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Review Article


Nutritional Aspects of Treatment in Epileptic Patients

Danesh SOLTANI, Majid GHAFFAR POUR, Abbas TAFAKHORI, Payam SARRAF, Sama BITARAFAN

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 1-12
https://doi.org/10.22037/ijcn.v10i3.9224

How to Cite This Article: Soltani D, Ghaffar pour M, Tafakhori A, Sarraf P, Bitarafan S. Nutritional Aspects of Treatment in Epileptic Patients. Iran J Child Neurol. Summer 2016; 10(3): 1-12.

 

Abstract
Epilepsy is a neurological disorder characterized by interruption of normal neuronal functions that is manifested by behavioral disorders, changing of awareness level, and presence of some sensory, autonomic and motor symptoms or signs. It is resulted from many different causes. Many antiepileptic drugs (AEDs) are considered to manage epileptic attacks. Some of them  hange
metabolism and absorption of many nutrients. Therefore, epileptic patients may be in higher risk of nutrient deficiency and its unwelcome effects. In the present paper, we intend to review the relationship between nutrition and epilepsy in two aspects. In one aspect we discuss the nutritional status in epileptic patients, the causes of nutritional deficiencies and the way of compensation of the nutrient deficiencies. It will guide these patients to have a healthy life. In another aspect we explain the role of some nutrients and specific diets in management of epileptic attacks. It can help to better control of epileptic attacks in these patients.

 

References

1. Gragnani A, Müller BR, Oliveira AF, Ferreira LM. Burns and epilepsy–review and case report. Burns 2014;41:e15–e18.

2. Carlson C, Dugan P, Kirsch HE, Friedman D, Investigators E. Sex differences in seizure types and symptoms.EpilepsyBehav 2014; 41:103-8.

3. Speed D, O’Brien TJ, Palotie A, Shkura K, Marson AG, Balding DJ, et al. Describing the genetic architecture of epilepsy through heritability analysis. Brain 2014; 137:2680-9.

4. Poduri A, Sheidley BR, Shostak S, Ottman R. Genetic testing in the epilepsies developments and dilemmas. Nat Rev Neurol 2014; 10:293-9.

5. Malkan A, Beran RG. An appraisal of the new operational definition of epilepsy-Then and now. Epilepsy Behav 2014; 41:217-20.

6. Wong VC, Fung C, Kwong AK. SCN2A mutation in a Chinese boy with infantile spasm-response to Modified Atkins Diet. Brain Dev 2014; 37:729-732.

7. Rogawski MA. KCNQ2/KCNQ3 K. channels and the molecular pathogenesis of epilepsy: implications for therapy. Trends Neurosci 2000; 23:393-8.

8. Annegers JF, Hauser WA, Coan SP, Rocca WA. A population-based study of seizures after traumatic brain injuries. N Engl J Med 1998; 338:20-24.

9. Falconer Ma, Serafetinides Ea, Corsellis Jn. Etiology and pathogenesis of temporal lobe epilepsy. Arch Neurol 1964; 10:233-48.

10. Menon B, Shorvon SD. Ischaemic stroke in adults and epilepsy. Epilepsy Res 2009; 87:1-11.

11. Annegers J, Hauser W, Beghi E, Nicolosi A, Kurland L. The risk of unprovoked seizures after encephalitis and meningitis. Neurology 1988; 38:1407-10.

12. Matera G, Labate A, Quirino A, Lamberti AG, Borzì G, Barreca GS, et al. Chronic neuroborreliosis by B. garinii: an unusual case presenting with epilepsy and multifocal brain MRI lesions. New Microbiol 2014; 37:393-97.

13. Rajneesh KF, Binder DK. Tumor-associated epilepsy. Neurosurg Focus 2009; 27:E4.

14. Kovac S, Abramov AY, Walker MC. Energy depletion in seizures: Anaplerosis as a strategy for future therapies. Neuropharmacology 2013; 69:96-104.

15. Prasad C, Rupar T, Prasad AN. Pyruvate dehydrogenase deficiency and epilepsy. Brain Dev 2011; 33:856-65.

16. Seven M, Basaran SY, Cengiz M, Unal S, Yuksel A. Deficiency of selenium and zinc as a causative factor for idiopathic intractable epilepsy. Epilepsy Res 2013; 104:35-39.

17. Xiang J, Jiang Y. Regulation of Cu-Zn superoxide dismutase on SCN2A in SH-SY5Y cells as a potential therapy for temporal lobe epilepsy. Mol Med Rep 2014; 9:16-22.

18. Mintzer S, Skidmore CT, Sperling MR. B-Vitamin deficiency in patients treated with antiepileptic drugs. Epilepsy Behav 2012; 24:341-4.

19. Apeland T, Mansoor MA, Pentieva K, McNulty H, Strandjord RE. Fasting and post-methionine loading concentrations of homocysteine, vitamin B2, and vitamin B6 in patients on antiepileptic drugs. Clin Chem 2003;49:1005-8.

20. Brodie MJ, Mintzer S, Pack AM, Gidal BE, Vecht CJ, Schmidt D. Enzyme induction with antiepileptic drugs: cause forconcern? Epilepsia 2013; 54:11-27.

21. Miziak B, Blaszczyk B, Chroscinska-Krawczyk M, Danilkiewicz G, Jagiello-Wójtowicz E, Czuczwar SJ. The problem of osteoporosis in epileptic patients taking antiepileptic drugs. Expert Opin Drug Saf 2014; 13:1-12.

22. Gough H, Goggin T, Bissessar A, Baker M, Crowley M, Callaghan N. A comparative study of the relative influence of different anticonvulsant drugs, UV exposure and diet on vitamin D and calcium metabolism in outpatients with epilepsy. QJM 1986; 59:569-77.

23. Hahn TJ. 6 Drug-induced disorders of vitamin D and mineral metabolism. Clin Endocrinol Metab 1980; 9:107-29.

24. Roe DA. Diet and Drug Interactions. In: Monika Grejniec, editor. Drug-induced nutritional deficiencies.1st ed. New York: Van Nostrand Reinhold; 1989:83-103.

25. Beerhorst K, Tan I, Krom M, Verschuure P, Aldenkamp A. Antiepileptic drugs and high prevalence of low bone mineral density in a group of in patients with chronic epilepsy. ActaNeurolScand 2013; 128:273-80.

26. Shen C, Chen F, Zhang Y, Guo Y, Ding M. Association between useof antiepileptic drugs and fracture risk: A systematic review and meta-analysis. Bone 2014; 64: 246–53.

27. Perreault S, Dragomir A, Blais L, Moride Y, Rossignol M, Ste- Marie LG, et al. Population- based study of the effectiveness of bone- specific drugs inreducing the risk of osteoporotic fracture. Pharmacoepidemiol Drug Saf 2008; 17:248–59.

28. Ahmad BS, Hill KD, O’Brien TJ, Gorelik A, Habib N, Wark JD. Falls and fractures in patients chronically treated with antiepileptic drugs. Neurology 2012; 79:145-51.

29. Nicholas JM, Ridsdale L, Richardson MP, Grieve AP, Gulliford MC. Fracture risk with use of liver enzyme inducing antiepileptic drugs in people with active epilepsy: cohort study using the general practice research database. Seizure 2013; 22:37-42.

30. Beerhorst K, Schouwenaars F, Tan I, Aldenkamp A. Epilepsy: fractures and the role of cumulative antiepileptic drug load. Acta Neurolo Scand 2012; 125:54-9.

31. Weinstein RS, Bryce GF, Sappington LJ, King DW, Gallagher BB. Decreased Serum Ionized Calcium and Normal Vitamin D Metabolite Levels with Anticonvulsant Drug Treatment. J Clin Endocrinol Metab1984; 58:1003-9.

32. Fitzpatrick LA. Pathophysiology of bone loss in patients receiving anticonvulsant therapy. Epilepsy Behav 2004; 5:3-15.

33. Pack AM, Olarte LS, Morrell MJ, Flaster E, Resor SR, Shane E. Bone mineral density in an outpatient population receiving enzyme-inducing antiepileptic drugs. Epilepsy Behav 2003; 4:169-74.

34. Phabphal K, Geater A, Limapichat K, Sathirapanya P, Setthawatcharawanich S, Leelawattana R. Effect of switching hepatic enzyme- inducer antiepileptic drug to levetiracetam on bone mineral density, 25 hydroxy vitamin D, and parathyroid hormone in young adult patients with epilepsy. Epilepsia 2013; 54:e94-e8.

35. Richens A, Rowe D. Disturbance of calcium metabolism by anticonvulsant drugs. BMJ 1970; 4:73-76.

36. Hahn TJ, Hendin BA, Scharp CR, Haddad Jr JG. Effect of chronic anticonvulsant therapy on serum 25-hydroxycalciferol levels in adults. N Engl J Med 1972; 287:900-4.

37. Bouillon R, Reynaert J, Claes JH, Lissens W, De Moor P. The effect of anticonvulsant therapy on serum levels of 25-hydroxy-vitamin D, calcium, and parathyroid hormone. Clin Endocrinol Metab 1975; 41:1130-5

38. Lifshitz F, Maclaren NK. Vitamin D-dependent rickets in institutionalized, mentally retarded children receiving long-term anticonvulsant therapy .I.A survey of 288 patients. J Pediatr 1973; 83:612-20.

39. Deb S, Cowie VA, Tsanaclis LM, Richens A. Calcium homeostasis in mentally handicapped epileptic patients. J Intellectual Disabil Res 1985; 29:403-10.

40. Teagarden DL, Meador KJ, Loring DW. Low vitamin D levels are common in patients with epilepsy. Epilepsy res 2014; 108:1352-6.

41. Petty SJ,O’brien T, Wark J. Anti-epileptic medication and bone health. Osteoporis Int 2007; 18:129-42.

42. Wu FJ, Sheu SY, Lin HC. Osteoporosis is associated with antiepileptic drugs: a population- based study. Epileptic Disord 2014; 16:333-42.

43. Lazzari AA, Dussault PM, Thakore- James M, Gagnon D, Baker E, Davis SA, et al. Prevention of bone loss and vertebral fractures in patients with chronic epilepsy-Antiepileptic drug and osteoporosis prevention trial. Epilepsia 2013; 54:1997-2004.

44. Christiansen C, Rødbro P, Lund M. Incidence of anticonvulsant osteomalacia and effect of vitamin D: controlled therapeutic trial. BMJ 1973; 4:695-701.

45. Krause K, Bonjour J, Berlit P, Kynast G, Schmidt-Gayk H, Schellenberg B. Effect of long-term treatment with antiepileptic drugs on the vitamin status. Drug Nutr Interact 1987; 5:317-43.

46. Schwaninger M, Ringleb P, Winter R, Kohl B, Fiehn W, Rieser PA, et al. Elevated plasma concentrations of homocysteine in antiepileptic drug treatment. Epilepsia 1999; 40:345-50.

47. Apeland T, Mansoor MA, Strandjord RE, Kristensen O. Homocysteine concentrations and methionine loading in patients on antiepileptic drugs. Acta Neurol Scand 2000; 101:217-23.

48. Apeland T, Mansoor MA, Strandjord RE, Vefring H, Kristensen O. Folate, homocysteine and methionine loading inpatients on carbamazepine. Acta neurol scand 2001; 103:294-9.

49. Apeland T, Mansoor MA, Strandjord RE. Antiepileptic drugs as independent predictors of plasma total homocysteine levels. Epilepsy Res 2001; 47:27-35.

50. Apeland T, Mansoor MA, Pentieva K, McNulty H, Seljeflot I, Strandjord RE. The effect of B-vitamins on hyperhomocysteinemia in patients on antiepileptic drugs. Epilepsy Res 2002; 51:237-47.

51. Linnebank M, Moskau S, Semmler A, Widman G, Stoffel- Wagner B, Weller M, et al. Antiepileptic drugs interact with folate and vitamin B12 serum levels. Ann Neurol 2011; 69:352-9.

52. Scheinfeld N. Phenytoin in cutaneous medicine: Its uses and side effects. Dermatol Online J 2003; 9:6-22.

53. Reynolds E, Chanarin I, Milner G, Matthews D. Anticonvulsant therapy, folic acid and vitamin B12 metabolism and mental symptoms. Epilepsia 1966; 7:261-70.

54. Krause K-H, Kochen W, Berlit P, Bonjour J-P. Excretion of organic acids associated with biotin deficiency in chronic anticonvulsant therapy. Int J Vitam Nutr Res 1984; 54:217-22.

55. .Mock DM, Mock NI, Nelson RP, Lombard KA. Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. J Pediatr Gastroenterol Nutr 1998; 26:245-50.

56. Krause KH, Berlit P, Bonjour JP. Imparied biotin status in anticonvulsant therapy. Ann Neurol 1982; 12:485-6.

57. Mock DM, Dyken ME. Biotin catabolism is accelerated in adults receiving long-term therapy with anticonvulsants. Neurology 1997; 49:1444-7.

58. Gillman MA, Sandyk R. Nicotinic acid deficiency induced by sodium valproate. S Afr Med J 1984; 65:986.

59. Semmler A, Moskau-Hartmann S, Stoffel-Wagner B, Elger C, Linnebank M. Homocysteine plasma levels in patients treated with antiepileptic drugs depend on folate and vitamin B12 serum levels, but not on genetic variants of homocysteine metabolism. Clin Chem Lab Med 2013; 51:665-9.

60. Ray K. Epilepsy: Antiepileptic drugs reduce vitamin B12 and folate levels. Nature Rev Neurol 2011; 7:125.

61. Hoffbrand A, Necheles T. Mechanism of folate deficiency in patients receiving phenytoin. The Lancet 1968; 292:528-30.

62. Zahn C. Neurologic care of pregnant women with epilepsy. Epilepsia. 1998;39:S26-S31.

63. Belcastro V, Striano P. Antiepileptic drugs, hyperhomocysteinemia and B-vitamins supplementation in patients with epilepsy. Epilepsy res 2012; 102:1-7.

64. Bochyńska A, Lipczyńska-Łojkowska W, Gugała-Iwaniuk M, Lechowicz W, Restel M, Graban A, et al. The effect of vitamin B supplementation on homocysteine metabolism and clinical state of patients withchronic epilepsy treated with carbamazepine and valproic acid. Seizure 2012; 21:276-81.

65. Bailey LB. Folate in health and disease: in: Taylor and Francis group, editor. folate and neurological disease. 2nd ed. CRC Press; 2009; 325-355.

66. Paknahad Z, Chitsaz A, Zadeh AH, Sheklabadi E. Effects of common anti-epileptic drugs on the serum levels of homocysteine and folic acid. Int J Prev Med 2012; 3:S186–S190.

67. Jeeja MC, Jayakrishnan T, Narayanan PV, Kumar MSV, Thejus T, Anilakumari VP. Folic acid supplementation on homocysteine levels in children taking antiepileptic drugs: A randomized controlled trial. J PharmacolPharmacother 2014; 5:93-99.

68. Coburn SP. Location and turnover of vitamin B6 pools and vitamin B6 requirements of Humansa. Ann N Y AcadSci 1990; 585:76–85.

69. Kretsch MJ, Sauberlich HE, Newbrun E. Electroencephalographic changes and periodontal status during short-term vitamin B-6 depletion of young, nonpregnant women. Am J ClinNutr 1991; 53:1266-74.

70. Attilakos A, Papakonstantinou E, Schulpis K, Voudris K, Katsarou E, Mastroyianni S, et al. Early effect of sodium valproate and carbamazepine monotherapy on homocysteine metabolism in children with epilepsy. Epilepsy Res 2006; 71:229-32.

71. Apeland T, Froyland ES, Kristensen O, Strandjord RE, Mansoor MA. Drug-induced pertubation of the aminothiol redox-status in patients with epilepsy: improvement by B-vitamins. Epilepsy Res 2008; 82:1-6.

72. Sawicka-Glazer E, Czuczwar SJ. Vitamin C: A new auxiliary treatment of epilepsy? Pharmacol Rep 2014; 66: 529–533.

73. Ullah I, Badshah H, Naseer MI, Lee HY, Kim MO. Thymoquinone and Vitamin C Attenuates Pentylenetetrazole-Induced Seizures Via Activation of GABAB1 Receptor in Adult Rats Cortex and Hippocampus. Neuromolecular Med2014; 17:1-12.

74. Dubick MA, Keen CL. Alterations in tissue trace element and ascorbic acid metabolism in phenytoin-fed rats and mice. J Nutr1985; 115:1481-7.

75. Wilcox RE, Riffee WH, Goldman C-PL, Young RK. Effects of ascorbate on a dopaminergic response: Apomorphine-induced modification of pentylenetetrazol induced seizures in mice. Psychopharmacology 1984; 83:48-50.

76. Fex G, Larsson K, Andersson A, Berggren-Söderlund M. Low serum concentrationof all-trans and 13-cis retinoic acids in patients treated with phenytoin, carbamazepine and valproate. Arch Toxicol 1995; 69:572-4.

77. Leo MA, Lowe N, Lieber CS. Decreased hepatic vitamin A after drug administration in men and in rats. Am J Clin Nutr 1984; 40:1131-6.

78. Cornelissen M, Steegers-Theunissen R, Kollée L, Eskes T, Vogels-Mentink G, Motohara K, et al. Increased incidence of neonatal vitamin K deficiency resulting from maternal anticonvulsant therapy. Am J Obstet Gynecol 1993; 168:923-8.

79. Cornelissen M, Steegers-Theunissen R, Kollee L, Eskes T, Motohara K, Monnens L. Supplementation of vitamin K in pregnant women receiving anticonvulsant therapy prevents neonatal vitamin K deficiency. Am J Obstet Gynecol1993; 168:884-8.

80. Nazıroğlu M, Yürekli VA. Effects of antiepileptic drugs on antioxidant and oxidant molecular pathways: focus on trace elements. Cell Mol Neurobiol 2013; 33:589-99.

81. Hurd R, Van Rinsvelt H, Wilder B, Karas B, Maenhaut W, De Reu L. Selenium, zinc, and copper changes with valproic acid Possible relation to drug side effects. Neurology 1984; 34:1393-95.

82. Palm R, Hallmans G. Zinc and copper metabolism in phenytoin therapy. Epilepsia 1982; 23:453-61.

83. Lewis-Jones M, Evans S, Culshaw M. Cutaneous manifestations of zinc deficiency during treatment with anticonvulsants. BMJ (Clinical research ed) 1985; 290:603-604.

84. Kuzuya T, Hasegawa T, Shimizu K, Nabeshima T. Effect of anti-epileptic drugs on serum zinc and copper concentrations in epileptic patients. Int J Clin Pharmacol Ther Toxicol 1993; 31:61-5.

85. Liu C-S, Wu H-M, Kao S-H, Wei Y-H. Serum trace elements, glutathione, copper/zinc superoxide dismutase, and lipid peroxidation in epileptic patients with phenytoin or carbamazepine monotherapy. Clin Neuropharmacol 1998; 21:62-4.

86. Castro-Gago M, Pérez-Gay L, Gómez-Lado C, Castiñeiras-Ramos DE, Otero-Martínez S, Rodríguez-Segade S. The influence of valproic acid and carbamazepine treatment on serum biotin and zinc levels and on biotinidase activity. J Child Neurol 2011; 26:1522-4.

87. Yuen W, Whiteoak R, Thompson R. Zinc concentrations in leucocytes of patients receiving antiepileptic drugs. J Clin Pathol 1988; 41:553-5.

88. Ghose K, Taylor A. Hypercupraemia induced by antiepileptic drugs. Hum Exp Toxicol 1983; 2:519-29.

89. Morris DR, Levenson CW. Ion channels and zinc: mechanisms of neurotoxicity and neurodegeneration. J Toxicol 2012; 201:1-6.

90. Gower- Winter SD, Levenson CW. Zinc in the central nervous system: from molecules to behavior. Biofactors 2012; 38:186-93.

91. Yorulmaz H, Şeker FB, Demir G, Yalçın İE, Öztaş B. The Effects of Zinc Treatment on the Blood–Brain Barrier Permeability and Brain Element Levels During Convulsions. Biol Trace Elem Res 2013; 151:256-62.

92. Wojciak RW, Mojs E, Stanislawska-Kubiak M, Samborski W. The serum zinc, copper, iron, and chromium concentrations in epileptic children. Epilepsy Res 2013; 104:40-4.

93. Kessler SK, Gallagher PR, Shellhaas RA, Clancy RR, Bergqvist A. Early EEG improvementafter ketogenic diet initiation. Epilepsy Res 2011; 94:94-101.

94. Wilder R, editor. The effects of ketonemia on the course of epilepsy. Mayo Clin Proc 1921; 2: 307-308.

95. Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: a systematic review of efficacy. Pediatrics 2000; 105:46-53.

96. Freeman JM, Kossoff EH, Hartman AL. The ketogenic diet: one decade later. Pediatrics 2007; 119:535-43.

97. Danial NN, Hartman AL, Stafstrom CE, Thio LL. How does the ketogenic diet work? Four potential mechanisms. J Child Neurol 2013; 28:1027-33.

98. Klepper J. GLUT1 deficiency syndrome in clinical practice. Epilepsy res 2012; 100:272-7.

99. Neal EG, Chaffe H, Schwartz RH, Lawson MS, Edwards N, FitzsimmonsG, et al. The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. Lancet Neurol 2008; 7:500-6.

100.Lutas A, Yellen G. The ketogenic diet: metabolic influences on brain excitability and epilepsy. Trends Neurosci 2013; 36:32-40.

101.Hartman AL, Gasior M, Vining EP, Rogawski MA. The neuropharmacology of the ketogenic diet. Pediatr Neurol 2007; 36:281-92.

102.Stafstrom CE, Rho JM. The ketogenic diet as a treatment paradigm for diverse neurological disorders. Front Pharmacol 2012; 3:1-8.

103.Yoon J-R, Lee EJ, Kim HD, Lee JH, Kang H-C. Polyunsaturated fatty acid-enriched diet therapy for a child with epilepsy. Brain Dev 2014; 36:163-6.

104.Huttenlocher PR. Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy. Pediatr Res 1976; 10:536-40.

105.Owen O, Morgan A, Kemp H, Sullivan J, Herrera M, Cahill Jr G. Brain metabolism during fasting. J Clin Invest 1967; 46:1589-95.

106.Smith AL, Satterthwaite HS, Sokoloff L. Induction of Brain D (m)-β-Hydroxybutyrate Dehydrogenase Activity by Fasting. Science 1969; 163:79-81.

107.Vining EP. Clinical efficacy of the ketogenic diet. Epilepsy Res 1999; 37:181-90.

108.YmC L, Wang H. Medium-chain triglyceride ketogenic diet, an effective treatment for drug-resistant  epilepsy and a comparison with other ketogenic diets. Biomed J2013;36:9-15.

109.Huttenlocher P, Wilbourn A, SignoreJ. Medium- chain triglycerides as a therapy for intractable childhood epilepsy. Neurology 1971; 21:1526-632.

110. Bach AC, Babayan VK. Medium-chain triglycerides: an update. Am J Clin Nutr 1982; 36:950-62.

111. Wlaź P, Socała K, Nieoczym D, Żarnowski T, Żarnowska I, Czuczwar SJ, et al. Acute anticonvulsant effects of capric acid in seizure tests in mice. Prog Neuropsychopharmacol Biol Psychiatry 2015; 57:110-6.

112. Chang P, Zuckermann AM, Williams S, Close AJ, Cano- Jaimez M, McEvoy JP, et al. Seizure control by derivatives of medium chain fatty acids associated with the ketogenic diet show novel branching-point structure for enhanced potency. J Pharmacol Exp Ther 2015; 352:43-52.

113. Henderson ST. Ketone bodies as a therapeutic for Alzheimer’s disease. Neurotherapeutics 2008; 5:470-80.

114. Johnson RC, Young SK, Cotter R, Lin L, Rowe W. Medium-chain-triglyceride lipid emulsion: metabolism and tissue distribution. Am J Clin Nutr 1990; 52:502-8.

115. McGarry JD, Foster DW. The Regulation of Ketogenesis from Octanoic Acid The Role Of The  Tricarboxylic Acid Cycle And Fatty Acid Synthesis. J Biol Chem 1971;246:1149-59.

116. Papamandjaris AA, MacDougall DE, Jones PJ. Medium chain fatty acid metabolism and energy expenditure: obesity treatment implications. Life Sci 1998; 62:1203-15.

117. Samson Jr FE, Dahl N, Dahl DR. A study on the narcotic action of theshort chain fatty acids. J Clin Invest 1956;35:1291-8.

118. Ebert D, Haller RG, Walton ME. Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy. J Neurosci 2003; 23:5928-35.

119. Edmond J, Higa TA, Korsak RA, Bergner E, Lee WNP. Fatty acid transport and utilization for the developing brain. J Neurochem 1998; 70:1227-34.

120.Rapoport SI. In vivo fatty acid incorporation into brain phosholipids in relation to plasma availability, signal transduction and membrane remodeling. J Mol Neurosci 2001; 16:243-61.

121.Spector R. Fatty Acid Transport Through the Blood- Brain Barrier. J Neurochem 1988; 50:639-43.

122.Walker C, McCandless D, McGarry J, Schenker S. Cerebral energy metabolism in short-chain fatty acidinduced coma. J Lab Clin Med 1970; 76:569-83.

123.Hughes SD, Kanabus M, Anderson G, Hargreaves IP, Rutherford T, Donnell MO, et al. The ketogenic diet

component decanoic acid increases mitochondrial citrate synthase and complex I activity in neuronal cells. J Neurochem 2014; 129:426-33.

124.Kamata Y, Shiraga H, Tai A, Kawamoto Y, GohdaE. Induction of neurite outgrowth in PC12 cells by the medium-chain fatty acid octanoic acid. Neuroscience 2007; 146:1073-81.

125.Jiang W, Van Cleemput J, Sheerin AH, Ji SP, Zhang Y, Saucier DM, et al. Involvement of extracellular regulated kinase and p38 kinase in hippocampal seizure tolerance. J Neurosci Res 2005; 81:581-8.

126.Jung S, Bullis JB, Lau IH, Jones TD, Warner LN, Poolos NP. Downregulation of dendritic HCN channel gating in epilepsy is mediated by altered phosphorylation signaling. J Neurosci 2010; 30:6678-88.

127.Scheffer IE. Genetics of the epilepsies: channelopathies and beyond. Epilepsia.2011;52:192-3.

128.Genton P. When antiepileptic drugs aggravate epilepsy. Brain Dev 2000; 22:75-80.

129.Dressler A, Trimmel-Schwahofer P, Reithofer E, Mühlebner A, Gröppel G, Reiter-Fink E, et al. Efficacy and tolerability of the ketogenic diet in Dravet syndrome- Comparison with various standard antiepileptic drug regimen. Epilepsy Res 2015; 109:81-9.

130.Dahlin M, Hjelte L, Nilsson S, Åmark P. Plasma phospholipid fatty acids are influenced by a ketogenic diet enriched with n-3 fatty acids in children with epilepsy. Epilepsy Res 2007; 73:199-207.

131.DeGiorgio CM, MillerPR, Harper R, Gornbein J, Schrader L, Soss J, et al. Fish oil (n-3 fatty acids) in drug resistant epilepsy: a randomised placebo-controlled crossover study. J Neurol Neurosurg Psychiatry 2015; 86:670-5.

132.Taha AY, Burnham WM, AuvinS. Polyunsaturated fatty acids and epilepsy. Epilepsia 2010; 51:1348-58.

133.Taha A, Ryan MAA, Cunnane SC. Despite transient ketosis, the classic high-fat ketogenic diet induces marked changes in fatty acid metabolism in rats. Metabolism 2005; 54:1127-32.

134.Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia 2007; 48:43-58.

135.Bough KJ, Wetherington J, Hassel B, Pare JF, Gawryluk JW, Greene JG, et al. Mitochondrial biogenesis in the anticonvulsant mechanism of theketogenic diet. Ann Neurol 2006; 60:223-35.

136.Kossoff EH, Zupec- Kania BA, Amark PE, Ballaban- Gil KR, Christina Bergqvist A, Blackford R, et al. Optimal clinical management of children receiving the ketogenic diet: recommendations of the International Ketogenic Diet Study Group. Epilepsia 2009; 50:304-17.

137.Bergqvist A, Schall JI, Stallings VA. Vitamin D status in children with intractable epilepsy, and impact of the ketogenic diet. Epilepsia 2007; 48:66-71.

138.Sharma S, Jain P. The ketogenic diet and other dietary treatments for refractory epilepsy in children. Ann Indian Acad Neurol 2014; 17:253-8.

139.Kim JT, Kang H-C, Song J-E, Lee MJ, Lee YJ, Lee EJ, et al. Catch-up growth after long-term implementation and weaning from ketogenic diet in pediatric epileptic patients. Clin Nutr 2013; 32:98-103.

140.Mosek A, Natour H, Neufeld MY, Shiff Y, Vaisman N. Ketogenic diet treatment in adults with refractory epilepsy: a prospective pilot study. Seizure 2009; 18:30-3.

141.Klein P, Janousek J, Barber A, Weissberger R. Ketogenic diet treatment in adults with refractory epilepsy. Epilepsy Behav 2010; 19:575-9.

142.Berry- Kravis E, Booth G, Sanchez AC, Woodbury- Kolb J. Carnitine levels and theketogenic diet. Epilepsia 2001; 42:1445-51.

143.Schwartz RH, Eaton J, Bower B, Aynsley- Green A. Ketogenic Diets In The Treatment Of Epilepsy: Short-Term Clinical Effects. Dev Med Child Neurol 1989; 31:145-51.

144.Chesney D, Brouhard BH, Wyllie E, Powaski K. Biochemical abnormalities of the ketogenic diet in children. Clin Pediatr 1999; 38:107-9.

145.Kang HC, Chung DE, Kim DW, Kim HD. Early- and late onset complications of the ketogenic diet for intractable epilepsy. Epilepsia 2004; 45:1116-23.

146.Wheless JW. The ketogenic diet: an effective medical therapy with side effects. J Child Neurol 2001; 16:633-5.

147.Fraser D, Whiting S, Andrew R, Macdonald E, Musa– Veloso K, Cunnane S. Elevated polyunsaturated fatty acids in blood serum obtained from children on the ketogenic diet. Neurology 2003; 60:1026-9.

148.Freeman J, Veggiotti P, Lanzi G, Tagliabue A, Perucca E. The ketogenic diet: from molecular mechanisms to clinical effects. Epilepsy Res 2006; 68:145-80.

149.Lin Q, Ruuska SE, Shaw NS, Dong D, Noy N. Ligand selectivity of the peroxisome proliferator-activated receptor α. Biochemistry 1999; 38:185-90.

150.Nei M, Ngo L, Sirven JI, Sperling MR. Ketogenic diet in adolescents and adults with epilepsy. Seizure 2014;23:439-442.

151.Schoeler NE, Wood S, Aldridge V, Sander JW, Cross JH, Sisodiya SM. Ketogenic dietary therapies for adults with epilepsy: Feasibility and classification of response. Epilepsy Behav 2014; 37:77-81.

152.Kossoff EH, McGrogan JR, Bluml RM, Pillas DJ, Rubenstein JE, Vining EP. A modified Atkins diet is effective for the treatment of intractable pediatric epilepsy. Epilepsia 2006; 47:421-4.

153.Pfeifer HH, Thiele EA. Low-glycemic-index treatment: a liberalized ketogenicdiet for treatment of intractable epilepsy. Neurology 2005; 65:1810-2.

154.Coppola G, D’Aniello A, Messana T, Di Pasquale F, della Corte R, Pascotto A, et al. Low glycemic index diet in children and young adults with refractory epilepsy: first Italian experience. Seizure 2011; 20:526-8.

155.Kossoff EH, Turner Z, Bluml RM, Pyzik PL, Vining EP. A randomized, crossover comparison of daily carbohydrate limits using the modified Atkins diet. Epilepsy Behav 2007; 10:432-6.

156.Kossoff EH, Dorward JL. The modified Atkins diet. Epilepsia 2008; 49:37-41.

157.Sharma S, Sankhyan N, Gulati S, Agarwala A. Use of the modified Atkins diet in infantile spasms refractory to firstline treatment. Seizure 2012; 21:45-8.

158.Sharma S, Sankhyan N, Gulati S, Agarwala A. Use of the modified Atkins diet for treatment of refractory childhood epilepsy: a randomized controlled trial. Epilepsia 2013; 54:481-6.

159.Karimzadeh P, Sedighi M, Beheshti M, Azargashb E, Ghofrani M, Abdollahe-Gorgi F. Low Glycemic Index Treatment in pediatric refractory epilepsy: The first Middle East report. Seizure 2014; 23:570-2.

 

Diagnosis and Management of Multiple Sclerosis in Children

Mohammad Reza NAJAFI, Mohammad Amin NAJAFI, Zahra NASR

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 13-23
https://doi.org/10.22037/ijcn.v10i3.8423

How to Cite This Article: Najafi MR, Najafi MA, Nasr Z. Diagnosis and Management of Multiple Sclerosis in Children. Iran J Child Neurol. Summer 2016; 10(3): 13-23.

Abstract

Growing evidence indicates the safety and well toleration of treatment by Disease-modifying in children suffering multiple sclerosis (MS). The treatment is not straight forward in a great number of patients, thus patients with pediatric MS must be managed by experienced specialized centers. Common treatments of multiple sclerosis for adults are first-line therapies. These therapies (firstline) are safe for children. Failure in treatment that leads to therapy alteration is almost prevalent in pediatric MS. Toleration against current second-line therapies has been shown in multiple sclerosis children. Oral agents have not been assessed in children MS patients. Although clinical trials in children are insufficient, immunomodulating managed children, experience a side effect similar to the adult MS patients. However, further prospective clinical studies, with large sample size and long follow-up are needed to distinguish the benefits and probable side effects of pediatric MS therapies.

 

References

  1. Julian L, Serafin D, Charvet L, Ackerson J, Benedict R, Braaten E, et al. Cognitive Impairment Occurs in Children and Adolescents With Multiple Sclerosis Results From a United States Network.J Child Neurol 2013;28(1):102-7.
  2. Inaloo S, Haghbin S. Multiple sclerosis in children. Iran J Child Neurol 2013;7(2):1-10. Epub 2014/03/26.
  3. Patel Y, Bhise V, Krupp L. Pediatric multiple sclerosis. Ann Indian Acad Neurol 2009;12(4):238.
  4. Saadatnia M, Najafi MR, Najafi F, Davoudi V, Keyhanian K, Maghzi AH. CD24 gene allele variation is not associated with oligoclonal IgG bands and IgG index of multiple sclerosis patients. Neuroimmunomodulation 2012;19(3):195-9.
  5. Inaloo S, Haghbin S. Multiple Sclerosis in Children. Iran J Child Neurol 2013 Spring; 7(2): 1–10.
  6. Jutta Gartner PH. MS disease-modifying therapies in children: ECTRIMS 2010;8:21-4.
  7. Kornek B A-EF, Rostasy K, Milos RI. Natalizumab therapy for highly active pediatric multiple sclerosis. JAMA Neurol 2013;Apr;70(4):469-75.
  8. Yeh E, Weinstock-Guttman B, Ramanathan M, Ramasamy D, Willis L, Cox J, et al. Magnetic resonance imaging characteristics of children and adults with paediatric-onset multiple sclerosis. Brain 2009;132(12):3392-400.
  9. Chabas D, Green AJ, Waubant E. Pediatric multiple sclerosis. NeuroRx 2006;3(2):264-75.
  10. McDonald WI, Compston A, Edan G, Goodkin D, Hartung HP, Lublin FD, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol 2001;50(1):121-7.
  11. Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 2011;69(2):292-302.
  12. 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.
  13. Krupp LB, Tardieu M, Amato MP, Banwell B, Chitnis T, Dale RC, et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler2013 Sep;19(10):1261-7. doi: 10.1177/1352458513484547.
  14. Krupp LB, Banwell B, Tenembaum S. Consensus definitions proposed for pediatric multiple sclerosis and related disorders. Neurology 2007;68(16 suppl 2):S7-S12.
  15. Amato M, Goretti B, Ghezzi A, Lori S, Zipoli V, Portaccio E, et al. Cognitive and psychosocial features of childhood and juvenile MS. Neurology 2008;70(20):1891-7.
  16. Ghezzi A, Amato M, Capobianco M, Gallo P, Marrosu G, Martinelli V, et al. Disease-modifying drugs in childhood-juvenile multiple sclerosis: results of an Italian co-operative study. Mult Scler 2005;11(4):420-4.
  17. Mikaeloff Y, Caridade G, Tardieu M, Suissa S. Effectiveness of early beta interferon on the first attack after confirmed multiple sclerosis: a comparative cohort study. Eur J Paediatr Neurol 2008;12(3):205-9.
  18. Callen D, Shroff M, Branson H, Lotze T, Li D, Stephens D, et al. MRI in the diagnosis of pediatric multiple sclerosis. Neurology 2009;72(11):961-7.
  19. Jacobs LD, Cookfair DL, Rudick RA, Herndon RM, Richert JR, Salazar AM, et al. Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. Ann Neurol 1996;39(3):285-94.
  20. Pohl D, Rostasy K, Gärtner J, Hanefeld F. Treatment of early onset multiple sclerosis with subcutaneous interferon beta-1a. Neurology 2005;64(5):888-90.
  21. Banwell B, Reder A, Krupp L, Tenembaum S, Eraksoy M, Alexey B, et al. Safety and tolerability of interferon beta-1b in pediatric multiple sclerosis. Neurology 2006;66(4):472-6.
  22. Tenembaum SN, Segura MJ. Interferon beta-1a treatment in childhood and juvenile-onset multiple sclerosis. Neurology 2006;67(3):511-3.
  23. Pohl D, Waubant E, Banwell B, Chabas D, Chitnis T, Weinstock-Guttman B, et al. Treatment of pediatric multiple sclerosis and variants. Neurology 2007;68(16 suppl 2):S54-S65.
  24. Kornek B, Bernert G, Balassy C, Geldner J, Prayer D, Feucht M. Glatiramer acetate treatment in patients with childhood and juvenile onset multiple sclerosis. Neuropediatrics 2003;34(03):120-6.
  25. Ghezzi A. Immunomodulatory treatment of early onset multiple sclerosis: results of an Italian Co-operative Study. Neurol Sci 2005;26(4):s183-s6.
  26. Tenembaum SN, Banwell B, Pohl D, Krupp LB, Boyko A, Meinel M, et al. Subcutaneous Interferon Beta-1a in Pediatric Multiple Sclerosis A Retrospective Study.J Child Neurol 2013:0883073813488828.
  27. Sloka JS, Stefanelli M. The mechanism of action of methylprednisolone in the treatment of multiple sclerosis. Mult Scler (Houndmills, Basingstoke, England) 2005;11(4):425-32. Epub 2005/07/27.
  28. Gorman MP, Healy BC, Polgar-Turcsanyi M, Chitnis T. Increased relapse rate in pediatric-onset compared with  adult-onset multiple sclerosis. Arch Neurol 2009;66(1):54.
  29. Shahar E, Andraus J, Savitzki D, Pilar G, Zelnik N. Outcome of Severe Encephalomyelitis in Children Effect of High-Dose Methylprednisolone and Immunoglobulins. J Child Neurol 2002;17(11):810-4.
  30. Spalice A, Properzi E, Faro VL, Acampora B, Iannetti P. Intravenous immunoglobulin and interferon: successful treatment of optic neuritis in pediatric multiple sclerosis. J Child Neurol 2004;19(8):623-6.
  31. Koziolek M, Mühlhausen J, Friede T, Ellenberger D, Sigler M, Huppke B, et al. Therapeutic Apheresis in Pediatric Patients with Acute CNS Inflammatory Demyelinating Disease. Blood Purification 2013;36(2):92-7.
  32. Najafi F, Ghaffarpour M, Najafi M, Aghamohammadi A, Saadatnia M. Prognostic value of intrathecal IgG synthesis in multiple sclerosis: a study in 54 patients. Tehran University Medical Journal 2008;66(1):1-6.
  33. Yeh E KL, Ness J, Chabas D, et al. Breakthrough disease in pediatric MS patients: a pediatric network experience: Annual Meeting of the American Academy of Neurology. Seattle WA: 2009.
  34. Yeh EA. Diagnosis and treatment of multiple sclerosis in pediatric and adolescent patients: current status and future therapies. Adolesc Health Med Ther 2010;1:61-71.
  35. Borriello G, Prosperini L, Luchetti A, Pozzilli C. Natalizumab treatment in pediatric multiple sclerosis: a case report. Eur J Paediatr Neurol 2009;13(1):67-71.
  36. Huppke P, Stark W, Zurcher C, Huppke B, Bruck W, Gartner J. Natalizumab use in pediatric multiple sclerosis. Arch Neurol 2008;65(12):1655.
  37. Makhani N, Gorman M, Branson H, Stazzone L, Banwell B, Chitnis T. Cyclophosphamide therapy in pediatric multiple sclerosis. Neurology 2009;72(24):2076-82.
  38. Rice GP, Hartung H-P, Calabresi PA. Anti-α4 integrin therapy for multiple sclerosis Mechanisms and rationale. Neurology 2005;64(8):1336-42.
  39. Polman CH, O’Connor PW, Havrdova E, Hutchinson M, Kappos L, Miller DH, et al. A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med 2006;354(9):899-910.
  40. Ghezzi A, Pozzilli C, Grimaldi L, Morra VB, Bortolon F, Capra R, et al. Safety and efficacy of natalizumab in children with multiple sclerosis. Neurology   2010;75(10):912-7.
  41. Sousa L, de Sa J, Sa MJ, Cerqueira JJ, Martins-Silva A, En Nombre Del Portugal Experience With Natalizumab Study Group Snapshot EN. The efficacy and safety of natalizumab for the treatment of multiple sclerosis in Portugal.: a retrospective study. Revista de Neurologia 2014;59(9):399-406. Epub 2014/10/25. Estudio retrospectivo de la eficacia y seguridad del natalizumab en el tratamiento de la esclerosis multiple en Portugal.
  42. Huppke P, Stark W, Zürcher C, Huppke B, Brück W, Gärtner J. Natalizumab use in pediatric multiple sclerosis. Arch Neurol 2008;65(12):1655-8.
  43. Hauser SL, Dawson DM, Lehrich JR, Beal MF, Kevy SV, Propper RD, et al. Intensive immunosuppression in progressive multiple sclerosis. A randomized, three-arm study of high-dose intravenous cyclophosphamide, plasma exchange, and ACTH. N Engl J Med 1983;308(4):173-80. Epub 1983/01/27.
  44. Weiner HL, Mackin GA, Orav EJ, Hafler DA, Dawson DM, LaPierre Y, et al. Intermittent cyclophosphamide pulse therapy in progressive multiple sclerosis: final report of the Northeast Cooperative Multiple Sclerosis
  45. Treatment Group. Neurology 1993;43(5):910-8. Epub 1993/05/01.
  46. Hauser SL, Waubant E, Arnold DL, Vollmer T, Antel J, Fox RJ, et al. B-cell depletion with rituximab in relapsing–remitting multiple sclerosis. N Engl J Med 2008;358(7):676-88.
  47. Tzaribachev N, Koetter I, Kuemmerle-Deschner JB, Schedel J. Rituximab for the treatment of refractory pediatric autoimmune diseases: a case series. Cases J 2009;2:6609.
  48. Carson KR, Focosi D, Major EO, Petrini M, Richey EA, West DP, et al. Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients
  49. treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. Lancet Oncology 2009;10(8):816-24.
  50. Beres SJ, Graves J, Waubant E. Rituximab Use in Pediatric Central Demyelinating Disease. Pediatr Neurol 2014 Jul;51(1):114-8.
  51. Wynn D, Kaufman M, Montalban X, Vollmer T, Simon J, Elkins J, et al. Daclizumab in active relapsing multiple  sclerosis (CHOICE study): a phase 2, randomised, double-blind, placebo-controlled, add-on trial with interferon beta. Lancet Neurol 2010;9(4):381-90.
  52. Bielekova B, Howard T, Packer AN, Richert N, Blevins G, Ohayon J, et al. Effect of anti-CD25 antibody daclizumab in the inhibition of inflammation and stabilization of disease progression in multiple sclerosis. Arch Neurol 2009;66(4):483-9.
  53. Rose JW, Watt HE, White AT, Carlson NG. Treatment of multiple sclerosis with an anti–interleukin-2 receptor monoclonal antibody. Ann Neurol 2004;56(6):864-7.
  54. Ali E, Healy B, Stazzone L, Brown B, Weiner H, Khoury S. Daclizumab in treatment of multiple sclerosis patients. Mult Scler 2009;15(2):272-4.
  55. Gorman MP, Tillema J-M, Ciliax AM, Guttmann CR, Chitnis T. Daclizumab use in patients with pediatric multiple sclerosis. Arch Neurol 2012;69(1):78-81.
  56. Gorelik L, Lerner M, Bixler S, Crossman M, Schlain B, Simon K, et al. Anti-JC virus antibodies: implications for PML risk stratification. Ann Neurol 2010;68(3):295-303.
  57. Bloomgren G, Richman S, Hotermans C, Subramanyam M, Goelz S, Natarajan A, et al. Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Engl J Med 2012;366(20):1870-80.
  58. Sørensen PS, Bertolotto A, Edan G, Giovannoni G, Gold R, Havrdova E, et al. Risk stratification for progressive multifocal leukoencephalopathy in patients treated with natalizumab. Mult Scler 2012;18(2):143-52.
  59. Yildirim-Toruner C, Diamond B. Current and novel therapeutics in the treatment of systemic lupus erythematosus. J Allergy Clin Immunol 2011;127(2):303-12.
  60. Zappitelli M, Duffy CM, Bernard C, Gupta IR. Evaluation of activity, chronicity and tubulointerstitial indices for childhood lupus nephritis. Pediatr Nephrol 2008;23(1):83-91.
  61. Di Filippo S. Anti-IL-2 receptor antibody vs. polyclonal anti-lymphocyte antibody as induction therapy in Pediatr Transplant. Pediatr Transplant 2005;9(3):373-80.
  62. Gallagher M, Quinones K, Cervantes-Castaneda RA, Yilmaz T, Foster CS. Biological response modifier therapy for refractory childhood uveitis. Br J Ophthalmol 2007;91(10):1341-4.
  63. Giovannoni G, Comi G, Cook S, Rammohan K, Rieckmann P, Sørensen PS, et al. A placebo-controlled trial of oral cladribine for relapsing multiple sclerosis. N Engl J Med 2010;362(5):416-26.
  64. Kappos L, Radue E-W, O’Connor P, Polman C, Hohlfeld R, Calabresi P, et al. A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med 2010;362(5):387-401.
  65. Chun J, Hartung H-P. Mechanism of action of oral fingolimod (FTY720) in multiple sclerosis. Clin Neuropharmacoll 2010;33(2):91.
  66. Comi G, O’connor P, Montalban X, Antel J, Radue E, Karlsson G, et al. Phase II study of oral fingolimod (FTY720) in multiple sclerosis: 3-year results. Mult Scler 2010;16(2):197-207.
  67. Cohen JA, Barkhof F, Comi G, Hartung H-P, Khatri BO, Montalban X, et al. Oral fingolimod or intramuscular interferon for relapsing multiple sclerosis.N Engl J Med 2010;362(5):402-15.
  68. Mehling M, Lindberg R, Raulf F, Kuhle J, Hess C, Kappos L, et al. Th17 central memory T cells are reduced by FTY720 in patients with multiple sclerosis. Neurology 2010;75(5):403-10.
  69. Edwards JC, Szczepański L, Szechiński J, Filipowicz-Sosnowska A, Emery P, Close DR, et al. Efficacy of B-cell–targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med 2004;350(25):2572-81.

Research Article


Neurological Manifestations of Renal Diseases in Children in Qazvin/ Iran

Reza DALIRANI, Abolfazl MAHYAR, Parviz AYAZI, Ghazaleh AHMADI

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 24-27
https://doi.org/10.22037/ijcn.v10i3.9030

 

 

How to Cite This Article: Dalirani R, Mahyar A, Ayazi P, Ahmadi Gh. Neurological Manifestations of Renal Diseases in

Children in Qazvin/ Iran. Iran J Child Neurol. Summer 2016; 10(3):24-27.

Abstract

Objective

Renal diseases are one of the most common causes of referrals and admissions of children, hence it is important to know their neurological presentations. This study aimed to determine neurological presentations of renal diseases in children.

Material & Methods

A total of 634 children with renal diseases, admitted to Qazvin Pediatric Hospital, Qazvin, central Iran from 2011 to 2013 were studied. Neurological presentations of patients were established and the results were analyzed using statistical tests.

Results

Neurological presentations were found in 18 (2.8%) out of 634 patients, of whom 15 had febrile seizures, two thromboembolism, and one encephalopathy. Among patients with urinary tract infection (UTI), 2.6% had febrile seizures, 11.1% of those with glomerulonephritis had encephalopathy, and 3.7% of those with nephrotic syndrome had cerebral thromboembolism.

Conclusion

Results showed neurological presentations in 2.8% of children with renal diseases, and febrile seizure as the most common presentation.

 

References

 

1.      Elder JS. Urinary tract infection. In: Kliegman RM, Stanton RE, Schor NF, Geme III JW St, Behrman RE. Nelson Textbook of Pediatrics. 19th ed. Phila, Saunders; 2011: 1838-1846.

2.      Bhoobun S, Jalloh AA, Jacobsen KH. Cerebral venous thrombosis in a child with nephrotic syndrome: case report. Pan Afr Med J 2012;13:57.

3.      Lee P, Verrier Jones K. Urinary tract infection in febrile convulsions. Arch Dis Child 1991; 66(11):1287-90.

4.      Bensman A, Dunand O, Ulinski T: Urinary tract infection. In: Avner ED, Harman WE, Niaudet P, Yoshikawa N, Pediatric Nephrology. Berlin, Springer. 2009:1007-1025.

5.      Anochie I, Eke F, Okpere A. Childhood nephrotic syndrome: change in pattern and response to steroids. J Natl Med Assoc 2006; 98(12):1977-81.

6.      Pan GC, Avner ED. Glomerulonephritis Associated with Infections. In: Kliegman RM, Stanton RE, Schor NF, Geme III JW St, Behrman RE. Nelson Textbook of Pediatrics. 19th ed. Phila, Saunders; 2011: 1783-6.

7.      Salvadori M, Bertoni E. Update on hemolytic uremic syndrome: Diagnostic and therapeutic recommendations. World J Nephrol 2013 6; 2(3): 56-7.

8.      Shinnar S. Febrile seizures. In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice. 4th ed. Philadelphia: Mosby, 2006:1079-86.

9.      Bryce A. Kerlin, Rose Ayoob, William E. Smoyer. Epidemiology and Pathophysiology of Nephrotic Syndrome–Associated Thromboembolic Disease. Clin J Am Soc Nephrol 2012 ; 7(3): 513–520.

10.  Faigle R, Sutter R, Kaplan PW. The electroencephalography of encephalopathy in patients with endocrine and metabolic disorders. J Clin Neurophysiol 2013;30(5):10.1097. doi:10.1097/WNP.0b013e3182a73db9.

11.  Momen AA, Monajemzadeh SM, Gholamian M. The Frequency of Urinary Tract Infection among Children with Febrile Convulsions. Iran J Child Neurol 2011; 5(3): 29-32.

12.  Burn D J, Bates D. Neurology and the kidney. J Neurol Neurosurg Psychiatr 1998;65:810–821.

13.  Orth SR, Ritz E. The nephrotic syndrome. N Engl J Med 1998;338: 1202-11.

14.  Zaffanello M, Franchini M. Thromboembolism in childhood nephritic syndrome: a rare but serious complication. Hematology 2007; 12:69-73.

15.  Sébire G, Tabarki B, Saunders DE, et al. Cerebral venous sinus thrombosis in children: risk factors, presentation, diagnosis and outcome. Brain 2005; 128 (3):477–89.

16.  Joel F, Denis G, deVeber Gabrielle D V. Cerebral sinovenous thrombosis and idiopathic nephrotic syndrome in childhood: report of four new cases and review of the literature. Eur J Pediatr 2006; 165(10):709–716.

17.  Nathanson S, Kwon T, Elmaleh M et al. Acute neurological involvement in diarrhea-associated hemolytic uremic syndrome. Clin J Am Soc Nephrol 2010 ;5(7):1218-28.

 

 

Effects of Abnormal Oral Reflexes on Speech Articulation in Persian Speaking Children with Spastic Cerebral Palsy

Hooshang DADGAR, Mohammad Reza HADIAN, Ortega Adriana LIRA

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 28-34
https://doi.org/10.22037/ijcn.v10i3.8519

How to Cite This Article: Dadgar H, HadianMR, Lira OA. Effects of Abnormal Oral Reflexes on Speech Articulation in Persian Speaking Children with Spastic Cerebral Palsy. Iran J Child Neurol. Summer 2016; 10(3):28-34.

Abstract

Objective

The purpose of this study was to investigate the relationship between the presence of abnormal oral reflexes and speech sound production in children with severe cerebral palsy.

Materials&Methods

Seven oral reflexes such as, rooting, mouth-opening, biting, chewing, lip, tongue, and suckling were examined in 52Persian-speaking monolingual children with spastic cerebral palsy (ages 5-10 yr).Phonetic information tests were administered to investigate their ability for articulation of the speech sounds.

Results

A significant relationship between three (i.e. the chewing, lip, and biting reflexes) out of the seven abnormal oral reflexes and the speech articulation was noticed. The presence of the chewing reflex was associated with deficits in production of /s, z, š,č/ sounds. The lip reflex was associated with deficits in the production of /p, m, r, j, f, č/ sounds. The biting reflex was associated with deficits in the production of /z, l, y and š/ sounds. No significant relationship was found between the rooting, mouth-opening, tongue, and suckling reflexes and sound articulation.

Conclusion

The presence of abnormal reflexes in the children with spastic cerebral palsy would suggest a correlation between these reflexes and sound articulation in Iranian children with spastic cerebral palsy. Hence, these observations might suggest some disturbances in normal speech development. 

References

 

  1. Surveillance of Cerebral Palsy in Europe (SCPE) Collaborative Group. Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Dev Med Child Neurol 2000; 42:816–24.
  2. Karen W Krigger. Cerebral Palsy: An Overview. American Family Physician 2006; 73, 1; 91-100.
  3. O’Shea Michael T. Cerebral palsy in very preterm infants: New epidemiological insights. Mental retardation and developmental disabilities research. Reviews2002; 8: 135–145.
  4. Krageloh-Mann AIngeborg, Cans B Christine. Cerebral palsy updates. Brain & Development 2009;31 537–544.
  5. Andersen GL, Irgens LM, Haagaas I, Skranes JS, Meberg AE, Vik T. Cerebral palsy in Norway: Prevalence, subtypes and severity. Eur J Paediatr Neurol. 2008 Jan;12(1):4-13.
  6. Nordmark E, H gglund G, Lagergren J. Cerebral palsy in southern Sweden: Prevalence and clinical features, ActaPaediatrica 2001; 90: 271 – 1276.
  7. Pfeifer LI, Silva DB, Funayama CA, Santos JL. Classification of CerebralPalsy: Association between gender, age, motor type, topography and Gross Motor Function. Arq Neuropsiquiatr2009; 67(4):1057-1061.
  8. Hagberg B. Nosology and classification of cerebral palsy. Giorn Neuropsich Eta Evol Suppl 1989; 4:12–17.
  9. Otapowicz D, Sobaniec W, Kułak W, Sendrowski K. Severity of dysarthric speech in children with infantile cerebral palsy in correlation with the brain CT and MRI. Adv Med Sci 2007; Vol. 52 • Suppl. 1
  10. Selassie GR, Viggedal G, Olsson I, Jennische M. Speech, language, and cognition in preschool children with epilepsy. Dev Med Child Neurol 2008; 50: 432–438.
  11. Bjornson KF, McLaughlin JF, Loeser JD, Nowak-Cooperman KM, Russel M, Bader KA, Desmond SA.Oral motor, communication, and nutritional status of children during intrathecal baclofen therapy: a descriptive pilot study. Arch Phys Med Rehabil2003; 84:500-6.
  12. Mysak ED. Neuro speech therapy for the cerebral palsy (3rd ed). New York: Teacher college Press;1980.p.87-8,p.110-112.
  13. Sheppard JJ, Mysak ED. Ontogeny of infantile oral reflexes and emerging chewing. Child Dev 1984; 55:831-843.
  14. Sheppard JJ. Cranio-oropharyngeal motor patterns in dysarthria associated with cerebral palsy. J speech Hear Res 1964; 7:373-380.
  15. International Phonetic Alphabet: Handbook of the International Phonetic Association: A guide to the use of the International Phonetic AlphabetCambridge, U.K. & New York, NY: Cambridge University Press.1999.
  16. Damerchi Z, Jalilehvand N, Bakhtiari B, Keyhani MR.Development of Phonetic inventory in 2-to-6 year-old Farsi speaking children. Research in Rehabilitation Sciences2010;5:1.42-47. (In Persian).
  17. Dos Santos MT, Nogueira ML. Infantile reflexes and their effects on dental caries and oral hygiene in cerebral palsy individuals. J Oral Rehabil2005; 32; 880–885.
  18. Love RJ, Hagerman EL, Taimi EG. Speech performance, dysphagia and oral reflexes in cerebral palsy. J Speech Hear Disord 1980; 45(1):59-75.
  19. Platt LJ, Andrews G,Young M, Quinn PT. Dysarthria of adult cerebral palsy: Intelligibility and articulatory impairment. J Speech Hear Res 1980; 23(1):28-40.
  20. McFarland DH, Baum SR. Incomplete compensation to articulatory perturbation. J AcoustSoc Am1995; 97:1865-1873.
  21. Irwin OC. Communication variables of cerebral palsy and mentally retarded children. Springfield,IL: C.C. Thomas 1972.
  22. Shelley I, Velleman, Marilyn m, Vihman, phonology development in infancy and early childhood: implications for theories of language learning. In: Martha C. Pennington,editors. Phonology in Context. Basingstoke: Palgrave Macmillan;2006.p.34.
  23. Ingram TT. Clinical significance of the infantile feeding reflexes. Dev Med Child Neurol 1992; 4:159–169.
  24. Hixon T, Hardy J. Restricted motility of speech articulation in cerebral palsy. J Speech Hearing Dis1964; 29:293-306.
  25. Dubner R, Sessle BJ, Storey AT. The neural basis of oral and facial function. New York: Plenum Press. 1978.p.483.

 

Comparing Mental Health of School-Age Children with and without Epilepsy

Farshid SHAMSAEI, Fatemeh CHERAGHI, Gholamreza ZAMANI

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 35-41
https://doi.org/10.22037/ijcn.v10i3.8432

How to Cite This Article: Shamsaei F, Cheraghi F, Zamani Ghr. Comparing Mental Health of School-Age Children with and without Epilepsy: A Case Control Study. Iran J Child Neurol. Summer 2016; 10(3):35-41.

 

Abstract

Objective

Mental health problems frequently occur in children with epilepsy but the diagnosis is frequently missed and therapeutic opportunities are often lost. The aim of this study was to compare mental health statues between school-aged children with epilepsy and the healthy group.

Materials & Methods

In this case, control study, 120 children aged 6 to 12 years with idiopathic epilepsy and 240 healthy control groups were followed up. Children with epilepsy were enrolled from Iranian Epilepsy Association in 2014. The parent version of Child Symptom Inventory-4 questionnaire was used. Mean comparisons were performed using Student’s t test while effect sizes were estimated by Cohen’s d coefficient. The Chi-Square test was used to assess the difference between frequency distribution of demographic variables in both groups. The significance level was considered less than 0.05.

Results

There were statistically significant differences between children with epilepsy and control group as for attention deficit hyperactivity disorder, generalized anxiety disorder, major depression, separation anxiety, social phobia, motor and vocal tics and oppositional defiant disorder.

Conclusion

The carefully evaluating and prospectively following the psychopathology symptom of children with epilepsy are critical for early identification, prevention and treatment.

References

  1. Valizadeh L, Barzegar M, Akbarbegloo M, Zamanzadeh V, Rahiminia E, Ferguson CF. The relationship between psychosocial care and attitudes toward illness in adolescents with epilepsy. Epilepsy Behav 2013; 27(1):267-71.
  2. Russ SA, Larson K, Halfon N. A national profile of childhood epilepsy and seizure disorder. Pediatrics 2002; 129(2):256-264.
  3. Kotsopoulos IA, van Merode T, Kessels FG, de Krom MC, Knottnerus, JA. Systematic review and meta-analysis of incidence studies of epilepsy and unprovoked seizures. Epilepsia 2002; 43(11):402–1409.
  4. Sayehmiri K, Tavan H, Sayehmiri F, Mohamadi I, Carson KV. Prevalence of Epilepsy in Iran: A Meta-Analysis and Systematic Review. Iran J Child Neurol 2014; 8(4): 9–17.
  5. Salpekar JA, Dunn DW. Psychiatric and psychosocial consequences of pediatric epilepsy. Semin Pediatr Neurol 2007; 14(4): 181-8.
  6. Ott D, Siddarth P, Gurbani S, Koh S, Tournay A, Shields WD, Caplan R. Behavioral disorders in pediatric epilepsy: unmet psychiatric need. Epilepsia 2003; 44(4): 591-597.
  7. Davies S, Heyman I, Goodman R. A population survey of mental health problems in children with epilepsy. Dev Med Child Neurol 2003; 45(5):292-295.
  8. Maia Filho HS, Costa CRM, Gomes MM. Epilepsia e Saúde Mental na Infância. J Epilep Clin Neurophysiol 2006; 12(2):79-88.
  9. Gaitatzis A, Carroll K, Majeed A, Sander J. The epidemiology of the comorbidity of epilepsy in the general population. Epilepsia 2004; 45(2):1613-1622.
  10. Jones JE, Watson R, Sheth R, Caplan R, Koehn M, Seidenberg M, Hermann B. Psychiatric comorbidity in children with new onset epilepsy. Dev Med Child Neurol 2007; 49(7):493-7.
  11. Gadow KD, Sprafkin J. Child symptom inventory-4 Screening and norms manual. Stony Brook, NY: checkmate Plus Ltd, 2002.
  12. Dulcan MK, Mina K. Dulcan’s Textbook of Child and Adolescent Psychiatry. 1st ed, American Psychiatric Pub, 2010.
  13. Jafari N, Mohammadi MR, Khanbani M, Farid S, Chiti P. Effect of Play Therapy on Behavioral Problems of Maladjusted Preschool Children. Iran J Psychiatry 2011 6(1): 37–42.
  14. Hermann B, Jones J, Dabbs K, Allen CA, Sheth R, Fine J, McMillan A, Seidenberg M. The frequency, complications and etiology of ADHD in new onset pediatric epilepsy. Brain 2007; 130(Pt 12):3135-48.
  15. Kaner AM. Psychiatric Comorbidity in Children with Epilepsy … or Is It: Epilepsy Comorbidity in Children with Psychiatric Disorders? Epilepsy Curr 2008; 8(1): 10–12.
  16. Williams J Steel C, Sharp GB, DelosReyes E, Phillips T, Bates S, Lange B, Griebel ML. Parental anxiety and quality of life in children with epilepsy. Epilepsy Behav 2003; 4(5): 483–486.
  17. Stefanello S, Marín-Léon L, Fernandes PT, Li LM, Botega NJ. Depression and anxiety in a community sample with epilepsy in Brazil. Arq Neuropsiquiatria 2011; 69 (2):342-348.
  18. Dunn DW, Austin JK, Perkins SM. Prevalence of psychopathology in childhood epilepsy: categorical and dimensional measures. Dev Med Child Neurol 2009; 51(5):364-372.
  19. McDermott S, Mani S, Krishnaswami S. A population-based analysis of specific behavior problems associated with childhood seizures. J Epilepsy 1995; 8(2):110–118.
  20. Davies S, HeymanI Goodman R. Apopulation survey of mental health problems in children with epilepsy. Dev Med Child Neurol 2003; 45(5):292-295.
  21. Parisi R, Moavero R, Verrotti A, Curatolo P. Attention deficit hyperactivity disorder in children with epilepsy. Brain Dev 2010; 32(1):10–16.


Phantom Limb Sensation (PLS) and Phantom Limb Pain (PLP) among Young Landmine Amputees

Mahtab POOR ZAMANY NEJAT KERMANY, Ehsan MODIRIAN, Mohammadreza SOROUSH, Mahdi MASOUMI, Maryam HOSSEINI

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 42-47
https://doi.org/10.22037/ijcn.v10i3.7323

How to Cite This Article: Poor Zamany Nejat Kermany M, Modirian E, Soroush M, Masoumi M, Hosseini M. Phantom Limb Sensation (PLS) and Phantom Limb Pain (PLP) Among Young Landmine Amputees. Iran J Child Neurol. Summer 2016; 10(3):42-47.

 

Abstract

Objective

To determine the frequency of phantom limb sensation (PLS) and phantom limb pain (PLP) in children and young adults suffering landmine-related amputation.

Materials & Methods

All youths with amputation due to landmine explosions participated in this study. The proportions of patients with phantom limb sensation/pain, intensity and frequency of pain were reported. Chi square test was used to examine the relationship between variables. Comparison of PLP and PLS between upper and lower amputation was done by unpaired t-test.

Results

There were 38 male and 3 female with the mean age of 15.8±2.4yr. The mean interval between injury and follow-up was 90.7±39.6 months. Twelve (44.4%) upper limb amputees and 11 (26.8%) lower limb amputees had PLS. Nine (33.3%) upper limb amputees and 7 (17.1%) lower limb amputees experienced PLP. Of 27 upper limb amputees, 6 (14.6%) and among 15 lower limb amputees, 6 (14.6%) had both PLS and PLP. One case suffered amputation of upper and lower limbs and was experiencing PLS and PLP in both parts. PLS had a significant difference between the upper and lower amputated groups. Significant relationship was observed between age of casualty and duration of injury with PLP.

Conclusion

Phantom limb sensation and pain in young survivors of landmine explosions appear to be common, even years after amputation.

 

References

 

  1. Nikolajsen L, Jensen TS. Phantom limb pain. Br J Anaesth 2001; 87:107-16.
  2. Tseng CC, Chen PY, Lee YC. Successful treatment of phantom limb pain and phantom limb sensation in the traumatic amputee using scalp acupuncture. Acupunct Med 2014;32(4):356-8.
  3. Davis RW. Phantom sensation, phantom pain, and stump pain. Arch Phys Med Rehabil 1993;74:79–91.
  4. Jensen TS, Krebs B, Nielsen J, Rasmussen P. Phantom limb, phantom pain and stump pain in amputees during the first 6 months following limb amputation. Pain 1983;17(3):243–256.
  5. Gupta R. FRCA, FFPMRCA, EDRA. Pain Management. Phantom Pain Syndromes. 2014, pp 71-74.
  6. Davidson JH, Khor KE, Jones LE. A cross-sectionalstudy of post-amputation pain in upper and lower limb amputees,experience of a tertiary referral amputee clinic. Disabil Rehabil 2010;32(22):1855-62.
  7. Hirsh AT, Dillworth TM, Ehde DM, Jensen MP. Sex differences in pain and psychological functioning inpersons with limb loss. J Pain. 2010; 11(1): 79–86.
  8. Anwar F. Phantom limb: Review of literature. KMUJ. 2013; 5(4): 207-12.
  9. Ephraim PL, Wegener ST, MacKenzie EJ, Dillingham TR, Pezzin LE. Phantom pain, residual limb pain, and back pain in amputees: results of a national survey. Arch Phys Med Rehabil 2005; 86(10):1910-19.
  10. Husum H, Resell K, Vorren G,Heng YV, Murad M, Gilbert M, et al. Chronic pain in land mine accident survivors in Cambodia and Kurdistan. SocSci Med 2002; 55(10):1813-6.
  11. Wartan SW, Hamann W, Wedley JR, McColl I. Phantom pain and sensation among British veteran amputees. Br J Anaesth 1997; 78(6):652-9.
  12. Krane EJ, Heller LB. The prevalence of phantom sensation and pain in pediatric amputees. J Pain Symptom Manage 1995; 10(1): 21-9.
  13. Wilkins KL, McGrath PJ, Finley GA, Katz J. Phantom limb sensations and phantom limb pain in child and adolescent amputees. Pain 1998; 78(1): 7–12.
  14. Mariane L. Simmel. Phantom experiences following amputation in childhood. J Neurol Neurosurg Psychiat 1962; 25(1): 69-78.
  15. Mohammadi Seilabipour N, Mohammadi Fallah S, Kazemi H, Shariat SV. Phantom limb correlates among amputee war veterans. Adv Cognitive Sci 2013; 15(2): 32-9.
  16. Modirian E, Shojaei H, Soroush MR, Masoumi M. Phantom pain in bilateral upper limb amputation. DisabilRehabil 2009; 31(22): 1878-81.
  17. Explosive remnants of war-Unicef. http://www.unicef. org/sowc2013/focus_war_remnants.html
  18. Rayegani SM, Aryanmehr A, Soroosh MR, Baghbani M. Phantom Pain, Phantom Sensation, and Spine Pain in Bilateral Lower Limb Amputees: Results of a National Survey of Iraq-Iran War Victims’ Health Status. JPO 2010; 22(3): 162-165.
  19. Subedi B, GrossbergGT. PhantomLimbPain:Mechanisms and Treatment Approaches. Pain Res Treat 2011, Article ID 864605, 8 pages.
  20. Laura L. Burgoyne, Catherine A. Billups, José L. JirónJr, Roland N. Kaddoum, Becky B. Wright, George B. Bikhazi, et al. Phantom limb pain in young cancer-related amputees: Recent experience at St. Jude Children’s Research Hospital. Clin J Pain 2012; 28(3): 222–5.
  21. Sin EI, Thong SY, Poon KH. Incidence of phantom limb phenomena after lower limb amputations in a Singapore tertiary hospital. Singapore Med J. 2013; 54(2): 75-81.
  22. Melzack R, Israel R, Lacroix R and Schultz G. Phantom limbs in people with congenital limb deficiency or amputation in early childhood. Brain 1997; 120(9): 1603– 20.
  23. Rahimi A, Mousavi B, Soroush M, Masumi M, Montazeri A. Pain and Health-Related Quality of Life in War Veterans with Bilateral Lower Limb Amputations. Trauma Mon2012; 17(2):282-286.
  24. Ketz AK. The experience of phantom limb pain in patients with combat-related traumatic amputations. Arch Phys Med Rehabil 2008, 89(6): 1127-32.
  25. Boyle M, Tebbi CK, Mindell ER, Mettlin CJ. Adolescent adjustment to amputation. Med Pediatr Oncol 1982; 10(3): 301-12.
  26. Patricia A. McGrath, Loretta M. Hillier. Phantom limb sensations in adolescents: A case study to illustrate the utility of sensation and pain logs in pediatric clinical practice. J Pain Symptom Manage 1992; 7(1): 46–53.
  27. Vida L. Tyc. Psychosocial adaptation of children and adolescents with limb deficiencies: A review. Clin Psychol Rev 1992; 12(3); 275–291. 

 

Predictors of Poor Seizure Control in Children Managed at a Tertiary Care Hospital of Eastern Nepal

Prakash POUDEL, Mohit CHITLANGIA, Rita POKHAREL

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 48-56
https://doi.org/10.22037/ijcn.v10i3.8776

How to Cite This Article: Poudel P, Chitlangia M, Pokharel R. Predictors of Poor Seizure Control in Children Managed at a Tertiary Care Hospital of Eastern Nepal Iran J Child Neurol. Summer 2016; 10(3):48-56.

 

Abstract

Objective

Various factors have been claimed to predict outcome of afebrile seizures in children. This study was aimed to find out the predictors of poor seizure control in children at a resource limited setting.

Materials & Methods

This prospective study was done from July 1st, 2009 to January 31st, 2012 at B.P. Koirala Institute of Health Sciences, Nepal. Children (1 month-20 yr of age) with afebrile seizures presenting to pediatric neurology clinic were studied.

Significant predictors on bivariate analysis were further analyzed with binary logistic model to find out the true predictors. Positive predictive values (PPVs) and negative predictive values (NPVs) for the true predictors were calculated.

Results

Out of 256 patients (male: female ratio 3:2) with afebrile seizures followed up for median duration of 27 (IQR 12-50) months, seizure was poorly controlled in 20% patients. Three factors predicted poor seizure control. They were frequent (≥1 per month) seizures at onset (OR 12.76, 95% CI 1.44-112.73, PPV 25%, NPV 98%); remote symptomatic etiology (OR 3.56, 95% CI 1.04-12.17, PPV 36%, NPV 92%); and need of more than one anticonvulsant drug (polytherapy) (OR 12.83, 95% CI 5.50-29.9, PPV 56%, NPV 96%). The strongest predictor was need of polytherapy. When all three factors were present, PPV and NPV for prediction of poor seizure control were 70% and 90% respectively.

Conclusion

Frequent seizures at onset, remote symptomatic etiology of seizure and need of polytherapy were associated with poor seizure control in children with afebrile seizures.

 

 References

  1. Sander JW, Shorvon SD. Epidemiology of the epilepsies. J Neurol Neurosurg Psychiatry 1996; 61:433-43.
  2. Johnston MV. Seizures in Childhood. In: Behman RE, Kleigman RM, Jenson HB, eds. Nelson Textbook of Pediatrics 17thed. Philadelphia: Saunders, 2004:1993-2005.
  3. Sillanpaa M. Remission of seizures and prediction of intractability in long-term follow-up. Epilepsia 1993; 34:930-6.
  4. Harrison RM, Taylor DC. Childhood seizures: a 25-year follow-up, social and medical prognosis. Lancet 1976; 1:948-51.
  5. Berg AT, Levy SR, Novotny EJ, Shinnar S. Predictors of intractable epilepsy in childhood: a case-control study. Epilepsia 1996; 37:24-30.
  6. Malik MA, Hamid MH, Ahmed TM, Ali Q. Predictors of intractable childhood epilepsy. J Coll Physicians Surg Pak 2008; 18:158-62.
  7. Kwong KL, Sung WY, Wong SN, So KT. Early predictors of medical intractability in childhood epilepsy. Pediatr Neurol 2003; 29:46-52.
  8. Chawla S, Aneja S, Kashyap R, Mallika V. Etiology and clinical predictors ofintractable epilepsy. Pediatr Neurol 2002; 27:186-91.
  9. Shinnar S, Berg AT, Moshe SL, O’Dell C, Alemany M, Newstein D et al. The risk of seizure recurrence after a first unprovoked afebrile seizure in childhood: an extended follow-up. Pediatrics 1996; 98:216-25.
  10. Shinnar S, Berg AT, Moshé SL, Petix M, Maytal J, Kang H et al. Risk of seizure recurrence following a first unprovoked seizure in childhood: a prospective study. Pediatrics 1990;85:1076-85.
  11. Sillanpää M, Schmidt D. Early seizure frequency and aetiology predict long-term medical outcome in childhood-onset epilepsy. Brain 2009; 132:989-98.
  12. Casetta I, Granieri E, Monetti VC, Gilli G, Tola MR, Paolino E et al. Early predictors of intractability in childhood epilepsy: a community-based case-control study in Copparo, Italy. Acta Neurol Scand 1999; 99:329-33.
  13. Stroink H, Brouwer OF, Arts WF, Geerts AT, Peters AC, van Donselaar CA. The first unprovoked, untreated seizure in childhood: a hospital based study of the accuracy of the diagnosis, rate of recurrence, and long term outcome after recurrence. Dutch study of epilepsy in childhood. J Neurol Neurosurg Psychiatry 1998; 64:595-600.
  14. Tripathi M, Padhy UP, Vibha D, Bhatia R, Padma Srivastava MV, Singh MB et al. Predictors of refractory epilepsy in north India: a case-control study. Seizure 2011; 20:779-83.
  15. Oskoui M, Webster RI, Zhang X, Shevell MI. Factors predictive of outcome in childhood epilepsy. J Child Neurol 2005; 20:898-904.
  16. Lohani S, Devkota UP, Rajbhandari H. Predictors of unfavourable seizure outcome in patients with epilepsy in Nepal. Can J Neurol Sci 2010; 37:76-80.
  17. Beume LA, Steinhoff BJ. Long-term outcome of difficult-to treat epilepsy in childhood. Neuropediatrics 2010; 41:135-9.
  18. Bouma PA, Peters AC, Brouwer OF. Long term course of childhood epilepsy following relapse after antiepileptic drug withdrawal. J Neurol Neurosurg Psychiatry 2002; 72:507-10.
  19. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia 1981; 22:489-501.
  20. Kwan P, Brodie MJ. Effectiveness of first antiepileptic drug. Epilepsia 2001; 42:1255-60.
  21. Dörks M, Langner I, Timmer A, Garbe E. Treatment of pediatric epilepsy in Germany: Antiepileptic drug utilization in children and adolescents with a focus on new antiepileptic drugs. Epilepsy Res 2013;103:45-53
  22. Herman ST. Single Unprovoked Seizures. Curr Treat Options Neurol 2004; 6:243-55.
  23. Boonluksiri P. Risk of recurrence following a first unprovoked seizure in Thai children. Neurol J Southeast Asia 2003; 8:25-9.
  24. Parra J, Augustijn PB, Greets Y, van Emde Boas W. Classification of Epileptic Seizures: A Comparison of Two Systems. Epilepsia 2001; 42:476-82.
  25. Eeg-Olofsson O. The development of the electroencephalogram in normal children and adolescents from the age of 1 through 21 years. Acta Paediatr Scand 1971; Suppl 208:1-46.

 

SerumTrace Elements in Febrile Seizure: A Case-Control Study

Kokab NAMAKIN, Mahmoud ZARDAST, Gholamreza SHARIFZADEH, Toktam ZARGARIAN, Samaneh BIDAR

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 57-60
https://doi.org/10.22037/ijcn.v10i3.9215

 How to Cite This Article: Namakin K, Zardast M, Sharifzadeh Gh, Bidar T, Zargarian S. Serum Trace Elements in Febrile Seizure: A Case-Control Study. Iran J Child Neurol. Summer 2016; 10(3):57-60.

 

 

Abstract

Objective

Febrile seizure (FS) is one of the most common neurological problems during childhood.Pathogenesis of febrile convulsion is unknown. This study investigated some trace elements among children admitted with FS compared with thoseof febrile without seizure attacks.

Materials & Methods

This case-control study was conducted on48 children (6 months to 5 yr old) diagnosed with febrile seizure as the cases and 48 age-matched febrile children as the control group. Serum levels of magnesium, calcium, sodium, potassium, and serum zinc were measured. Statistical analysis was performed with SPSS (version 15) using Student t-test.

Results

There were no significant differences between the cases and controls in terms of gender or age. The means of serum level of zinc, sodium, calcium and magnesium in the case group was lower than those of the control group. There was no significant difference onserum potassium mean level between the case and control groups.

Conclusion

Deficiency of trace elements was correlated significantly with febrile convulsion, while further investigations on trace elements are required.

References

References

  1. Martindale JL, Goldstein JN, Pallin DJ. Emergency department seizureepidemiology. Emerg Med Clin North Am 2011;29:15-27.
  2. Lee J-H, Hyun Kim J.Comparison of Serum Zinc Levels Measured by Inductively Coupled Plasma Mass Spectrometry in Preschool Children with Febrile and Afebrile Seizures. Ann Lab Med 2012;32:190-193 http://dx.doi.org/10.3343/alm.2012.32.3.190.
  3. Akbayram S, Cemek M, Büyükben A, Aymelek F, Karaman S, Yilmaz F, Dogan M,Caksen H. Major and minor bio-element status in children with febrile seizure. Bratisl Lek Listy 2012; 113 (7)421 – 423.
  4. Johnston MV. Seizures in children. In: Behrman RE, JensonHB, Stanton BF, editors. Nelson Textbook of Pediatrics.18thed. Philadelphia: Saunders, 2008:2457-73.
  5. Salehiomran MR, Mahzari M. Zinc status in febrile seizure: a case-control study. Iran J Child Neurol 2013; 7(4):20-23.
  6. Nadkarni J, Binaykiya I, Sharma U, Dwivedi R. Role of serum sodium levels in prediction of seizure recurrence within the same febrile illness.Neurology Asia 2011; 16(3): 195–197.
  7. Ganesh R, Janakiraman L. Serum zinc levels in children with simple febrile seizure. Clin Pediatr (Phila) 2008;47:164–166.
  8. Waqar Rabbani M, Ali I, Zahid Latif H, Basit A, Rabbani MA. Serum zinc level in children presenting with febrile seizures. Pak J Med Sci 2013;29(4):1008-11.
  9. Ehsanipour F, Talebi-Taher M, Harandi N, Kani K. Serumzinc level in children with febrile convulsion and itscomparison with that of control group. Iran J Pediatr2009;65-8.
  10. Amiri M, Farzin L, Moassesi ME, Sajadi F. Serum trace element levels in febrile convulsion. Biol Trace Elem Res 2010;135(1-3):38-44.
  11. Mohamed Aly IAR, Mohamed Kmal H, Soliman DR, Hassan Mohamed M. Iron profile parameters and serum zinc & copper levels in children with febrile convulsions in Banha. J Am Sci 2014;10(7): 1-4.
  12. Gattoo I, Harish R, Quyoom Hussain S. Correlation of serum zinc level with simple febrile seizures: a hospital based prospective case control study. Int J Pediatr 2015;3(2):16-.19.
  13. Sadeghzadeh M, Nabi S, Khoshnevisasl P, Mousavinasab N. The correlation between cerebrospinal fluid and levels of serum zinc and Ca in children with febrile seizure. J Comprehens Pediatr 2013; 3(5): 179-83.
  14. Osama N. Salah, Ehab R. Abdelraou, Marwa H. Abdelhameed Ahmed A, Dawood, Adel F,Kilany HA, Suzette I. Assessment of the Level of GABA and some trace elements in blood in children who suffer from familial febrile convulsions. Macedonian JMed Sci 2014; 7(1):68-73.
  15. Heydarian F, Ashrafzadeh F, Cam S. Simple febrile seizure: the role of serum sodium levels in prediction of seizure recurrence during thefirst 24 hours. Iran J Child Neurol2009; 3(2):31-4.

Relationship of Mothers’ Psychological Status with Development of Kindergarten Children

Firoozeh SAJEDI, Mahbobeh AHMADI DOULABI, Roshanak VAMEGHI, Mohammad Ali MAZAHERI, Alireza AKBARZADEH BAGHBAN

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 61-72
https://doi.org/10.22037/ijcn.v10i3.10340

How to Cite This Article: Firoozeh Sajedi F, Ahmadi Doulabi M, Vameghi R, Mazaheri MA, Akbarzadeh Baghban AR. Relationship of Mothers’ Psychological Status with Development of Kindergarten Children. Iran J Child Neurol. Summer 2016; 10(3):61-72.

 

Abstract

Objective

Given the importance of children’s development and the role of psychological status of mothers in this regard, this study investigated the relationship of mothers’ psychological status (stress, anxiety and depression) with the development of children aged 36-60 months.

Materials & Methods

This descriptive study was performed on 1036 mothers and their children, aged 36 to 60 months, in different kindergartens in Tehran City, Iran, in 2014-2015.

Participants were selected through multi-stage random sampling. The following instruments were used in this study: A demographic and obstetric specification questionnaire, children specification questionnaire, the Beck Depression Inventory, Spiel Berger Test, Perceived stress questionnaire and the Ages and Stages Questionnaire to determine the status of the children’s development.

Data were analyzed using SPSS20 software, Mann-Whitney; independent t-test and logistic-Regression model were used.

Results

The prevalence of developmental delay in children aged 36-60 months was 16.2%. The independent t-test showed a relationship between maternal stress and developmental delay in children. The Mann-Whitney test revealed a significant relation between mothers’ depression level and developmental delay in their children. There was a significant relation between trait anxiety and developmental delay in children. Moreover, a significant relation was found between maternal stress and developmental delay in fine motor skills.

The logistic regression model showed a significant relationship of child gender, economic and social states with developmental delay.

Conclusion

This study showed mothers’ psychological status probably is an effective factor in developmental delay. The assessment of mothers’ psychological status is suggested for early interventions.

 

References

  1. Irwin LG, Siddiqi A, Hertzman C. Early child development: a powerful equalizer. Final report to the WHO Commission on social determinants of health, Geneva. 2007.
  2. Guralnick MJ. Early Intervention for Children with Intellectual Disabilities: Current Knowledge and Future Prospects. J Appl Res Intellect Disabil 2005;18(4):313-24.
  3. Marmot M, Friel S, Bell R, Houweling TA, Taylor S. Commission on Social Determinants of Health. Closing the gap in a generation: health equity through action on the social determinants of health. Lance 2008 Nov 14;372(9650):1661-1669.
  4. Boyle CA, Boulet S, Schieve L, Cohen RA, Blumberg SJ, Yeargin-Allsopp M, Visser S, Kogan MD. Trends in the Prevalence of Developmental Disabilities in US Children, 1997–2008. Pediatrics 2011; 27: 1034-1042.
  5. Sherr EH, Shevell MI. Global developmental delay and mental retardation/ intellectual disability. In: Swaiman KF, Ashwal S, Ferriero DM, Schor NF.eds Pediatric neurology:principles and practice. 5th ed. Philadelphia: Elsevier Saunders, 2012:554–74.
  6. Al-Naddawi M, Ibraheem MF, Alwan SH, Causes of Global Developmental Delay in Children Welfare Teaching Hospital-Baghdad. IPMJ 2013;12(3):383-9.
  7. Vohr BR, O’Shea M, Wright LL, editors. Longitudinal multicenter follow-up of high-risk infants: why, who, when, and what to assess. Seminars in Perinatology; 2003: Elsevier.
  8. Rydz D, Srour M, Oskoui M, Marget N, Shiller M, Birnbaum R, et al. Screening for developmental delay in the setting of a community pediatric clinic: a rospective assessment of parent-report questionnaires. PEDIATRICS 2006;118(4):e1178-e86.
  9. Glascoe FP. Early detection of developmental and behavioral problems. Pediatr Rev 2000;21(8):272-80.
  10. Potijk MR, Kerstjens JM, Bos AF, Reijneveld SA, de Winter AF. Developmental delay in moderately preterm-born children with low socioeconomic status: risks multiply. Pediatrics 2013;163(5):1289-95.
  11. de Moura DR, Costa JC, Santos IS, Barros AJ, Matijasevich A, Halpern R, et al. Risk factors for suspected developmental delay at age 2 years in a Brazilian birth cohort. Paediatr Perinat Epidemiol 2010;24(3):211-21.
  12. Poon JK, Larosa AC, Pai GS. Developmental delay: timely identification and assessment. Indian Pediatr 2010;47(5):415-22.
  13. Tervo RC. Identifying patterns of developmental delays can help diagnose neurodevelopmental disorders. Clin Pediatr 2006;45(6):509-17.
  14. Afraz S, Ahmadi M, Sajedi F, Akbarzadeh Baghban A. Development Status of 4-24 Months Children Born to Teenage Mothers Referred to Health Care Centers in Yasuj, 2013. Yumsj 2015;20(3):253-63.
  15. Shahshahani S, Vameghi R, Azari N, Sajedi F, Kazemnejad A. Comparing the Results of Developmental Screening of 4-60 Months Old Children in Tehran Using ASQ & PDQ. Iran Rehab J 2011 Jul 15;9:3-7.
  16. Shaahmadi F, Khushemehri G, Arefi Z, Karimyan A, Heidari F. Developmental Delay and Its Effective Factors in Children Aged 4 to12 Months. In J Pediatr 2015 Jan 1;3(1.1):396-402.
  17. Karami K, Abbasi L, Moridi F, Falah F, Bayat Z, Pourvakhshoori N. Evaluation criteria and factors associated with the development of one year old children in Khorramabad. Iran J Pediatr 2015;1(3):57-64.
  18. Dorre F, Fattahi Bayat G. Evaluation of children’s development (4-60mo) with history of NICU admission based on ASQ in Amir kabir Hospital, Arak. J Ardabil Uni Med Sci 2011 Jun 15;11(2):143-50.
  19. Shahshahani S, Vameghi R, Azari N, Sajedi F, A. K. Developmental screening for children 60-4 months in Tehran using the Denver Developmental Screening Test 2 and Ages and Stages Questionnaires. Quarterly J Rehab 2011; 12 (3):65-71.
  20. Persha A, Arya S, Nagar R, Behera P, Verma R, Kishore M. Biological and psychosocial predictors of developmental delay in persons with intellectual disability: retrospective case-file study. APDRJ 2007;18(1):93-100.
  21. Sanders B, Schneiderman JU, Loken A, Lankenau SE, Bloom JJ. Gang youth as a vulnerable population for nursing intervention. Public Health Nurs 2009;26(4):346-52.
  22. To T, Guttmann A, Dick PT, Rosenfield JD, Parkin PC, Tassoudji M, et al. Risk markers for poor developmental attainment in young children: results from a longitudinal national survey. Arch Pediatr Adolesc Med 2004;158(7):643-9.
  23. Sameroff AJ, Seifer R, Barocas R, Zax M, Greenspan S. Intelligence quotient scores of 4-year-old children: Social-environmental risk factors. Pediatrics 1987;79(3):343-50.
  24. Delgado CE, Vagi SJ, Scott KG. Identification of early risk factors for developmental delay. Exceptionality 2007;15(2):119-36.
  25. Huggenberger HJ, Suter SE, Blumenthal TD, Schachinger Maternal social stress modulates the development of prepulse inhibition of startle in infants. Dev Cogn Neurosci 2013;3:84-90.
  26. Ceballo R, McLoyd VC. Social support and parenting in poor, dangerous neighborhoods. Child Dev 2002:1310-21.
  27. Conners-Burrow NA, Johnson B, Whiteside-Mansell Maternal substance abuse and children’s exposure to violence. Pediatrics Nursing 2009;24(5):360-8.
  28. Propper C, Rigg J. Socio-economic status and child behaviour: evidence from a contemporary UK cohort. Lse Sticerd Research Paper No Case 125. 2007.
  29. Berg-Nielsen TS, Vika A, Dahl AA. When adolescents disagree with their mothers: CBCL-YSR discrepancies related to maternal depression and adolescent self-esteem. Child Care Health Dev 2003;29(3):207-13.
  30. Koutra K, Chatzi L, Bagkeris M, Vassilaki M, Bitsios P, Kogevinas M. Antenatal and postnatal maternal mental health as determinants of infant neurodevelopment at 18 months of age in a mother–child cohort (Rhea Study) in Crete, Greece. Soc Psychiatry Psychiatr Epidemiol 2013;48(8):1335-45.
  31. Ordway MR. Depressed mothers as informants on child behavior: Methodological issues. Res Nurs Health 2011;34(6):520-32.
  32. Field T. Infants of depressed mothers. Infant Behav Dev 1995;18(1):1-13.
  33. Herring S, Gray K, Taffe J, Tonge B, Sweeney D, Einfeld Behaviour and emotional problems in toddlers with pervasive developmental disorders and developmental delay: associations with parental mental health and family functioning. J Intellectual Disabil Res 2006;50(12):874-82.
  34. Jakšić N, Ivezić E, Jokić-Begić N, Surányi Z, Stojanović-Špehar S. Factorial and diagnostic validity of the Beck Depression Inventory-II (BDI-II) In Croatian primary health care. J Clin Psychol Med Settings 2013;20(3):311-22.
  35. Hall BJ, Hood MM, Nackers LM, Azarbad L, Ivan I, Corsica J. Confirmatory factor analysis of the Beck Depression Inventory-II in bariatric surgery candidates. Psychol Assessment 2013;25(1):294.
  36. Razavi SH, Razavi-Ratki SK, Nojomi MM, Namiranian N. Depression and general anxiety in the prisoner of war’s children: a cross sectional study. Med J Islam Repub Iran 2012;26(4):179.
  37. Ghassemzadeh H, Mojtabai R, Karamghadiri N, Ebrahimkhani N. Psychometric properties of a Persian-language version of the Beck Depression Inventory-Second edition: BDI-II-PERSIAN. Depress Anxiety 2005;21(4):185-92.
  38. Cohen S, Kamarck T, Mermelstein R. A global measure of perceived stress. J Health Soc Behav 1983:385-96.
  39. Bastani F, Rahmatnejad L, Jahdi F, Haghani H. Breastfeeding self efficacy and perceived stress in primiparous mothers. IJN 2008;21(54):9-24.
  40. Bech P, Gormsen L, Loldrup D, Lunde M. The clinical effect of clomipramine in chronic idiopathic pain disorder revisited using the Spielberger State Anxiety Symptom Scale (SSASS) as outcome scale. J Affect Disord 2009;119(1):43-51.
  41. Court H, Greenland K, Margrain TH. Measuring Patient Anxiety in Primary Care: Rasch Analysis of the 6-item Spielberger State Anxiety Scale. Value in Health 2010;13(6):813-9.
  42. Nasiri AF, Salmalian H, Haji AM, Ahmadi AM. Association between prenatal anxiety and spontaneous preterm birth. JBUMS 2009;11(4):42-48.
  43. Shamaeian Razavi N, Bahri Binabaj N, Hoseiny Shahidy L, PourHeidari M. The effect of maternal position on labor pain. Ofogh-e-Danesh Journal 2006;12(2):16-21.
  44. Masoumi R, Lamieian M, Ghaedi S. Role of oxytocin in anxiety in the normal parturition. Zah J Res Med Sci 2008; 10(1):53-58.
  45. Kaviani H, Ahmadi Abhari A. Prevalence of anxiety disorders in Tehran city. Iran J Psychiatry Clin Psychol 2003;8(3):4-11.
  46. Zhang J, Gao Q. Validation of the trait anxiety scale for state-trait anxiety inventory in suicide victims and living controls of Chinese rural youths. Arch Suicide Res 2012;16(1):85-94.
  47. Elbers J, Macnab A, McLeod E. Article originale. Can J Rural Med 2008;13(1).
  48. Yu LM, Hey E, Doyle LW, Farrell B, Spark P, Altman DG, et al. Evaluation of the Ages and Stages Questionnaires identifying  children  with  neurosensory disability the Magpie Trial follow-up study. Acta Paediatrica 2007;96(12):1803-8.
  49. Lindsay NM, Healy GN, Colditz PB, Lingwood BE. Use of the Ages and Stages Questionnaire to predict outcome after hypoxic-ischaemic encephalopathy in the neonate. J Paediatr Child Health 2008;44(10):590-5.
  50. Squires J, Bricker D, Potter L. Revision of a parent-completed developmental screening tool: Ages and Stages Questionnaires. J Pediatr Psychol 1997;22(3):313-28.
  51. Glascoe FP. Screening for developmental and behavioral problems. Ment Retard Dev Disable Res Rev 2005;11(3):173-9.
  52. Richter J, Janson H. A validation study of the Norwegian version of the Ages and Stages Questionnaires. Acta Paediatr 2007;96(5):748-52.
  53. Vameghi R, Sajedi F, Mojembari AK, Habiollahi A, Lornezhad HR, Delavar B. Cross-cultural adaptation, validation and standardization of Ages and Stages Questionnaire (ASQ) in Iranian children. Iran J Publ Health 2013;42(5):522.
  54. Chiang T-L, Lin S-J, Shu B-C. Parental mental health and child development from six to thirty-six months in a birth cohort study in Taiwan. J Perinat Med 2009;37(4):397-402.
  55. Benjamin J, Sadock, Virginia A. Kaplan comprehensive Text book of psychiatry,7 th ed:Lippincott Williams.2000,1284-1338.
  56. Sajadi H, Vameghi M, Setare forozan A, Rafiey H, Mohgheghee Kamal SH, Nosrat abadi M. Prevalence, risk factors and interventions of depression during pregnancy in Iranian Studies (1997-2011): A systematic review. North Khorasan Univ Med Sci 2013;5(2):521-30.
  57. Ali NS, Mahmud S, Khan A, Ali BS. Impact of postpartum anxiety and depression on child’s mental development from two peri-urban communities of Karachi, Pakistan: a quasi-experimental study. Bmc Psychiatrry 2013;13(1):274.
  58. Hadley C, Tegegn A, Tessema F, Asefa M, Galea S. Parental symptoms of common mental disorders and children’s social, motor, and language development in sub-Saharan Africa. Ahb Ann Hum Biol 2008;35(3):259-75.
  59. Brennan PA, Hammen C, Andersen MJ, Bor W, Najman JM, Williams GM. Chronicity, severity, and timing of maternal depressive symptoms: relationships with child outcomes at age 5. Dev Psychol 2000;36(6):759.
  60. Coyl D, Roggman L, Newland L. Stress, maternal depression and negative mother-infant interactions in relation to infant attachment. Infant Ment Health J 2002; 23: 145-163.
  61. Brouwers EP, van Baar AL, Pop VJ. Maternal anxiety during pregnancy and subsequent infant development. Infant Behav Dev 2001;24(1):95-106.
  62. McLearn KT, Minkovitz CS, Strobino DM, Marks E, Hou W. The timing of maternal depressive symptoms and mothers’ parenting practices with young children: implications for pediatric practice. Pediatrics 2006;118(1):e174-e82.
  63. Van der Toorn SL, Huizink AC, Utens EM, Verhulst FC, Ormel J, Ferdinand RF. Maternal depressive symptoms, and not anxiety symptoms, are associated with positive mother–child reporting discrepancies of internalizing problems in children: a report on the TRAILS Study. Eur Child Adolesc Psychiatry 2010;19(4):379-88.
  64. Cooper PJ, Tomlinson M, Swartz L, Woolgar M, Murray L, Molteno C. Post-partum depression and the mother-infant relationship in a South African peri-urban settlement. Br J Psychiatry 1999;175(6):554-8.
  65. Tomlinson M, Cooper P, Murray L. The Mother–Infant Relationship and Infant Attachment in a South African Peri-Urban Settlement. Child Dev 2005;76(5):1044-54.
  66. DeMulder EK, Radke-Yarrow M. Attachment with affectively ill and well mothers: Concurrent behavioral correlates. Dev Psychopppathol 1991;3(03):227-42.
  67. Winnicott DW. The theory of the parent-infant relationship. Int Rev Psychoanal 1960;41(6):585-95.
  68. Petrozzi A, Gagliardi L. Anxious and depressive components of Edinburgh Postnatal Depression Scale in maternal postpartum psychological problems1). J Perinat Med 2013;41(4):343-8.
  69. Black MM, Baqui AH, Zaman K, McNary SW, Le K, Arifeen SE, et al. Depressive symptoms among rural Bangladeshi mothers: implications for infant development. J Child Psychol Psychiatry 2007;48(8):764-72.
  70. McCrory C, McNally S. The effect of pregnancy intention on maternal prenatal behaviours and parent and child health: results of an irish cohort study. Paediatr Perinat Epidmiol 2013;27(2):208-15.
  71. Field T. Infants of depressed mothers. Devpsychopathol 1992;4(01):49-66.
  72. Murray L, Cartwright W. The role of obstetric factors in postpartum depression. J Reprod Infant Psychhol 1993;11(4):215-9.
  73. Tronick EZ. Emotions and emotional communication in infants. Am Psychol 1989;44(2):112.
  74. Rovee-Collier C. Time windows in cognitive development. DEV Psychol 1995;31(2):147.
  75. van IJzendoorn M. Attachment at an early age (0-5) and its impact on children’s development. Encyclopedia on Early Childhood Development. 2005:1-5.
  76. Brody GH, Flor DL. Maternal resources, parenting practices, and child competence in rural, single-parent African American families. Child Dev 1998:803-16.
  77. Hane A, Fox N. Natural variations in maternal caregiving of human infants influence stress reactivity. Psychol Sci 2006;17:550-6.
  78. Keim SA, Daniels JL, Dole N, Herring AH, Siega-Riz AM, Scheidt PC. A prospective study of maternal anxiety, perceived stress, and depressive symptoms in relation to infant cognitive development. Early Hum Dev 2011;87(5):373-80.
  79. Kurstjens S, Wolke D. Effects of maternal depression on cognitive development of children over the first 7 years of life. J Child Psychol.Psychiatry 2001;42(05):623-36.
  80. Campbell SB, Cohn JF, Meyers T. Depression in first-time mothers: mother-infant interaction and depression chronicity. Dev Psychol 1995;31(3):349.
  81. Sameroff AJ, Seifer R, Baldwin A, Baldwin C. Stability of intelligence from preschool to adolescence: The influence of social and family risk factors. Child Dev 1993;64(1):80-97.
  82. Murray L, Halligan S, Cooper P. Effects of postnatal depression on mother–infant interactions and child development. Wiley-Blackwell Handbook of Infant Development, The, Volume 2, Second Edition 2010:192-220.

Neurometabolic Disorder Articles


Neurometabolic Diagnosis in Children who referred as Neurodevelopmental Delay (A Practical Criteria, in Iranian Pediatric Patients)

Parvaneh KARIMZADEH, Narjes JAFARI, Habibeh NEJAD BIGLARI, Sayena JABBEHDARI, Simin KHAYAT ZADEH, Farzad AHMAD ABADI, Azra LOTFI

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 73-81
https://doi.org/10.22037/ijcn.v10i3.10183

How to Cite This Article: Karimzadeh P, Jafari N, Nejad Biglari H, Jabbehdari J, Khayat Zadeh S, Ahmad Abadi F, Lotfi A. Neurometabolic Diagnosis in Children who referred as Neurodevelopmental Delay (A Practical Criteria, in Iranian Pediatric Patients). Iran J Child Neurol. Summer 2016; 10(3):73-81.

 

Objective

We aimed to investigate the clinical and para clinical manifestations of neuro metabolic disorders, in patients who presented by neuro developmental delay in their neuro developmental milestones.

Materials & Methods

The patients diagnosed as neuro developmental delay and regression with or without seizure at the Neurology Department of Mofid Children Hospital in Tehran, Iran between 2004 and 2014 were included in our study. These patients diagnosed as neuro developmental delay by pediatric neurologists in view of diagnostic /screening neuro developmental assessment tests. The patients who completed our inclusion criteria as neuro metabolic disorders were evaluated in terms of metabolic and genetic study in referral lab.

Results

Overall, 213 patients with neurometabolic disorders were diagnosed. 54.3% of patients were male. The average age of patients was 41 +-46.1 months. 71.4% of parent’s patients had consanguinity of marriages. Eighty seven percent of patients had developmental delay (or/and) regression. 55.5% of them had different type of seizures. Overall, 213 patients with 34 different neurometabolic disorders were diagnosed and classified in the 7 sub classes, consisting of:

1- organic acidemia and aminoacidopathy (122 patients), 2-storage disease (37 patients) 3- eukodystrophy (27 patients), other classes consisted: lipid oxidation disorders, urea cycle disorders, progressive myoclonic epilepsy; and peroxizomal disorders (27 patients).

Conclusion

In patients with developmental delay or regression, with or without seizure, abnormal neurologic exam along with positive family history of similar disorder or relative parents, abnormal brain imaging with specific patterns, neurometabolic disorders should be considered as one of the important treatable diseases.

 

References

  1. Brismar J. CT and MRI of the brain in inherited neurometabolic disorders. J Child Neurol 1992 Apr;7 Suppl:S112-31.
  2. Barkovich AJ. An approach to MRI of metabolic disorders in children. J Neuroradiol 2007; 34(2):75-88.
  3. Barkovich AJ. A magnetic resonance approach to metabolic disorders in childhood. Rev Neurol 2006 10;43 Suppl 1:S5-16.
  4. Zimmerman RA. Neuroimaging of inherited metabolic disorders producing seizures. Brain Dev 2011;33(9):734-44.
  5. Cakir B, Teksam M, Kosehan D, Akin K, Koktener A.Inborn errors of metabolism presenting in childhood. J Neuroimaging 2011;21(2):e117-33.
  6. Burton BK. Inborn errors of metabolism in infancy: a guide to diagnosis. Pediatrics 1998;102(6):E69.
  7. Iman G. Mahmoud M, Marwa M, Miral R, Marian G, Nevin W, Ameera E. Clinical, Neuroimaging, and Genetic Characteristics of Megalencephalic Leukoencephalopathy With Subcortical Cysts in Egyptian Patients. Pediatr Neurol 2014;140e-148.
  8. Sarar M, Ebtessam M, Melegy B, Iman T, Amany H, Khaled K. Neurometabolic Disorders-Related Early Childhood Epilepsy: A Single-Center Experience in Saudi Arabia. Pediatr Neurol 2015; xx, 1e9.
  9. Talebian A, Jahangiri M, Rabiee M, Masoudi N, Akbari H, Sadat Z. The Etiology and Clinical Evaluations of Neonatal Seizures in Kashan, IRAN. Iran J Child Neurol 2015;9(2):29-35.
  10. Vigevano F, Bartuli A. Infantile epileptic syndromes and metabolic etiologies. J Child Neurol 2002;17:3S9e13.
  11. Karimzadeh P. Approach to Neurometabolic Diseases from a Pediatric Neurological Point of View. Iran J Child Neurol 2015;9(1): 1-16.
  12. Hee Eun S, Houn Hahn S. Metabolic evaluation of children with global developmental delay. Korean J Pediatr 2015;58(4):117-122.
  13. Kroll R, Pagel M, Roman S, Barkovich A, D’Agostino A, Neuwelt E.White matter changes associated with feline GM2 gangliosidosis (Sandhoff disease): correlation of MR findings with pathologic and ultrastructural abnormalities. Am J Neuroradiol 1995;16(6):1219-26.
  14. Karimzadeh P, Jafari N, Nejad Biglari H, Jabbeh Dari S, Ahmad Abadi F, Alaee M,. GM2-Gangliosidosis (Sandhoff and Tay Sachs disease): Diagnosis and Neuroimaging Findings (An Iranian Pediatric Case Series). Iran J Child Neurol 2014;8(3):55-60.
  15. Wang Q, Ding Y, Liu Y, Li X, Wu T, Song J, et al.(Clinical and laboratory studies on 28 patients with glutaric aciduria type 1). Zhonghua Er Ke Za Zhi 2014 Jun;52(6):415-9.
  16. Karimzadeh P, Pirzadeh Z, Ahmadabadi F, Jafari N, Jabbehdari S, Nemati H,. Glutaric aciduria type 1: diagnosis and neuroimaging findings of this neurometabolic disorder in an Iranian pediatric case series. Int J Develop Dis 2014; 60(3): 1–6
  17. Weller S, Rosewich H, Gärtner J. Cerebral MRI as a valuable diagnostic tool in Zellweger spectrum patients. J Inherit Metab Dis 2008;31(2):270-80.
  18. Groeschel S, Kehrer C, Engel C, I Dali C, Bley A, Steinfeld R, et al. Metachromatic leukodystrophy; natural course of cerebral MRI changes in relation to clinical course. J Inherit Metab Dis 2011;34(5):1095-102.
  19. Klee D, Thimm E, Wittsack HJ, Schubert D, Primke R, Pentang G,et al. Structural white matter changes in adolescents and young adults with maple syrup urine disease. J Inherit Metab Dis 2013;36(6):945-53.
  20. Karimzadeh P. Approach to neurometabolic diseases from a pediatric neurological point of view. Iran J Child Neurol 2015;9(1):1-16.
  21. Leuzzi V1, Tosetti M, Montanaro D, Carducci C, Artiola C, Carducci C,et al. The pathogenesis of the white matter abnormalities in phenylketonuria. A multimodal 3.0 tesla MRI and magnetic resonance spectroscopy (1H MRS) study. J Inherit Metab Dis 2007;30(2):209-16. Epub 2007 Jan 23.
  22. Karimzadeh P, Ahmadabadi F, Jafari N, Shariatmadari F, Nemati H, Ahadi A, Karimi Dardashti S, Mirzarahimi M, Dastborhan Z, Zare Noghabi J. Study on MRI changes in phenylketonuria in patients referred to mofid hospital/ iran. Iran J Child Neurol 2014 ;8(2):53-6.
  23. Abdelhalim AN, Alberico RA, Barczykowski AL, Duffner PK. Patterns of magnetic resonance imaging abnormalities in symptomatic patients with Krabbe disease correspond to phenotype. Pediatr Neurol 2014;50(2):127-34.
  24. Santosh Rai PV, Suresh BV, Bhat IG, Sekhar M, Chakraborti S.Childhood adrenoleukodystrophy - Classic and variant - Review of clinical manifestations and magnetic resonance imaging. J Pediatr Neurosci 2013;8(3):192-7.
  25. George U, Varte N, Rathore S, Jain V, Goyal S. “Split thalamus”: Internal medullary involvement in Wilson’s disease. Neurol India 2010;58:680
  26. Oder W, Prayer L, Grimm G, Spatt J, Ferenci P, Kollegger H, et al. Wilson’s disease: evidence of subgroups derived from clinical findings and brain lesions. Neurology 1993;43:120-4.
  27. Bickel H.(Brain atrophy and disorders of the amino acid metabolism). Monatsschr Kinderheilkd 1967;115(4):254-8.
  28. Karimzadeh P, Jafari N, Alai M, Jabbehdari S, Nejad Biglari H. Homocystinuria: Diagnosis and Neuroimaging Findings of Iranian Pediatric patients. Iran J Child Neurol 2015;9(1):94-8.
  29. Sreenivasan P, Purushothaman KK.Radiological clue to diagnosis of Canavan disease. Indian J Pediatr 2013;80(1):75-7.
  30. Karimzadeh P, Jafari N, Nejad Biglari H, Rahimian E, Ahmadabadi F, Nemati H, Nasehi MM, Ghofrani M, Mollamohammadi M. The Clinical Features and Diagnosis of Canavan’s Disease: A Case Series of Iranian Patients. Iran J Child Neurol 2014 ;8(4):66-71.
  31. Nguyen HV, Ishak GE. Canavan disease - unusual imaging features in a child with mild clinical presentation. Pediatr Radiol 2014 Aug 9.
  32. Rogers T, al-Rayess M, O’Shea P, Ambler MW.Dysplasia of the corpus callosum in identical twins with nonketotic hyperglycinemia. Pediatr Pathol 1991;11(6):897-902.
  33. Johnson JA, Le KL, Palacios E.Propionic acidemia: case report and review of neurologic sequelae. Pediatr Neurol 2009;40(4):317-20.
  34. Karimzadeh P, Jafari N, Ahmad Abadi F, Jabbedari S, Taghdiri MM, Alaee MR, Ghofrani M, Tonekaboni SH, Nejad Biglari H. Propionic acidemia: diagnosis and neuroimaging findings of this neurometabolic disorder. Iran J Child Neurol 2014;8(1):58-61.
  35. 35.Desai S, Ganesan K, Hegde A.Biotinidase deficiency: a reversible metabolic encephalopathy. Neuroimaging and MR spectroscopic findings in a series of four patients. Pediatr Radiol 2008;38(8):848-56.
  36. Karimzadeh P, Ahmadabadi F, Jafari N, Jabbehdari S, Alaee MR, Ghofrani M, Taghdiri MM, Tonekaboni SH. Biotinidase deficiency: a reversible neurometabolic disorder (an Iranian pediatric case series). Iran J Child Neurol 2013;7(4):47-52.
  37. Brismar J, Ozand PT.CT and MR of the brain in disorders of the propionate and methylmalonate metabolism. Am J Neuroradiol 1994;15(8):1459-73.
  38. Karimzadeh P, Jafari N, Ahmad Abadi F, Jabbedari S, Taghdiri MM, Nemati H, Saket S, Shariatmadari SF, Alaee MR, Ghofrani M, Tonekaboni SH. Methylmalonic acidemia: diagnosis and neuroimaging findings of this neurometabolic disorder (an Iranian pediatric case series). Iran J Child Neurol 2013;7(3):63-6.

 

Case Report


Cerebellar Infarction in Childhood: Delayed-Onset Complication of Mild Head Trauma

Ibrahim Ilker OZ, Evrim BOZAY OZ, Ismail ÅžERIFOÄžLU, Nurullah KAYA, Oktay ERDEM

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 82-85
https://doi.org/10.22037/ijcn.v10i3.9955

How to Cite This Article: Oz II, Bozay Oz E, Şerifoğlu I, Kaya N, Erdem O. Cerebellar Infarction in Childhood: Delayed-Onset Complication of Mild Head Trauma. Iran J Child Neurol. Summer 2016; 10(3):82-85.

Objective
Cerebellar ischemic infarction is a rare complication of minor head trauma. Vertebral artery dissection, vasospasm or systemic hypo perfusion can cause infarct. However, underlying causes of the ischemic infarct cannot be explained in nearly half of cases. The accurate diagnosis is essential to ensure appropriate treatment. Here we report a five yr old boy patient of cerebellar infraction after minor head trauma, admitted to emergency serves of Bulent Ecevit University, Turkey in 2013. We aimed to remind minor head trauma that causes cerebellar infarction during childhood, and to review the important points of the diagnosis, which should be keep in mind.

 

References

  1. Schutzman SA, Greenes DS. Pediatric minor head trauma. Ann Emerg Med 2001;37(1):65-74.
  2. Shaffer L, Rich PM, Pohl KR, Ganesan V. Can mild head injury cause ischaemic stroke? Arch Dis Child 2003;88(3):267-9.
  3. Lin JJ, Lin KL, Chou ML, Wong AM, Wang HS. Cerebellar infarction in the territory of the superior cerebellar artery in children. Pediatr Neurol 2007;37(6):435-7.
  4. Matsumoto H, Kohno K. Posttraumatic cerebral infarction due to progressive occlusion of the internal carotid artery after minor head injury in childhood: a case report. Childs Nerv Syst 2011;27(7):1169-75.
  5. Williams LS, Garg BP, Cohen M, Fleck JD, Biller J. Subtypes of ischemic stroke in children and young adults. Neurology 1997;49(6):1541-5.
  6. Kieslich M, Fiedler A, Heller C, Kreuz W, Jacobi G. Minor head injury as cause and co-factor in the aetiology of stroke in childhood: a report of eight cases. J Neurol Neurosurg Psychiatry 2002;73(1):13-6.
  7. O’Brien NF, Reuter-Rice KE, Khanna S, Peterson BM, Quinto KB. Vasospasm in children with traumatic brain injury. Intensive Care Med 2010;36(4):680-7.
  8. Barkovich A, Schwartz E. Brain and Spine Injuries in Infancy and Childhood. In: Barkovich A, Raybaud C, editors. Pediatric Neuroimaging. 5th ed. Philidelphia, PA: Lippincott Williams & Wilkins; 2012. p. 335-8.
  9. Lansberg MG, Albers GW, Beaulieu C, Marks MP. Comparison of diffusion-weighted MRI and CT in acute stroke. Neurol 2000;54(8):1557-61. 

 

Hemispherectomy Procedure in Proteus Syndrome

Prastiya Indra GUNAWAN, Lusiana LUSIANA, Darto SAHARSO

Iranian Journal of Child Neurology, Vol. 10 No. 3 (2016), 5 June 2016, Page 86-90
https://doi.org/10.22037/ijcn.v10i3.9797

How to Cite This Article: Gunawan PI, Lusiana L, Saharso D. Hemispherectomy Procedure in Proteus Syndrome. Iran J Child Neurol.Summer 2016; 10(3):86-90

 

Objective

Proteus syndrome is a rare overgrowth disorder including bone, soft tissue, and skin. Central nervous system manifestations were reported in about 40% of the patients including hemimegalencephaly and the resultant hemicranial hyperplasia, convulsions and mental deficiency. We report a 1-month-old male baby referred to Pediatric Neurology Clinic Soetomo Hospital, Surabaya, Indonesia in 2014 presented recurrent seizures since birth with asymmetric dysmorphic face with the right side larger than the left, subcutaneous mass and linear nevi. Craniocervical MRI revealed hemimegalencephaly right cerebral hemisphere. Triple antiepileptic drugs were already given as well as the ketogenic diet, but the seizures persisted. The seizure then was resolved after hemispherectomy procedure.

References

  1. Beachkofsky TM, Sapp JC, Biesecker LG, Darling TN. Progressive overgrowth of the cerebriform connective tissue nevus in patients with Proteus syndrome. J Am Acad Dermatol 2010;63:799-804.
  2. Biesecker L. The challenges of Proteus syndrome: diagnosis and management. Eur J Hum Genet 2006;14:1151-7.
  3. Yamatogi Y, Ohtahara S. Early-infantile epileptic encephalopathy with suppression-bursts, Ohtahara syndrome; its overview referring to our 16 cases. Brain Dev 2002;24:13-23.
  4. Bastos H, da Silva PFS, de Albuquerque MAE, Mattos A, Riesgo RS, Ohlweiler L, et al. Proteus syndrome associated with hemimegalecephaly and Ohtahara syndrome: Report of two cases. Seizure 17(4):2008.
  5. Turner JT, Cohen MM, Jr., Biesecker LG. Reassessment of the Proteus syndrome literature: application of diagnostic criteria to published cases. Am J Med Genet A 2004;130A:111-22.
  6. Cohen MM, Jr. Proteus syndrome: clinical evidence for somatic mosaicism and selective review. Am J Med Genet 1993;47:645-52.
  7. Bilkay U, Tokat C, Ozek C, Gundogan H, Erdem O, Gurler T, et al. Proteus syndrome. Scand J Plast Reconstr Surg Hand Surg 2003;37:307-10.
  8. Biesecker LG, Happle R, Mulliken JB, Weksberg R, Graham JM, Jr., Viljoen DL, et al. Proteus syndrome: diagnostic criteria, differential diagnosis, and patient evaluation. Am J Med Genet 1999;84:389-95.
  9. Caraballo R, Bartuluchi M, Cersosimo R, Soraru A, Pomata H. Hemispherectomy in pediatric patients with epilepsy: a study of 45 cases with special emphasis on epileptic syndromes. Childs Nerv Syst 2011;27:2131-6.
  10. Moosa AN, Gupta A, Jehi L, Marashly A, Cosmo G, Lachhwani D, et al. Longitudinal seizure outcome and prognostic predictors after hemispherectomy in 170 children. Neurology 2013;80:253-60.