Cataplexy Mistaken for Seizures in a Patient With Undiagnosed Narcolepsy Type I.

Narcolepsy Type 1 is a sleep disorder, with cataplexy as its cardinal feature, characterized by sudden decrease or loss of muscle tone triggered by strong emotions. Cataplexy can be misdiagnosed as epileptic seizures given its clinical similarity to atonic seizures. The low prevalence of the disease added another layer of complexity in providing timely and accurate diagnosis. We report a case of a young man with recurrent episodes of falling and an inability to respond, initially misinterpreted as epileptic seizures due to findings in routine electroencephalography (EEG). Anti-seizure medications were ineffective, and subsequent ambulatory EEG revealed no epileptic activity during events. A detailed history uncovered symptoms of cataplexy and daytime sleepiness, leading to the correct diagnosis of narcolepsy type I confirmed by polysomnogram (PSG) and mean sleep latency test (MSLT). Discontinuation of anti-seizure medications and treatment with venlafaxine successfully resolved cataplexy. The case highlights the importance of a thorough clinical history in distinguishing cataplexy from seizures, as well as the caution against relying solely on EEG findings for epilepsy diagnosis. Ambulatory EEG can help exclude epileptic events, and PSG with MSLT are necessary to confirm narcolepsy type I.

Treatment of REM sleep behavior disorder with trazodone: report of 3 cases.

Rapid eye movement sleep behavior disorder is a sleep disturbance characterized by the absence of regular paralysis during rapid eye movement sleep, accompanied by dream enactment behavior. The available pharmacotherapy options for treating rapid eye movement sleep behavior disorder are limited, and the utilization of antidepressants has yielded mixed results. We report 3 cases of isolated rapid eye movement sleep behavior disorder improved with trazodone. Doses of 50-100 mg of trazodone at bedtime over 4-6 months resulted in significant clinical improvement. These cases highlight that trazodone could serve as a treatment for isolated rapid eye movement sleep behavior disorder that does not respond to traditional treatments at submaximal dosages. CITATION: Barrow J, Vendrame M. Treatment of REM sleep behavior disorder with trazodone: report of 3 cases. J Clin Sleep Med. 2024;20(5):821-823.

Perspective: A resident's role in promoting safe machine-learning tools in sleep medicine.

Residents and fellows can play a helpful role in promoting safe and effective machine-learning tools in sleep medicine. Here we highlight the importance of establishing ground truths, considering key variables, and prioritizing transparency and accountability in the development of machine-learning tools within the field of artificial intelligence. Through understanding, communication, and collaboration, in-training physicians have a meaningful opportunity to help progress the field toward safe machine-learning tools in sleep medicine. CITATION: Smith CM, Vendrame M. Perspective: a resident's role in promoting safe machine-learning tools in sleep medicine. J Clin Sleep Med. 2023;19(11):1985-1987.

Images: Irregular sleep-wake rhythm disorder in transgender individuals.

Growing evidence suggests that transgender individuals face a significant health disparity and are particularly vulnerable to sleep disorders. We present two patients who developed irregular sleep-wake rhythm disorder after gender reassignment and hormone replacement therapy. The growing interest in transgender health warrants further evaluation of the effects and frequency of all sleep disorders in this population. Efforts to address sleep disorders should consider assessing sleep disturbance in terms of sleep/wake patterns and schedules. CITATION: Kokash A, Vendrame M. Images: irregular sleep-wake rhythm disorder in transgender individuals. J Clin Sleep Med. 2023;19(11):1981-1984.

Seizure control with treatment of delayed sleep-wake phase disorder in juvenile myoclonic epilepsy: A case report.

Juvenile Myoclonic Epilepsy (JME) is an idiopathic generalized epilepsy associated with a characteristic sleep/wake rhythm, with the tendency to go to bed later at night, to get up later in the morning. In the pediatric population, we have previously observed specific circadian and sleep/wake patterns of generalized seizures (6 am-12 pm) and myoclonic seizures (in wakefulness, 6 am to noon). Delayed Sleep-Wake Phase Disorder (DSWPD) is characterized by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time. Here we present the case of a 20-year-old man with JME, diagnosed DSWPD (sleep schedule 3 am to 11 am), presenting with nocturnal seizures out of sleep, always between 5 and 6am. Improvements in seizure control (seizure frequency from 8 per month to 0 per month) were achieved with timed evening melatonin, combined with behavioral sleep-wake scheduling (sleep schedule 10 pm to 6 am) and morning light therapy. Recognition and characterization of DSWPD in JME, together with assessment of circadian and diurnal seizure patterns, may offer therapeutic consideration for better control of seizures.

A Case of Recurrent Hypersomnia With Autonomic Dysfunction.

ABSTRACT: We report the case of a 50-year-old man with disabling recurrent hypersomnia with autonomic instability due to catatonia in the setting of atypical bipolar disorder. Treatment with valproic acid for bipolar disorder resulted in complete resolution of symptoms.

Localization of sleep spindles, k-complexes, and vertex waves with subdural electrodes in children.

PURPOSE: To describe for the first time in children the localization of sleep spindles, K-complexes, and vertex waves using subdural electrodes. METHODS: We enrolled children who underwent presurgical evaluation of refractory epilepsy with subdural grid electrodes. We analyzed electroencephalogram data from subdural electrodes and simultaneous recording with Cz scalp electrode. Sleep spindles, K-complexes, and vertex waves were identified and localized based on their morphology on the subdural electrodes. RESULTS: Sixteen patients (9 boys; age range, 3-18 years) were enrolled in the study. The inter-rater reliability on identification and localization of maximal amplitude was high with an intraclass correlation coefficient of 0.85 for vertex waves, 0.94 for sleep spindles, and 0.91 for K-complexes. Sleep spindles presented maximum amplitude around the perirolandic area with a field extending to the frontal regions. K-complexes presented maximum amplitude around the perirolandic area with a field extending to the frontal regions. Vertex waves presented maximum amplitude around the perirolandic areas. CONCLUSIONS: In our series of pediatric patients, sleep spindles, K-complexes, and vertex waves were localized around the perirolandic area.

Comparison of pediatric patients with status epilepticus lasting 5-29 min versus ≥30 min.

The most common thresholds for considering prolonged seizures as status epilepticus (SE) are 5 and 30 min. It is unknown whether these different thresholds (5 or 30 min) identify patient populations with different electroclinical characteristics. We compared the characteristics of patients with SE lasting 5-29 min (SE5-29) with those with SE lasting ≥30 min (SE≥30). Inclusion criteria were the following: 1) 1 month to 21 years of age at the time of SE, 2) convulsive seizures, and 3) seizure duration ≥5 min. Exclusion criteria were the following: 1) exclusively neonatal seizures, 2) psychogenic nonepileptic seizures, or 3) incomplete information about seizure duration. Four hundred forty-five patients (50.1% male) with a median (p25-p75) age at SE of 5.5 (2.8-10.5) years were enrolled. Status epilepticus lasted for 5-29 min in 296 (66.5%) of subjects and for ≥30 min in 149 (33.5%). Patients with SE≥30 were younger than the patients with SE5-29 at the time of seizure onset (median: 1 versus 2.1 years, p=0.0007). Status epilepticus as the first seizure presentation was more frequent in patients with SE≥30 (24.2% versus 12.2%, p=0.002). There was a tendency towards a higher rate of abnormalities in the magnetic resonance imaging at baseline in patients with SE≥30 (70.5% versus 57.1%, p=0.061). Differences were not detected in seizure frequency, seizure types, presence of developmental delay, and electroencephalogram abnormalities at baseline. In the pediatric population, SE thresholds of either 5 or 30 min identify groups of patients with very similar electroclinical characteristics, which may influence future definitions of pediatric SE.

Central sleep apnea and complex sleep apnea in patients with epilepsy.

PURPOSE: We sought to examine the prevalence of central sleep apnea (CSA) and complex sleep apnea (CompSA) in patients with epilepsy and to examine their clinical profile, with respect to epilepsy type, etiology, medication use, and EEG abnormalities. METHODS: We undertook a retrospective analysis of 719 consecutive patients with epilepsy who underwent polysomnography (PSG) at our institution between 2004 and 2011. Of the 458 patients with complete data, we excluded 42 patients with congestive heart failure or left ventricular ejection fraction <40 %. Comparison of clinical and PSG variables between the three groups were conducted with Fisher exact test and analysis of variance. RESULTS: Out of 416 patients tested, 315 (75 %) had obstructive sleep apnea (OSA), 16 (3.7 %) had CSA, 33 (7.9 %) had CompSA. There were more males in the CSA and CompSA groups than in the OSA group (81.2, 81.8, and 59.6 %, respectively, p=0.04). Focal seizures were more prevalent in patients with CSA than in patients OSA or CompSA (62.5, 265, and 21.1 %, respectively, p=0.02). CONCLUSION: About 11 % of epilepsy patients have sleep-breathing disorders with central apneas, which is not higher than that in a general population. These data should be expanded with future research investigating the role of interictal, ictal, and postictal central apneas in epileptogenesis and epilepsy.

Insomnia and epilepsy: a questionnaire-based study.

STUDY OBJECTIVES: Although disturbed sleep has been frequently reported in patients with seizures, little is known about insomnia and epilepsy. The aims of this study were (1) to analyze the prevalence and degree of insomnia in patients with epilepsy, (2) to examine the clinical features and correlates of insomnia in these patients, and (3) to evaluate the impact of poor sleep on their quality of life. METHODS: One hundred-fifty-two patients with epilepsy (mean age 46 years) completed the following questionnaires: Insomnia Severity Index, Pittsburgh Sleep Quality Index, Beck Depression Inventory-II, Quality of Life in Epilepsy Inventory-31. Patients with other known sleep disorders, including obstructive sleep apnea, were excluded from the study. Regression analysis was conducted for adjusting for age, years since epilepsy onset, number of antiepileptic drugs, comorbidities, and depression scores. RESULTS: More than half of the participants (55%) suffered from insomnia and more than 70% were "poor sleepers." Insomnia and poor sleep quality were significantly correlated with the number of antiepileptic medications and scores of depressive symptoms. After controlling for covariates, insomnia and poor sleep quality were significant predictors of lower quality of life. CONCLUSION: These results suggest that insomnia and poor sleep are common in patients with epilepsy and may adversely impact quality of life. Further studies should examine whether improvements in sleep can improve seizure control and quality of life of these patients.

Clinical evolution of seizures: distribution across time of day and sleep/wakefulness cycle.

Seizures can evolve sequentially into different clinical phases. For example, a seizure may start as an aura (first phase), then evolve into a tonic seizure (second phase), and evolve further into a generalized tonic-clonic semiology (third phase). It is currently unknown whether specific seizure evolutions cluster at particular times of the day and/or during sleep/wakefulness. We aimed to describe the distribution of the clinical evolution of seizures across time of day and sleep/wake state. We included all patients with at least two seizure phases admitted for long-term electroencephalogram monitoring during a 5 year period. Two-hundred-and-fifteen patients (866 seizures) presented with two different phases and 87 patients (324 seizures) evolved into a third clinical phase. During phase two, evolution into clonic seizures differed across time (p = 0.047) with peaks at 0-3 h and 6-9 h and during sleep (p < 0.001), evolution into automotor seizures peaked during wakefulness (p = 0.015), evolution into tonic seizures differed across time (p = 0.005) with peaks at 21-12 h and during sleep (p = 0.0119), and generalized tonic-clonic seizures peaked during sleep (p = 0.0067). Findings remained statistically significant after multivariable analysis adjusting, separately, for potential confounders (semiology of the first phase, age, gender, days in the long-term electroencephalographic monitoring unit, abnormal neuroimaging, number of antiepileptic medications, and seizure localization). During phase three, seizure evolutions followed the same pattern of distribution as during phase two but differences did not reach statistical significance. Our data demonstrate that the evolution of seizures into different phases cluster at specific times of day and at specific phases of the sleep/wakefulness cycle.

Dacrystic seizures: demographic, semiologic, and etiologic insights from a multicenter study in long-term video-EEG monitoring units.

PURPOSE: To provide an estimate of the frequency of dacrystic seizures in video-electroencephalography (EEG) long-term monitoring units of tertiary referral epilepsy centers and to describe the clinical presentation of dacrystic seizures in relationship to the underlying etiology. METHODS: We screened clinical records and video-EEG reports for the diagnosis of dacrystic seizures of all patients admitted for video-EEG long-term monitoring at five epilepsy referral centers in the United States and Germany. Patients with a potential diagnosis of dacrystic seizures were identified, and their clinical charts and video-EEG recordings were reviewed. We included only patients with: (1) stereotyped lacrimation, sobbing, grimacing, yelling, or sad facial expression; (2) long-term video-EEG recordings (at least 12 h); and (3) at least one brain magnetic resonance imaging (MRI) study. KEY FINDINGS: Nine patients (four female) with dacrystic seizures were identified. Dacrystic seizures were identified in 0.06-0.53% of the patients admitted for long-term video-EEG monitoring depending on the specific center. Considering our study population as a whole, the frequency was 0.13%. The presence of dacrystic seizures without other accompanying clinical features was found in only one patient. Gelastic seizures accompanied dacrystic seizures in five cases, and a hypothalamic hamartoma was found in all of these five patients. The underlying etiology in the four patients with dacrystic seizures without gelastic seizures was left mesial temporal sclerosis (three patients) and a frontal glioblastoma (one patient). All patients had a difficult-to-control epilepsy as demonstrated by the following: (1) at least three different antiepileptic drugs were tried in each patient, (2) epilepsy was well controlled with antiepileptic drugs in only two patients, (3) six patients were considered for epilepsy surgery and three of them underwent a surgical/radiosurgical or radioablative procedure. Regarding outcome, antiepileptic drugs alone achieved seizure freedom in two patients and did not change seizure frequency in another patient. Radiosurgery led to moderately good seizure control in one patient and did not improve seizure control in another patient. Three patients were or are being considered for epilepsy surgery on last follow-up. One patient remains seizure free 3 years after epilepsy surgery. SIGNIFICANCE: Dacrystic seizures are a rare but clinically relevant finding during video-EEG monitoring. Our data show that when the patient has dacrystic and gelastic seizures, the cause is a hypothalamic hamartoma. In contrast, when dacrystic seizures are not accompanied by gelastic seizures the underlying lesion is most commonly located in the temporal cortex.

Circadian patterns of generalized tonic-clonic evolutions in pediatric epilepsy patients.

OBJECTIVE: To investigate the sleep/wake, day/night, and 24-h periodicity of pediatric evolution to generalized tonic-clonic seizures (GTC). METHODS: Charts of 407 consecutive patients aged 0-21 years undergoing continuous video-EEG monitoring for epilepsy were reviewed for the presence of GTC evolution. Seizures were characterized according to 2001 ILAE terminology. Charts were reviewed for EEG seizure localization, MRI lesion, and for seizure occurrence in 3-h time blocks, out of sleep or wakefulness, and during the day (6 AM-6 PM) or night. Analysis was done with binomial testing. Regression models were fitted using generalized estimating equations with patients as the cluster level variable. RESULTS: 71 patients (32 girls, mean age 12.63 ± 5.3 years) had 223 seizures with GTC evolution. Sleep/wake seizure distribution predicted tonic-clonic evolution better than time of day, with more occurring during sleep (p<0.001). Tonic-clonic evolution occurred most frequently between 12-3 AM and 6-9 AM (p<0.05). Patients with generalized EEG onset had more tonic-clonic evolution between 9 AM and 12 PM (p<0.05). Patients with extratemporal focal seizures were more likely to evolve during sleep (p<0.001); this pattern was not found in patients with temporal or generalized seizure onset on EEG. Patients without MRI lesions were more likely to evolve between 12 AM and 3 AM (p<0.05), in the sleeping state (p<0.001), and at night (p<0.05). Logistic regression revealed that sleep and older patient age were the most important predictors of GTC evolution. CONCLUSION: GTC evolution occurs most frequently out of sleep and in older patients. Our results may assist in seizure prediction, individualized treatment patterns, and potentially complication and SUDEP prevention.

Diurnal and sleep/wake patterns of epileptic spasms in different age groups.

PURPOSE: Epileptic spasms are seizures that occur predominantly in children and are characterized by clusters of brief axial movements. Epileptic spasms may occur in the context of a variety of syndromes. Previous research has found that epileptic spasms occur in a sleep/wake and diurnal rhythm. The purpose of this study was to identify these patterns in different age groups. METHODS: Charts of 2,021 patients with epilepsy undergoing video-electroencephalography (EEG) monitoring over a 10-year period were reviewed for presence of epileptic spasms and analyzed for their occurrence during the day (6 a.m. to 6 p.m.) or night, out of wake or sleep, and in 3-h time-blocks throughout the day. Exact epileptic spasm time, EEG localization, and the presence or absence of magnetic resonance imaging lesion were also recorded. Patients were separated into two age groups: A ages 3 and under, and over age 3. Statistical analysis of seizure occurrence in time bins was carried out using binomial calculations. p-Values <0.05 were taken as significant. Using exact seizure times, a generalized linear mixed model of the Poisson-family with a square root link function was used to calculate mean seizure times. Age, as a binary variable, and time, as a categorical variable, was treated as fixed effect predictors, and individual effects were modeled as random effects. For comparison between the two age groups, over age 3 and under age 3, seizure times were transformed into circular variables. A circular analysis of variance test was used to assess for the difference in mean seizure time, assuming a von Mises distribution of the circle. KEY FINDINGS: We analyzed 219 clusters of epileptic spasms in 51 patients (15 girls; mean age 2.15 ± 2.22 years). Forty-two patients younger than 3 years of age had 163 seizures and nine patients older than 3 years had 56 seizures. Epileptic spasms occurred predominantly during wakefulness (p < 0.001) and during daytime (p < 0.001). Epileptic spasms occurred most frequently between 9 a.m. and noon (p < 0.05) and between 3 p.m. and 6 p.m. (p < 0.001). Patients without magnetic resonance imaging lesions had most seizures between 9 a.m. and noon (p < 0.01) and 3 p.m. and 6 p.m. (p < 0.001). Thirty-seven patients had 157 epileptic spasms (71.2%) with generalized EEG patterns and 14 patients had 62 epileptic spasms (28.8%) with focal EEG patterns. Generalized EEG seizures occurred more frequently than focal EEG seizures (p < 0.001). Following age stratification, patients younger than 3 years had most epileptic spasms between 9 a.m. and noon (p < 0.05) and 3 p.m. and -6 p.m. (p < 0.01) and patients older than 3 years had most epileptic spasms between 6 a.m. and -9 a.m. (p < 0.05) and a second peak between 3 p.m. and 6 p.m., although the difference was not statistically significant due to insufficient numbers. Using continuous time analysis, the mean seizure time in the under age 3 and the over age 3 groups was 2:24 p.m. and 11:40 a.m. Using a circular analysis of variance test, the difference between mean seizure times in these groups was found to be statistically significant (p = 0.038). SIGNIFICANCE: Epileptic spasms occur more frequently in the waking state and daytime. Younger patients have epileptic spasms mostly between 9 a.m. and noon and 3 p.m. and -6 p.m., and older patients have epileptic spasms mostly between 6 a.m. and 9 a.m. These findings emphasize age-related changes in epileptic spasm pathophysiology or potentially evolution of disease with age.

Effect of treatment of obstructive sleep apnea on seizure outcomes in children with epilepsy.

A retrospective review of children with epilepsy and obstructive sleep apnea, treated surgically for their obstructive sleep apnea from January 2008-October 2010, was performed for age, sex, type of epilepsy, antiseizure medications, sleep-study data, and changes in seizure frequency. Twenty-seven subjects (median age, 5 years) with no adjustment to their medications around their time of surgery were identified. Three months after surgery, 10 (37%) patients became seizure-free, three (11%) demonstrated >50% seizure-reduction, and six (22%) exhibited an amelioration of seizure frequency. Two (7%) demonstrated unchanged seizure-frequency, and six (22%) manifested a worsening of seizure frequency. Median seizure frequency before surgery was 8.5 (interquartile range, 2-90), and after surgery, three (interquartile range, 0-75), with a 53% median seizure reduction. Multivariate analysis demonstrated a trend toward seizure freedom with each percentile increase in body mass index and early age of surgery. We conclude that obstructive sleep apnea surgery may decrease seizure frequency, especially in children with elevated body mass index scores and younger age at time of surgery.

Outcomes of epileptic spasms in patients aged less than 3 years: single-center United States experience.

Retrospective review was performed of children aged <3 years with epileptic spasms at our center from 2004-2010. Short-term (<6 months) and long-term (≥6 months) outcomes were assessed. We included 173 children (104 boys; median age of onset, 6.8 months) with epileptic spasms of known (62%) and unknown (38%) etiology. Treatments included adrenocorticotropic hormone (n = 103), vigabatrin (n = 82), phenobarbital (n = 34), and other agents (n = 121). Short-term treatment with adrenocorticotropic hormone and vigabatrin provided better epileptic spasm control in groups with known and unknown etiology than other agents. At follow-up (6-27 months), 54% of children manifested seizures, and 83% manifested developmental delay. Known etiology was a predictor of poor developmental outcome (P = 0.006), whereas bilateral/diffuse brain lesions predicted both poor development and seizures (P = 0.001 and 0.005, respectively). Initial presentations of epileptic spasms with hypotonia or developmental delay most strongly predicted both seizures and neurodevelopmental outcomes (P < 0.001). In a child presenting with epileptic spasms with developmental delay or hypotonia, no specific treatment may offer superior benefit.

Analysis of EEG patterns and genotypes in patients with Angelman syndrome.

We prospectively analyzed EEGs from participants in the ongoing NIH Rare Diseases Clinical Research Network Angelman Syndrome Natural History Study. Of the one-hundred-sixty enrolled patients (2006-2010), 115 had complete data (58 boys, median age 3.6 years). Distinct EEG findings were intermittent rhythmic delta waves (83.5%), interictal epileptiform discharges (74.2%), intermittent rhythmic theta waves (43.5%), and posterior rhythm slowing (43.5%). Centro-occipital and centro-temporal delta waves decreased with age (p=0.01, p=0.03). There were no specific correlations between EEG patterns and genotypes. A classification tree allowed the prediction of deletions class-1 (5.9 Mb) in patients with intermittent theta waves in <50% of EEG and interictal epileptiform abnormalities; UPD, UBE3A mutation or imprinting defects in patients with intermittent theta in <50% of EEG without interictal epileptiform abnormalities; deletions class-2 (5.0 Mb) in patients with >50% theta and normal posterior rhythm; atypical deletions in patients with >50% theta but abnormal posterior rhythm. EEG patterns are important biomarkers in Angelman syndrome and may suggest the underlying genetic etiology.

Effect of continuous positive airway pressure treatment on seizure control in patients with obstructive sleep apnea and epilepsy.

In patients with epilepsy, improvement in seizure control with treatment of coexisting obstructive sleep apnea (OSA) has been reported, but there is lack of data on the effect of continuous positive airway pressure (CPAP) compliance on seizure control in these patients. We examined the variability in seizure frequency in patients who were CPAP compliant and those who were not CPAP compliant. We undertook a retrospective review of clinical and polysomnographic data of adult patients with OSA and epilepsy seen at the Boston University Medical Center Epilepsy and Sleep Clinics between 2000 and 2010. Data were reviewed for CPAP compliance and seizure frequency after at least 6 months of CPAP use. Only patients with no changes in antiepileptic drug regimens during CPAP trial were included. Of the 660 patients identified, 41 fulfilled inclusion criteria, of whom 28 were CPAP compliant and 13 were not CPAP compliant. In the compliant group, CPAP use led to decreased seizure frequency from 1.8 per month to 1 per month (p = 0.01). In the noncompliant group, no significant difference in seizure frequency was noted between baseline (2.1 per month) and at follow-up (1.8 per month, p = 0.36). Sixteen of 28 CPAP-compliant subjects were seizure free, whereas only 3 of 13 non-CPAP compliant subjects were seizure free [relative risk (RR) 1.54, p = 0.05]. Patients with epilepsy and OSA not compliant with CPAP treatment are at higher risk of seizures than are CPAP-compliant patients. To validate this observation, further prospective studies are warranted.

Selective serotonin reuptake inhibitors and periodic limb movements of sleep.

Serotonin reuptake inhibitors may induce periodic limb movements of sleep in adults. We undertook a retrospective review of polysomnography data of 1,023 children acquired at our institution over 1 year to assess whether children receiving serotonin reuptake inhibitors have a higher risk of periodic limb movements of sleep than children that are not treated with these medications. Periodic limb movements of sleep were found in 13 (31.7%) of 41 children receiving serotonin reuptake inhibitors and in 77 (7.8%) of 982 children not receiving serotonin reuptake inhibitors (odds ratio 5.45). Furthermore, the median periodic limb movement index in patients receiving serotonin reuptake inhibitors was significantly higher than patients not receiving serotonin reuptake inhibitors (11.2 and 6.5 respectively; P < 0.05). Children receiving serotonin reuptake inhibitors are at risk of periodic limb movements of sleep. Appropriate clinical judgment and medical management may result in better control of periodic limb movements of sleep and improved quality of life in these patients.