Comparison of Diffuse Weighted Imaging and Fluid Attenuation Inversion Recovery Sequences of MRI in Brain Multiple Sclerosis Plaques Detection

How to Cite This Article: Nafisi-Moghadam R, Rahimdel A, Shanbehzadeh T, Fallah R. Comparison of Diffuse Weighted Imaging and Fluid Attenuation Inversion Recovery Sequences of MRI in Brain Multiple Sclerosis Plaques Detection. Iran J Child Neurol. Winter 2017; 11(1):13-20.AbstractObjectiveSuitable magnetic resonance imaging (MRI) techniques from conventional to new devices can help physicians in diagnosis and follow up of Multiple Sclerosis (MS) patients. The aim of present research was to compare effectiveness of Fluid Attenuation Inversion Recovery (FLAIR) sequence of conventional MRI and Diffuse Weighted Imaging (DWI) sequence as a new technique in detection of brain MS plaques. Materials&MethodsIn this analytic cross sectional study, sample size was assessed as 40 people to detect any significant difference between two sequences with a level of 0.05.DWI and FLAIR sequences of without contrast brain MRI of consecutive MS patients referred to MRI center of Shahid Sadoughi Hospital, Yazd, Iran from January to May 2012, were evaluated. ResultsThirty-two females and 8 males with mean age of 35.20±9.80 yr (range =11-66 yr) were evaluated and finally 340 plaques including 127(37.2%) in T2WI, 127(37.2%) in FLAIR, 63(18.5%) in DWI and 24(7.1%) in T1WI were detected. FLAIR sequence was more efficient than DWI in detection of brain MS plaques, oval, round, amorphous plaque shapes, frontal and occipital lobes, periventricular, intracapsular, corpus callosum, centrum semiovale, subcortical, basal ganglia plaques and diameter of detected MS plaques in DWI sequence was smaller than in FLAIR. ConclusionOld lesion can be detected by conventional MRI and new techniques might be more useful in early inflammatory phase of MS and assessment of experimental treatments.References1. Inglese M, Bester M. Diffusion imaging in multiple sclerosis: research and clinical implications. NMRBiomed 2010;23(7):865-72. 2. Inaloo S, Haghbin S. Multiple Sclerosis in Children. Iran J Child Neurol 2013;7(2):1-10.3. Polman CH, Reingold SC, Edan G, Filippi M, Hartung HP, Kappos L, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the McDonald criteria. Ann Neurol 2005;58(6):840-6.4. Sahraian MA, Eshaghi A. Role of MRI in diagnosis and treatment of multiple sclerosis. Clin Neurol Neurosurg 2010 ;112(7):609-15.5. Miller DH; Steering Committee of MAGNIMS. Role of MRI in diagnosing multiple sclerosis: magnetic resonance imaging is valuable. BMJ 2006, 29;332(7548):1034. 6. Rovira A, León A. MR in the diagnosis and monitoring of multiple sclerosis: an overview. Eur J Radiol 2008;67(3):409-14.7. Bakshi R, Thompson AJ, Rocca MA, Pelletier D, Dousset V, Barkhof F, Inglese M, Guttmann CR, Horsfield MA, Filippi M. MRI in multiple sclerosis: current status and future prospects. Lancet Neurol 2008 ;7(7):615-25.8. Nielsen JM, Korteweg T, Barkhof F, Uitdehaag BM, Polman CH. Over diagnosis of multiple sclerosis and magnetic resonance imaging criteria. Ann Neurol 2005;58(5):781-3.9. Zecca C, Cereda C, Wetzel S, Tschuor S, Staedler C, Santini F, Nadarajah N, Bassetti CL, Gobbi C. Diffusion weighted imaging in acute demyelinating myelopathy. Neuroradiology 2012;54(6):573-8.10. Lo CP, Kao HW, Chen SY, Chu CM, Hsu CC, Chen YC, Lin WC, Liu DW, Hsu WL. Comparison of diffusion weighted imaging and contrast-enhanced T1-weighted imaging on a single baseline MRI for demonstrating dissemination in time in multiple sclerosis. BMC Neurol 2014,7;14:100.11. Miabi Z, Midia M, Midia R, Moghinan D. Anatomical distribution of central nervous system plaques in multiple sclerosis: an Iranian experience. Pak J Biol Sci 2010;13(24):1195-20112. Miabi Z, Hashemi H, Moghinan Hokmabad D, Samimi K. Diffusion-weighted and conventinal MRI in detection of multiple sclerosis lesion in brain : a comparative study.Tehran University Medical Journal (TUMJ)2006;64(5):51- 65.13. Poloni G, Minagar A, Haacke EM, Zivadinov R. Recent developments in imaging of multiple sclerosis. Neurologist 2011;17(4):185-204.14. Filippi M, Rocca MA. MRI aspects of the “inflammatory phase” of multiple sclerosis. Neurol Sci 2003 ;24 Suppl 5:S275-8. 15. Filippi M, Rocca MA, De Stefano N, Enzinger C, Fisher E, Horsfield MA, Inglese M, Pelletier D, Comi G. Magnetic resonance techniques in multiple sclerosis: the present and the future. Arch Neurol 2011 ;68(12):1514- 20.16. Bhatt A, Masih A, Grothous HF, Farooq MU, Naravetla B, Kassab MY. Diffusion-weighted imaging: not all that glitters is gold. South Med J 2009 ;102(9):923-8. 17. Wilson M, Morgan PS, Lin X, Turner BP, Blumhardt LD. Quantitative diffusion weighted magnetic resonance imaging, cerebral atrophy, and disability in multiple sclerosis. J Neurol Neurosurg Psychiatry 2001;70(3):318- 22.18. Cheng GX, Wu HW, Zhang J, Liang LN, Zhang XL. MRI diagnosis of multiple cerebral sclerosis. Nan Fang Yi Ke Da Xue Xue Bao. 2008;28(8):1372-5. [Article in Chinese]

Relationship between Bone Density and Biochemical Markers of Bone among Two Groups Taking Carbamazepine and Sodium Valproate for Epilepsy in Comparison with Healthy Individuals in Yazd

Introduction: Chronic antiepileptic therapy has been associated with metabolic bone diseases including osteomalacia and osteoporosis. The aim of this study was to determine frequency of changes in biochemical and bone mineral density (BMD) in adults receiving valproaic acid (VPA) & carbamazepine (CBZ). Methods: In a cross sectional study evaluating adults (age 20- 50 y) epileptic patients receiving valproic acid or carbamazepine for at least 2 years. This study was conducted from May 2014 to May 2015 in Shahid Sadoughi Hospital of Yazd University of Medical Science, Yazd, Iran. Bone metabolism was evaluated by measurement of serum calcium (Ca), phosphorus (P), alkaline phosphatase (ALP) and parathormone hormone (PTH), BMD at lumbar and femoral measured by dual energy X ray absorptiometry (DXA). SPSS software (version 18) was used for data analysis. The t-test was used for quantitative data, and the chi-squared test was used for the qualitative variables. Results: Eighty two epileptic patients (mean age: 31.67±10.69 year) treated with either carbamazepine (n=41) or valproate sodium (n=41) were studied. Normal serum Ca and P levels were observed in 98.8% and 97.6% of patients respectively. Serum ALP and PTH were normal in 97.6% and 97.6% of patients. Means of Ca and P in CBZ group were significantly lower than VPA group (Ca: 9.02 vs. 9.1, p-value: 0.03 and P: 3.54 vs. 3.76 p- value: 0.004). BMD values at lumbar spine were not significant in either group (T. score CBZ: -0.43± 0.744 vs. T. score VPA: -0.615± 0.904 and p-value: 0.333) and were significantly higher than Iranian normal population BMD value at femoral neck in CBZ group was lower than VPA group (T. score CBZ: -0.707± 0.896 vs. T. score VPA: - 0.297± 0.850 p-value: 0.04). Dosage of CBZ and VPA did not correlate with BMD and biochemical parameters. Duration of CBZ use had correlation with increased ALP and duration of VPA use had correlation with decreased BMD in adult patients. Conclusion: long term anti-epileptic drug treatment either with CBZ and VPA which has unknown effects on skeletal mineralization and induces a state of decreased bone mineral density BMD values at femoral neck were significant in CBZ group Therefore regular screening for monitoring of biochemical markers of bone turnover and BMD with DXA during the treat period is recommended. In addition, Ca supplement could be considered for all patients with epilepsy upon initiation of CBZ and VPA therapy

Comparison between Intravenous Sodium Valproate and Subcutaneous Sumatriptan for Treatment of Acute Migraine Attacks; Double-Blind Randomized Clinical Trial

Background: Sodium valproate (SV) has been approved for migraine prophylaxis and its intravenous form is used to treat acute migraine attacks. We compared the efficacy and safety of intravenous SV and subcutaneous Sumatriptan in managing acute migraine attacks. Methods: This double-blind randomized clinical trial divided 90 patients into two groups: one group received 400 mg of intravenous SV and the second group received 6 mg of subcutaneous Sumatriptan. Headache severity before treatment and half an hour, one hour, and two hours after treatment was measured based on the VNRS in the groups. Associated symptoms, i.e., photophobia, phonophobia, nausea, and vomiting, were assayed on admission and 2 hours after treatment. Side effects of the drugs were checked 2 hours after injection. Obtained data from the groups were compared. Results: In both groups, pain decrement at the mentioned time points was significant (P0.05), indicating the similar effect of both drugs on pain improvement. In the SV group, photophobia, phonophobia, nausea, and vomiting were improved significantly, while in the Sumatriptan group, only photophobia and vomiting were decreased significantly, indicating the advantage of SV in improving the associated symptoms. Nausea, vomiting, facial paresthesia, and hypotension were more significantly frequent in the Sumatriptan group than in the SV group (P<0.05). Conclusion: Intravenous SV (400 mg) was as effective as subcutaneous Sumatriptan in the treatment of acute migraine attacks, but with more improvement in associated symptoms and with fewer side effects. Trial Registration Number: IRCT201108025943N