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The Neurology of Benign Paroxysmal Torticollis of Infancy: Report of 10 New Cases and Review of the Literature N. Paul Rosman, Laurie M. Douglass, Uzma M. Sharif and Jan Paolini J Child Neurol 2009; 24; 155 DOI: 10.1177/0883073808322338 The online version of this article can be found at: http://jcn.sagepub.com/cgi/content/abstract/24/2/155

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Original Article

The Neurology of Benign Paroxysmal Torticollis of Infancy: Report of 10 New Cases and Review of the Literature

Journal of Child Neurology Volume 24 Number 2 February 2009 155-160 # 2009 Sage Publications 10.1177/0883073808322338 http://jcn.sagepub.com hosted at http://online.sagepub.com

N. Paul Rosman, MD, Laurie M. Douglass, MD, Uzma M. Sharif, MD, and Jan Paolini, RN, PNP Benign paroxysmal torticollis is an under-recognized cause of torticollis of early infancy. The attacks usually last for less than 1 week, recur from every few days to every few months, improve by age 2 years, and end by age 3. There very frequently is a family history of migraine. We did a detailed analysis of 10 cases of benign paroxysmal torticollis, seen over 5 years, and compared our findings with those in the 103 cases in the literature. Detailed neurodevelopmental assessments, available only in our cases, showed accompanying gross motor delays in 5/10 children, with

additional fine motor delays in 3/5. As the benign paroxysmal torticollis improved, so did the gross motor delays in 3/5, and the fine motor delays in 1/3. In all of our cases, at least 2 other family members had migraine. Benign paroxysmal torticollis is likely an age-sensitive, migrainerelated disorder, commonly accompanied by delayed motor development.

B

comprehensive analysis of the available data. Feedback from referring practitioners and their families has prompted us to prepare an in-depth review of our own experiences with benign paroxysmal torticollis and a summary of the world’s literature.

enign paroxysmal torticollis of infancy is a clinically striking disorder, characterized by recurrent episodes of cervical dystonia. Because benign paroxysmal torticollis inevitably remits, it is called ‘‘benign,’’ but while it is ongoing, it is most distressing to the parents and to the child, particularly since no treatment helps. The disorder is almost certainly under-recognized by pediatric practitioners, who often order extensive and unrewarding testing. The clinical features of benign paroxysmal torticollis encompass a broad spectrum. Since the first report close to 40 years ago,1 there have been numerous case reports from throughout the globe, but there has been no

Received April 2, 2008. Received revised May 26, 2008. Accepted for publication May 27, 2008. From the Departments of Pediatrics and Neurology, Division of Pediatric Neurology, Boston Medical Center, Massachusetts (NPR, LMD); Tufts Medical Center, Boston, Massachusetts (NPR, LMD, UMS, JP); Children’s Hospital of Wisconsin, Milwaukee, Wisconsin (UMS); and Massachusetts General Hospital, Boston, Massachusetts (JP). The authors have no conflicts of interest to disclose with regard to this article. Address correspondence to: N. Paul Rosman, MD, Boston Medical Center Place Dowling 3-South, Boston, MA 02118; e-mail: npaul.rosman@ bmc.org. Rosman NP, Douglass LM, Sharif UM, Paolini J. The neurology of benign paroxysmal torticollis of infancy: report of 10 new cases and review of the literature. J Child Neurol. 2009;24:155-160.

Keywords: torticollis; development

paroxysmal;

migraine;

motor

Methods We reviewed in detail all cases of benign paroxysmal torticollis that we had seen during a 5-year period (2000-2005) at the Floating Hospital for Children, Tufts Medical Center and in the Department of Pediatrics, Boston Medical Center. We then searched the literature, using PubMed and Medline, for all reported cases of benign paroxysmal torticollis, regardless of language. We limited our review to only those cases where clinical information and laboratory data accompanied the reports.1-22

Results We were referred 10 children with benign paroxysmal torticollis during the 5-year period; we did detailed neurodevelopmental evaluations on all children and followed them for periods ranging from 20 to 79 months. We found 103 cases of benign paroxysmal torticollis in the literature with sufficient information to include in this review (Table 1).

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156 Journal of Child Neurology / Vol. 24, No. 2, February 2009

Table 1.

Clinical Findings in Benign Paroxysmal Torticollis of Infancy Our 10 Cases (Mean; Median)

Clinical features Gender Age of onset (months) Duration of episodes (days) Time to peak intensity (days) Interval between episodes (days) Age when episodes began to improve (months) Age of last episode (months) Duration of follow-up (months) Torticollis always/usually on same side Alternation between sides in successive episodes Tortipelvis always/sometimes Persistence during sleep, always/sometimes Signs and symptoms accompanying torticollis Irritability Limb dystonia Vomiting Pallor Vertigo/ataxia Apathy/drowsiness Gaze abnormalities Early gross motor delay (severity) Early fine motor delay (severity) Abnormal audiometry Abnormal calorics Family histories Benign paroxysmal torticollis Migraine Car and/or other motion sickness Recurrent dizziness/vertigo Global developmental delay Gross motor delay/clumsiness Sequelae Persisting gross motor delay (severity) Persisting fine motor delay (severity) Headache Vertigo/ataxia

M/F 6/4 0.5-4.5 (2.4; 2.3) 5-10.5 (8.0; 7.5) 1-10 (4.3; 3.3) 1.5-18 (8.7; 7.3) 5-24 (13.4; 13.0) 10-32 (18.6; 18.0); 1 ongoing at 58 months 20-79 (49.6; 47.5) always 1/10; usually 5/10 always 2/10; usually 5/10 always 4/10; sometimes 3/10 always 8/9; sometimes 1/9 4/10 4/10 2/10 1/10

A Total of 103 Cases From Literature (Mean; Median)

M/F 43/60; 58% girls 0.25-30 (5.9; 5.0);75% by 7 months <1-30; (4.5; 2.0); 75%  6 days 7-150 (37.1; 30.0); 75%  45 days 8-36 (20.8; 21.0); 75% by 24 months 3.5-60 (31.4; 36.0);75% by 36 months

always 10 cases; usually 8 cases 25 cases

30 cases 2 cases 36 cases 18 cases 24 cases 12 cases 7 cases

5/10 (moderate 2; mild 3) 3/10 (mild); all with gross motor delay 3/24 9/31 1/10 (other torticollis in 2/10) 10/10 6/10 7/9 1/9 2/9

6 cases 39 cases 13 cases

4/5 (mild/moderate 1; mild 3) 2/3 (mild 2) 2/9 2/9

2/20 0/20 12 cases 5 cases

Summary of Our 10 Cases of Benign Paroxysmal Torticollis Clinical features. There were 6 boys and 4 girls seen. Gestational ages ranged from 35 to 40 weeks (mean 38.2 weeks; median 39.5 weeks). The perinatal course was uneventful in 8 cases. In the other 2 cases, perinatal difficulties necessitated cesarean section. The childrenâ&#x20AC;&#x2122;s ages at the onset of the first attack of torticollis ranged from 2 weeks to 4.5 months (mean 2.4 months; median 2.3 months). The duration of the episodes of torticollis ranged from 5 to 10.5 days (mean 8.0 days; median 7.5 days). The number of days during an episode before the torticollis reached peak intensity ranged from 1 to 10 days (mean 4.3 days; median 3.3 days). The frequency of the episodes varied from every 1.5 to 18 days (mean 8.7 days; median 7.3 days). Clinical improvement (decreased frequency, decreased duration, or decreased severity of the episodes)

began between ages 5 months and 24 months (mean 13.4 months; median 13.0 months). The age when the episodes ended (in 9/10 patients) ranged from 10 to 32 months (mean 18.6 months; median 18.0 months); in 1 patient, the episodes were continuing at age 58 months. Children were followed to ages from 20 to 79 months (mean 49.6 months; median 47.5 months). Search for triggering factors was largely negative, though 7 children had at least 1 episode of otitis media and 2 of those 7 had 5 episodes (mean 1.8 episodes; median 1.0 episode). In 5 cases, the torticollis was right sided, usually (4 cases) or always (1 case); in 1, it was usually left sided. In 7 cases, the torticollis alternated sides with successive attacks, usually (5 cases) or always (2 cases). In 7 cases, there was accompanying tortipelvis, always (4) or sometimes (3). The torticollis persisted during sleep, always (8 cases)

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The Neurology of Benign Paroxysmal Torticollis of Infancy / Rosman et al

or sometimes (1 case). Associated symptoms during attacks of torticollis included irritability (4 cases), upper limb dystonia (4 cases, with accompanying irritability in 3 of the 4), vomiting (2 cases) and pallor (1 case). Accompanying neurological abnormalities included gross motor delay in 5 children (moderate in 2, mild in 3), with accompanying mild fine motor delay in 3 of those 5. Head circumferences ranged from the 7th percentile to greater than the 97th percentile (mean 70th percentile; median 85th percentile). A total of 8 children had magnetic resonance imaging of brain; 7 were normal, whereas in 1, there was incidental bilateral temporal lobe hypoplasia. Family histories. Family histories were mostly negative for torticollis. In 1 boy whose benign paroxysmal torticollis began at 1.5 months, his younger sister developed benign paroxysmal torticollis at age 5 weeks; also, their maternal second cousin had torticollis in infancy. In a girl with benign paroxysmal torticollis, a maternal cousin had torticollis in infancy. The brother of another girl with benign paroxysmal torticollis developed a head tilt at times of fatigue, and a maternal great aunt had a head tilt. No patient had a family history of paroxysmal vertigo. All 10 patients had family histories of migraine affecting at least 2 other family members. In 8 of the 10, at least 1 parent had migraine (3 fathers, 6 mothers). Both patients whose parents did not have migraine, however, had second-degree relatives with migraine, as did 7 other patients. First-degree or second-degree family members of 6/10 cases had carsickness and/or other motion sickness. There was no family history of recurrent abdominal pain, except in 1 maternal aunt. There was no family history of recurrent vomiting, except for gastroesophageal reflux in the brother of 1 case. First-degree or second-degree family members in 7/9 cases had recurrent dizziness or vertigo. No family members had a history of alternating hemiplegia. There were no family members with global developmental delay, except for 1 autistic maternal second cousin. In 1 of our cases with persisting mild gross motor delay, several family members were said to be awkward as adults, while in another case where the child showed no gross motor delay, the mother was said to be awkward. Sequelae. Although there was persisting gross motor delay in 4/5 children, in 3/5 there was improvement: 1 from moderate to mild/moderate (by 36 months), 1 from moderate to mild (by 77 months), and 1 from mild to normal (by 36 months). In 2 children, mild gross motor delay persisted (at 59 and 62 months). In the 3 children with fine motor delay, 1 resolved (by 59 months), and in 2 it persisted (at 36 and 62 months). All 10 children had normal initial speech and language development, but in 2, mild dysarthria was noted later (at 62 and 70 months). One child had recurrent nocturnal headaches. Two had paroxysmal vertigo; in one, on awakening from sleep, often

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with a headache; in the other, during the daytime, with accompanying ataxia. No child had recurrent vomiting. Review of 103 Cases of Benign Paroxysmal Torticollis From the Literature Clinical features. There were 22 reports on 103 patients, with the number of cases in these reports ranging from 1 to 22. These included 60 girls and 43 boys. The childâ&#x20AC;&#x2122;s age with the first attack of torticollis ranged from 1 week to 30 months (mean 5.9 months; median 5.0 months). A total of 75% of the episodes began within the first 7 months of life and 95% within the first 14 months. The average duration of the episodes ranged from 10 minutes to 30 days (mean 4.5 days; median 2.0 days). A total of 75% of the episodes lasted 6 days or less and 90% 14 days or less. The frequency of the episodes ranged from 1 every 7 days to 1 every 5 months (mean 37.1 days; median 30.0 days). A total of 75% of the attacks recurred every 45 days or less and 90% every 75 days or less. Improvement began between ages 8 and 36 months (mean 20.8 months; median 21.0 months), with improvement seen by age 2 years in 75% and by 3 years in 95%. The age when the episodes stopped ranged from 3.5 to 60 months (mean 31.4 months; median 36.0 months). A total of 75% of the attacks stopped by 3 years and 95% by 4. Laterality of the torticollis was commented on in 18 cases; in all 18, it always (10) or usually (8) remained on the same side. Associated symptoms were reported in 74/103 cases (72%). Because in most reports, only the presence (and not the absence) of accompanying symptoms was recorded, it was not possible to determine the true frequency of each symptom. Thus, we could record only the number of cases in which each symptom was reported. Commonly reported symptoms were tortipelvis (25 cases), vomiting (36 cases), irritability (30 cases), vertigo and/or ataxia (usually indistinguishable; 24 cases), and pallor (18 cases). Less frequent symptoms were apathy or drowsiness (12 cases), gaze abnormalities (7 cases), limb dystonia (2 cases), and nystagmus (1 case). Audiometry was normal in 21 cases and abnormal in 3. Calorics were normal in 17 cases, abnormal in 9 (including the 3 with abnormal audiometry), and inconclusive in 5. A total of 12 of these abnormal test results (calorics 9, audiometry 3) came from the original report of benign paroxysmal torticollis.1 There were 3 additional reported cases of benign paroxysmal torticollis, in whom caloric testing indicated unilateral vestibular dysfunction, but there was no accompanying clinical information.23 Radiological studies were normal, including cervical spine films (29 cases), skull films (13 cases), computed cranial tomography (16 cases), magnetic resonance imaging of brain (6 cases), ultrasonography (2 cases), and angiography (1 case). Electroencephalograms were normal

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158 Journal of Child Neurology / Vol. 24, No. 2, February 2009

in 43/45 patients; in one child, occipital spikes were seen, but only during attacks; in another, the electroencephalogram showed ‘‘nonspecific abnormalities.’’ Family histories. There was a family history of benign paroxysmal torticollis in 6 cases. A family history of migraine was reported in 39 cases. There was a family history of motion sickness in 13 cases, with 12/13 from 1 report.3 Sequelae. Long-term outcome data were available in some cases. A total of 18/20 had normal gross motor development (one had immature gross motor skills, while another was ‘‘clumsy’’); 20/20 had normal fine motor development; 19/19 had normal speech and language development; 19/20 had normal cognition (the 20th had been born 2 months prematurely); 12 patients had recurrent headaches, some of them migrainous; 5 had recurrent vertigo; and 1 had cyclic vomiting.

benign paroxysmal torticollis in whom cold-water calorics produced an asymmetric response, suggesting unilateral vestibular dysfunction, but there was no accompanying clinical information.23 In all other reports, however, caloric testing has been normal or inconclusive (22/31 cases), and audiometry has been normal (21/24 cases). In the apparently only abnormal electromyographic (EMG) study in benign paroxysmal torticollis, continuous electrical discharges were seen over the ipsilateral sternomastoid muscle and over the contralateral trapezius muscle, suggesting that benign paroxysmal torticollis was a form of idiopathic paroxysmal infantile dystonia.5 By contrast, EMGs in 7 children with benign paroxysmal torticollis, with onset between 1 and 5 years, were normal.4

Discussion

A large number of studies have excluded many potential causes for benign paroxysmal torticollis. Abnormalities of the cervical spine, including recurrent atlantoaxial dislocation, atlanto-occipital fusion, Klippel–Feil syndrome and hemivertebrae, have been ruled out.1,6-10 Epileptiform activity has been sought on many electroencephalograms, but was found in only 1/45 cases.1,3,7-11 There has been no evidence for cervical adenitis, myositis, or fibrositis,6 nor has a superior oblique palsy, which can cause head deviation as in benign paroxysmal torticollis24 been seen.6 In many children with benign paroxysmal torticollis, Sandifer syndrome (reflux esophagitis), with or without a hiatus hernia, has been suspected25 but none has been found.8,12,13 There have been no cases of benign paroxysmal torticollis with a cervical spinal cord tumor6 or a posterior fossa brain tumor1,6,8,11,14 seen on neuroimaging. Of possible metabolic causes, glutaric aciduria has most often been considered, but not found.13 Paroxysmal torticollis can occur in children given phenothiazines or metoclopramide,26 but there have been no reported adverse drug reactions in any of these cases.

Benign paroxysmal torticollis was first described in 1969 by Snyder, who reported 12 cases, with onset in infancy in 11 of the 12. Nine had abnormal calorics bilaterally, suggesting that benign paroxysmal torticollis was caused by a disturbance of vestibular function, originating in the labyrinth or in its sensory innervation.1 In most subsequent reports, however, caloric (and audiometric) testing has been normal. Benign paroxysmal torticollis is not a frequent cause of torticollis; in 700 cases of primary torticollis followed from 1970 to 1988, only 7 (1%) were ones of benign paroxysmal torticollis.4 Individual attacks are distressful to the child, but unfortunately, no symptomatic treatment has been shown to help, including meclizine, dimenhydrinate, and chlorpromazine.1 Happily, however, in most children the attacks cease by age 3 years (Table 1). Many differing etiologies for benign paroxysmal torticollis have been considered. These fall into 3 categories: (1) possible causes of benign paroxysmal torticollis supported by abnormal laboratory test results; (2) possible causes of benign paroxysmal torticollis excluded by negative laboratory testing; (3) clinical findings indicating that benign paroxysmal torticollis is a forerunner of later migraine and/or a brain-based disorder associated with delayed neurological maturation. Benign Paroxysmal Torticollis With Abnormal Laboratory Test Results There have been 2 studies of benign paroxysmal torticollis suggesting it is a labyrinthine disorder, localized to the labyrinth itself or to its vestibular nerve supply. The first of these was the original report by Snyder; in 9 of his 12 patients, ice-water calorics failed to induce expected nystagmus in either ear; additionally, hearing was reduced in 3 of those 9.1 Eviatar briefly reported 3 children with

Benign Paroxysmal Torticollis With Negative Laboratory Test Results

Benign Paroxysmal Torticollis as a Forerunner to Migraine and/or as a Neurodevelopmental Disorder Benign paroxysmal torticollis’ close link to migraine and its invariable disappearance as the child grows older suggest strongly that benign paroxysmal torticollis is an age-sensitive neurodevelopmental disorder. Longitudinal studies have shown that some children with benign paroxysmal torticollis later develop benign paroxysmal vertigo, followed in sequence by cyclic vomiting and/or abdominal migraine, and eventually more classical cephalic migraine.15 Several authors consider benign paroxysmal torticollis to be an infantile form of benign paroxysmal vertigo.27 Others have viewed benign paroxysmal torticollis as a migraine precursor or equivalent2 or more specifically, as a form

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The Neurology of Benign Paroxysmal Torticollis of Infancy / Rosman et al

of basilar migraine.13,16 Dual etiologies have also been suggested, either vascular (with a family history of migraine), or labyrinthine or vestibular (with no such family history).12 In all of our 10 cases of benign paroxysmal torticollis, there was a history of migraine in at least 2 other family members, and often in more. In 8 of our 10 patients, at least 1 parent had migraine and at least 1 second-degree relative had migraine in 9 of our 10 patients. Family histories of migraine were present in at least 39 of the 103 cases of benign paroxysmal torticollis reported in the literature. The prevalence of migraine in the general population varies by age, ranging from 3% in early grade school children to 20% in older adolescents and adults.28,29 It has been suggested that the preponderance in girls of benign paroxysmal torticollis, seen also in migraine, indicates a causative genetic role, providing additional support for a benign paroxysmal torticollisâ&#x20AC;&#x201C;migraine link.13 The possibility of a genetic defect in these cases was suggested in 2001 by Ducros et al who found mutations in the CACNA1A gene, which encodes a neuronal calcium channel, present in 50% of families with hemiplegic migraine, including all such cases with permanent cerebellar signs.30 A year before, Drigo et al had speculated that benign paroxysmal torticollis might be caused by an ionic channel pathology, such as those thought to underlie familial hemiplegic migraine, alternating hemiplegia and episodic ataxia.3 Consistent with this thinking, Giffin et al suggested in 2002 that benign paroxysmal torticollis was a migraine equivalent, related to familial hemiplegic migraine, linked to a CACNA1A mutation on chromosome 19.2 Acknowledging the possible presence of a genetic defect in at least some cases of benign paroxysmal torticollis, it has been suggested that benign paroxysmal torticollis is a developmentally sensitive disorder associated with immaturity of the central nervous system.6,13 Some have suggested that the pathology resides in central vestibular structures and/or in their connections.3,13,16 Alternatively, it has been thought that the disorder is one of disturbed axial tone, which increases in a paroxysmal and asymmetric fashion, ipsilateral to the side of the paroxysmal torticollis. Such changes in axial tone are thought to be central in origin, possibly under the influence of the basal ganglia.4 Indeed, our cases support strongly this last speculation. Half of our cases (5/10) showed gross motor delay accompanying their benign paroxysmal torticollis, with associated fine motor delay in 3/5. As the children grew older, improvement was seen in 3 of the 5 with gross motor delay and in 1 of the 3 with fine motor delay. These gross motor delays, which may be of frontal lobe origin, may also be contributed to by the torticollis and tortipelvis seen in these children because such asymmetry in axial tone interferes with the childâ&#x20AC;&#x2122;s acquisition of large motor skills. In that regard, it is of interest that the 5 children with benign paroxysmal torticollis in whom gross motor development was delayed had more frequent accompanying

159

tortipelvis (4/5 vs 3/5 cases), had episodes with a longer mean duration (8.6 vs 7.4 days) and were of an older mean age when the episodes stopped (23.6 vs 21.4 months) than the children with benign paroxysmal torticollis without gross motor delay. These motor delays could not be explained by family history, for such delay was found in only 1 of the 5 families of our children with gross motor delay. Such motor delays have not been reported in other benign paroxysmal torticollis cases in the literature, perhaps because detailed neurodevelopmental examinations have not been done. Furthermore, each of our 10 cases had a strong family history of migraine, affecting at least 2 other family members. Additionally, there was a family history of car/ motion sickness in 6 cases and recurrent dizziness/vertigo in 7, both frequent migraine accompaniments. In the 103 cases reported in the literature, there was a family history of migraine in at least 39 cases, and car/motion sickness in at least 13 cases. The strong relationship of benign paroxysmal torticollis to migraine provides further support for the potential importance of neurological immaturity in benign paroxysmal torticollis, for 25% to 40% of childhood migraineurs become migraine-free on long-term follow-up.28,31 It thus would appear that maturational changes in the central nervous system may underlie the inevitable disappearance of benign paroxysmal torticollis as the affected child grows older.

Conclusion Benign paroxysmal torticollis is an important cause of torticollis, and doubtlessly under-recognized by pediatric practitioners. Benign paroxysmal torticollis begins in early infancy, with recurrent episodes of cervical dystonia, usually lasting days, with recurrences in days to months, with improvement within 2 years and resolution within 3 years. Frequent accompaniments include irritability, vomiting, pallor, ataxia, tortipelvis, and delayed gross and fine motor development. Laboratory studies are usually negative and no treatment has been effective. Migraine is very frequent in other family members and benign paroxysmal torticollis itself is a frequent forerunner of later migraine. These data indicate that benign paroxysmal torticollis is probably an age-sensitive, migraine-related disorder, which may be associated with delayed motor development. The symptoms of benign paroxysmal torticollis invariably disappear, and this is often accompanied by an acceleration in the childâ&#x20AC;&#x2122;s motor development.

References 1. Snyder CH. Paroxysmal torticollis in infancy: a possible form of labyrinthitis. Am J Dis Child. 1969;117:458-460.

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2. Giffin NJ, Benton S, Goadsby PJ. Benign paroxysmal torticollis of infancy: four new cases and linkage to CACNA1A mutation. Develop Med Child Neurol. 2002;44:490-493. 3. Drigo P, Carli G, Laverda AM. Benign paroxysmal torticollis of infancy. Brain Dev. 2000;22:169-172. 4. Nikolic V, Banic M. Paroxysmal torticollis in the developmental age. Med Pregl. 1989;42:99-101. 5. Kimura S, Nezu A. Electromyographic study in an infant with benign paroxysmal torticollis. Pediatr Neurol. 1998;19:236-238. 6. Gourley IM. Paroxysmal torticollis in infancy. Can Med Assoc J. 1971;105:504-505. 7. Hanukoglu A, Somekh E, Fried D. Benign paroxysmal torticollis in infancy. Clin Pediatr. 1984;23:272-274. 8. Cohen HA, Nussinovitch M, Ashkenasi A, Straussberg R, Kauschanksy A, Frydman M. Benign paroxysmal torticollis in infancy. Pediatr Neurol. 1993;9:488-490. 9. Balslev T, Flarup M, Ostergaard JR, Haslam RH. Benign paroxysmal torticollis. Recurrent involuntary twisting of the head in infants and young children. Ugeskr Laeger. 1998;160:5365-5367. 10. Dimitrijevic L, Colovic H, Zivkovic V. Benign paroxysmal torticollis in infancy. Vojnosanit Pregl. 2006;63:69-71. 11. Casella LB, Casella EB, Baldacci ER, Ramos JL. Benign paroxysmal torticollis of infancy: diagnosis and clinical evolution of six patients. Arq Neuropsiquiatr. 2006;64:845-848. 12. Lipson EH, Robertson WC. Paroxysmal torticollis of infancy: familial occurrence. Am J Dis Child. 1978;132:422-423. 13. Sanner G, Bergstrom B. Benign paroxysmal torticollis in infancy. Acta Paediatr Scand. 1979;68:219-223. 14. Del Cuore F. Torcicollo parossistico benigno nellâ&#x20AC;&#x2122;infanzia. Pediatr Med Chir. 1997;19:69-70. 15. Al-Twaijri WA, Shevell MI. Pediatric migraine equivalents: occurrence and clinical features in practice. Pediatr Neurol. 2002;26:365-368. 16. Deonna T, Martin D. Benign paroxysmal torticollis in infancy. Arch Dis Child. 1981;56:912-919.

17. Bratt HD, Menelaus MB. Benign paroxysmal torticollis of infancy. J Bone Joint Surg Br. 1992;74:449-451. 18. Chaves-Carballo E. Paroxysmal torticollis. Semin Pediatr Neurol. 1996;3:255-256. 19. Ishida T, Hattori S, Ueda T, Nanba H. Benign paroxysmal torticollis in infancy: case report. No To Hattatsu. 1990;22: 274-278. 20. Poddar U, Singh S, Kumar L. Paroxysmal torticollis of infancy. Ind Pediatr. 1999;36:86-88. 21. Roulet E, Deonna T. Benign paroxysmal torticollis in infancy. Develop Med Child Neurol. 1988;30:407-412. 22. Scagni P, Morello M, Pagliero R, Pecco P. Benign paroxysmal torticollis of infancy: a case report. Minerva Pediatr. 2006;58: 499-501. 23. Eviatar L. Benign paroxysmal torticollis. Pediatr Neurol. 1994;11:72. 24. Raab EL. Paroxysmal torticollis in infancy. Am J Dis Child. 1970;119:378. 25. Murphy WJ, Gellis SS. Torticollis with hiatus hernia: Sandifer syndrome. Am J Dis Child. 1977;131:564-565. 26. Casteels-van Daele M. Paroxysmal torticollis in infancy. Am J Dis Child. 1970;120:88. 27. Dunn DW, Snyder CH. Benign paroxysmal vertigo. Am J Dis Child. 1976;130:1099-1100. 28. Bille B. Migraine in childhood and its prognosis. Cephalalgia. 1981;1:71-75. 29. Pakalnis A. Current therapies in childhood and adolescent migraine. J Child Neurol. 2007;22:1288-1292. 30. Ducros A, Denier C, Joutel A, et al. The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel. N Engl J Med. 2001;345:17-24. 31. Kienbacher C, Wober C, Zesch HE, et al. Clinical features, classification, and prognosis of migraine and tension-type headache in children and adolescents: a long-term follow-up study. Cephalalgia. 2006;26:820-830.

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Journal of Child Neurology