Participation of Iranian Cerebral Palsy Children in Life Areas: A Systematic Review Article

Marzieh PASHMDARFARD, Malek AMINI, Afsoon HASSANI MEHRABAN

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 1-12
https://doi.org/10.22037/ijcn.v11i1.11761

How to Cite This Article: Pashmdarfard M, Amini M, Hassani Mehraban A. Participation of Iranian Cerebral Palsy Children in Life Areas: A Systematic Review. Iran J Child Neurol. Winter 2017; 11(1):1-12.

 Abstract

Objective

Cerebral palsy (CP) is the most common cause of chronic disability that restricts participation in areas of occupations for children. The main aim of rehabilitation is enhancement of their clients for participation in occupations. The aim of this study was to overview of the factors influencing the participations of children with CP in Iran.

 Materials & Methods

A systematic, evidence-based process (Duffy 2005) was used. For data gathering electronic databases including Google scholar and Iranian and foreigner famous journals in the fields of pediatrics, were used. The main key words for search were Activity of Daily Living (ADL), Instrumental Activity of Daily Living (IADL), play, leisure, work, rest/sleep, social participation, and education. All the papers of this study were about the factors influencing the participation of Iranian CP children during 2000-2016. Totally, 156 articles were found eligible as for Iranian CP children study, of which 100 articles were discarded. Because of repetitive and duplicability of some articles, 17 articles were removed as well.

 Results

The most studies about Iranian CP children participations in life areas were in the ADL area of participation (N=12), and the lowest articles were in the area in the field of: Work (N=2), play (N=2), and sleep/rest (N=2). Most of the occupational therapists do not focus on the all life areas.

 Conclusion

In Iran, many researchers do not pay attention to the participation of CP children. Many articles just paid attention to the sensory, motor or cognitive components of their clients.


Refereneces

1.Trabacca A, Vespino T, Di Liddo A, Russo L. Multidisciplinary rehabilitation for patients with cerebral
palsy: improving long-term care. J Multidiscip Health c 2016;22(9):455-462.
2. shubhra M, Deborah J. cerebral palsy. In: Braddom RL, editors. physical Medicine & Rehabilitation. 3rd ed.
Elsevier; 2007. p.1243-61.
3. Van Nieuwenhuizen O, Platenga NJ, Kasteel TE. Epilepsy in cerebral palsy: etiology, classification and prevalence. Europe Paed Neural Soc 1997;1(2-3):111-5.
4. Oriady Zanjani M. Cerebral palsy in viewpoint of speech language pathology nature, assessment and treatment. Hamedan: Nooreelm; 2005.
5. Joghataei M, Kazem M. Assessment the level of community needs in welfare services on the whole
country. 1st ed. Tehran: University of Social Welfare and Rehabilitation Sciences; 1990.p.123-5.
6. Vohr BR, Wright LL, Dusick AM. Differences and outcomes of extremely low birth weight infants. Pediatrics 2004;113(4):781-9.
7. sharifi A, Kamali M, Chabok A. Rehabilitation Needs of People with Cerebral Palsy: a qualitativeStudy. Med J Islam Repub Iran 2014;28:1-10.
8. labaf S, Shamsoddini A, Hollisaz MT, Sobhani V, Shakibaee A. Effects of Neurodevelopmental Therapy on
Gross Motor Function in Children with Cerebral Palsy. Iran J Child Neurol 2015;9(1):36-41.
9. Shamsoddini A. comparison between the effect of neurodevelopmental treatment and sensory integration therapy on gross motor function in children with Cerebral Palsy. Iran J Child Neurology 2010;14(1):31-8.
10. American Occupational Therapy Association. Occupational Therapy Practice Framework: Domain and Process, 3rd Edition. Am J Occup Therapy 2014;48:3-48.
11. Bradley L, Law M. systematically reviewing the evidence. In: Law M, editors. Evidence-based rehabilitation: A guide to practice. 2nd ed. USA: Slack Incorporated; 2008. p.143-7.
12. Dalvand H, Dehghan L, Feizy A, Amirsalai S, Bagheri H. Effects of the bobath technique, conductive education and education to parents in activities of daily living in children with cerebral palsy. Hong Kong J Occup Therapy 2009;19(1):14–9.
13. Nurani Gharaborghe S, Sarhady M, Hosseini SMS, Mortazavi SS. Relationship between Quality of Life and Gross Motor Function in Children with Cerebral Palsy (Ages 4-12) Medical Journal of Tabriz University of Medical Sciences and Health Services 2015;37(2):48-53.
14. Afshar S, Rassafiani M, Hosseini S.A. Effect of Occupational Therapy Home Program on Activities of Daily Living of 5-12 Years Old Children. J Rehabil 2013 13(4):117-23.
15. Lewandowska A, Zajchowska J, Iwaniszyn J, Huk J, Świeboda P, Filip R. Functioning of the family of a child suffering from cerebral palsy. J Pre-Clin Clin Res. 2012; 6(1): 50-53.
16. Razavi Afzal Z-S, Rassafiani M, Sarfaraz Z, Malekpour M, Salehi, M. A Survey on caregivers’ knowledge about special caring for 1-to-5 year-old children with cerebral palsy and their compliance with these practices. J Res Rehabil Sci 2013;9(4):618-28.
17. Rassafiani M, Sahaf R. Hypertonicity in Children with Cerebral Palsy: a New Perspective. Iran Rehabil J 2011;9:66-74.
18. Poursadoughi A, Dadkhah A, Pourmohamadreza-Tajrishi M, Biglarian A. Psycho-Rehabilitation Method (Dohsahou) and Quality of Life in Children with Cerebral Palsy. Iran Rehabil J 2015;13(2):28-33.
19. Salehi Dehno N, Noorizadeh Dehkordi S, Dadgoo M, Salehi M. Association between spasticity and the level of motor function with quality of life in community dwelling Iranian young adults with spastic cerebral palsy. Med J Islam Repub Iran 2012;26(4):150-6.
20. Noori M, Pishyareh E, Hosseini SA, Akbarfahimi N, Rahgozar M. Relationship between upper extremity function and quality of life in the children with spastic cerebral palsy in Capital of Iran. Pajouhan Scientific Journal 2015;13(3):41-8.
21. Dalvand H, Rassafiani M, Hosseini S.A. Handling challenges in the children with cerebral palsy: A qualitative content analysis. J Res Rehabil Sci 2013;9(8):1267-80.
22. Balouchy R, Ghaeni S. Physical Fitness of The Children Infected With Cerebral Paralysis Through A work-group of “Therapists - Children - Parents”. Scientific Journal of Ilam University of Medical Sciences 2009;17(3):16-23.
23. Dalvand H, Rassafiani M, Hosseini S.A. Handling in the Children with Cerebral Palsy: A Review of Ideas and Practices (A Literature Review). J Rehabil 2012;13(5):8- 17.
24. Hassani M, Hassani Mehraban A, Taghizadeh G, Aliabadi F, Ramezani S. Enjoyment of participation in formal and informal activities among students with cerebral palsy and healthy students. J Kermanshah Univ Med Sci 2015;19(3):160-7.
25. Nobakht Z, Rassafiani M, Rezasoltani P. Influence of child’s disability on encountering environmental barriers to Participation of children with cerebral palsy. J Res Rehabil Sci 2013;9(2):286-94.
26. Ghasemzadeh R, Kamali M, Chabok A, Falahi M, Shirani M. Accessibility to the public facilities: a mean to achieve civil rights of the people with disabilities in Iran. Iran Rehabil J 2008;6(7,8):73-82.
27. PourRanjbar M, Keshavarz L, Sharifian E, Farahani A. Barriers for Wheelchair-User Disabled People to Participate in Leisure Physical Activities in Southeast of Iran. Journal of Kerman University of Medical Sciences 2015;22(5):555-68.
28. Hassani Mehraban A, Hassani M, Amini M. The Comparison of Participation in School-Aged Cerebral Palsy Children and normal Peers: A Preliminary Study. Iran J Pediatr 2016 June; 26(3):e5303. doi: 10.5812/ijp.5303
29. Nobakht Z, Rassafiani M, Rezasoltani P, Sahaf R, Yazdani F. Environmental barriers to social participation of children with cerebral palsy in Tehran. Iran Rehabil J 2013;11:40-5.
30. Abbaskhanian A , Rashedi V , Delpak A, Vameghi R, Gharib M. Rehabilitation Interventions for Children with Cerebral Palsy: A Systematic Review. J Pediatr Rev 2015;3(1):1-8.
31. Amini M, Hassani Mehraban A, Haghni H, Asgharnezhad AA, Khayatzadeh Mahani M. Development and validation of Iranian children’s participation assessment scale. Med J Islam Repub Iran 2016 (20 February). Vol. 30:333.
32. Rosenberg L, Jarus T, Bart O. Development and initial validation of the children participation questionnaire(CPQ). Disability Rehabil 2010;32(20):1633-44.
33. Amini M, Hassani Mehraban A, Rostamzade O. Translation, cultural adaptation, face, content and convergent validity of children participation questionnaire into Persian. J Rehabil Med 2016; 5(2): 151-157.
34. Soleimani F, Vameghi R, Kazemnejad A, Akbar Fahimi N, Nobakht Z, Rassafiani M. Psychometric Properties of the Persian Version of Cerebral Palsy Quality of Life Questionnaire for Children. Iran J Child Neurol 2015;9(1):76-86.


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

Reza NAFISI-MOGHADAM, Abolghasem RAHIMDEL, Tahereh SHANBEH-ZADEH, Razieh FALLAH

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 13-20
https://doi.org/10.22037/ijcn.v11i1.6287

How to Cite This Article: Nafisi-Moghadam R, Rahimdel A, Shanbehzadeh T, Fallah R. Comparison of Diffuse Weighted Imaging and Fluid Attenuation Inversion Recovery Sequences of MRI in Brain Multiple Sclerosis Plaques Detection. Iran J Child Neurol. Winter 2017; 11(1):13-20.

Abstract

Objective

Suitable magnetic resonance imaging (MRI) techniques from conventional to new devices can help physicians in diagnosis and follow up of Multiple Sclerosis (MS) patients. The aim of present research was to compare effectiveness of Fluid Attenuation Inversion Recovery (FLAIR) sequence of conventional MRI and Diffuse Weighted Imaging (DWI) sequence as a new technique in detection of brain MS plaques.

 

Materials&Methods

In this analytic cross sectional study, sample size was assessed as 40 people to detect any significant difference between two sequences with a level of 0.05.

DWI and FLAIR sequences of without contrast brain MRI of consecutive MS patients referred to MRI center of Shahid Sadoughi Hospital, Yazd, Iran from January to May 2012, were evaluated.

 Results

Thirty-two females and 8 males with mean age of 35.20±9.80 yr (range =11-66 yr) were evaluated and finally 340 plaques including 127(37.2%) in T2WI, 127(37.2%) in FLAIR, 63(18.5%) in DWI and 24(7.1%) in T1WI were detected. FLAIR sequence was more efficient than DWI in detection of brain MS plaques, oval, round, amorphous plaque shapes, frontal and occipital lobes, periventricular, intracapsular, corpus callosum, centrum semiovale, subcortical, basal ganglia plaques and diameter of detected MS plaques in DWI sequence was smaller than in FLAIR.

 Conclusion

Old lesion can be detected by conventional MRI and new techniques might be more useful in early inflammatory phase of MS and assessment of experimental treatments.

References

1. Inglese M, Bester M. Diffusion imaging in multiple sclerosis: research and clinical implications. NMR
Biomed 2010;23(7):865-72.
2. Inaloo S, Haghbin S. Multiple Sclerosis in Children. Iran J Child Neurol 2013;7(2):1-10.
3. Polman CH, Reingold SC, Edan G, Filippi M, Hartung HP, Kappos L, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the McDonald criteria. Ann Neurol 2005;58(6):840-6.
4. Sahraian MA, Eshaghi A. Role of MRI in diagnosis and treatment of multiple sclerosis. Clin Neurol Neurosurg 2010 ;112(7):609-15.
5. Miller DH; Steering Committee of MAGNIMS. Role of MRI in diagnosing multiple sclerosis: magnetic resonance imaging is valuable. BMJ 2006, 29;332(7548):1034.
6. Rovira A, León A. MR in the diagnosis and monitoring of multiple sclerosis: an overview. Eur J Radiol 2008;67(3):409-14.
7. Bakshi R, Thompson AJ, Rocca MA, Pelletier D, Dousset V, Barkhof F, Inglese M, Guttmann CR, Horsfield MA, Filippi M. MRI in multiple sclerosis: current status and future prospects. Lancet Neurol 2008 ;7(7):615-25.
8. Nielsen JM, Korteweg T, Barkhof F, Uitdehaag BM, Polman CH. Over diagnosis of multiple sclerosis and magnetic resonance imaging criteria. Ann Neurol 2005;58(5):781-3.
9. Zecca C, Cereda C, Wetzel S, Tschuor S, Staedler C, Santini F, Nadarajah N, Bassetti CL, Gobbi C. Diffusion weighted imaging in acute demyelinating myelopathy. Neuroradiology 2012;54(6):573-8.
10. Lo CP, Kao HW, Chen SY, Chu CM, Hsu CC, Chen YC, Lin WC, Liu DW, Hsu WL. Comparison of diffusion weighted imaging and contrast-enhanced T1-weighted imaging on a single baseline MRI for demonstrating dissemination in time in multiple sclerosis. BMC Neurol 2014,7;14:100.
11. Miabi Z, Midia M, Midia R, Moghinan D. Anatomical distribution of central nervous system plaques in multiple sclerosis: an Iranian experience. Pak J Biol Sci 2010;13(24):1195-201
12. Miabi Z, Hashemi H, Moghinan Hokmabad D, Samimi K. Diffusion-weighted and conventinal MRI in detection of multiple sclerosis lesion in brain : a comparative study.Tehran University Medical Journal (TUMJ)
2006;64(5):51- 65.
13. Poloni G, Minagar A, Haacke EM, Zivadinov R. Recent developments in imaging of multiple sclerosis. Neurologist 2011;17(4):185-204.
14. Filippi M, Rocca MA. MRI aspects of the “inflammatory phase” of multiple sclerosis. Neurol Sci 2003 ;24 Suppl 5:S275-8.
15. Filippi M, Rocca MA, De Stefano N, Enzinger C, Fisher E, Horsfield MA, Inglese M, Pelletier D, Comi G. Magnetic resonance techniques in multiple sclerosis: the present and the future. Arch Neurol 2011 ;68(12):1514- 20.
16. Bhatt A, Masih A, Grothous HF, Farooq MU, Naravetla B, Kassab MY. Diffusion-weighted imaging: not all that glitters is gold. South Med J 2009 ;102(9):923-8.
17. Wilson M, Morgan PS, Lin X, Turner BP, Blumhardt LD. Quantitative diffusion weighted magnetic resonance imaging, cerebral atrophy, and disability in multiple sclerosis. J Neurol Neurosurg Psychiatry 2001;70(3):318- 22.
18. Cheng GX, Wu HW, Zhang J, Liang LN, Zhang XL. MRI diagnosis of multiple cerebral sclerosis. Nan Fang Yi Ke Da Xue Xue Bao. 2008;28(8):1372-5. [Article in Chinese]

 

Childhood Epilepsy; Prognostic Factors in Predicting the Treatment Failure

Mohammad Mehdi TAGHDIRI, Mahmoud OMIDBEIGI, Sina ASAADI, Mohammad GHOFRANI

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 21-28
https://doi.org/10.22037/ijcn.v11i1.10956

How to Cite This Article: Taghdiri MM, Omidbeigi M, Asaadi S, Mohebbi M, Azarghashb E, Ghofrani M. Childhood Epilepsy; Prognostic Factors in Predicting the Treatment Failure. Iran J Child Neurol. Winter 2017; 11(1):21-28.


Abstract

Objective

We aimed to find the prognostic factors to detect the patients who fail the treatment of epilepsy, in the early stages of the disease.

Materials & Methods

This study was done on the epileptic patients attending the Neurology Clinic of Mofid Children’s Hospital, Tehran, Iran from September 2013 to October 2014. After defining the criteria for exclusion and inclusion, the patients were divided to two groups based on responding to the medical treatment for their epilepsy and indices were recorded for all the patients to be used in the statistical analyses.

Results

The patients’ age ranged from 1 to 15 yr. There was 188 patients with refractory seizure in group 1 (experimental group) and 178 patient with well controlled seizure in group 2(control group).There was a significant different between serum drug level in both groups and patients with refractory seizure group had a lower serum drug level than control group. In both groups tonic-clonic was the most common type of seizure. Also the prevalence of brain imaging Abnormalityand other neurologic disorders was significantly higher in patients with refractory seizure in compare with control group.

Conclusion

Children with seizure who suffer from refractory epilepsy need more attention and exact observation by the medical staff.

 References

 

1. Kozyrskyj AL, Prasad AN. The burden of seizures in Manitoba children: a population-based study. Can J Neurol Sci 2004;31:48-52.
2. Camfield PR, Camfield CS, Gordon Kandet al. If a first antiepileptic drug fails to control a child’s epilepsy, what are the chances of success with the next drug? J Pediatr 1997; 131:821-4.
3. Arts WF, Brouwer OF, Peters ACet al. Course and prognosis of childhood epilepsy: 5-year follow-up of the Dutch study of epilepsy in childhood. Brain 2004;127:1774–84.
4. Berg AT, Shinnar S, Levy SR, et al. Early Development of intractable epilepsy in children: a prospective study. Neurology 2001;56:1445–52.
5. Berg AT, Vickrey BG, Testa FM, et al. How long does it take for epilepsy to become intractable? A prospective investigation. Ann Neurol 2006;60:73–9.
6. Kwan P, Brodie M. Early identification of refractory epilepsy. N Eng J Med2000;342:314–9.
7. Mohanraj R, Brodie MJ. Diagnosing refractory epilepsy: response to sequential treatment schedules. Eur J Neurol 2006;13:277–82.
8. Berg A. Identification of Pharmacoresistant Epilepsy. Neurol Clin 2009;27(4):1003-1013.
9. Luciano AL, Shorvon SD. Results of treatment changes in patients with apparently drug-resistant chronic epilepsy. Ann Neurol 2007;62:375–381.
10. Carpay HA, Arts WF, GeertsAT, et al. Epilepsy in childhood: An audit of clinical practice. Arch Neurol 1998;55:668–73.
11. Dudley RW, Penney SJ, Buckley DJ. First-drug treatment failures in children newly diagnosed with epilepsy. Pediatr Neurol 2009;40:71–7.
12. Berg AT, Vickrey BG, Testa FM, et al. How long does it take epilepsy to become intractable? A prospective investigation. Ann Neurol 2006;60:73–79.
13. Spooner CG, Berkovic SF, Mitchell LA, et al. New onset temporal lobe epilepsy in children: lesion on MRI predicts poor seizure outcome. Neurology 2006;67:2147–2153.
14. Robinson RO, Baird G, Robinson Get al. Landau– Kleffner syndrome: course and correlates with outcome. Dev Med Child Neurol2001;43:243-7.
15. Berg AT, Shinnar S, Levy SR, et al. Defining early seizure outcomesin pediatric epilepsy: the good, the bad and the in-between. Epilepsy Res 2001;43:75-84.
16. Shinnar S, Berg AT. Does antiepileptic drug therapy prevent the development of ‘‘chronic’’ epilepsy? Epilepsia 1996;37:701-8.Neurol Clin 2009;27(4):1003-1013.
17. Engel J. The goal of epilepsy therapy: no seizures, no side effects,as soon as possible. CNS Spectrums 2004;9:95–97.
18. Mathern GW, Pretorius JK, Babb TL. Influence of the type ofinitial precipitating injury and at what age it occurs on courseand outcome in patients with temporal lobe seizures. J Neurosurg1995;82:220 –227.
19. Cross JH, Jaykar P, Nordli D and et al. Propose criteria for referraland evaluation of children for epilepsy surgery: recommendations of the Subcomission for Pediatric Epilepsy Surgery. Epilepsia2006;47:953–959.
20. Weiner HL, Carlson C, Ridgway EBet al. Epilepsy surgery inyoung children with tuberous sclerosis: results of a novel approach. Pediatrics 2006;117:1494 –1502.
21. Del Felice A, Beghi E, Boero G, La Neve A, Bogliun G, De Palo A, et al. Early versus late remission in a cohort of patients with newly diagnosed epilepsy. Epilepsia 2010;51(1):37-42.
22. Levy SR, Novotny EJ, Shinnar S. Predictors of intractable epilepsy in childhood: a case–control study. Epilepsia 1996;37:24–30.
23. Berg AT, Shinnar S, Levy SR and et al. Smith- Rappaport S, Beckerman B. Early development of intractable epilepsy in children: a prospective study. Neurology2001;56:1445–52.
24. Casetta I, Granieri E, Monetti VC et al. Early predictors of intractability in childhood epilepsy: a community-based
case–control study in Copparo, Italy. Acta Neurologica Scandinavica 1999;99:329–33.
25. Chawla S, Aneja S, Kashyap Ret al. Etiology and clinical predictors ofintractable epilepsy. Pediatric Neurology 2002;27:186–91.
26. Ko TS, Holmes GL. EEG and clinical predictors of medically intractable childhood epilepsy. Clin Neurophysiol 1999;110:1245–51.
27. Kwong KL, Sung WY, Wong SN, et al. Early predictors of medical intractability in childhood epilepsy. Pediatr Neurol2003;29:46–52.
28. Oskoui M, Webster RI, Zhang X and et al. Factors predictive of outcome inchildhood epilepsy. J Child Neurol 2005;20:898–904.
29. Seker Yilmaz B, Okuyaz C, Komur M. Predictors of Intractable Childhood Epilepsy. Pediatr Neurol 2013;48(1):52-55.
30. Kim S, Park K, Kim S, Kwon O, No S. Presence of epileptiform discharges on initial EEGs are associated with failure of retention on first antiepileptic drug in newly diagnosed cryptogenic partial epilepsy: A 2-year observational study. Seizure 2010;19(9):536-539.
31. Callaghan B, Anand K, Hesdorffer D, Hauser W, French J. Likelihood of seizure remission in an adult population with refractory epilepsy. Ann Neurol 2007;62(4):382- 389.
32. Arhan E, Serdaroglu A, Kurt A, Aslanyavrusu M. Drug treatment failures and effectivity in children with newly diagnosed epilepsy. Seizure 2010;19(9):553-557.

The Impact of Dynamic Seating on Classroom Behavior of Students with Autism Spectrum Disorder

Nader MATINSADR, Hojjat Allah HAGHGOO, Sayyed Ali SAMADI, Mehdi RASSAFIANI, Enayatollah BAKHSHI, Hossein HASSANABADI

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 29-36
https://doi.org/10.22037/ijcn.v11i1.11193

How to Cite This Article: Matin Sadr N, Haghgoo H, Samadi S.A, Rassafiani M, Bakhshi E, Hassanabadi H. The Impact of Dynamic Seating on Classroom Behavior of Students with Autism Spectrum Disorder. Iran J Child Neurol. Winter 2017; 11(1):29-36.

 

Abstract

Objective

Children with autism have sitting and on-task behavior problems in class. In this study, the effect of three alternative classroom-seating devices such as regular classroom chairs, therapy balls, and air cushions were examined on students’ classroom behavior.

Materials & Methods

15 students with autism participated in this A1-B-A2-C multiple treatments study from Mashhad’s Tabasom School, Mashhad, Iran in 2014. Students’ behaviors were video recorded in three phases: sitting on their common chairs during phase A, air-sit cushioned in phase B, and ball chairs in phase C. Sitting times and on-task behaviors were quantified by momentary time sampling and compared during different phases for important changes during 8 wk.

Additionally, the Gilliam Autism Rating Scale-Second Edition test was used to examine stereotyped movements, social and communication skills of the students in the before and after research.

 Results

Significant increases in in-seat behaviors in 86.7% (thirteen out of 15) of the students and on-task behaviors in 53.3% of the students (eight out of 15) when seated on therapy balls. Air cushions had no significant effects on in-seat/on-task behaviors. The results also showed significant decrease in stereotyped movement and increase in communication and social skills of these students. The teachers also preferred the use of the balls and/or air-cushioned chairs for their students.

Conclusion

Therapy ball chairs facilitated in-seat behavior and decreased autism related behavior of the students with Autism Spectrum Disorder in class.

References

1. Elsabbagh, M., Divan, G., Koh, Y. J., Kim, Y. S., Kauchali, S., Marcín, C., ... & Yasamy, M. T. Global prevalence of autism and other pervasive developmental disorders. Autism Res, 2012; 5(3): 160-179.
2. Ghanizadeh A. A preliminary study on screening prevalence of pervasive developmental disorder in school children in Iran. J Autism Dev Disord 2008; 38(4):759- 63.
3. Ivory DM. The Impact of Dynamic Furniture on Classroom Performance: A Pilot Study: University of Puget Sound; 2011.
4. Dunn W. The sensations of everyday life: Empirical, theoretical, and pragmatic considerations. Am J Occup Ther 2001;55(6):608-20.
5. Schilling DL, Schwartz IS. Alternative seating for young children with autism spectrum disorder: Effects on classroom behavior. J Autism Dev Disord 2004;34(4):423- 32.
6. Dunn WW. Habit: What’s the Brain Got To Do with It? OTJR 2000;20(1):6S-20S.
7. Ayres A. Sensory integration and learning disabilities. Los Ángeles: WPS 1972:474-89.
8. Schaaf RC, Hunt J, Benevides T. Occupational Therapy Using Sensory Integration to Improve Participation of a Child With Autism. Am J Occup Ther 2012 Sep- Oct;66(5):547-55.
9. Tunstall H.R. Effects of Alternative Seating on the Academic Engagement of Children With Autism: East Carolina University; 2010.
10. Bagatell N, Mirigliani G, Patterson C, Reyes Y, Test L. Effectiveness of therapy ball chairs on classroom participation in children with autism spectrum disorders. Am J Occup Ther 2010;64(6):895-903.
11. Hemmingson H, Borell L. Environmental barriers in mainstream schools. Child Care Health Dev 2002;28(1):57-63.
12. Fedewa A, Davis MA, Ahn S. Effects of stability balls on children’s on-task behavior, academic achievement, and discipline referrals: a randomized controlled trial. Am J Occup Ther 2015;69(2):6902220020p1-p9.
13. Winkler, Charlotte A. The Graduate School Univel’sity of Wisconsin-Stout Menomonie, WI: University of Wisconsin; 2010.
14. Pfeiffer B, Henry A, Miller S, Witherell S. Effectiveness of disc ‘o’sit cushions on attention to task in second-grade students with attention difficulties. Am J Occup Ther 2008;62(3):274-81.
15. Fedewa AL, Erwin HE. Stability Balls and Students With Attention and Hyperactivity Concerns: Implications for On-Task and In-Seat Behavior. Am J Occup Ther 2011;65(4):393-9.
16. Schilling DL. Alternative seating devices for children with ADHD: Effects on classroom behavior. Pediatr Phys Ther 2006;18(1):81.
17. Samadi SA, McConkey R. The utility of the Gilliam autism rating scale for identifying Iranian children with autism. Disabil Rehabil 2014;36(6):452-6.
18. Kuhn D, Lewis S. The Effect of Dynamic Seating on Classroom Behavior for Students in a General Education Classroom. 2013. http://soundideas.pugetsound.edu/cgi/
viewcontent.cgi?article=1079&context=ms_occ_therapy
19. Schilling DL, Washington K, Billingsley FF, Deitz J. Classroom seating for children with attention deficit hyperactivity disorder: Therapy balls versus chairs. Am J Occup Ther 2003;57(5):534-41.
20. Hodgetts S, Hodgetts W. Somatosensory stimulation interventions for children with autism: Literature review and clinical considerations. Can J Occup Ther 2007;74(5):393-400.
21. Watling RL, Dietz J. Immediate effect of Ayres’s sensory integration–based occupational therapy intervention on children with autism spectrum disorders. Am J Occup Ther 2007;61(5):574-83.
22. Gamache-Hulsmans G. Stability Ball use in the Classroom Affect on On Task Behaviour and Handwriting Written By: Ginette Gamache-Hulsmans Banff Elementary School May 03, 2007.
23. Greenspan SI, Wieder S. Developmental patterns and outcomes in infants and children with disorders in relating and communicating: A chart review of 200 cases of children with autistic spectrum diagnoses. J Dev Learn Disord 1997;1:87-142.
24. Umeda C, Deitz J. Effects of therapy cushions on classroom behaviors of children with autism spectrum disorder. Am J Occup Ther 2011;65(2):152-9.
25. Samadi, S. A., & McConkey, R.. Screening for autism in Iranian preschoolers: Contrasting M-CHAT and a scale developed in Iran. J. Autism Dev. Disord 2015; 45(9), 2908-2916.
26. Samadi, S. A., Mohammad, M. P., Ghanimi, F., & McConkey, R. The challenges of screening pre-school children for autism spectrum disorders in Iran. Disabil. Rehabil, 2016; 1-9.


Morphological Changes of Anterior Cerebral Artery (ACA) in Hydrocephalic Pediatric Patients

Sait OZTURK, Erdogan AYAN, Metin KAPLAN

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 37-42
https://doi.org/10.22037/ijcn.v11i1.11167

How to Cite This Article: Ozturk S, Ayan E, Kaplan M. Morphological Changes of Anterior Cerebral (ACA) Artery in Hydrocephalic Pediatric Patients. Iran J Child Neurol. Winter 2017; 11(1):37-42.

 

Abstract

Objective

The morphology of anterior cerebral artery (ACA) in patients with hydrocephalus (HCP) was analyzed, and its importance was discussed in maintaining cerebral perfusion.

Materials & Methods

A total of 84 cases in 2 groups between 0 and 3 months, followed-up at Firat Universitesi Hastanesi, Beyin Cerrahisi Klinigi, Elazig, Turkiye due to in 2010-2013, were enrolled. Two groups were created for the study. Group 1; patients with HCP and Group 2; as control group without HCP. In both groups, the length of the A2 segment of ACA was measured from its origin to the junction of the genu and body portions of the corpus callosum on T2 mid-sagittal magnetic resonance (MR) scans. For all cases, axial MR imaging scans were used to calculate Evans’ index (EI), and the cases were divided into three groups: Group A, EI ≥50%; Group B, EI of 40-50% and Group C, EI <40%. The two groups (Groups 1 and 2) were compared with respect to ACA length, and the correlation with the EI was quantified. P values below 0.05 were considered statistically significant.

Results

Mean length of ACA was 57.3 mm in Group 1 and 37.5 mm in Group 2. EI increased as the length of ACA increased. A statistical comparison of the two groups revealed that the ACA length was significantly greater in Group 1. The relationship between EI and ACA length was statistically significant.

Conclusion

Reducing ventricular size appears to be an important factor in addition to reducing intracranial pressure in an attempt to maintain normal cerebral perfusion(CP).

References

1. Westra SJ, Lazareff J, Curran JG, Sayre JW, Kawamoto H Jr. Transcranial Doppler ultrasonography to evaluate need for cerebrospinal fluid drainage in hydrocephalic children. J Ultrasound Med 1998; 17): 561-569.
2. Kolarovszki B, Zubor P, Kolarovszka H, Benco M, Richterova R, Matasova K. The assessment of intracranial dynamics by transcranial Doppler sonography in perioperative period in paediatric hydrocephalus. Arch Gynecol Obstet 2013; 287: 229-238.
3. Tritton DJ. Fluid Mechanics. Physical fluid Dynamics. Tritton, DJ: 2nd ed. Oxford, Clarendon Press 1988; pp:536-540.
4. de Oliveira RS, Machado HR. Transcranial color-coded Doppler ultrasonography for evaluation of children with hydrocephalus. Neurosurg Focus 2003; 15: ECP3.
5. Kempley ST, Gamsu HR. Changes in cerebral artery blood flow velocity after intermittent cerebrospinal fluid drainage. Arch Dis Child 1993; 69: 74-76.
6. Hanlo PW, Gooskens RH, Nijhuis IJ, Faber JA, Peters RJ, van Huffelen AC and et al. Value of transcranial Doppler indices in predicting raised ICP in infantile hydrocephalus. A study with review of the literature. Childs Nerv Syst 1995; 11: 595-603.
7. Nishimaki S, Yoda H, Seki K, Kawakami T, Akamatsu H, Iwasaki Y. Cerebral blood flow velocities in the anterior cerebral arteries and basilar artery in hydrocephalus before and after treatment. Surg Neurol 1990; 34: 373- 377.
8. Wang B, Cheng Z, Mu X, Fan B, Guo Z. Preoperative and postoperative transcranial Doppler sonographic evaluations of the cerebral hemodynamics of craniostenosis. J Craniofac Surg 2010; 21: 432-435.
9. Bell SR, Vo AH, Armanda RA. Applied neurovascular anatomy of the brain and skull. In: Hurst RW, Rosenwasser RH, editors. Interventional Neuroradiology. New York: Informa; 2008: pp: 22-27.
10. Kaplan M, Berilgen MS, Erol FS, Artas H, Serhatlioglu S, Ozveren MF. Relationship between Clinical Grade, Cerebral Blood Flow, and Electroencephalographic Alterations in Patients with Chronic Subdural Hemorrhage. Neurosurgery Q 2006; 16: 157-160.
11. Riggo JD, Kolarovszki B, Richterova R, Kolarovszka H, Sutovsky J, Durdikc P. Measurement of the blood flow velocity in the pericallosal artery of children with hydrocephalus by transcranial Doppler ultrasonography-preliminary results. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2007; 151: 285-289.
12. Zenger MN, Kabataş S, Zenger S, Cakmakçi H. The value of power Doppler ultrasonography in the differential diagnosis of intracranial extraaxial fluid collections. Diagn Interv Radiol. 2007; 13: 61-63.
13. Kaplan M, Erol FS, Bozgeyik Z, Koparan M: The effectiveness of simple drainage technique in improvement of cerebral blood flow in patients with chronic subdural hemorrhage. Turk Neurosurg 2007; 17: 202-206.
14. Rozenfeld A. Ultrasound in diagnostics of blood vessels: the role of the assessment of both extra- and intracranial flows by Doppler ultrasonography. Neurol Neurochir Pol 1994; 28: 51-66.
15. Miller SP, Cozzio CC, Goldstein RB, Ferriero DM, Partridge JC, Vigneron DB and et al. Comparing the diagnosis of white matter injury in premature newborns with serial MR imaging and transfontanel ultrasonography findings. AJNR Am J Neuroradiol 2003; 24: 1661-1669.


Frequency and Causes of Hypotonia in Neonatal Period with the Gestational Age of More Than 36 Weeks in NICU of Mofid Children Hospital, Tehran, Iran During 2012-2014

Nosratollah SEYED SHAHABI, Hossain FAKHRAEE, Mohammad KAZEMIAN, Abolfazl AFJEH, Minoo FALLAHI, Maryam SHARIATI, Fatemeh GORJI

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 43-49
https://doi.org/10.22037/ijcn.v11i1.10989

How to Cite This Article: Seyed Shahabi N, Fakhraee H, Kazemian M, Afjeh A, Fallahi M, Shariati M, Gorji F. Frequency and Causes of Hypotonia in Neonatal Period with the Gestational Age of More Than 36 Weeks in NICU of Mofid Children Hospital, Tehran, Iran During 2012-2014. Iran J Child Neurol. Winter 2017; 11(1):43-49.

 

Abstract

Objective

Hypotonia is a serious neurologic problem in neonatal period. Although hypotonia is a nonspecific clinical finding but it is the most common motor disorder in the newborn. The objective of this study was to determine the frequency of neonatal hypotonia then to ascertain of the most common causes.

Materials & Methods

This cross –sectional prospective study was carried out on the 3281 term infants hospitalized in conventional and NICU of Mofid Children Hospital, Tehran, Iran during 2012-2014. Diagnosis was made by history, physical & neurological examination and accessible diagnostic tests.

Results

Fifty nine hypotonic neonates were identified, forty seven (79.66%) had central hypotonia (Hypoxic ischemic encephalopathy (n= 2), other causes of encephalopathy (n=2), intracranial hemorrhage (n=4), CNS abnormalities (n= 7), chromosomal disorders (n=4), syndromic–nonsyndromic (n=8), and metabolic diseases (n=8). Peripheral hypotonic recognized in 6 infants (10.17%); spinal muscular atrophy (n= 1), and myopathy (n= 5). Six cases (10.17%) remained unclassified. Twelve infants had transient hypotonia. In final study, 18 of 59 infants (30%) died, nearly 90% before one year of age. Twenty-eight (47%) infants found developmental disorders and only 13 (22%) infants achieved normal development in their follow up.

Conclusion

Neonatal hypotonia is a common event in neonatal period. A majority of diagnosis is obtained by history and physical examination. Neuroimaging, genetic and metabolic tests were also important in diagnosis. Genetic, syndromic–nonsyndromic, and metabolic disorders were the most causes of neonatal hypotonia.

References

1.Miller VS, Delgado M, Iannaccone ST. Neonatal hypotonia Seminar in neurology 1993; 13 (1):73-83.
2. Laugal V, Cossee M, MJ. de Saint –Martin A, Echaniz- Laguna A, Mandel JL, Astruc D, Messer FMJ. Diagnostic approach to neonatal hypotonia: retrospective study on144neonates.Eur J Pediatr 2008; 167:517-523.
3. Birdi K, Prasad C, Chodirker B, Chudly AE, The floppy infant: retrospective analysis of clinical experience (1990-2000) in a tertiary care facility. J Chlid Neurol 2005; 20: 803-808.
4. Johnston HM.The floppy weak infant revisited. Brain Dev 2003; 25:55-58.
5. Crawford TO. Clinical Evaluation of the Floppy infant. Pediatric Annal 1992;16:348-354.
6. Richer LP, Shevell MI, Miller SP. Diagnostic profile of neonatal hypotonia; An 11 year study. Peditric Neurol 2001; 25:32-37.
7. Paro–Panjan D. Congenital hypotonia is there an algorithm. J Child Neurology 2004;19 (6):439-442.
8. Griggs RC, Mendell JR, Miller RG. Cngenital myopathies.in: Evaluation and treatment of myopathies. Philadelphia:FA Davis C; 1995:211-46
9. Nada Zadeh and Louanne Hudgings. The Genetic Approach to hypotonia in the neonate. NeoReviews 2009; 10; e600-e607.
10. Bodenstiener JB. The evaluation of the hypotonic infant Seminar in PediatricNeurology 2008;15:10-20.
11. Dubowitz V. Thomas NH. The natural history of type 1(severe) spinal muscular dystrophy. Neuromuscular Disord. 1994;4:497-50212.
12. Jimenez E, Garcia – Cazoria A, Colomer J, Nascimento A, Ieiondo M, Compistol J. Hypotonia in the neonatal period: 12 years experience.[Article in Spanish] Rev Neurol 2013 Jan16:56 (2):72-8.


A Psychometric Study of the Bayley Scales of Infant and Toddler Development in Persian Language Children

Nadia AZARI, Farin SOLEIMANI, Roshanak VAMEGHI, Firouzeh SAJEDI, Soheila SHAHSHAHANI, Hossein KARIMI, Adis KRASKIAN, Amin SHAHROHI, Robab TEYMOURI, Masoud GHARIB

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 50-56
https://doi.org/10.22037/ijcn.v11i1.12056

How to Cite This Article: Azari. N, Soleimani F, Vameghi R, Sajedi F, Shahshahani S, Karimi H, Kraskian A, Shahrokhi A, Teymouri R, Gharib M. A Psychometric Study of the Bayley Scales of Infant and Toddler Development in Persian Language Children. Iran J Child Neurol. Winter 2017; 11(1):50-56.

Abstract

Objective

Bayley Scales of infant & toddler development is a well-known diagnostic developmental assessment tool for children aged 1–42 months. Our aim was investigating the validity & reliability of this scale in Persian speaking children.

Materials & Methods

The method was descriptive-analytic. Translation- back translation and cultural adaptation was done. Content & face validity of translated scale was determined by experts’ opinions. Overall, 403 children aged 1 to 42 months were recruited from health centers of Tehran, Iran during years of 2013- 2014 for developmental assessment in cognitive, communicative (receptive & expressive) and motor (fine & gross) domains. Reliability of scale was calculated through three methods; internal consistency using Cronbach’s alpha coefficient, test-retest and interrater methods. Construct validity was calculated using factor analysis and comparison of the mean scores methods.

Results

Cultural and linguistic changes were made in items of all domains especially on communication subscale. Content and face validity of the test were approved by experts’ opinions. Cronbach’s alpha coefficient was above 0.74 in all domains.

Pearson correlation coefficient in various domains, were ≥ 0.982 in test retest method, and ≥0.993 in inter-rater method. Construct validity of the test was approved by factor analysis. Moreover, the mean scores for the different age groups were compared and statistically significant differences were observed between mean scores of different age groups, that confirms validity of the test.

Conclusion

The Bayley Scales of Infant and Toddler Development is a valid and reliable tool for child developmental assessment in Persian language children.

References

1. Boyle CA, Boulet S, Schieve LA, Cohen RA, Blumberg SJ, Yeargin-Allsopp M, et al. Trends in the prevalence of developmental disabilities in US children, 1997–2008. Pediatrics 2011:peds. 2010-989.
2. Sajedi F, Doulabi MA, Vameghi R, Baghban AA, Mazaheri MA, Mahmodi Z, et al. Development of Children in Iran: A Systematic Review and Meta-Analysis. Glob J Health Sci 2015 Dec 18;8(8):51251.
3. Soleimani F, Vameghi R, Biglarian A, Rahgozar M. Prevalence of motor developmental disorders in children in Alborz Province, Iran in 2010. Iran Red Crescent Med J 2014 Dec 25;16(12):e16711.
4. Soleimani F, Vameghi R, Biglarian A. Antenatal and Intrapartum Risk Factors for Cerebral Palsy in Term and Near-term Newborns. Arch Iran Med 2013;16(4): 213 – 216.
5. Soleimani F, Vameghi R, Biglarian A, Daneshmandan N : Risk factors Associated with Cerebral Palsy in Children Born in Eastern and Northern Districts of Tehran. Iran Red Crescent Med J 2010; 12 (4):428-432.
6. Fischer VJ, Morris J, Martines J. Developmental Screening Tools: Feasibility of Use at Primary Healthcare Level in Low-and Middle-income Settings. J Health Popul Nutr 2014 Jun;32(2):314-26.
7. Blauw-Hospers CH, Hadders-Algra M. A systematic review of the effects of early intervention on motor development. Dev Med Child Neurol 2005 Jun;47(6):421-32.
8. Nordhov SM, Ronning JA, Dahl LB, Ulvund SE, Tunby J, Kaaresen PI. Early intervention improves cognitive outcomes for preterm infants: randomized controlled trial. Pediatrics 2010 Nov;126(5):e1088-94.
9. Bailey DB, Jr., Hebbeler K, Scarborough A, Spiker D, Mallik S. First experiences with early intervention: a national perspective. Pediatrics 2004 Apr;113(4):887-96.
10. Raju TN, Higgins RD, Stark AR, Leveno KJ. Optimizing care and outcome for late-preterm (near-term) infants: a summary of the workshop sponsored by the National Institute of Child Health and Human Development. Pediatrics 2006;118(3):1207-14.
11. First LR, Palfrey JS. The infant or young child with developmental delay. N Engl J Med 1994 Feb 17;330(7):478-83.
12. Dobrez D, Sasso AL, Holl J, Shalowitz M, Leon S, Budetti P. Estimating the cost of developmental and behavioral screening of preschool children in general pediatric practice. Pediatric 2001;108(4):913-22.
13. Torras-Mana M, Guillamon-Valenzuela M, Ramirez-Mallafre A, Brun-Gasca C, Fornieles-Deu A. Usefulness of the Bayley scales of infant and toddler development, third edition, in the early diagnosis of language disorder. Psicothema 2014;26(3):349-56.
14. Gladstone M, Lancaster GA, Jones A, Maleta K, Mtitimila E, Ashorn P, et al. Can Western developmental screening tools be modified for use in a rural Malawian setting? Arch Dis Child. 2008 Jan;93(1):23-9.
15. Lipkin PH, Cartwright JD, Desch LW, Duby JC, Elias ER, Johnson CP, et al. Role of the medical home in family-centered early intervention services. Pediatrics 2007;120(5):1153-8.
16. Johnson S, Marlow N. Developmental screen or developmental testing? Early Hum Dev 2006 Mar;82(3):173-83.
17. Vameghi R, Sajedi F, Kraskian Mojembari A, Habiollahi A, Lornezhad HR, Delavar B. Cross-Cultural Adaptation, Validation and Standardization of Ages and Stages Questionnaire (ASQ) in Iranian Children. Iran J Public Health 2013 May 1;42(5):522-8.
18. Shahshahani S, Vameghi R, Azari N, Sajedi F, Kazemnejad A. Validity and Reliability Determination of Denver Developmental Screening Test-II in 0-6 Year-Olds in Tehran. Iran J Pediatr 2010 Sep;20(3):313-22.
19. Abubakar A, Holding P, Van Baar A, Newton C, van de Vijver FJ. Monitoring psychomotor development in a resourcelimited setting: an evaluation of the Kilifi Developmental Inventory. Ann Trop Paediatr 2008 Sep;28(3):217-26.
20. Harris SR, Megens AM, Backman CL, Hayes VE. Stability of the Bayley II Scales of Infant Development in a sample of low-risk and high-risk infants. Dev Med Child Neurol 2005 Dec;47(12):820-3.
21. Albers CA, Grieve AJ. Review of Bayley Scales of Infant and Toddler Development. J Psychoeduc Assess 2007 Jun;25(2):180-190. DOI: 10.1177/0734282906297199.
22. Godamunne P, Liyanage C, Wimaladharmasooriya N, Pathmeswaran A, Wickremasinghe AR, Patterson C, et al. Comparison of performance of Sri Lankan and US children on cognitive and motor scales of the Bayley scales of infant development. BMC Res Notes 2014 May 16;7:300.
23. Deroma L, Bin M, Tognin V, Rosolen V, Valent F, Barbone F, et al. [Interrater reliability of the Bayley III test in the Italian Northern-Adriatic Cohort II]. Epidemiol Prev 2013 Jul-Oct;37(4-5):297-302.
24. Zakaria S, Seok CB, Sombuling A, Ahmad MS, Hashmi SI. Reliability and Validity for Malay Version of Bayley Scales of Infant and Toddler Development-(Bayley- III): Preliminary Study. International Proceedings of Economics Development & Research 2012;40.
25. Yu YT, Hsieh WS, Hsu CH, Chen LC, Lee WT, Chiu NC, et al. A psychometric study of the Bayley Scales of Infant and Toddler Development - 3rd Edition for term and preterm Taiwanese infants. Res Dev Disabil 2013 Nov;34(11):3875-83.
26. Acton BV, Biggs WS, Creighton DE, Penner KA, Switzer HN, Thomas JHP, et al. Overestimating neurodevelopment using the Bayley-III after early complex cardiac surgery. Pediatrics 2011 Oct;128(4):e794-800.
27. Anderson PJ, De Luca CR, Hutchinson E, Roberts G, Doyle LW. Underestimation of developmental delay by the new Bayley-III Scale. Arch Pediatr Adolesc Med 2010 Apr;164(4):352-6.
28. Campbell SK, Zawacki L, Rankin KM, Yoder JC, Shapiro N, Li Z, et al. Concurrent validity of the TIMP and the Bayley III scales at 6 weeks corrected age. Pediatr Phys Ther 2013 Winter;25(4):395-401.
29. Visser L, Ruiter SAJ, Van der Meulen BF, Ruijssenaars WAJJM, Timmerman ME. Validity and suitability of the Bayley-III Low Motor/Vision version: A comparative study among young children with and without motor and/or visual impairments. Res Dev Disabil 2013 Nov;34(11):3736-45.
30. Soleimani F, Azari N, Vameghi R, Sajedi F, Shahshahani S, Karimi H, Kraskian A, Shahrokhi A, Teymouri R, Gharib M. Is the Bayley Scales of Infant and Toddler Developmental Screening Test, valid and reliable for Persian speaking children? Iran J Pediatr 2016 October; 26(5):83-90.


Inter and Intra Rater Reliability of the 10 Meter Walk Test in the Community Dweller Adults with Spastic Cerebral Palsy

Fariba BAHRAMI, Shohreh NOORIZADEHDEHKORDI, Mehdi DADGOO

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 57-64
https://doi.org/10.22037/ijcn.v11i1.9669

How to Cite This Article: Bahrami F, Noorizadeh Dehkordi SH, Dadgoo M. Inter and Intra Rater Reliability of the 10 Meter Walk Test in the Community Dweller Adults with Spastic Cerebral Palsy. Iran J Child Neurol.Winter 2017; 11(1): 57-64.

 

Abstract

Objective

We aimed to investigation the intra-rater and inter-raters reliability of the 10 meter walk test (10 MWT) in adults with spastic cerebral palsy (CP).

Materials&Methods

Thirty ambulatory adults with spastic CP in the summer of 2014 participated (19 men, 11 women; mean age 28 ± 7 yr, range 18- 46 yr). Individuals were non-randomly selected by convenient sampling from the Ra’ad Rehabilitation Goodwill Complex in Tehran, Iran. They had GMFCS levels below IV (I, II, and III). Retest interval for inter-raters study lasted a week. During the tests, participants walked with their maximum speed. Intra class correlation coefficients (ICC) estimated reliability.

Results

The 10 MWT ICC for intra-rater was 0.98 (95% confidence interval (CI) 0.96-0.99) for participants, and >0.89 in GMFCS subgroups (95% confidence interval (CI) lower bound>0.67). The 10 MWT inter-raters’ ICC was 0.998 (95% confidence interval (CI) 0/996-0/999), and >0.993 in GMFCS subgroups (95% confidence interval (CI) lower bound>0.977). Standard error of the measurement (SEM) values for both studies was small (0.02< SEM< 0.07).

Conclusion

Excellent intra-rater and inter-raters reliability of the 10 MWT in adults with CP, especially in the moderate motor impairments (GMFCS level III), indicates that this tool can be used in clinics to assess the results of interventions.

References

1. Bottos M, Feliciangeli A, Sciuto L, Gericke C, Vianello A. Functional status of adults with cerebral palsy and implications for treatment of children. Dev Med Child Neurol 2001; 43:516-28.
2. Andersson C, Mattsson E. Adults with cerebral palsy: a survey describing problems, needs, and resources, with special emphasis on locomotion. Dev Med Child Neurol 2001; 43:76-82.
3. Murphy KP, Molnar GE, Lankasky K. Medical and Functional Status of Adults with Cerebral Palsy. Dev Med Child Neurol 1995; 37:1075-84.
4. Rapp Jr CE, Torres MM. The adult with cerebral palsy. Arch Family Med 2000; 9:466.
5. Peters DM, Fritz SL, Krotish DE. Assessing the reliability and validity of a shorter walk test compared with the 10-meter walk test for measurements of gait speed in healthy, older adults. J Geriatr Phys Ther 2013; 36:24-30.
6. Fritz S, Lusardi M. White paper:“walking speed: the sixth vital sign”. J Geriatr Phys Ther 2009; 32:2-5.
7. Lord SE, McPherson K, McNaughton HK, Rochester L, Weatherall M. Community ambulation after stroke: how important and obtainable is it and what measures appear predictive? Arch Phys Med Rehabil 2004; 85:234-9.
8. Maki BE. Gait changes in older adults: predictors of falls or indicators of fear. J Am Geriatr Soc 1997; 45:313-20.
9. Tyson S, Connell L. The psychometric properties and clinical utility of measures of walking and mobility in neurological conditions: a systematic review. Clin Rehabil 2009; 23:1018-33.
10. Bohannon RW. Comfortable and maximum walking speed of adults aged 20—79 years: reference values and determinants. Age Ageing 1997; 26:15-9.
11. Judith G, Claudia L, Hubertus VH. Test-retest reliability of gait parameters in children with neurological gait disorders. International Neurorehabilitation Symposium 2013, Science City, ETH Zurich.
12. Watson MJ. Refining the ten-metre walking test for use with neurologically impaired people. Physiotherapy
2002; 88:386-97.
13. van Loo MA, Moseley AM, Bosman JM, de Bie RA, Hassett L. Test-re-test reliability of walking speed, step length and step width measurement after traumatic brain injury: a pilot study. Brain Inj 2004 Oct; 18:1041-8.
14. Steffen T, Seney M. Test-retest reliability and minimal detectable change on balance and ambulation tests, the 36-item short-form health survey, and the unified Parkinson disease rating scale in people with parkinsonism. Phys Ther 2008 Jun; 88:733-46.
15. Pirpiris M, Wilkinson AJ, Rodda J, Nguyen TC, Baker RJ, Nattrass GR, et al. Walking speed in children and young adults with neuromuscular disease: comparison between two assessment methods. J Pediatr Orthop 2003 May-Jun; 23:302-7.
16. Collen FM, Wade DT, Bradshaw CM. Mobility after stroke: reliability of measures of impairment and disability. Int Disability Stud 1990 Jan-Mar; 12 :6-9.
17. Bowden MG, Behrman AL. Step Activity Monitor: accuracy and test-retest reliability in persons with incomplete spinal cord injury. J Rehabil Res Dev 2007; 44:355-62.
18. Scivoletto G, Tamburella F, Laurenza L, Foti C, Ditunno J, molinari M. Validity and Reliability of the 10-m walk test and the 6 min walk test in spinal cord injury patients. Spinal Cord 49:736-40.
19. Thompson P, Beath T, Bell J, Jacobson G, Phair T, Salbach NM, et al. Test-retest reliability of the 10 meter fast walk test and 6 minute walk test in ambulatory school aged children with cerebral palsy. Dev Med Child Neurol 2008;50:370-6.
20. Palisano R, Rosenbaum P, Walter S, Russell D, Wood E, Galuppi B. Development and reliability of a system to classify gross motor function in children with cerebral palsy. Dev Med Child Neurol 1997; 39:214-23.
21. Graham JE, Ostir GV, Fisher SR, Ottenbacher KJ. Assessing walking speed in clinical research: a systematic review. J Eval Clin Pract 2008; 14:552-62.
22. Portney LG, Watkins MP. Foundations of clinical research: applications to practice, FA Davis; 2015 Mar 18. 23. Stratford PW.Getting more from the literature: estimating the standard error of measurement from reliability studies. Physiother Can 2004; 56: 27-30.
24. Bland JM, Altman DG. Statistic and random error in repeated measurements of temporal and distance parameters of gait after stroke. Arch Phys Med Rehabil 1997; 78: 725-29.
25. Wolf S, Catlin P, Gage K, Gurucharri K, et al. Establishing the reliability and validity of measurements of walking time using the Emory Functional Ambulation Profile. Phys ther 1999; 79:1122-33.


Feasible Relation between Glutathione Peroxidase and Febrile Seizure

Abolfazl MAHYAR, Parviz AYAZI, Reza DALIRANI, Behzad MOHAMMAD HOSEINI, Mohammad Reza SAROOKHANI, Amir JAVADI, Shiva ESMAEILY

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 65-69
https://doi.org/10.22037/ijcn.v11i1.11458

How to Cite This Article: Mahyar A, Ayazi P, Dalirani R, Mohammad Hoseini B, Sarookhani MR, Javadi A, Esmaeily Sh. Feasible Relation between Glutathione Peroxidase and Febrile Seizure. Iran J Child Neurol. Winter 2017; 11(1):65-69.

Abstract

Objective

We aimed to determine the relationship between serum glutathione peroxidase and febrile seizure.

Materials & Methods

In this case-control study, 43 children with simple febrile seizure (case group) were compared with 43 febrile children without seizure (control group) in terms of serum glutathione peroxidase level, measured by ELISA method. This study was conducted in Qazvin Children Hospital, Qazvin University of Medical Sciences in Qazvin, Iran in 2012-2013. The results were analyzed and compared in two groups.

Results

From 43 children 24 (53%) were male and 19 (47%) were female in children with simple febrile seizure, and 26 (60%) were male and 17 (40%) were female in febrile children without seizure (control group) (P=0.827). Serum glutathione peroxidase level was 166 U/ml (SD=107) in the case group and 141 U/ml (SD=90.5) in the control group of no significant difference.

Conclusion

There was no significant relationship between serum glutathione peroxidase and simple febrile seizure. Thus, it seems that glutathione peroxidase, an essential component of antioxidant system, does not play any role in the pathogenesis of simple febrile seizure.

References

1. Duffner PK, Baumann RJ, Berman P, Green JL, Schneider S, Hodgson ES, etal. Febrile seizures: clinical practice guideline for the long-term management of the child with simple febrile seizures. Pediatrics 2008 ;121:1281-6.Midline doi: 10.1542/peds.2008-0939.
2.Shinnar S. Febrile seizures. In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice. 4th ed. Philadelphia: Mosby, 2006:1079-86.
3. Mikati M A. Febrile seizures.In: Kliegman RM, Stanton B F, GemeIII J WS, Schor NF , Behrman RE. Nelson textbook of pediatrics.19th ed. Philadelphia: Saunders, 2011:2017-19.
4. Hara K, Tanabe T, Aomatsu T, Inoue N, Tamaki H, Okamoto N ,etal. Febrile seizures associated with influenza A. Brain and Development 2007;29: 30-38.
5. Sugai K.Current management of febrile seizures in Japan: An overview . Brain and Development 2010; 32: 64-7. Midline doi: 10.1016/j.braindev.2009.09.019.
6. Camfield P, Camfield C, Kurlemann G. Febrile seizures, epileptic syndromes in infancy, childhood, and adolescence. 3th ed. London: John Libbey & Co Ltd,2002:145–52.
7. Sapir D, Leitner Y, Harel S, Kraumer U. Unprovoked seizures after complex febrile convulsions. Brain Dev 2000; 22:484–6.
8. Kumari PL, Nair MK, Nair SM, Kailas L, Geetha S. Iron deficiency as a risk factor for simple febrile seizures--a case control study. Indian Pediatr 2012; 49:17-9.
9. Tutuncuoglu S, Kutukculer N, Kepe L, Coker C, Berdeli A, Tekgul H. Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions. Pediatr Int 2001;43:235-9.
10. Ashrafi MR, Shams S, Nouri M, Mohseni M, Shabanian R, Yekaninejad MS, etal. A probable causative factor for an old problem: selenium and glutathione peroxidase appear to play important roles in epilepsy pathogenesis. Epilepsia 2007 ;48:1750-5.
11. Willmore IJ, Rubin JJ. Antiperoxidant pretreatment and iron-induced epileptiform discharges in the rat: EEG and histopathologic studies. Neurology1981; 31:63–69.
12.Irshad M, Chaudhuri PS. Oxidant-antioxidant system: role and significance in human body. Indian J Exp Biol 2002 ;40:1233-9.
13.Rayman MP.The importance of selenium to human health. Lancet 2000;356:233-41.
14.Patel M. Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures. Free Radical Biology & Medicine 2004;37:1951–1962.
15.Li-Ping L, Patel M. Seizure induced changes in mitochondrial redox status. Free Radical Biology & Medicine 2006;40:316–322.
16. Weber GF, Maertens P, Meng XZ, Pippenger CE. Glutathione peroxidase deficiency and childhood seizures. Lancet 1991 15; 337:1443-4.
17. Sudha K, Rao AV, Rao A. Oxidative stress and antioxidants in epilepsy. Clin Chim Acta 2001; 303:19-24.
18. Verrotti A, Basciani F, Trotta D, Pomilio MP, Morgese G, Chiarelli F.Serum Copper, Zinc, Selenium, Glutathione peroxidase and Superoxide dismutase levels in epileptic children before and after 1 year of sodium valproate and carbamazepine therapy. Epilepsy Res 2002;48:71-5.
19. Ben-Menachem E. Kyllerman M, Marklund S. Superoxide dismutase and glutathione peroxidase function in progressive myoclonus epilepsies. Epilepsy Res 2000;40:33-9.
20. Turkdogan D, Toplan S, Karakoc Y. Lipid peroxidation and antioxidative enzyme activities in childhood epilepsy. J Child Neurol 2002; 17:673-6.
21.Naziroglu M, Kutluhan S, Yilmaz M. Selenium and topiramate modulates brain microsomal oxidative stress values, Ca2+-ATPase activity, and EEG records in pentylenetetrazol-induced seizures in rats. J Membr Biol 2008;225:39-49.
22.Naziroglu M. Role of selenium on calcium signaling and oxidative stress-induced molecular pathways in epilepsy. Neurochem Res 2009; 34:2181-91.Medline doi: 10.1007/s11064-009-0015-8.
23.Brigelius-Flohé R, Maiorino M.Glutathione peroxidases. Biochim Biophys Acta 2013 ;1830:3289-303.
24. Harapin I, Bauer M, Bedrica L, Potoanjak D. Correlation between gluthathione peroxidase activity and the quantity of selenium in the whole blood of beef calves. Acta Vet Brno 2000; 69: 87–92.Medline. doi: 10.1016/j.bbagen.2012.11.020.
25.Koller LD, South PJ, Exon JH, Whitbeck GA, Maas J. Comparison of selenium levels and glutathione peroxidase activity in bovine whole blood. Can J Comp Med 1984 ;48:431-3.


Association of a Novel Nonsense Mutation in KIAA1279 with Goldberg-Shprintzen Syndrome

Shadab SALEHPOUR, Feyzollah HASHEMI-GORJI, Ziba SOLTANI, Soudeh GHAFOURI-FARD, Mohammad MIRYOUNESI

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 70-74
https://doi.org/10.22037/ijcn.v11i1.12498

How to Cite This Article: Salehpour Sh, Hashemi-Gorji F, Soltani Z, Ghafouri-Fard S, Miryounesi M. Association of a Novel Nonsense Mutation in KIAA1279 with Goldberg-Shprintzen Syndrome. Iran J Child Neurol. Winter 2017; 11(1):70-74.

Abstract

Goldberg-Shprintzen syndrome (OMIM 609460) (GOSHS) is an autosomal recessive multiple congenital anomaly syndrome distinguished by intellectual disability, microcephaly, and dysmorphic facial characteristics. Most affected individuals also have Hirschsprung disease and/or gyral abnormalities of the brain. This syndrome has been associated with KIAA1279 gene mutations at 10q22.1. Here we report a 16 yr old male patient referred to Center for Comprehensive Genetic Services, Tehran, Iran in 2015 with cardinal features of GOSHS in addition to refractory seizures. Whole exome sequencing in the patient revealed a novel nonsense (stop gain) homozygous mutation in KIAA1279 gene (KIAA1279: NM_015634:exon6:c.C976T:p.Q326X).

Considering the wide range of phenotypic variations in GOSHS, relying on phenotypic characteristics for discrimination of GOSH from similar syndromes may lead to misdiagnosis. Consequently, molecular diagnostic tools would help in accurate diagnosis of such overlapping phenotypes.

References

1. Goldberg R, Shprintzen R. Hirschsprung megacolon and cleft palate in two sibs. J Craniofac Genet Dev Biol 1980;1(2):185-9.
2. Yomo A, Taira T, Kondo I. Goldberg-Shprintzen syndrome: Hirschsprung disease, hypotonia, and ptosis in sibs. Am J Med Genet 1991;41(2):188-91.
3. Drevillon L, Megarbane A, Demeer B, Matar C, Benit P, Briand-Suleau A, et al. KBP-cytoskeleton interactions underlie developmental anomalies in Goldberg-Shprintzen syndrome. Hum Mol Genet 2013;22(12):2387-99.
4. Brooks AS, Bertoli-Avella AM, Burzynski GM, Breedveld GJ, Osinga J, Boven LG, et al. Homozygous nonsense mutations in KIAA1279 are associated with malformations of the central and enteric nervous systems. Am J Med Genet 2005;77(1):120-6.
5. Blatch GL, Lassle M. The tetratricopeptide repeat: a structural motif mediating protein-protein interactions. BioEssays 1999;21(11):932-9.
6. Alves MM, Burzynski G, Delalande J-M, Osinga J, van der Goot A, Dolga AM, et al. KBP interacts with SCG10, linking Goldberg–Shprintzen syndrome to microtubule dynamics and neuronal differentiation. Hum Mol Genet 2010:ddq280.
7. Valence S, Poirier K, Lebrun N, Saillour Y, Sonigo P, Bessières B, et al. Homozygous truncating mutation of the KBP gene, encoding a KIF1B-binding protein, in a familial case of fetal polymicrogyria. Neurogenetics
2013;14(3-4):215-24.
8. Murphy HR, Carver MJ, Brooks AS, Kenny SE, Ellis IH. Two brothers with Goldberg-Shprintzen syndrome. Clinl Dysmorphol 2006;15(3):165-9.


Acute Necrotizing Encephalopathy of Childhood (ANEC): A Case Report

Afagh HASSANZADEH RAD, Vahid AMINZADEH

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 75-77
https://doi.org/10.22037/ijcn.v11i1.10862

How to Cite This Article: Hassanzadeh Rad A, Aminzadeh V. Acute Necrotizing Encephalopathy of Childhood (ANEC): A Case Report. Iran
J Child Neurol. Winter 2017; 11(1):75-77.

Abstract

Acute Necrotizing Encephalopathy of childhood (ANEC) is a specific type of encephalopathy. After viral infection, it can be diagnosed by bilateral symmetrical lesions predominantly observed in thalami & brainstem of infants & children.

Although, it is commonly occurred in Japanese and Taiwanese population. The goal of this article is to report a rare case of ANEC in a 15 months old girl infant from Thaleghani Hospital, Ramian, Gorgan, northern Iran.

References

1. Mizuguchi M, Mizuguchi M, Abe J, et al. Acute necrotising encephalopathy of childhood: a new syndrome presenting with multifocal, symmetric brain lesions. J Neurol, Neurosurg Psychiatr 1995;58(5):555-561.
2. Mizuguchi M. Acute necrotizing encephalopathy of childhood: a novel form of acute encephalopathy prevalent in Japan & Taiwan. Brain Dev 1997;19:81-82.
3. Narra R, Mandapalli A, Kamaraju SK. Acute Necrotizing Encephalopathy in an Adult. J Clin Imag Sci 2015;5:20. doi:10.4103/2156-7514.156117.
4. Kim JH1, Kim IO, Lim MK, et al. Acute necrotizing encephalopathy in Korean infants and children: imaging findings and diverse clinical outcome. Korean J Radiol 2004 Jul-Sep;5(3):171-7.
5. Salehiomran MR, Nooreddini H, Baghdadi F. Acute Necrotizing Encephalopathy of Childhood; A Case Report. Iran J Child Neurol 2013;7(2):51-54.
6. Protheroe SM ,Mellor DH. Imaging in influenza A encephalitis. Arch Dis Child 1991;66:702-705.
7. Barkovich AJ. Infections of the nervous system. Pediatic neuroimaging 3rd ed. Philadelphia:Lippincoot Williams &Wilkins, 2000:744-746.
8. Kumar S1, Misra UK, Kalita J, et al. MRI in Japanese encephalitis.Neuroradiology 1997:39:180-184.
9. Abe T1, Kojima K, Shoji H, et al. Japanese encephalitis. J MRI 1998;8:755-761.
10. Fenichel G. Clinical pediatric neurology; 4th ed. 2002:54.


Ataxia Oculomotor Apraxia Type 1 in the Siblings of a Family: A Novel Mutation

Parvaneh KARIMZADEH, Simin KHAYYATZADEH, Shaghayegh Sadat ESMAIL NEJAD, Masoud HOUSHMAND, MOHAMMAD GHFORANI

Iranian Journal of Child Neurology, Vol. 11 No. 1 (2017), 29 October 2016 , Page 78-81
https://doi.org/10.22037/ijcn.v11i1.11820

How to Cite This Article: Karimzadeh P, khayatzadeh kakhki S,Esmail Nejad Sh. S., Houshmand M,Ghofrani M. Ataxia oculomotor apraxia 1 in two siblings of a family:a novel mutation. Iran J Child Neurol.Winter 2017; 11(1):78-81.

Abstract

Although AOA1 (ataxia oculomotor apraxia1) is one of the most common causes of autosomal recessive cerebellar ataxias in Japanese population, it is reported from all over the world. The clinical manifestations are similar to ataxia telangiectasia in which non-neurological manifestations are absent and include almost 10% of autosomal recessive cerebellar ataxias. Dysarthria and gait disorder are the most two common and typical manifestations. Oculomotor apraxia is usually seen a few years after the manifestations start. APTX gene on 9p13.3 chromosome is expressed in the cells of all human body tissues and different mutations had been discovered. Here we report two siblings (a girl and a boy) of consanguineous parents visited at Mofid Pediatrics Hospital in 2015, with history of gait ataxia, titubation, tremor, and oculomotor apraxia around five yr old and after that. The brother showed symptoms of disease earlier and more severe than his sister did. After ruling out the common etiologies of progressive ataxia, we did genetic study for AOA1 that showed a homozygous frameshift mutation as c.418_418 del was found. This mutation was not reported before so this was a new mutation in APTX gene.

References

1. Jafar-Nejad P, Maririch SM, Zoghbi HM .The cerebellum and hereditary ataxias. In: Swaiman KF, Ashwal S, Ferriero DM, Schor NF. Swaiman’s Pediatric Neurology Principles, and Practice.15th ed. 2012.P.939-952.
2. Pina-Garza JE. Ataxias. In:Pina-Garza JE. Fenichel Clinical pediatric neurology. 7th ed. 2013.P.215-231.
3. Le Ber I, Moreira MC, Rivaud-Péchoux S, Chamayou C, Ochsner F, Kuntzer T, et al. Cerebellar ataxia with oculomotor apraxia type 1: clinical and genetic studies. Brain 2003; 126:2761-72.
4. Coutinho P, Barbot C. Ataxia with Oculomotor Apraxia Type 1. 2002 Jun 11 [Updated 2015 Mar 19]. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2016. Available from: https:// www.ncbi.nlm.nih.gov/books/NBK1456/
5. Shahwan A, Byrd PJ, Taylor AM, Nestor T, Ryan S, King MD. Atypical presentation of ataxia-oculomotor apraxia type 1. Dev Med Child Neurol 2006 Jun; 48(6):529-32.
6. Shimazaki H, Takiyama Y, Sakoe K, Ikeguchi K, Niijima K, et al. Early-onset ataxia with ocular motor apraxia and hypoalbuminemia: the aprataxin gene mutations. Neurology 2002; 59(4):590-5.
7. Yokoseki A, Ishihara T, Koyama A, Shiga A, Yamada M, Suzuki C,and et al. Genotype-phenotype correlations in early onset ataxia with ocular motor apraxia and hypoalbuminaemia. Brain 2011; 134:1387-99.
8. Moreira MC, Barbot C, Tachi N, Kozuka N, Mendonça P, Barros J, Coutinho P, Sequeiros J, Koenig M. Homozygosity mapping of Portuguese and Japanese forms of ataxia-oculomotor apraxia to 9p13, and evidence for genetic heterogeneity. Am J Hum Genet 2001; 68(2):501-8.