Long-Term Evaluation of Cannabidiol in Pediatric Drug-Resistant Epilepsy: A Real-Time Single-Center Retrospective Study

Jong Ho Cha; Haeryung Kim; Young Ho Kim; Seungbok Lee; Soo Yeon Kim; Byung Chan Lim; Jong-Hee Chae; Ki Joong Kim; Woo Joong Kim

doi:10.26815/acn.2025.00997

Ann Child Neurol > Volume 34(1); 2026 > Article

Cha, Kim, Kim, Lee, Kim, Lim, Chae, Kim, and Kim: Long-Term Evaluation of Cannabidiol in Pediatric Drug-Resistant Epilepsy: A Real-Time Single-Center Retrospective Study

Original article

Annals of Child Neurology 2026;34(1):66-74.

Published online: December 31, 2025

DOI: https://doi.org/10.26815/acn.2025.00997

Long-Term Evaluation of Cannabidiol in Pediatric Drug-Resistant Epilepsy: A Real-Time Single-Center Retrospective Study

Jong Ho Cha, MD¹

, Haeryung Kim, MD¹, Young Ho Kim, MD¹, Seungbok Lee, MD^1,², Soo Yeon Kim, MD^1,², Byung Chan Lim, MD¹, Jong-Hee Chae, MD^1,², Ki Joong Kim, MD¹, Woo Joong Kim, MD¹

¹Department of Pediatrics, Seoul National University Children’s Hospital, Seoul National University College of Medicine, Seoul, Korea

²Department of Genomic Medicine, Seoul National University Hospital, Seoul, Korea

Corresponding author: Woo Joong Kim, MD Department of Pediatrics, Seoul National University Children's Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 03080, Korea
Tel: +82-2-6960-1300 Fax: +82-2-6960-1072 E-mail: rainkim23@gmail.com

Received June 10, 2025 Revised August 30, 2025 Accepted September 16, 2025

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose

Cannabidiol (CBD) is a promising treatment option for pediatric drug-resistant epilepsy (DRE). The aim of this study was to assess the tolerability and safety of CBD in a single-center retrospective cohort based on real-world clinical experience.

Methods

This study included 71 pediatric patients (median age, 8.9 years; interquartile range [IQR], 6.2 to 14.0) with Lennox-Gastaut syndrome who received purified CBD (Epidiolex, GW Pharmaceuticals) between March 2019 and July 2024. All patients had previously failed treatment with more than five anti-seizure medications (ASMs). Responder rate (≥50% seizure frequency reduction), retention rate, adverse effects (AEs), and predictors of favorable treatment response were analyzed over a median follow-up of 21.3 months (IQR, 2.8 to 38.5).

Results

The initial responder rate during the first 3 months was 45.1%, which increased to 70.8% at 18 months and 63.0% at 24 months. The retention rate at 24 months was 52.4% (33/71). Seven patients (9.9%) achieved seizure freedom beyond 24 months of CBD therapy, and five of these patients were able to reduce their concomitant ASM burden. AEs were observed in 39.4% (28/71) of patients, with the most frequent being somnolence (20 cases) and increased seizure frequency (six cases); 92.9% of AEs occurred within the first 3 months of treatment. No serious AEs requiring treatment discontinuation were identified.

Conclusion

In this real-world study, CBD demonstrated potential as an adjunctive therapy with manageable AEs. These findings highlight that CBD can reduce seizure frequency while maintaining tolerability in pediatric patients with DRE.

Keywords: Cannabidiol; Lennox Gastaut syndrome; Retrospective studies; Drug resistant epilepsy

Introduction

Approximately one-third of pediatric patients with epilepsy develop drug resistance, which often progresses to intractable epilepsy and significantly impairs quality of life. Although many anti-seizure medications (ASMs) have been introduced in recent decades, none have substantially decreased the incidence of drug-resistant epilepsy (DRE).

Cannabinoids, derived from the Cannabis sativa plant, have long been recognized for their potential therapeutic effects in epilepsy [1]. Cannabidiol (CBD), a major cannabinoid, has demonstrated notable anti-seizure activity. Several mechanisms have been proposed for CBD’s anti-seizure effects, including modulation of the endocannabinoid system, activation of the transient receptor potential vanilloid type-1 channel, and regulation of intracellular Ca²⁺ [2-4]. However, its exact mechanism of action has not yet been fully elucidated.

Two double-blind randomized controlled trials reported that adjunctive CBD therapy produced greater reductions in seizure frequency than placebo in patients with Lennox-Gastaut syndrome (LGS) [5,6]. Subsequently, the U.S. Food and Drug Administration approved purified CBD (Epidiolex; GW Pharmaceuticals, Cambridge, UK) for the treatment of pediatric DRE associated with Lennox-Gastaut syndrome (LGS). In South Korea, the National Health Insurance Service has covered cannabidiol for patients aged ≥2 years with Lennox-Gastaut syndrome or Dravet syndrome since 2021. Eligibility criteria included drug-refractoriness, documented failure of at least five ASMs, and concomitant clobazam use.

Previous open-label studies suggested that CBD may effectively reduce seizure frequency in pediatric DRE and demonstrated favorable safety and tolerability profiles [7-9]. However, these studies were limited by short follow-up durations and strict enrollment conditions. Several long-term open-label studies also reported encouraging efficacy and tolerability, but such trials remain susceptible to selection bias [10,11].

Therefore, evidence regarding the long-term use of CBD in pediatric patients in real-world clinical practice remains scarce. To our knowledge, very few studies have specifically targeted pediatric populations, and none have reported extended real-life clinical outcomes. To address this gap, we aimed to evaluate the long-term effects of CBD on seizure frequency reduction and tolerability in pediatric DRE, and to identify potential factors associated with a favorable treatment response.

Materials and Methods

1. Study participants

This retrospective cohort study included pediatric patients with LGS, aged 2 to 18 years, who were treated with CBD at the Department of Child Neurology, Seoul National University Children’s Hospital, between March 2019 and July 2024. Patients were followed until December 31, 2024, or were censored at the time of their last CBD prescription.

Patient selection was defined as follows: (1) patients who continued to experience intractable seizures despite treatment with more than two ASMs, and (2) patients who had tried more than five conventional ASMs—including valproate, clobazam, topiramate, stiripentol, clonazepam, levetiracetam, zonisamide, ethosuximide, phenobarbital, lamotrigine, and rufinamide—but failed to achieve seizure freedom. All patients received concomitant clobazam, unless it had previously been discontinued due to unavoidable adverse effects. A selection flow diagram of study participants is shown in Fig. 1. Of the 91 patients prescribed CBD, six were excluded due to incomplete records, five discontinued the medication because of reimbursement issue, and nine changed either the dosage or number of ASMs within 4 weeks prior to CBD initiation. The final study population comprised 71 patients. During follow-up, we excluded patients who were lost to follow-up, discontinued CBD owing to adverse effects, or had incomplete treatment duration. Patients diagnosed with LGS exhibited the characteristic clinical features of multiple seizure types, abnormal electroencephalogram (EEG) findings, and cognitive impairment [12].

Medical records from outpatient visits were retrospectively reviewed. Clinical data included age at seizure onset, comorbidities, epilepsy etiology, EEG findings, genetic variants, and history of concomitant ASMs. Outpatient visits typically occurred every 2 weeks during the 1st month, followed by visits every 3 months.

2. Ethical statements

This study was approved by the Institutional Review Board of Seoul National University Hospital (IRB No. 2411-054-1585). The requirement for informed consent was waived due to the retrospective nature of the study.

3. Cannabidiol

Patients were treated with highly purified CBD (100 mg/mL oral solution; Epidiolex), manufactured by GW Pharmaceuticals. Treatment began at a median dose of 6.5 mg/kg/day (interquartile range [IQR], 4.7 to 7.7). Clinicians increased the dose to 10-20 mg/kg/day while assessing drug tolerance and safety over a median titration period of 1 month (IQR, 1 to 3).

4. Outcome measurements

For primary outcomes, seizure reduction rate was calculated relative to baseline seizure frequency at 3, 6, 12, 24, and 36 months after CBD initiation. Outcomes were categorized as no reduction, <50% reduction, ≥50% reduction, or seizure freedom. Responder rate was defined as the proportion of patients achieving either seizure freedom or ≥50% seizure reduction compared with baseline (defined as seizure frequency at CBD initiation). The initial responder rate was assessed over the first 3 months of treatment. Patients who discontinued CBD due to adverse effects were excluded from the denominator. Treatment effectiveness was also evaluated by comparing the number and dosage of concomitant ASMs between baseline and the final visit. Safety outcomes included treatment-emergent adverse effects, regardless of whether CBD was discontinued. Adverse effects were assessed through parental reports and laboratory evaluations, including complete blood counts, serum electrolytes, and blood chemistry analyses.

Treatment retention rate, defined as the proportion of patients continuing CBD therapy, was calculated at each time point. All reasons for discontinuation, including adverse effects, lack of efficacy, and loss to follow-up, were considered.

5. Statistical analysis

Patient characteristics, including baseline seizure frequency, seizure frequency after 3 months, and history of concomitant ASMs, were compared between initial responders and non-responders. Categorical variables were analyzed using the chi-square test, while continuous variables were analyzed using the Mann-Whitney U test, as appropriate. Logistic regression analysis was then performed to identify clinical factors associated with initial response. Variables that reached statistical significance in univariate analyses (chi-square or Mann-Whitney U tests) were included in the multivariable model, adjusted for sex and the total number of prior ASM trials. A P<0.05 was considered statistically significant. All analyses were conducted using R version 4.2.1 (R Foundation for Statistical Computing, Vienna, Austria) and GraphPad Prism version 8.0 (GraphPad Software Inc., San Diego, CA, USA).

Results

1. Study population

The demographic characteristics of the patients are summarized in Table 1. The study population consisted of 71 pediatric patients with LGS. The median age at CBD initiation was 8.9 years (IQR, 6.2 to 14.0). The median titration period to reach the final dosage was 1 month (IQR, 1 to 3), and the median duration of CBD use was 21.3 months (IQR, 2.8 to 38.5). A total of 41 patients (57.7%) used CBD for more than 12 months, and 33 patients (46.5%) continued for more than 24 months.

Seizures began at a median age of 12 months (IQR, 4.5 to 42.5), and 21 patients (29.6%) were diagnosed with infantile epileptic spasms syndrome. In total, 14 patients had genetic etiologies, and 18 had structural etiologies. Twenty genetic variants were identified, including chromosomal deletions, duplications, and pathogenic single-nucleotide variants (Supplementary Table 1).

Of the 71 patients, 32 (45.1%) were initial responders. Comparisons between initial responders and non-responders are shown in Table 2. The two groups did not differ significantly in most clinical characteristics, except that infantile epileptic spasms syndrome was less frequent in the responder group than in the non-responder group (15.6% vs. 41.0%, P=0.04). The ASM profiles administered before CBD therapy are provided in Supplementary Table 2. All patients had previously used or were currently using clobazam. The most frequently administered ASM was levetiracetam (61/71, 85.9%), followed by valproic acid (56/71, 78.9%) and topiramate (46/71, 64.8%).

2. Treatment retention

The retention rate among patients who received CBD for longer than 3 months was 74.6%. The retention rates at 6, 12, 18, and 24 months were 67.1%, 59.4%, 57.4%, and 52.4%, respectively (Fig. 2A). During the study period, 28 patients (39.5%) discontinued CBD. Among these, 15 patients discontinued treatment because of adverse effects, and two of the nine patients with no treatment response also discontinued therapy within the first 6 months (Fig. 2B).

3. Responder rate

Temporal changes in seizure reduction are shown in Fig. 2A. The initial responder rate was 45.1% during the first 3 months, increasing to 68.0% at 6 months and peaking at 70.8% at 18 months. The responder rate then decreased to 63.0% at 24 months and further to 46.5% at 36 months. Patients who discontinued CBD within the first 3 months were categorized as ‘no effect’ at the 3-month evaluation. Among the initial responders, five patients (15.6%) reduced the number of concomitant ASMs, and four patients (12.5%) reduced ASM dosages (Table 2). Of the 33 patients (46.5%) who maintained CBD treatment for more than 24 months, 29 achieved ≥50% seizure reduction. Of these 29, 21 had already achieved this reduction within the first 3 months, and 24 within the first 6 months.

Table 3 summarizes the clinical course of seven patients who achieved seizure freedom after 24 months of CBD therapy. Three patients (SNUH_CBD1, SNUH_CBD3, and SNUH_CBD6) attained seizure freedom within 12 months of initiation and sustained it for at least 24 months. Two patients (SNUH_CBD2 and SNUH_CBD5) achieved seizure freedom after 2 years, while two others (SNUH_CBD4 and SNUH_CBD7) did so after 3 years. At the time of CBD initiation, these patients were receiving two to five concomitant ASMs. With seizure freedom, five were able to taper or discontinue at least one ASM. All seven patients had achieved ≥50% seizure reduction within the first 6 months of treatment.

4. Adverse effects

During the study period, 33 adverse events were reported in 28 patients (39.4%) (Fig. 3). The most frequent adverse events were somnolence (20 cases), increased seizure frequency (six cases), and vomiting (three cases). Most patients (26/28, 92.9%) experienced adverse effects within the first 3 months of CBD initiation. Among the affected patients, 15 discontinued CBD, three reduced the dosage with subsequent improvement, and 10 continued at the same dosage. In the three cases where the CBD dose was reduced, patients maintained seizure reduction while symptoms improved.

One patient (SNUH_CBD6 in Table 3) developed elevated liver enzyme levels after 12 months of treatment, with aspartate aminotransferase and alanine aminotransferase levels reaching 608 and 491 IU/L, respectively. This patient had a history of neonatal seizures and started CBD at 3 years of age. Genetic testing revealed a de novo ARX mutation, consistent with developmental and epileptic encephalopathy. Six months after CBD initiation, baclofen was added to manage spasticity. At 12 months, routine laboratory testing showed elevated liver enzymes without signs of infection or other causes. Given the substantial seizure reduction since CBD initiation, the dosage (14 mg/kg/day) was maintained, and serial monitoring was performed. The abnormalities resolved spontaneously, and CBD therapy was continued without further escalation.

5. Predictors of responders

Significant variables, including age at seizure onset and latency from seizure onset to CBD initiation, were selected for regression analysis (Supplementary Table 3). No significant risk factors were identified for an initial response. However, factors associated with ≥50% seizure reduction at 6 months included earlier seizure onset (odds ratio [OR], 0.97; 95% confidence interval [CI], 0.94 to 0.99) and ≥50% reduction at 3 months (OR, 64.11; 95% CI, 10.89 to 377.3).

Discussion

This study was conducted to investigate the real-time clinical experience of CBD in pediatric patients with DRE. The initial responder rate was 46.1%, and seven patients (9.9%) achieved seizure freedom lasting more than 24 months. During the observation period, more than half of the patients continued CBD treatment for over 12 months, and no life-threatening or organ-damaging adverse effects were reported as reasons for discontinuation.

The effect of CBD in real-world clinical practice has been reported in several countries. A recent German study of 126 patients showed that ≥50% seizure reduction was achieved in 47.5% of patients at 3 months and in 45.5% at 12 months [11]. Szaflarski et al. [13] followed 892 patients for 4 years of CBD use and found that 58% achieved ≥50% seizure reduction, which was higher than our findings. This discrepancy likely reflects differences in study populations; our cohort consisted of pediatric patients with DRE who had failed more than five conventional ASMs. Despite the longer treatment histories and heavier ASM burden compared with previous studies, our cohort still showed a meaningful response to CBD, supporting its potential as a treatment option for severe DRE. Our results also indicated a decline in sustained seizure reduction beyond 24 months of treatment. Nevertheless, many patients continued CBD therapy, with a median treatment duration of 21.3 months. Among the 33 patients who maintained treatment for more than 24 months, 29 achieved ≥50% seizure reduction. Thus, while long-term sustained seizure reduction requires further validation, our findings suggest that extended CBD treatment may remain effective, underscoring the need for studies with longer follow-up to assess its long-term efficacy and safety.

In our CBD treatment protocol, which involved dose titration up to 10-20 mg/kg/day according to patient tolerance, some patients were unable to complete titration. Compared with the study by Szaflarski et al. [13], the overall incidence of adverse effects was lower in our cohort (26/45 [58%] vs. 28/71 [39.4%]), whereas the incidence of adverse effects leading to discontinuation was slightly higher (9/45 [20%] vs. 15/71 [21.1%]). We did not observe adverse effects commonly reported in prior studies, such as diarrhea, pyrexia, and fatigue [14]. Importantly, patients who reduced their CBD dose because of adverse effects continued to maintain seizure reduction even after dose adjustment. Since most adverse effects occurred within the first 3 months, especially during initial dosing and titration, our findings highlight the importance of individualized titration. Excluding one case of hepatitis, no life-threatening or organ-damaging adverse effects were identified that necessitated discontinuation.

Our study cohort represented a population with severe DRE, characterized by a median of seven prior ASM trials and ongoing use of a median of four concomitant ASMs at CBD initiation. Many patients had previously discontinued other therapies due to adverse effects, leaving few viable pharmacological options. In addition, these patients were highly vulnerable to drug-drug interactions. Although adverse effects were reported in 39.4% (28/71) of patients, most were minor and reversible. These results suggest that CBD may provide a safe and effective therapeutic option for pediatric patients with DRE.

In this study, seven patients (9.9%) achieved sustained seizure freedom after 24 months of CBD therapy, and five of them were able to taper or reduce concomitant ASM dosages. Patel et al. [15] examined long-term seizure reduction in 54 pediatric patients with DRE and followed outcomes for up to 60 months. Their study found that six patients (12.5%) achieved greater than 90% seizure reduction over time. Our findings are consistent with previous reports, showing that patients who achieved ≥50% seizure reduction within the first 6 months of treatment were more likely to maintain seizure reduction over the long term.

We did not identify any significant factors associated with initial responders in our regression analysis. Nevertheless, later seizure onset may be related to achieving ≥50% seizure reduction within the first 6 months. A previous report indicated that predictors of early favorable outcomes included seizure frequency reductions with CBD-enriched oil and younger age at CBD initiation [16,17]. In our study, no significant associations were observed between early treatment response and clinical variables such as seizure type, seizure frequency at onset, or etiology. The relationship between seizure onset age and CBD response could not be fully elucidated within the current study design. Given the potential confounding factors that may influence CBD response, the identification of a single clinically significant predictor is unlikely, particularly since LGS encompasses a wide range of etiologies and seizure types.

This study has several limitations. First, as a single-center, open-label study, we were unable to include a control group for comparison. Furthermore, seizure frequency was reported subjectively by parents, which warrants caution when attributing seizure reduction solely to CBD. To mitigate this limitation, we excluded patients who experienced changes in concomitant ASMs during the 4 weeks prior to CBD initiation; however, controlled studies are needed to confirm the effects of CBD. Second, evaluating the impact of CBD on cognition and neurodevelopment remains a critical issue in pediatric care. In our cohort, the majority of patients were bedridden or had severe cognitive impairment, limiting the assessment of neurodevelopmental outcomes. Future research should address the influence of CBD on cognitive development and quality of life. Third, responder rates in our study may be biased. The initial responder rate could have been underestimated due to early dropouts within the first 3 months of CBD use, while subsequent responder rates may have been overestimated because censored patients were excluded from the analysis.

In conclusion, based on a 5-year, single-center real-world experience, CBD appears to be a promising treatment option for pediatric patients with DRE, showing favorable tolerability and without severe adverse effects. Our findings highlight CBD as both a safe and effective ASM in this highly refractory population.

Supplementary material

Supplementary materials related to this article can be found online at https://doi.org/10.26815/acn.2025.00997

Supplementary Table 1.

Confirmed genetic variants of the study population

acn-2025-00997-Supplementary-Table-1.pdf

Supplementary Table 2.

Comparison of total ASM trials between patients with and without an initial response

acn-2025-00997-Supplementary-Table-2.pdf

Supplementary Table 3.

Logistic regression analysis of predictors for CBD responders

acn-2025-00997-Supplementary-Table-3.pdf

Conflicts of interest

Ki Joong Kim and Jong-Hee Chae are editorial board members of the journal, but they were not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.

Author contribution

Conceptualization: JHC and WJK. Data curation: WJK. Formal analysis: JHC. Funding acquisition: WJK. Methodology: JHC, HK, YHK, and WJK. Project administration: WJK. Visualization: JHC and WJK. Writing - original draft: JHC and WJK. Writing - review & editing: SL, SYK, BCL, JHC, and KJK.

Fig. 1.

Study flow diagram. LGS, Lennox-Gastaut syndrome; CBD, cannabidiol; DRE, drug-resistant epilepsy; ASM, anti-seizure medication.

Fig. 2.

Temporal trends of retention rates, seizure reduction outcomes, and responder rates during cannabidiol (CBD) treatment. (A) Retention rates and seizure reduction outcomes at each time point. The left axis shows the proportions of seizure-frequency groups, categorized into seizure freedom, ≥50% reduction, <50% reduction, and no effect. The right axis shows the line graph representing the retention rate. (B) Kaplan-Meier curve for CBD treatment retention.

Fig. 3.

Adverse effect (AE) profiles of the study population. (A) AE reports, (B) number of AE reports, (C) timing of the AE, (D) AE management. CBD, cannabidiol.

Table 1.

Demographic and clinical characteristics of the study population

Variable	Study population (n=71)
Age at CBD initiation (yr)	8.9 (6.2-14.0)
Sex
Male	44 (62.0)
Female	27 (38.0)
Seizure onset age (mo)	12.0 (4.5-42.5)
Baseline monthly seizure frequency
<4/mo (<1/wk)	1 (1.4)
4-20/mo (1-5/wk)	2 (2.8)
30-150/mo (1-5/day)	30 (42.3)
180-300/mo (6-10/day)	18 (25.4)
>300/mo (>10/day)	20 (28.2)
Median duration of CBD (mo)	21.3 (2.8-38.5)
Initial dose (mg/kg/dose)	6.5 (4.7-7.7)
Titration period (mo)	1 (1-3)
Concomitant number of ASMs	4 (3-5)
Previous number of ASMs	7 (6, 8)
VNS	10 (14.1)
KD	26 (36.6)
Epilepsy surgery	8 (11.3)
Etiology
Structural	18 (25.4)
HIE	5
Lissencephaly	2
Brain hemorrhage	2
Focal cortical dysplasia	2
Hemimegalencephaly	2
Moyamoya disease	1
Pachygyria	2
Brain tumor	1
Brain infarction	1
Immunologic	4 (5.6)
Autoimmune encephalitis	3
Rasmussen encephalitis	1
Genetic	15 (21.1)
Infection	2 (2.8)
Unknown	32 (45.1)

Values are presented as median (interquartile range) or number (%).

CBD, cannabidiol; ASM, anti-seizure medication; VNS, vagus nerve stimulation; KD, ketogenic diet; HIE, hypoxic ischemic encephalopathy.

Table 2.

Comparison of patient characteristics stratified by early response

Variable	Initial non-responder (n=39)	Initial responder (n=32)	P value
Sex			1.00
Male	15 (38.5)	12 (37.5)
Female	24 (61.5)	20 (62.5)
Age of CBD initiation (yr)	9.9 (6.8-14.2)	8.1 (5.9-12.9)	0.54
Seizure onset age (mo)	12.0 (4.5-35.5)	12.0 (4.5-49.0)	0.95
Latency from seizure onset to CBD initiation (yr)	6.9 (5.0-10.1)	5.9 (3.9-9.4)	0.45
Initial dosage (mg/kg/day)	6.7 (5.1-9.3)	6.1 (3.8-7.1)	0.10
Seizure type^a
Spasms	16 (41.0)	5 (15.6)	0.04
Tonic	23 (59.0)	26 (81.2)	0.08
Tonic-clonic	10 (25.6)	7 (21.9)	0.93
Absence	8 (20.5)	9 (28.1)	0.64
Atonic	8 (20.5)	4 (12.5)	0.56
Myoclonic	14 (35.9)	11 (34.4)	1.00
EEG background			0.50
Normal background	14 (36.8)	16 (50.0)
Focal dysfunction	3 (7.9)	2 (6.2)
Diffuse cerebral dysfunction	22 (56.4)	14 (43.8)
EEG abnormality			0.56
Normal	0	0
IED, focal	14 (35.9)	12 (37.5)
IED, generalized	11 (28.2)	12 (37.5)
IED, generalized and focal	14 (35.9)	8 (25.0)
Baseline monthly seizure frequency			1.00
<4/mo (<1/wk)	1 (2.6)	0
4-20/mo (1-5/wk)	1 (2.6)	1 (3.1)
30-150/mo (1-5/day)	16 (41.0)	14 (43.8)
180-300/mo (6-10/day)	10 (25.6)	8 (25.0)
≥300/mo (≥10/day)	11 (28.2)	9 (28.1)
Concomitant number of ASMs	4 (3-5)	4 (4-5)	0.89
Total number of past ASM trials	7 (6-8)	6 (6-8)	0.06
Decreased number of concomitant ASMs	1 (2.6)	5 (15.6)
Decreased dosage of concomitant ASMs	1 (2.6)	4 (12.5)	0.25

Values are presented as number (%) or median (interquartile range).

CBD, cannabidiol; EEG, electroencephalogram; IED, interictal epileptifom discharge; ASM, anti-seizure medication.

^aPatient could have more than one seizure type.

Table 3.

Clinical characteristics of patients who achieved seizure freedom after 24 months of CBD usage

Subject no.	Sex/sz onset age	Age at CBD initiation (yr)	Monthly sz frequency	Seizure types	Concomitant no. of ASMs	Achievement of sz freedom (mo)^a	CBD duration (yr)	Concomitant no. of ASMs	Comorbidities
SNUH_CBD1	M/6 mo	14	150	T, Abs	6	6	2.1	5 (CLB stopped, PER tapered)	Preterm infants (33+3 weeks, 1.9 kg), HIE, PVL
SNUH_CBD2	M/60 mo	17	300	T. Abs. My	3	24	3.5	2 (PER stopped)	MR (FSIQ 68)
SNUH_CBD3	F/5 mo	8	360	T, My	4	12	2.8	4	HIE
SNUH_CBD4	F/21 mo	8	60	T, Abs	3	36	3.6	3 (VPA tapered)
SNUH_CBD5	F/16 mo	5	120	T	3	24	3.9	2 (OXC stopped)	Preterm infants (26+2 weeks, 1.02 kg)
SNUH_CBD6	M/3 day	3	300	Sp, T, GTC	2	3	2.0	2	DEE (ARX)
SNUH_CBD7	M/12 mo	6	210	T, Abs	4	36	3.8	2 (CLB, PER stopped)	MR (FSIQ 46) 1q deletion

CBD, cannabidiol; sz, seizure; ASM, anti-seizure medication; SNUH, Seoul National University Hospital; T, tonic seizure; Abs, absence seizure; CLB, clobazam; PER, perampanel; HIE, hypoxic ischemic encephalopathy; PVL, periventricular leukomalacia; My, myoclonic seizure; MR; mental retardation; FSIQ, full scale intelligent quotient; VPA, valproic acid; OXC, oxcarbazepine; Sp, spasms; GTC, generalized tonic-clonic seizure; DEE, developmental epileptic encephalopathy.

^aAfter CBD initiation.

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