- Email: [email protected]
P211 The evaluation of tension-type headache, migraine and others type of headache in the adolescent by Midas measurement
Posters
S85
P208 Characterization of interstitial middle 6q deletions in two adult patients with mental retardation and seizures E. Andermann1,2,7 , F. Andermann5,2,6 , M. Veilleux5,2 , J. Lavoie3,4 , D. Amrom1,2 *. 1 Neurogenetics Unit, Montreal Neurological Hospital and Institute, Montreal, Canada; 2 Department of Neurology & Neurosurgery, McGill University, Canada; 3 Cytogenetics Laboratory, Montreal Children’s Hospital, Canada; 4 Department of Pathology, McGill University, Canada; 5 Epilepsy Service & Seizure Clinic, Montreal Neurological Hospital and Institute; 6 Department of Paediatrics, McGill Unversity, Canada; 7 Department of Human Genetics, McGill University, Canada Objectives: Clinical, epilepsy, and array CGH characterization in two patients with interstitial 6q deletion, followed until adulthood. Methods: Detailed review of the medical records; oligonucleotide microarray analysis of genomic DNA; fluorescence in situ hybridization (FISH) analysis to confirm the deletion. Results: A 22-year-old woman, product of an uneventful fullterm pregnancy had initially normal developmental milestones, but speech delay was observed at age 4. She developed febrile atypical absences at age 3, and later afebrile atypical absences, relatively well controlled with valproic acid. Evaluation showed mild mental deficiency, generalized epileptiform discharges on EEG, and at age 13 some periventricular leukomalacia on MRI. At age 22, mild facial dysmorphism, microcephaly, mild mental retardation and atypical absences, poorly controlled on valproic acid and topiramate, are noted. A standard karyotype at 4 years revealed a chr6q deletion. Microarray analysis detected a single copy loss of 360 oligonucleotide probes at 6q22.1−6q22.33 (12.8 Mb, at least 32 OMIM genes), confirmed by FISH. A 31-year-old man, born after an uneventful fullterm pregnancy had at age 8 months febrile seizures and developmental delay. At age 14, facial dysmorphism, hyperextensible joints, and mild quadriparesis were recorded. In his late twenties, he developed stimulus-sensitive myoclonic jerks which have increased in frequency over the past two years. Evaluation showed background rhythm dysfunction but no ictal abnormalies on EEG, mild nonspecific cerebellar vermian atrophy/hypoplasia on MRI. Initial karyotype at one year of age was reported as normal. Cytogenetic studies at age 30 revealed a chr6q22.1-q22.2 deletion. Microarray analysis detected a single copy loss of 164 oligonucleotide probes at 6q21−6q22.31 (7.6 Mb, at least 18 OMIM genes), confirmed by FISH. Conclusions: CGH microarray is an excellent method to refine the genotype-phenotype correlations. This is the first report of epilepsy associated with 6q interstitial middle deletions, representing separate clinical entities from the one associated with 6q terminal deletions. P209 Refractory status epilepticus and vacuolised bone marrow precursors: metabolic disorder or treatment toxicity? K. Pelc3 *, A. Ferster2 , A. Demulder2 , C. Fonteyne1 , J. Papadopoulos5 , S.G. Boyd4 , B. Dan3 . 1 Paediatric Intensive Care Unit, Hopital Universitaire des Enfants Reine Fabiola, ˆ Universit´e Libre de Bruxelles, Brussels, Belgium; 2 Haematology, Hopital Universitaire des Enfants Reine Fabiola, Universit´e Libre ˆ de Bruxelles, Brussels, Belgium; 4 Clinical Neurophysiology, Great Ormond Street Hospital for Children, London, United Kingdom; 5 Paediatric Intensive Care Unit, Clinique de Jolimont, La Louvi`ere, Belgium A subset of children has been status epilepticus that lasts for despite treatment with multiple inducing medications. In three
described with refractory several weeks or months, anticonvulsant and comaunrelated boys aged 5−9
years with refractory status epilepticus of unknown aetiology, we documented highly stereotyped electroclinical sequences consisting of a run of high amplitude fast spiking activity followed by slower rhythmic bursts of spikes correlated with clinical myoclonic jerks. Such sequences were triggered by flash, touch or noise stimulation. This electroclinical state was abolished by halogenated anaesthetic agents (isoflurane or halothane) but not by thiopentone, thiopentone withdrawal, chlormethiazole, methylprednisolone, vigabatrin, topiramate, lignocaine, or ketamine. In all three patients, we found severe bone marrow abnormalities with hemophagocytosis highly suggestive of Pearson syndrome. Mitochondrial DNA was normal in all three patients. After halogenated withdrawal, repeat bone marrow smear normalised in the two patients in whom it was obtained. We discuss whether this is an expression of a metabolic disorder otherwise manifesting with refractory status epilepticus or results from bone marrow toxicity of halogenated agents. P210 Withdrawn P211 The evaluation of tension-type headache, migraine and others type of headache in the adolescent by Midas measurement S. Kılıc¸ 1 *, O. Derman1 , S. Aysun1 , T. Kutluk1 . 1 Hacettepe University, Faculty of Medicine, Pediatrics The aim of this study is to get information about the evaluation of tension-type headache, migraine and others type of headache in the adolescent by Midas Questionnaire, comparing it with migraine type headache, and the seriousness of tension-type headache. In this study, 82 adolescent complaining about headache, who were between 10−16 years old and admitted to the Adolescent Unit of Hacettepe University I˙hsan Dogramacı Children ˘ Hospital, were asked the question about characteristics of headache (such as age, gender, education, how long months/years is that they have headache, the frequency and severity of the headache, the location of the pain, whether it diffuses or not, when it happens during a day, the features of the pain, the volume of the pain, presence of aura, the factors that stimulate the headache, the findings that accompany the pain, whether analgesic or sleeping relieves the pain, car sickness history, the family history in terms of headache, epilepsy, depression. Midas Questionnaire was applied to each patient. The patients who had tension-type headache, migraine type headache and psychogenic headache were identified based on the results of the questionnaire. The degree of the volume of the headache of the patients who had tension-type headache and migraine type headache were scored. The scores were indicated as the total number the lost days in the last 3 months: • Scores 0−5: Degree 1 • Scores 6−10: Degree 2 • Scores 11−20: Degree 3 • Scores 21 and beyond: Degree 4 In our study 45 tension-type headache, 20 migraine type headache, 10 psychogenic headache and 7 undefined headache are determined. Tension-type headache are found more than migraine type headache. Based on the Midas scoring it is found out that tension headache more likely to be in degree 1 volume whereas migraine type headache is more common in degree 4. According to Midas scoring, no significant difference is detected in the degrees of headache volume between boys and girls. As the frequency of the headache increases Midas degree importantly increases. Midas volume degree is observed to increase if there is aura history and daily activities are affected. There is no statistically important difference between either accompanying findings or response to analgesics.
S86 Reference(s) [1] Kınık E. Adolesan Hastaya Yakla¸sım. In: Kale G, Kutluk T (ed), Katkı Pediatri Dergisi, Ankara, 2000; 21 (6); 713 719. [2] Erdine S. Agrı. ˘ Alemdar Ofset. I˙stanbul 2000. [3] Silberstein SD, Lipton BR, Dolessio DJ. Wolf’s headache and other head pain. Oxford University press. Seventh edition 2001. [4] Olesen J, Tfelt-Hanser P, Welch K.M.A. The Headache. Raven Press New York 1993. [5] Dweis H: Headache and facial pain. In: R.T. Johnson, J.W. Griffin, J.C. McArthur (Eds): Current Therapy in Neurologic Disease. Mosby; 2002;pp.81−88. [6] Silberstein SD, Lipton RB: Epidemiology of migraine. Neuroepidemiology 1993; 12: 170 194. [7] Mortimer MJ, Kay J, Jaron A. Epidemiology of headache and childhood migraine in an urban general practice using Ad Hoc Vahlqurt and IHS criteria. Dev Med Child Neurol. 1992; 34: 1095 1101. [8] Birrer RB, Fleisher JM, Cortese I ve ark. An urban primary school health programme. NY State J Med 1991; 91: 339 341. [9] Aysun S., Yetuk ¨ M. Clinical Experience on Headache in Children: Analysis of 92 Cases. J. Child Neurology 1998;13:202 210. [10] Mauskop A. Headache in children. N Y State Med 1992; 92:24. [11] Abu-Arefeh I, Russel G. Prevalence of headache and migraine in school children. BMJ 1994; 309: 765 769. [12] Sillanpaa M. Prevalence of migraine and other headache in Finnish children starting school. Headache 1976; 15: 288 290. [13] Alparslan Y. Sivas I˙li Merkezinde 7−14 Ya¸s Grubu I˙lko¨ gretim ˘ ¨ Cocuklarında ¸ Migren Ba¸s Agrısı Prevelansına, Klinik Ozelliklerine ˘ ˙ ˙ ve Renk Gorme Defekti Ile Olan Birlikteligine Ili¸skin Tarama ¨ ˘ ¨ Calı¸ ¸ sması. Uzmanlık Tezi, Cumhuriyet Universitesi, 2001. [14] Lewis DW. Headache in the pediatric emergency department. Winner P, Rothner DA. Headache in Children and Adolecents. Canada, B.C. Decker, 2001:163 181. [15] Mangini F. Headache and Facial Pain Thieme Stuttgart. New York 1999. [16] Winner P. Pediatric headaches: what’s new? Current Opinion in Neurology 1999; 12: 299 272. [17] Olesen J. Goadsby PJ. Synthesis of migraine mechanisms. The Headaches. Olesen J, Tfelt-Hansen P, Welch KMA.2. Baskı, Wolters Kluwer Company, Philadelphia, 2000:331 336. [18] Moscowitz MA. Neurogenic versus vascular mechanism in migraine headaches. Trend Pharmacol. Sci. 1992;13: 307 311. [19] Lauritzen M. Pathophysiology of migraine aura: the spreading depression theory. Brain 1994; 117:199 210. [20] Bolay H, Reuter U, Dunn A, Huang Z, Boas D, Moskowitz A. Intrinsic brain activity triggers trigeminal meningial afferens in a migraine model. Nature Medicine 2002, 8: 136 142. [21] Lassen LH, Ashina M, Christiansen I, Ulrich V, Olesen J. Nitric oxide synthase inhibition in migraine. Lancet 1997; 349: 401 402. [22] Olesen J. Clinical and pathophysiological observations in migraine and tension-type headache explained by integration of vascular, supraspinal and myofascial inputs. Pain 1991; 46: 125 132. [23] Ophoff RA, Terwindt GM, Vergouwe MN ve ark. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in calcium channel gene CACNLIA4. Cell 1996;87: 543 552. [24] De Fusco M, Marconi R, Silvestri L ve ark. Haploinsufficiency of ATPIA2 encoding the Na-K pump alpha2 subunit gene is responsible for familial hemiplegic migraine type 2. Nature Genet 2003; 33: 192 196. [25] Hammalainen ML. Medical and dietary management of headache and migraine. Abu Arefeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 136 148. [26] Hershey AD, Powers SW, Vockel AL, LeCates S, Kabbouche MA, Maynard MK: PedMIDAS: development of a questionnaire to assess disability of migraines in children. Neurology 2001:57: 2034 2039. [27] Lewis DW, Winner P. Migraine, migraine variants, and other primary headache syndromes. Winner P, Rothner DA eds. Headache in Children and Adolecents. Canada, B.C. Decker, 2001: 60−86. [28] Rothner AD. Childhood migraine: clinical features, classifications and diagnostic criteria. Abu-Arafeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 54−65. [29] Lewis DW, Lake A. Psychologic and nonpharmacologic treatment of headache. Winner P, Rothner DA eds. Headache in Children and Adolecents. Canada, B.C. Decker, 2001: 126 141. [30] Aaltolen K, Hamalainen ML, Hoppu K. Migraine attacks an sleep in children. Cephalalgia 2000;20: 580 584.
Posters [31] Herman C, Kim M, Blanchard EB. Behavioral and prophylactic pharmacological intervention studies of pediatric migraine: an exploratory meta-analysis. Pain 1995; 60: 239 255. [32] Osterhaus S. Psychological treatment of paediatric headache. AbuArafeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 149 174. [33] Grazzi L. Headache in children and adolescents: conventional and unconventional approches to treatment. Neurol. Sci. 2004;25: S223-S225. [34] Lewis DW, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S. Practice parameter: pharmacological treatment of migraine headache in children and adolescents: report of the American Academy of Neurology Quality Standarts Subcommittee and the Practice Committee of the Child Neurology Society. Neurology 2004: 63: 2215 2224. [35] Damen L. Brujin JK, Verhagen AP, Berger MY, Passchier P, Koes BW. Symptomatic treatment of migraine in children: a systematic review of medication trials. Pediatrics 2005; 116: 295 302. [36] Stewart W.F., Lipton R.B., Dowson A.J., Sawyer J. Development and testing of the Migraine Disability Assessment (MI˙DAS) Questionnaire to assess headache related disability. Neurology. Volume 56(6) Supplement 1, March 2001, S20-S28 ¨ Tunc¸ T. (2005) A ¨ U ¨ cler [37] Gedikoglu U., ¸ S., I˙nan L., Co¸skun O., ˘ Preliminary Study: Validity and Reliability of Turkish Translation of Migraine Disability Assessment (MIDAS) Questionnaire in Turkish Patients with Chronic Tension Type Headache. Intern. J. Neuroscience, 116: 1337 1345, 2006. [38] Senbil N., Aydın O.F., Kuyucu N. Assessment of migraine disability using the Migraine Disability Assessment (MI˙DAS) Questionnaire. Current Opinion in Neurology Volume 17 (3) June 2004. [39] Stewart WF, Lipton RB, Kolodner K. Migraine disability assessment (MIDAS) score: relation to headache frequency, pain intensity and headache symptoms. Headache 2003; 43 (3): 258 265. [40] D’Amico D, Grazzi L, Usai S, Andrasik F, Leone M, Rigamonti A, Bussone G. Use of the Migraine Disability Assessment Questionnaire in children and adolescents with headache: an I˙talian pilot study. Headache 2003; 43 (7): 767 773 [41] Demirkırkan M.K., Ellidokuz H., Bol ¨ uk ¨ A. Prevalance and Clinical Characteristics of Migraine in University Students in Turkey. Tohoku J. Exp. Med., 2006, 208, 87−92. [42] Lipton R.B., Stewart W.F., Sawyer J., Edmeads J.G. Clinical utility of an instrument assessing migraine disability: The Migraine Disability Assessment (MI˙DAS) Questionnaire. Headache 2001; 41: 854 861. [43] Iigaya M., Sakai F., Kolodner K.B., Lipton R.B., Stewart W.F. Reliability and Validity of the Japanese Migraine Disability Assessment (MI˙DAS) Questionnaire. Headache. 2003; 43: 343 352. [44] Stewart W.F., Lipton R.B., Whyte J., Dowson A., Kolodner K., Liberman J., Sawyer J. An international study to assess reliability of the Migraine Disability Assessment (MI˙DAS score. Neurology 1999 Sep 22; 53(5): 988 994. [45] Bigal M.E., Rapoport A.M., Lipton R.B., Stewart J.T., Sheftell F.D. Assessment of Migraine Disability Using the Migraine Disability Assessment (MI˙DAS) Questionnaire: A Comparison of Chronic Migraine With Episodic Migraine. Headache 2003: 43: 336 342. ¨ [46] Bıcakcı ¸ S., ¸ Over F., Aslan K., Bozdemir N., Saatci ¸ E., Sarıca Y. Headache Characteristics in Senior Medical Students in Turkey. Tohoku J. Exp. Med., 2007, 213, 277 282. [47] Sanvito W.L., Monzillo P.H., Peres M.F., Martinelli M.O., Fera M.P., Gouveia D.A. The epidemiologyof migraine in medical students. Headache. 1996 May; 36(5): 316 319. [48] da Costa M.Z., Soares C.B., Heinisch L.M., Heinisch R.H. Frequencyof headache in the medical students of Santa Catarina’s Federal University. Headache. 2000 Oct.; 40 (9): 740 744. [49] Mitsikostas D.D., Gatzonis S., Thomas A., Kalfakis N., Ilias A., Papageoergiou C. An epidemiological study of headaches among medical students in Athens. Headache. 1996 Oct; 36 (9): 561 564. [50] Amayo E.O., Jowi J.O., Njeru E.K. Headache associated disability in medical students at the Kenyatta National Hospital, Nairobi. East. Afr. Med. J. 2002 Oct.; 79(10): 519 523. [51] Stewart W.F., Lipton R.B., Kolodner K., Liberman J., Sawyer J. Reliability of the migraine disability assessment score in a population based sample of headache sufferers. Cephalalgia. 1999 Mar; 19(2): 107 114.
S85
P208 Characterization of interstitial middle 6q deletions in two adult patients with mental retardation and seizures E. Andermann1,2,7 , F. Andermann5,2,6 , M. Veilleux5,2 , J. Lavoie3,4 , D. Amrom1,2 *. 1 Neurogenetics Unit, Montreal Neurological Hospital and Institute, Montreal, Canada; 2 Department of Neurology & Neurosurgery, McGill University, Canada; 3 Cytogenetics Laboratory, Montreal Children’s Hospital, Canada; 4 Department of Pathology, McGill University, Canada; 5 Epilepsy Service & Seizure Clinic, Montreal Neurological Hospital and Institute; 6 Department of Paediatrics, McGill Unversity, Canada; 7 Department of Human Genetics, McGill University, Canada Objectives: Clinical, epilepsy, and array CGH characterization in two patients with interstitial 6q deletion, followed until adulthood. Methods: Detailed review of the medical records; oligonucleotide microarray analysis of genomic DNA; fluorescence in situ hybridization (FISH) analysis to confirm the deletion. Results: A 22-year-old woman, product of an uneventful fullterm pregnancy had initially normal developmental milestones, but speech delay was observed at age 4. She developed febrile atypical absences at age 3, and later afebrile atypical absences, relatively well controlled with valproic acid. Evaluation showed mild mental deficiency, generalized epileptiform discharges on EEG, and at age 13 some periventricular leukomalacia on MRI. At age 22, mild facial dysmorphism, microcephaly, mild mental retardation and atypical absences, poorly controlled on valproic acid and topiramate, are noted. A standard karyotype at 4 years revealed a chr6q deletion. Microarray analysis detected a single copy loss of 360 oligonucleotide probes at 6q22.1−6q22.33 (12.8 Mb, at least 32 OMIM genes), confirmed by FISH. A 31-year-old man, born after an uneventful fullterm pregnancy had at age 8 months febrile seizures and developmental delay. At age 14, facial dysmorphism, hyperextensible joints, and mild quadriparesis were recorded. In his late twenties, he developed stimulus-sensitive myoclonic jerks which have increased in frequency over the past two years. Evaluation showed background rhythm dysfunction but no ictal abnormalies on EEG, mild nonspecific cerebellar vermian atrophy/hypoplasia on MRI. Initial karyotype at one year of age was reported as normal. Cytogenetic studies at age 30 revealed a chr6q22.1-q22.2 deletion. Microarray analysis detected a single copy loss of 164 oligonucleotide probes at 6q21−6q22.31 (7.6 Mb, at least 18 OMIM genes), confirmed by FISH. Conclusions: CGH microarray is an excellent method to refine the genotype-phenotype correlations. This is the first report of epilepsy associated with 6q interstitial middle deletions, representing separate clinical entities from the one associated with 6q terminal deletions. P209 Refractory status epilepticus and vacuolised bone marrow precursors: metabolic disorder or treatment toxicity? K. Pelc3 *, A. Ferster2 , A. Demulder2 , C. Fonteyne1 , J. Papadopoulos5 , S.G. Boyd4 , B. Dan3 . 1 Paediatric Intensive Care Unit, Hopital Universitaire des Enfants Reine Fabiola, ˆ Universit´e Libre de Bruxelles, Brussels, Belgium; 2 Haematology, Hopital Universitaire des Enfants Reine Fabiola, Universit´e Libre ˆ de Bruxelles, Brussels, Belgium; 4 Clinical Neurophysiology, Great Ormond Street Hospital for Children, London, United Kingdom; 5 Paediatric Intensive Care Unit, Clinique de Jolimont, La Louvi`ere, Belgium A subset of children has been status epilepticus that lasts for despite treatment with multiple inducing medications. In three
described with refractory several weeks or months, anticonvulsant and comaunrelated boys aged 5−9
years with refractory status epilepticus of unknown aetiology, we documented highly stereotyped electroclinical sequences consisting of a run of high amplitude fast spiking activity followed by slower rhythmic bursts of spikes correlated with clinical myoclonic jerks. Such sequences were triggered by flash, touch or noise stimulation. This electroclinical state was abolished by halogenated anaesthetic agents (isoflurane or halothane) but not by thiopentone, thiopentone withdrawal, chlormethiazole, methylprednisolone, vigabatrin, topiramate, lignocaine, or ketamine. In all three patients, we found severe bone marrow abnormalities with hemophagocytosis highly suggestive of Pearson syndrome. Mitochondrial DNA was normal in all three patients. After halogenated withdrawal, repeat bone marrow smear normalised in the two patients in whom it was obtained. We discuss whether this is an expression of a metabolic disorder otherwise manifesting with refractory status epilepticus or results from bone marrow toxicity of halogenated agents. P210 Withdrawn P211 The evaluation of tension-type headache, migraine and others type of headache in the adolescent by Midas measurement S. Kılıc¸ 1 *, O. Derman1 , S. Aysun1 , T. Kutluk1 . 1 Hacettepe University, Faculty of Medicine, Pediatrics The aim of this study is to get information about the evaluation of tension-type headache, migraine and others type of headache in the adolescent by Midas Questionnaire, comparing it with migraine type headache, and the seriousness of tension-type headache. In this study, 82 adolescent complaining about headache, who were between 10−16 years old and admitted to the Adolescent Unit of Hacettepe University I˙hsan Dogramacı Children ˘ Hospital, were asked the question about characteristics of headache (such as age, gender, education, how long months/years is that they have headache, the frequency and severity of the headache, the location of the pain, whether it diffuses or not, when it happens during a day, the features of the pain, the volume of the pain, presence of aura, the factors that stimulate the headache, the findings that accompany the pain, whether analgesic or sleeping relieves the pain, car sickness history, the family history in terms of headache, epilepsy, depression. Midas Questionnaire was applied to each patient. The patients who had tension-type headache, migraine type headache and psychogenic headache were identified based on the results of the questionnaire. The degree of the volume of the headache of the patients who had tension-type headache and migraine type headache were scored. The scores were indicated as the total number the lost days in the last 3 months: • Scores 0−5: Degree 1 • Scores 6−10: Degree 2 • Scores 11−20: Degree 3 • Scores 21 and beyond: Degree 4 In our study 45 tension-type headache, 20 migraine type headache, 10 psychogenic headache and 7 undefined headache are determined. Tension-type headache are found more than migraine type headache. Based on the Midas scoring it is found out that tension headache more likely to be in degree 1 volume whereas migraine type headache is more common in degree 4. According to Midas scoring, no significant difference is detected in the degrees of headache volume between boys and girls. As the frequency of the headache increases Midas degree importantly increases. Midas volume degree is observed to increase if there is aura history and daily activities are affected. There is no statistically important difference between either accompanying findings or response to analgesics.
S86 Reference(s) [1] Kınık E. Adolesan Hastaya Yakla¸sım. In: Kale G, Kutluk T (ed), Katkı Pediatri Dergisi, Ankara, 2000; 21 (6); 713 719. [2] Erdine S. Agrı. ˘ Alemdar Ofset. I˙stanbul 2000. [3] Silberstein SD, Lipton BR, Dolessio DJ. Wolf’s headache and other head pain. Oxford University press. Seventh edition 2001. [4] Olesen J, Tfelt-Hanser P, Welch K.M.A. The Headache. Raven Press New York 1993. [5] Dweis H: Headache and facial pain. In: R.T. Johnson, J.W. Griffin, J.C. McArthur (Eds): Current Therapy in Neurologic Disease. Mosby; 2002;pp.81−88. [6] Silberstein SD, Lipton RB: Epidemiology of migraine. Neuroepidemiology 1993; 12: 170 194. [7] Mortimer MJ, Kay J, Jaron A. Epidemiology of headache and childhood migraine in an urban general practice using Ad Hoc Vahlqurt and IHS criteria. Dev Med Child Neurol. 1992; 34: 1095 1101. [8] Birrer RB, Fleisher JM, Cortese I ve ark. An urban primary school health programme. NY State J Med 1991; 91: 339 341. [9] Aysun S., Yetuk ¨ M. Clinical Experience on Headache in Children: Analysis of 92 Cases. J. Child Neurology 1998;13:202 210. [10] Mauskop A. Headache in children. N Y State Med 1992; 92:24. [11] Abu-Arefeh I, Russel G. Prevalence of headache and migraine in school children. BMJ 1994; 309: 765 769. [12] Sillanpaa M. Prevalence of migraine and other headache in Finnish children starting school. Headache 1976; 15: 288 290. [13] Alparslan Y. Sivas I˙li Merkezinde 7−14 Ya¸s Grubu I˙lko¨ gretim ˘ ¨ Cocuklarında ¸ Migren Ba¸s Agrısı Prevelansına, Klinik Ozelliklerine ˘ ˙ ˙ ve Renk Gorme Defekti Ile Olan Birlikteligine Ili¸skin Tarama ¨ ˘ ¨ Calı¸ ¸ sması. Uzmanlık Tezi, Cumhuriyet Universitesi, 2001. [14] Lewis DW. Headache in the pediatric emergency department. Winner P, Rothner DA. Headache in Children and Adolecents. Canada, B.C. Decker, 2001:163 181. [15] Mangini F. Headache and Facial Pain Thieme Stuttgart. New York 1999. [16] Winner P. Pediatric headaches: what’s new? Current Opinion in Neurology 1999; 12: 299 272. [17] Olesen J. Goadsby PJ. Synthesis of migraine mechanisms. The Headaches. Olesen J, Tfelt-Hansen P, Welch KMA.2. Baskı, Wolters Kluwer Company, Philadelphia, 2000:331 336. [18] Moscowitz MA. Neurogenic versus vascular mechanism in migraine headaches. Trend Pharmacol. Sci. 1992;13: 307 311. [19] Lauritzen M. Pathophysiology of migraine aura: the spreading depression theory. Brain 1994; 117:199 210. [20] Bolay H, Reuter U, Dunn A, Huang Z, Boas D, Moskowitz A. Intrinsic brain activity triggers trigeminal meningial afferens in a migraine model. Nature Medicine 2002, 8: 136 142. [21] Lassen LH, Ashina M, Christiansen I, Ulrich V, Olesen J. Nitric oxide synthase inhibition in migraine. Lancet 1997; 349: 401 402. [22] Olesen J. Clinical and pathophysiological observations in migraine and tension-type headache explained by integration of vascular, supraspinal and myofascial inputs. Pain 1991; 46: 125 132. [23] Ophoff RA, Terwindt GM, Vergouwe MN ve ark. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in calcium channel gene CACNLIA4. Cell 1996;87: 543 552. [24] De Fusco M, Marconi R, Silvestri L ve ark. Haploinsufficiency of ATPIA2 encoding the Na-K pump alpha2 subunit gene is responsible for familial hemiplegic migraine type 2. Nature Genet 2003; 33: 192 196. [25] Hammalainen ML. Medical and dietary management of headache and migraine. Abu Arefeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 136 148. [26] Hershey AD, Powers SW, Vockel AL, LeCates S, Kabbouche MA, Maynard MK: PedMIDAS: development of a questionnaire to assess disability of migraines in children. Neurology 2001:57: 2034 2039. [27] Lewis DW, Winner P. Migraine, migraine variants, and other primary headache syndromes. Winner P, Rothner DA eds. Headache in Children and Adolecents. Canada, B.C. Decker, 2001: 60−86. [28] Rothner AD. Childhood migraine: clinical features, classifications and diagnostic criteria. Abu-Arafeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 54−65. [29] Lewis DW, Lake A. Psychologic and nonpharmacologic treatment of headache. Winner P, Rothner DA eds. Headache in Children and Adolecents. Canada, B.C. Decker, 2001: 126 141. [30] Aaltolen K, Hamalainen ML, Hoppu K. Migraine attacks an sleep in children. Cephalalgia 2000;20: 580 584.
Posters [31] Herman C, Kim M, Blanchard EB. Behavioral and prophylactic pharmacological intervention studies of pediatric migraine: an exploratory meta-analysis. Pain 1995; 60: 239 255. [32] Osterhaus S. Psychological treatment of paediatric headache. AbuArafeh I. Childhood Headache. Lavenham Pres. Ltd. London 2002, 149 174. [33] Grazzi L. Headache in children and adolescents: conventional and unconventional approches to treatment. Neurol. Sci. 2004;25: S223-S225. [34] Lewis DW, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S. Practice parameter: pharmacological treatment of migraine headache in children and adolescents: report of the American Academy of Neurology Quality Standarts Subcommittee and the Practice Committee of the Child Neurology Society. Neurology 2004: 63: 2215 2224. [35] Damen L. Brujin JK, Verhagen AP, Berger MY, Passchier P, Koes BW. Symptomatic treatment of migraine in children: a systematic review of medication trials. Pediatrics 2005; 116: 295 302. [36] Stewart W.F., Lipton R.B., Dowson A.J., Sawyer J. Development and testing of the Migraine Disability Assessment (MI˙DAS) Questionnaire to assess headache related disability. Neurology. Volume 56(6) Supplement 1, March 2001, S20-S28 ¨ Tunc¸ T. (2005) A ¨ U ¨ cler [37] Gedikoglu U., ¸ S., I˙nan L., Co¸skun O., ˘ Preliminary Study: Validity and Reliability of Turkish Translation of Migraine Disability Assessment (MIDAS) Questionnaire in Turkish Patients with Chronic Tension Type Headache. Intern. J. Neuroscience, 116: 1337 1345, 2006. [38] Senbil N., Aydın O.F., Kuyucu N. Assessment of migraine disability using the Migraine Disability Assessment (MI˙DAS) Questionnaire. Current Opinion in Neurology Volume 17 (3) June 2004. [39] Stewart WF, Lipton RB, Kolodner K. Migraine disability assessment (MIDAS) score: relation to headache frequency, pain intensity and headache symptoms. Headache 2003; 43 (3): 258 265. [40] D’Amico D, Grazzi L, Usai S, Andrasik F, Leone M, Rigamonti A, Bussone G. Use of the Migraine Disability Assessment Questionnaire in children and adolescents with headache: an I˙talian pilot study. Headache 2003; 43 (7): 767 773 [41] Demirkırkan M.K., Ellidokuz H., Bol ¨ uk ¨ A. Prevalance and Clinical Characteristics of Migraine in University Students in Turkey. Tohoku J. Exp. Med., 2006, 208, 87−92. [42] Lipton R.B., Stewart W.F., Sawyer J., Edmeads J.G. Clinical utility of an instrument assessing migraine disability: The Migraine Disability Assessment (MI˙DAS) Questionnaire. Headache 2001; 41: 854 861. [43] Iigaya M., Sakai F., Kolodner K.B., Lipton R.B., Stewart W.F. Reliability and Validity of the Japanese Migraine Disability Assessment (MI˙DAS) Questionnaire. Headache. 2003; 43: 343 352. [44] Stewart W.F., Lipton R.B., Whyte J., Dowson A., Kolodner K., Liberman J., Sawyer J. An international study to assess reliability of the Migraine Disability Assessment (MI˙DAS score. Neurology 1999 Sep 22; 53(5): 988 994. [45] Bigal M.E., Rapoport A.M., Lipton R.B., Stewart J.T., Sheftell F.D. Assessment of Migraine Disability Using the Migraine Disability Assessment (MI˙DAS) Questionnaire: A Comparison of Chronic Migraine With Episodic Migraine. Headache 2003: 43: 336 342. ¨ [46] Bıcakcı ¸ S., ¸ Over F., Aslan K., Bozdemir N., Saatci ¸ E., Sarıca Y. Headache Characteristics in Senior Medical Students in Turkey. Tohoku J. Exp. Med., 2007, 213, 277 282. [47] Sanvito W.L., Monzillo P.H., Peres M.F., Martinelli M.O., Fera M.P., Gouveia D.A. The epidemiologyof migraine in medical students. Headache. 1996 May; 36(5): 316 319. [48] da Costa M.Z., Soares C.B., Heinisch L.M., Heinisch R.H. Frequencyof headache in the medical students of Santa Catarina’s Federal University. Headache. 2000 Oct.; 40 (9): 740 744. [49] Mitsikostas D.D., Gatzonis S., Thomas A., Kalfakis N., Ilias A., Papageoergiou C. An epidemiological study of headaches among medical students in Athens. Headache. 1996 Oct; 36 (9): 561 564. [50] Amayo E.O., Jowi J.O., Njeru E.K. Headache associated disability in medical students at the Kenyatta National Hospital, Nairobi. East. Afr. Med. J. 2002 Oct.; 79(10): 519 523. [51] Stewart W.F., Lipton R.B., Kolodner K., Liberman J., Sawyer J. Reliability of the migraine disability assessment score in a population based sample of headache sufferers. Cephalalgia. 1999 Mar; 19(2): 107 114.