Sleep Myoclonus Research Articles

NON EPILEPTIC PAROXYSMAL EVENTS IMITATING EPILEPSY IN CHILDREN

Differential diagnosis of epileptic seizures with non epileptic paroxysmal events often have serious difficulties. The most various states which are observed at somatic, neurologic, psychiatric disorders and even at healthy children imitate an epilepsy. Objective. Evaluation of reliability of the diagnosis “epilepsy” in patients referred to the epilepsy center. Material and methods. 2015 patients referred to our epilepsy center for evaluation and treatment for 3-year period. Age from 0 to 21 years. Methods of diagnosis: clinical examination, video-EEG monitoring (VEEG) of 6 to 120 hours, brain MRI. Results. The diagnosis of “epilepsy” was reliably confirmed in 1552 patients (77%). Among these, 101 (6,5%) patients were diagnosed late (later than 6 months from the onset with seizures frequency more often than 1 time per month). At 463 (23%) patients overdiagnosis has been established – the diagnosis epilepsy with the current seizures was established unreasonably. Among them we have identified the following 3 groups: healthy children – 57 patients (12.3%); somatic and neurological disorders – 323 patients (70%); psychogenic non-epileptic seizures (PNES) – 83 patients (18%). The most frequently seizures was imitated by hyperkinetic movement disorders – 40.4% (187 patients), including paroxysmal dyskinesia, hyperkinetic eye movements, pathological nonepileptic myoclonus, jitteriness, shuddering attacks, benign neonatal sleep myoclonus, tics, hyperekplexia, benign myoclonus of early infancy, benign paroxysmal torticollis, spasmus nutans. Among the frequent reasons of over-diagnosis of epilepsy were also parasomnias and PNES. Conclusions. The most frequent diagnostic errors were linked to the lack of objective information about the nature of paroxysms and misinterpretation of the EEG. VEEG is the most valuable tool in the differential diagnosis of epilepsy

Benign neonatal sleep myoclonus

Benign neonatal sleep myoclonus (BNSM), first described in 1982 by Coulter and Allen [1], is the non-epileptic condition most frequently confused with epileptic seizures during infancy. The etiology is uncertain: transient dysfunction of the serotoninergic system, a benign disturbance of the brainstem reticular activating system involved with initiation and synchronization of sleep and a genetic predisposition have been suggested by some authors. However none of these mechanisms has been proved [1,2]. The prevalence is also unknown, but it is thought that the condition is under-recognized. It was first described in three boys and in most subsequent publications, the condition was more commonly described in boys. Very recently, it has been shown that BNSM is extremely frequent in the newborn offspring of opiate-dependent mothers [3]. Myoclonic jerks usually present within a few days of birth. In a detailed study of 38 patients with BNSM the jerks appeared within the first 16 days, (median 3 days) and remitted in the first 10 months (median 2 months) of life [4]. It is usually said that the jerks disappear by the age of 3 months, but Egger et al. [5] demonstrated that the condition could persist for months and years. In the first description of BNSM myoclonus was reported to be bilateral, synchronous, and to mainly involve the distal parts of the upper extremities, with flexion of fingers, wrist, and elbow [1]. It is usually de-

Paroxysmal non-epileptic events in infants and toddlers: A phenomenologic analysis.

The aim of this study was to analyze in detail the clinical phenomenology of paroxysmal non-epileptic events (PNEE) in infants and toddlers. We studied all children aged ≤2 years who were diagnosed with PNEE based on video-electroencephalographic (VEEG) recordings. We analyzed the following four clinical domains of each clinical event: (i) motor manifestations (body/limb jerking, complex motor, and asymmetric limb posturing); (ii) oral/vocal (crying, vocalization, sighing); (iii) behavioral change (arrest of activity, staring); (iv) and autonomic (facial flushing, breath holding). Thirty-one of 81 (38.3%) infants and toddlers had 38 PNEE recorded during the study period (12 girls and 19 boys, mean age 10.5 months). The predominant clinical features were as follows: motor in 26/38 events, oral/verbal in 14/38 events, behavioral in 11/38 events, and autonomic in 8/38 events. Epileptic seizures and PNEE coexisted in four children (12.9%). Seventeen children (54.8%) had one or more risk factors suggestive of epilepsy. Twelve children (38.7%) had a normal neurologic examination, 10 (32.3%) had developmental delay, and eight (25.8%) had a family history of epilepsy or seizures. VEEG recorded PNEE in nearly 40% of 81 infants and toddlers referred for unclear paroxysmal events in our cohort. Non-epileptic staring spells and benign sleep myoclonus were the most common events recorded, followed by shuddering attacks and infantile masturbation. In addition, greater than one-half of the infants and toddlers had risk factors, raising a concern for epilepsy in the family and prompting the VEEG evaluation, suggesting that paroxysmal non-epileptic seizures may frequently coexist in young children with epilepsy.

Acute movement disorders in children: experience from a developing country.

We describe acute movement disorders in 92 children, aged 5 days to 15 years, from an Indian tertiary hospital. Eighty-nine children had hyperkinetic movement disorders, with myoclonus in 25, dystonia in 21, choreoathetosis in 19, tremors in 15, and tics in 2. Tetany and tetanus were seen in 5 and 2 children, respectively. Hypokinetic movement disorders included acute parkinsonism in 3 children. Noninflammatory and inflammatory etiology were present in 60 and 32 children, respectively. Benign neonatal sleep myoclonus in 16 and opsoclonus myoclonus syndrome in 7 accounted for the majority of myoclonus cases. Vitamin B12 deficiency in 13 infants was the most common cause of tremors. Rheumatic fever and encephalitis were the most common causes of acute choreoathetosis. Acute dystonia had metabolic etiology in 6 and encephalitis and drugs in 3 each. Psychogenic movement disorders were seen in 4 cases only, although these patients may be underreported.

Enterovirus 71 outbreak in Northern Sydney, 2013: case series and initial response.

Enteroviruses are a common cause of childhood disease which may manifest in a variety of ways. Enterovirus 71 (EV71) is a subtype of enterovirus which can cause meningoencephalomyelitis resulting in neurological sequelae including lethargy, weakness, ataxia, sleep myoclonus, urinary retention and, in severe cases, cardiorespiratory collapse due to neurogenic pulmonary oedema. EV71 was responsible for outbreaks in South East Asia in 1997-1998, in Western Australia in 1999 and in Sydney in 2000-2001. In 2013, we are experiencing another EV71 outbreak in Sydney. This study describes the discovery of a new outbreak in Sydney's Northern Beaches, the clinical findings as well as the public health response. Thirty-seven children in total presented with presumed EV71 to the Northern Beaches Health Service from December 2012 to April 2013. Most children presented with a prodrome lasting 2-7 days prior to seeking medical attention. Sleep myoclonus was a common presenting sign occurring in 65%. Neurological signs were subtle in the majority of children and were at times missed by clinicians on a child's first presentation. Forty-six per cent of children who presented to Northern Beaches Health Service during this outbreak required a transfer to a tertiary paediatric centre for more intensive care. The public health investigation was important in establishing that the disease was widespread throughout the community and not as a result to exposure to a single child care setting. Identification of risk factors enabled more targeted communication to medical practitioners, child care centres and parents within the local community. EV71 is in Australia and all clinicians seeing children in primary, secondary and tertiary care centres need to be aware of the disease, the subtle nature of initial symptoms and the potentially devastating consequences.

Benign neonatal sleep myoclonus: our experience of 15 Japanese cases.

Benign neonatal sleep myoclonus is a non-epileptic movement disorder that may mimic neonatal seizures. The aim of this study was to clarify the clinical manifestations and outcomes in Japanese infants with benign neonatal sleep myoclonus. We reviewed the clinical manifestations and outcomes in 15 consecutive patients with benign neonatal sleep myoclonus (males: 10), including three paired familial cases, referred to our center between 1996 and 2011. The diagnosis of benign neonatal sleep myoclonus was based on a neonatal onset, characteristic myoclonic jerks that occurred during sleep, and normal electroencephalogram findings. All were healthy full-term neonates at birth. The age at onset ranged from 1 to 18 days (median: 7 days). Prior to referral to our center (3-8 weeks), two infants had been placed on antiepileptic drugs, without effects. During the clinical course, the myoclonic jerks resolved by 6 months in 14 of the 15 patients. On follow-up (final evaluation, mean: 38 months), all but one patient (speech delay) showed normal development. None developed epilepsy. Of note, migraine occurred after 5 years of age in three children, including one who developed cyclic vomiting syndrome, evolving to migraine. Another boy developed cyclic vomiting syndrome, a precursor of migraine, before 1 year, and was being followed. A high incidence of migraine was observed in five (42%) of 12 parents whose detailed family history was available. Our study suggests that benign neonatal sleep myoclonus is related to migraine. With the high rate of familial cases, further genetic study, including migraine-related gene analysis, is necessary to determine the underlying mechanism responsible for benign neonatal sleep myoclonus.

Monosomy 1p36 – A multifaceted and still enigmatic syndrome: Four clinically diverse cases with shared white matter abnormalities

Monosomy 1p36 is the most common subtelomeric deletion syndrome seen in humans. Uniform features of the syndrome include early developmental delay and consequent intellectual disability, muscular hypotonia, and characteristic dysmorphic facial features. The gene-rich nature of the chromosomal band, inconsistent deletion sizes and overlapping clinical features have complicated relevant genotype–phenotype correlations. We describe four patients with isolated chromosome 1p36 deletions. All patients shared white matter abnormalities, allowing us to narrow the critical region for white matter involvement to the deletion size of up to 2.5 Mb from the telomere. We hypothesise that there might be a gene(s) responsible for myelin development in the 1p36 subtelomeric region. Other significant clinical findings were progressive spastic paraparesis, epileptic encephalopathy, various skeletal anomalies, Prader-Willi-like phenotype, neoplastic changes – a haemangioma and a benign skin tumour, and in one case, sleep myoclonus, a clinical entity not previously described in association with 1p36 monosomy. Combined with prior studies, our results suggest that the clinical features seen in monosomy 1p36 have more complex causes than a classical contiguous gene deletion syndrome.

Study of neck myoclonus isolated and associated to other involuntary movements during the sleep

Introduction We assessed the frequency and characteristics of neck myoclonus during sleep in a prospective sleep- disorder cohort, and investigated its correlates and associations with other involuntary movements. Materials and methods We studied 51 consecutive patients with parasomnia or hipersomnia (37 men; mean age 54 ± 18) undergoing routine time-synchronized videopolysomnography at the sleep laboratory. Neck myoclonus was defined as sudden, non-sustained dorsal or ventral flexion or version of the head to one side with varying amplitude from mild to intense. We differentiated between isolated neck myoclonus and that associated to other involuntary movements in the limbs or body. We excluded neck movements preceded by arousals, positional change, apnea o periodic legs movements. Results Ninety-six per cent of the patients had at least one neck myoclonus during sleep. The mean number of neck myoclonus was 1.18/h sleep (IC 95%: 0.65 ∼ 1.72). Movements were more frequent during REM sleep than NREM (1.16 and 0.36 respectively, p: 0.016). Isolated and associated neck myoclonus occurred with similar frequency (isolated 4.0 ± 5.7 and associated 4.7 ± 7.1). About half of the neck myoclonic movements were accompanied by simultaneous movements of other body parts, predominantly in the arms (mean 1.8 ± 2.5), and approximately 50% of them induced an arousal. The number of patients was too small to establish a study by ages. Conclusion In the sleep laboratory neck myoclonus is observed in most patients but it occurs occasionally, most of then in REM sleep. Isolated neck myocloni are as frequent as neck myocloni associated with other movements in the body, especially arm movements. Acknowledgements We thank Dr. Joan Santamaria for his scientific supervission.

YouTube as a Source of Information for Children with Paroxysmal Episodes

Whereas to date the internet is a main source of information for many parents, there are no restrictions regarding data presentation. Thus, the aim of this study was to assess the quality of internet material concerning paroxysmal episodes.We rated videos on YouTube for several conditions like infantile spasms, absence seizures, Sandifer syndrome, sleep myoclonus, and shuddering attacks. Videos were classified into different categories of certainty of diagnosis according to expert opinion based on a 4 point Likert scale followed by calculation of interrater reliability. Also the quality of supplemental information was assessed, as well as whether videos were helpful from a neuropaediatrican's point of view in counselling patients and their parents.In sleep myoclonus, absences and infantile spasms correlation between title of videos and classification by expert opinion was good. There was more discrepancy with the videos concerning Sandifer syndrome and shuddering attacks. Interrater reliability was low for Sandifer syndrome, fair for absences, shuddering attacks and sleep myoclonus and moderate for infantile spasms. Some supplemental information was rated to be helpful but other information was found to be misleading or even unsettling for patients and their parents.We consider that video material on YouTube can generally not be considered as helpful for parents because of a significant disagreement between experts, even for the most well defined disorders in our study.

Seizures in Newborn: An Update

Neonatal seizure is the most prominent neurological dysfunction in the neonatal period which constitutes a medical emergency. Seizures result from excessive depolarization of neurons within the nervous system. Tonic, clonic, subtle and myoclonic are the different forms of neonatal seizure. Among the causes hypoxic ischemic encephalopathy is the commonest. Jitteriness and benign neonatal sleep myoclonus should be differentiated from the neonatal seizure. Proper history taking and meticulous examination should aimed to identify the seizure and find out the aetiology. Important investigations include blood sugar, serum electrolytes (Na, Ca, Mg), arterial blood gas, anion gap, cerebrospinal fluid examination, ultrasound examination of the head and electroencephalography. Upon identification of common metabolic derangements like hypoglycaemia, hypocalcaemia, hypomagnesemia, they are treated as per recommended protocol. The rest of the symptomatic seizures (nonmetabolic) are treated with phenobarbitone. If seizures failed to respond or recur after Phenobarbitone therapy, Phenytoin, Midozolam are the subsequent options. As the recurrence rate is relatively small and the potential toxicities are high on developing brain, the good practice is to stop anticonvulsant as early as possible. Neonatal seizures have an adverse effect on neurodevelopmental outcome and predispose to cognitive, behavioral, or epileptic complications in later life. DOI: http://dx.doi.org/10.3329/jssmc.v4i1.12000 J Shaheed Suhrawardy Med Coll, 2012;4(1):26-31

Paroxysmal nonepileptic events in pediatric patients confirmed by long-term video-EEG monitoring — Single tertiary center review of 143 patients

The purpose of the study was to evaluate the clinical characteristics of paroxysmal nonepileptic events (PNEs) in pediatric patients. Reports of 1108 patients who underwent long-term video-EEG monitoring at Seoul National University Children's Hospital were reviewed retrospectively. One hundred forty-three (12.9%) patients were diagnosed as having PNEs. The most common type of PNE was staring. Staring, tonic posturing, sleep myoclonus, and sleep-related disorders were more common in patients younger than 6years old. Psychogenic nonepileptic seizure was the most common PNE in patients older than 6years. Patients who were younger than 6years old showed shorter disease duration and more varied types of PNEs when compared to older patients (6years old or older). Presence of epilepsy was not significantly related to clinical difference in PNEs. In patients with developmental delay, staring and tonic posture were significantly more frequent than patients without developmental delay. Thirty-two patients without concurrent epilepsy were misdiagnosed with epilepsy, and AEDs were discontinued after the correct diagnosis of PNEs. Whenever the diagnosis of paroxysmal abnormal behavior is uncertain, correct diagnosis should be made using long-term video-EEG monitoring, especially in younger pediatric patients and patients with developmental delay.

Benign Neonatal Sleep Myoclonus

Benign neonatal sleep myoclonus is an uncommon, nonepileptic disorder characterized by myoclonic jerks appearing in the neonatal period that occur predominantly during sleep. Although self-limiting, the disorder is frequently confused with epileptic neonatal seizures. A few familial cases have been reported; however the genetics has not been studied. We ascertained 3 families with 2 or more affected individuals and analyzed the pedigrees. We used microsatellite markers to determine if the disorder was possibly linked to KCNQ2 or KCNQ3, the 2 genes that cause most cases of benign familial neonatal seizures, a disorder that it could be easily confused with. The 3 pedigrees, including one with 4 affected individuals, were suggestive of autosomal dominant inheritance. The loci for KCNQ2 and KCNQ3 were excluded in the 2 larger families. We conclude that benign neonatal sleep myoclonus can show autosomal dominant inheritance and is not allelic with benign familial neonatal seizures.

Paroxysmal non‐epileptic motor events in childhood: a clinical and video‐EEG–polymyographic study

The aim of this article was to describe the phenomenology and polymyographic features of paroxysmal non-epileptic motor events (PNMEs) observed in a series of typically developing and children with neurological impairment. We conducted a retrospective evaluation of 63 individuals (29 females; 34 males) affected by PNMEs at the National Neurological Institute 'C. Besta' between 2006 and 2008. Individuals were included in the study if they had PNMEs documented by a video-electroencephalography-polymyographic study and were aged between 1 month and 18 years (mean age at the time of video-electroencephalography-polymyography: 5y 10mo). In 45 of the 63 participants (71%), PNMEs were associated with other neurological conditions (secondary) including epilepsy, whereas in 18 participants PNME was the only neurological symptom (primary). Clinical features allowed classification of the motor disturbance into usual movement disorder categories in 31 individuals (49%); in the remaining 32 (51%), the movement disorder was characterized on the basis of polymyographic pattern of 'jerks' or 'sustained contraction'. The most frequent PNMEs were paroxysmal dyskinesias, followed by startle, stereotypies, shuddering, sleep myoclonus, psychogenic movement disorders, and benign myoclonus of early infancy; the last syndrome was also observed in children with neurological impairment. In eight participants, PNMEs remained unclassified. PNMEs may occur in both healthy and children with neurological impairment and are caused by a wide range of static and progressive conditions. In the majority of children with neurological impairment with associated epilepsy, the PNMEs do not fit into the usual movement disorders categories. A video-electroencephalography-polymyography is therefore useful for characterizing them.

Benign convulsions in newborns and infants: Occurrence, clinical course and prognosis

Background During early development severe epilepsies may appear, some with well established occurrence. Benign non-epileptic and epileptic paroxysmal syndromes with excellent prognosis occur in the same period. There are no exact data on their occurrence. Aim We have reviewed medical histories of children with benign non-epileptic or benign epileptic events: benign myoclonus of early infancy, benign neonatal sleep myoclonus, benign sleep myoclonus in infancy, benign partial epilepsy in infancy (BPEI) and benign infantile familial convulsions (BIFC) were established. The occurrence, clinical characteristics and prognosis of these syndromes were evaluated. Methods Inclusion criteria were met in 31 children. Research included retrospective analysis of clinical characteristics, laboratory values, neuroimaging and neurophysiological assessments, followed by evaluation of psychosocial development with the use of the Strengths and Difficulties Questionnaire (SDQ), fulfilled by parents. Results In our group the incidence of benign non-epileptic convulsions was 6.69 per 10 000 live births and the incidence of benign epileptic convulsions was 1.35 per 10 000. Male/female ratio in the group of children with non-epileptic events was 2.1:1. Among non-epileptic group 5 out of 23 children and among epileptic group 3 out of 8 children had minimal, mild or moderate abnormalities at neurological assessment at the time of the first clinical examination. Nonspecific changes in laboratory values were seen in 6 out of 23 in the non-epileptic and in 1 out of 8 children in the epileptic group. Neurophysiological assessments showed subtle changes in 4/23 in the non-epileptic and 6/8 in the epileptic group. Neuroimaging was not optimal in 5/23 with non-epileptic and 3/8 with epileptic events. Analysis of SDQ did not show significant deviations in psyhosocial development. Statistically significant deviation was observed only in relations with peers ( p = 0.009). Conclusions Benign neonatal and infantile convulsions are more frequent than severe epilepsies of the same age period. Results show higher proportion of males with benign non-epileptic conditions. No deviations in further development was found. Laboratory values, neuroimaging and neurophysiological assessments were normal or nonspecifically changed.

Benign neonatal sleep myoclonus: A case with a spinal generator?

Benign neonatal sleep myoclonus (BNSM) is characterized by 1) neonatal onset, 2) myoclonic jerks occurring only during sleep, 3) abrupt and consistent cessation of jerks with arousal, 4) absence of electroencephalographic seizures, and 5) good outcome.1 The estimated incidence varies between 0.8 and 3.0 cases per 1,000 births.2 Procedures like repetitive sound, tactile stimuli, or rocking have been reported to provoke or worsen myoclonus.3 It is very important to differentiate BNSM from epilepsy, as it occurs in neurologically healthy neonates, usually disappears before 6 months of age, and requires no treatment. We report a child with BNSM in whom EEG was combined with polymyography and back-averaging, in an attempt to further characterize and analyze the myoclonus, as the pathophysiologic mechanism is unknown. ### Case report. A boy was born at 39 weeks of gestation following an uncomplicated pregnancy. At the time of delivery he had mild asphyxia due to a nuchal cord. Apgar scores …

A descriptive analysis of neck myoclonus during routine polysomnography.

Although episodes of neck myoclonus (head jerks) in REM sleep have a characteristic appearance, they have so far not been described systematically in video-polysomnography. This study assesses the occurrence, frequency, and characteristics of neck myoclonus in REM sleep in a prospective sleep disorder cohort, and investigates clinical correlates and associations with medication. University hospital sleep disorders center. Two-hundred twenty-eight mixed sleep disorder patients. Not applicable. REM sleep was screened visually for short "stripe-shaped" movement-induced artifacts visible vertically over the EEG leads in polysomnographic registration. If such artifact was present, the synchronized video was inspected for the presence of neck myoclonus. Out of 205 patients, 54.6% (n = 112) had neck myoclonus during REM sleep. The mean neck myoclonus index was 1.0 +/- 2.7/h REM sleep. Younger patients had a higher neck myoclonus index than older patients (< 45 years versus 45-60 years versus > 60 years: 1.8 +/- 4.2 versus 0.6 +/- 1.1 versus 0.5 +/- 1.1; P = 0.004). Ninety-five percent of subjects < 45 years had a neck myoclonus index between 0 and 9.4/h; 95% of subjects > 45 years had a neck myoclonus index between 0 and 2.7/h. Patients on benzodiazepine treatment had no neck myoclonus (0/112 vs. 13/93; P < 0.001). In 23 patients, additional surface neck EMG was performed. EMG activation associated with neck myoclonus had a mean duration of 0.6 +/- 0.4 sec. Correlation between duration of neck EMG activation and movement-induced EEG artifact duration was very high (rho = 0.96; P < 0.001). Neck myoclonus is common during REM sleep and more frequent in younger individuals. This could indicate that neck myoclonus during REM sleep is a physiological phenomenon. If there is a cut-off distinguishing normal from excessive has to be investigated in further studies.

Benign Neonatal Sleep Myoclonus: A Review of the Literature

Neurologically normal term infants sometimes present with repetitive, rhythmic myoclonic jerks that occur during sleep. The condition, which is traditionally resolved by 3 months of age with no sequelae, is termed benign neonatal sleep myoclonus. The goal of this review was to synthesize the published literature on benign neonatal sleep myoclonus. The US National Library of Medicine database and the Web-based search engine Google, through June 2009, were used as data sources. All articles published after the seminal description in 1982 as full-length articles or letters were collected. Reports that were published in languages other than English, French, German, Italian, Portuguese, or Spanish were not considered. We included 24 reports in which 164 term-born (96%) or near-term-born (4%) infants were described. Neonatal sleep myoclonus occurred in all sleep stages, disappeared after arousal, and was induced by rocking the infant or repetitive sound stimuli. Furthermore, in affected infants, jerks stopped or even worsened by holding the limbs or on medication with antiepileptic drugs. Finally, benign neonatal sleep myoclonus did not resolve by 3 months of age in one-third of the infants. This review provides new insights into the clinical features and natural course of benign neonatal sleep myoclonus. The most significant limitation of the review comes from the small number of reported cases.

P181 Sleep myoclonus in a child with brainstem damage: a video polysomnographic study

P181 Sleep myoclonus in a child with brainstem damage: a video polysomnographic study

Benign Neonatal Sleep Myoclonus: History and Semiology

Benign neonatal sleep myoclonus is a condition characterized by myoclonus occurring during sleep. Reported here are 18 cases of infants who had electroencephalographic monitoring, with myoclonic events recorded in 17 cases. In all cases, onset was within days to a few weeks of birth. In no case was the diagnosis of sleep myoclonus considered by the referring primary care physician. Myoclonus was evident during sleep in all 18 infants, but in two of them it was observed also during the transition from sleep to awakening. The behavioral features of the disorder were more varied than previously described: four of the infants had lateralized myoclonus and two had myoclonus involving the head and face. In most of the children, the duration of myoclonus was brief, but in two cases the paroxysmal events lasted more than 30 minutes. None of the children had electroencephalographic abnormalities during the myoclonus. The condition was short-lived, with the myoclonus resolving in most children within 3 months of onset. Benign neonatal sleep myoclonus is an under-recognized condition but one that has a consistently favorable outcome. Infants with the condition should not be treated with antiepileptic drugs.

Benign neonatal sleep myoclonus in newborn infants of opioid dependent mothers

The aim of our study was to evaluate the incidence, duration and risk factors for benign neonatal sleep myoclonus (BNSM) in infants with neonatal abstinence syndrome (NAS) treated with opioids or sedatives, compared with control infants. This is a single centre observational case control study. Seventy-eight near term and term infants with neonatal opiate abstinence syndrome confirmed by meconium analysis were included. Exclusion criteria were cerebral malformation, intracranial haemorrhage and perinatal asphyxia. The babies were assessed eight hourly with a modified Finnegan score that included sleep myoclonus. Seventy-eight infants not exposed to opiates during pregnancy, hospitalized for at least 14 days and matched for gestational age were used as controls. The median gestational age was 38 (1)/(7) (95% CI: 35 (3)/(7)-41 (2)/(7)) weeks, birth weight 2730 (95% CI: 1890-3600) g, umbilical artery pH 7.25 (CI 7.10-7.37) and Apgar score at 5 minutes 9 (95% CI: 7-10). The control infants did not differ in these characteristics. Sleep myoclonus was diagnosed in 52 (67%) of the infants with NAS and 2 (2.6%) of the controls (OR 26 [95% CI: 7-223], p < 0.001). Myoclonus appeared as early as day 2 and as late as day 56 of life (median day 6) and lasted for 1 to 93 days (median 13 days). All infants had serum glucose > 2.5 mmol/L at first occurrence. The neurological examinations as well as cerebral ultrasound scans were normal. An electroencephalogram (EEG) carried out in 18 infants showed no signs of epileptic activity. BNSM has a high incidence in infants with NAS. The diagnosis can be made clinically. In the absence of other neurological symptoms further investigations such as EEG are not necessary and anticonvulsive treatment is not indicated.