The relationship between dietary profile and adherence to the Mediterranean diet with EDSS and quality of life in multiple sclerosis patients: a retrospective cross-sectional study.

BACKGROUND: Multiple sclerosis (MS), one of the main neurological causes of disability seen at young ages, affects the quality of life of patients. Studies on which dietary pattern or consumption of food groups may have an impact on quality of life for MS patients are insufficient. The study was conducted to determine the relationship between adherence to Mediterranean diet and consumption levels of food groups on quality of life in multiple sclerosis patients. METHODS: This study was conducted with 95 patients, 76 females and 19 males, aged 18-65 years, who had been diagnosed with MS for at least 2 years and did not have any other chronic disease. Food Frequency Questionnaire, Mediterranean Diet Adherence Screener (MEDAS), Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Quality of Life-54 Instrument (MS-QoL-54) used as tools. Data were analyzed by SPSS 25.0. RESULTS: Adherence to the Mediterranean diet was associated with EDSS and physical and mental quality of life parameters (CPH and CMH), independent of progression. It was associated with EDSS and CMH in progressive MS. A statistically significant negative weak correlation was found between daily milk and oilseed consumption and EDSS. Daily fruit consumption was associated with CMH, and vegetable consumption was associated with both CPH and CMH. CONCLUSIONS: The Mediterranean diet may be an effective nutritional model in MS patients and may be related to the disability level and quality of life of the patients. Some food groups can be associated with the quality of life and disability level of MS patients.

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. CONCLUSION: 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.

Seizure as a neurologic complication after liver transplant.

OBJECTIVES: Seizure is a common complication after liver transplant and has been reported to occur in up to 42% of patients in different case series. Multiple factors can trigger seizures, including immunosuppressive toxicity, sepsis, metabolic imbalance, and structural brain lesions. The aim of this retrospective study was to evaluate seizure types and associated factors in adult liver transplant patients. MATERIALS AND METHODS: We retrospectively evaluated the medical records of 142 adult patients who received a liver transplant between 2005 and 2013. We recorded demographic data, immunosuppressive treatment, seizure type, cause, recurrence, and treatment. RESULTS: Of the 146 patients, 23 (15.7%) had a seizure after the liver transplant. This group included 10 females and 13 males, with ages ranging between 18 and 63 (39.9 ± 14.8 y). Generalized tonic-clonic seizures were the most common, occurring in 20 patients (87%). We observed complex partial seizure and status epilepticus in 1 and 2 patients. Immunosuppressive drug-related seizure occurred in 8 patients (34.8%) with normal drug blood levels, and all but 1 of these patients experienced seizure within the first week after transplant. Multiple factors (26.1%), metabolic imbalance (17.4%), structural lesion (13%), and sepsis (8.7%) were the other factors identified as underlying conditions. CONCLUSIONS: In conclusion, seizure occurred in a significant proportion of patients who underwent liver transplant. Immunosuppressive drugs were the most common factor associated with seizure occurrence and drug cessation prevented seizure recurrence.

High sensitivity C-reactive protein and cerebral white matter hyperintensities on magnetic resonance imaging in migraine patients.

BACKGROUND: Migraine is a common headache disorder that may be associated with vascular disease and cerebral white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) scan. High sensitivity C-reactive protein (hs-CRP) is a marker of inflammation that may predict subclinical atherosclerosis. However, the relation between migraine, vascular risks, and WMHs is unknown. We evaluated hs-CRP levels and the relation between hs-CRP level and WMHs in adult migraine patients. METHODS: This case-control study included 432 subjects (216 migraine patients [without aura, 143 patients; with aura, 73 patients]; 216 healthy control subjects without migraine; age range 18-50 y). Migraine diagnosis was determined according to the International Classification of Headache Disorders II diagnostic criteria. The migraine patients and control subjects had no known vascular risk factors, inflammatory disease, or comorbid disease. The presence and number of WMHs on MRI scans were determined, and serum hs-CRP levels were measured by latex-enhanced immunoturbidimetry. RESULTS: Mean hs-CRP level was significantly greater in migraine patients (1.94 ± 2.03 mg/L) than control subjects (0.82 ± 0.58 mg/L; P ≤ .0001). The mean number of WMHs per subject and the presence of WMHs was significantly greater in migraine patients (69 patients [31.9%]; 1.68 ± 3.12 mg/dL) than control subjects (21 subjects [9.7%]; 0.3 ± 1.3; P ≤ .001). However, there was no correlation between hs-CRP level and WMHs in migraine patients (r = 0.024; not significant). The presence of WMHs was increased 4.35-fold in migraine patients (odds ratio 4.35, P ≤ .001). CONCLUSIONS: High hs-CRP level may be a marker of the proinflammatory state in migraine patients. However, the absence of correlation between hs-CRP level and WMHs suggests that hs-CRP is not causally involved in the pathogenesis of WMHs in migraine patients. The WMHs were located mostly in the frontal lobe and subcortical area.

Lysosomal rupture, necroapoptotic interactions and potential crosstalk between cysteine proteases in neurons shortly after focal ischemia.

Ischemic cell death is a complex process and the initial distinction between apoptosis and necrosis appears to be an oversimplification. We previously reported that in ischemic neurons with disrupted plasmalemma, apoptotic mechanisms were also active. In the present study, we investigated cellular co-localization of another necrotic feature, lysosomal rupture, with apoptotic mechanisms in the mouse brain and assessed the potential interactions between cysteine proteases. The lysosomal enzymes were spilled into the cytoplasm 1-4h after ischemia/reperfusion, suggesting that lysosomal membrane integrity was rapidly lost, as occurs in necrosis. The same neurons also exhibited caspase-3 and Bid cleavage, and cytochrome-c release. Caspase-3 activity preceded cathepsin-B leakage in most neurons, and declined by 12h, while lysosomal leakage continued to increase. Concurrent inhibition of cathepsin-B and caspase-3 provided significantly better neuroprotection than obtained with separate use of each inhibitor. These data suggest that necrotic and apoptotic mechanisms may act both in concert as well as independently within the same cell beginning at the onset of ischemia to ensure the demise of damaged neurons. Therefore, combined inhibition of cysteine proteases may abrogate potential shifts between alternative death pathways and improve the success of stroke treatments.

Apoptotic and necrotic death mechanisms are concomitantly activated in the same cell after cerebral ischemia.

BACKGROUND AND PURPOSE: Both necrotic and apoptotic cell death mechanisms are activated after cerebral ischemia. However, whether they are concomitantly active in the same cell or in discrete cell populations is not known. METHODS: We investigated activation of both pathways at the cellular level in mice brains subjected to transient or permanent focal ischemia. RESULTS: Four hours after ischemia, diffuse cathepsin-B spillage into cytoplasm, suggesting lysosomal leakage, was observed within neurons immunoreactive for the active form of caspase-3 (p20). Ischemic neurons with a leaky plasma membrane (positive for propidium iodide) were colabeled with caspase-cleaved actin fragment and exhibited TUNEL-positive nuclei having apoptotic morphology. At 72 hours, up to 27% of cells with caspase activity displayed morphological features suggestive of secondary necrosis. CONCLUSIONS: These data, demonstrating an early and concurrent increase in caspase-3 and cathepsin-B activities followed by appearance of caspase-cleavage products, DNA fragmentation, and membrane disintegration, suggest that subroutines of necrotic and apoptotic cell death are concomitantly activated in ischemic neurons and that the dominant cell death phenotype is determined by the relative speed of each process.

Loss of NeuN immunoreactivity after cerebral ischemia does not indicate neuronal cell loss: a cautionary note.

NeuN immunoreactivity is used as a specific marker for neurons. The number of NeuN-positive cells decreases under pathological conditions. This finding is usually considered as an evidence of neuronal loss. However, decrease in NeuN labeling may also be caused by depletion of the protein or loss of its antigenicity. Hence, we have investigated the morphological features of neurons that lost NeuN immunoreactivity and the NeuN protein levels in mouse brain after cerebral ischemia. The number of NeuN-labeled cells was decreased 6 h after a mild ischemic insult (30 min middle cerebral artery occlusion) in penumbral and core regions. Hematoxylin and eosin (H&E) staining of adjacent sections showed that neurons in the penumbra were not disintegrated but displayed early ischemic changes. The nuclear NeuN staining was dramatically reduced or lost in some neurons. However, Hoechst 33258 staining of the same sections revealed that these nuclei were preserved with an intact membrane. Labeling of neurons that had lost NeuN-positivity with antibodies against caspase-3-p20, which is constitutively not present but emerges in neurons after ischemia, disclosed that these neurons still preserved their integrity. Moreover, Western blots showed that NeuN protein levels were not decreased, suggesting that reduced NeuN antigenicity accounted for loss of immunoreactivity in this mild brain injury model. Supporting this idea, NeuN labeling was partially restored after antigenic retrieval. In conclusion, since NeuN immunoreactivity readily decreases after metabolic perturbations, reduced NeuN labeling should not be taken as an indicator of neuronal loss and, quantitative analysis based on NeuN-positivity should be used cautiously after central nervous system (CNS) injury.

Suspected lamotrigine-induced toxic epidermal necrolysis.

Toxic epidermal necrolysis and Stevens-Johnson syndrome are rare, life treating cutaneous reactions. Most cases of toxic epidermal necrolysis are drug induced. The drugs with the highest estimated incidence include co-trimoxazloe (trimethoprim-sulfamethoxazole), sulfadoxine-pyrethamine, and carbamazepine. Among other drugs, the reported reaction rates are relatively low for lamotrigine and sulbactam-ampicillin. We describe a patient who developed toxic epidermal necrolysis after either administration of lamotrigine or of ampicillin.

Serial analysis of soluble intercellular adhesion molecule-1 level in relapsing-remitting multiple sclerosis patients during IFN-beta1b treatment.

In this controlled study, we investigated the serum and cerebrospinal fluid (CSF) levels of soluble intercellular adhesion molecule-1 (sICAM-1) in relapsing-remitting multiple sclerosis (RRMS) patients and changes in the levels of this adhesion molecule during interferon-beta1b (IFN-beta1b) treatment. We also investigated the changes in the levels of sICAM-1 in correlation with disease activity and with findings on magnetic resonance images (MRI). The study included 24 patients (16 females and 8 males) who were confirmed to have RRMS based on the criteria of Poser et al. Sixteen of the patients received IFN-beta1b (Betaseron, Berlex Laboratories, Schering AG Germany, Berlin) treatment, and 8 did not receive this therapy. The levels of sICAM-1 in the MS patients' serum and CSF were significantly higher than levels in individuals with noninflammatory neurologic disease (p = 0.0081 and p = 0.0001, respectively). In the first 3 months of the study, MS patients treated with IFN-beta1b showed a significant rise in sICAM-1 levels (p = 0.0023), whereas their untreated counterparts showed no significant change. Neither of the groups showed a significant correlation between sICAM-1 level and disease activity demonstrated by MRI or between sICAM-1 level and clinical disease activity. The findings suggest that IFN-beta1b treatment may have a short-term upregulating effect on sICAM-1.

Osmotic myelinolysis in a normonatremic patient.

Osmotic demyelination syndrome is usually associated with hyponatremia or rapid correction of this condition. The prognosis is usually fatal. We treated a 34-year-old chronic renal failure patient who did not have hyponatremia but developed severe pontine myelinolysis demonstrated with MRI. Serial MRI revealed gradual reduction of the lesions over 2 months. This case demonstrates that osmotic demyelination syndrome is not always associated with hyponatremia, and that, although the prognosis is usually poor, some patients recover.