carotid artery revascularization procedure, between 2001 and 2013 in Baskent University Hospital, Ankara, Turkey. Carotid artery stenting or CEA procedures were performed in patients with asymptomatic carotid stenosis (≥70%) or symptomatic stenosis (≥50%). Demographic data, procedural details, and clinical outcomes were recorded. Primary outcome measures were in 30-day stroke/transient ischemic attacks (TIA)/amaurosis fugax or death. Secondary outcome measures were nerve injury, bleeding complications, length of stay in hospital, stroke, restenosis (ICA patency), and all-cause death during long-term follow-up. Results: One hundred ninety-four CEA and 115 CAS procedures were performed for symptomatic and/or asymptomatic carotid artery stenosis. There is no significant differences 30-day mortality and neurologic morbidity between CAS (13%) and CEA procedures (7.7%). Length of stay in hospital were significantly longer in CEA group (p=0.001). In the post-procedural follow up, only in symptomatic patients, restenosis rate was higher in the CEA group (p=.045). The other endpoints did not differ significantly. Conclusions: Endovascular stent treatment of carotid artery atherosclerotic disease is an alternative for vascular surgery, especially for patients that are high risk for standard CEA. The increasing experience, development of cerebral protection systems and new treatment protocols increases CAS feasibility.

Aspirin resistance in cerebrovascular disease and the role of glycoprotein IIIa polymorphism in Turkish stroke patients.

Aspirin resistance occurs in 5–45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P = 0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100 mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36–60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke.

Relationship between white matter hyperintensities and retinal nerve fiber layer, choroid, and ganglion cell layer thickness in migraine patients:

Aim To compare the relationship between white matter hyperintensities (WMH) on brain magnetic resonance imaging and retinal nerve fiber layer (RNFL), choroid, and ganglion cell layer (GCL) thicknesses in migraine patients and healthy subjects. We also assessed the role of cerebral hypoperfusion in the formation of these WMH lesions. Methods We enrolled 35 migraine patients without WMH, 37 migraine patients with WMH, and 37 healthy control subjects examined in the Neurology outpatient clinic of our tertiary center from May to December 2015. RFNL, choroid, and GCL thicknesses were measured by optic coherence tomography. Results There were no differences in the RFNL, choroid, or GCL thicknesses between migraine patients with and without WMH (p > 0.05). Choroid layer thicknesses were significantly lower in migraine patients compared to control subjects (p < 0.05), while there were no differences in RFNL and GCL thicknesses (p > 0.05). Conclusions The ‘only cerebral hypoperfusion’ theory was insufficient to explain the pathophysiology of WMH lesions in migraine patients. In addition, the thinning of the choroid thicknesses in migraine patients suggests a potential causative role for cerebral hypoperfusion and decreased perfusion pressure of the choroid layer.

Prevalence and Treatment of Neuropathic Pain in Kidney and Liver Transplant Recipients.

OBJECTIVES Neurologic complications are common after kidney and liver transplant. Neurologic complications affect mortality and morbidity in transplant recipients, and neuropathic pain is an important symptom affecting a patients quality of life. The aim of the present study was to provide readers with our experience regarding causes and treatment of neuropathic pain in patients undergoing kidney and liver transplant at our transplantation center. MATERIALS AND METHODS The medical data of 553 kidney transplant recipients and 258 liver transplant recipients who received transplant procedures at the Baskent University Transplantation Center between 2008 and May 2016 were retrospectively reviewed. Fifty-one patients who were examined by an expert neurologist and diagnosed with neuropathic pain on the basis of clinical, neurologic examination, and laboratory findings were included for analyses. RESULTS Among 811 transplant recipients, 51 patients (6.2%) were diagnosed with neuropathic pain. Of these, 22 were female and 38 were male patients, and 42 were kidney transplant recipients and 9 were liver transplant recipients. Causes of neuropathic pain included uremia, diabetes mellitus, ischemic peripheral arterial disease, inflammatory neuropathy, vasculitis, discopathy, postherpetic neuralgia, carpal tunnel syndrome, and multiple myeloma. Patients with symptoms too mild to affect daily life activities were treated conservatively. Plasmapheresis, gabapentin, pregabalin, alpha-lipoic acid, and duloxetine were administered as treatment modalities and medications. CONCLUSIONS Neuropathic pain was lower in our transplant recipients than in the general population. Treatment medications were effective for transplant recipients at lower doses for the management of neuropathic pain impairing quality of life than doses for the general population.

Lentiform fork sign in a case with end-stage renal disease and metabolic acidosis

A 61-year-old woman admitted to our hospital with acute onset of confusion, speech, and gait disturbance. She had previous history of diabetes and end-stage renal disease, and she was on oral antidiabetic medication and regular hemodialysis for 4 months. Neurologic examination demonstrated dysarthria, postural instability, and bradykinesia. Laboratory examination showed elevated blood urea nitrogen (55 mg/dl) and creatinine (5.8 mg/dl), metabolic acidosis (pH: 7.09, HCO3: 5.6 mmol/l), and normal glucose level. Brain computerized tomography performed at the first day of admission revealed bilateral hypodensities on basal ganglia (Fig. 1). She received treatment for metabolic imbalance, and hemodialysis was continued three times a week, without any additional treatment for brain lesions. Brain magnetic resonance imaging (MRI) was performed on a 1.5 T unit (Siemens Symphony, Erlangen, Germany) including T1-weighted, T2-weighted, fluidattenuated inversion recovery (FLAIR), and diffusionweighted images (DWI) at the forth day of admission. On brain MRI, T2-weighted and FLAIR images showed bilateral and symmetric basal ganglia hyperintensities and also increased signal on DWI with increased apparent diffusion coefficient values, which were compatible with vasogenic edema (Fig. 2) [1]. Metabolic acidosis gradually improved with treatment, and she was discharged after 2 weeks. Follow-up evaluation performed at first month of initial presentation, showed only mild bradykinesia on neurologic examination, and brain MRI revealed remarkable resolution of the previously described lesions (Fig. 2).