Unaware and unrestrained: binge-eating behavior in epileptic absence seizures

Abstract

Background

Binge-eating disorder (BED) frequently co-occurs with dissociative symptoms and psychiatric comorbidities, yet potential neurological underpinnings remain underexplored.

Case presentation

We report an 18-year-old female with BED presenting with frequent binge episodes accompanied by memory lapses and altered consciousness. Initially attributed to dissociation, comprehensive evaluation revealed previously undiagnosed absence epilepsy, confirmed by EEG and neuroimaging. Neuropsychological assessment demonstrated significant impairments in working memory, processing speed, and divided attention. Treatment with lamotrigine (200 mg/day) resulted in complete remission of binges occurring during absence seizures and substantial cognitive improvements across multiple domains.

Conclusions

This case highlights the critical importance of neurological evaluation in eating disorder patients presenting with altered consciousness or memory lapses. The temporal relationship between seizures and binge episodes, coupled with treatment response, suggests potential neurobiological mechanisms linking epileptic activity to disinhibited eating behaviors. Clinicians should maintain heightened awareness of possible epilepsy-eating disorder comorbidity and consider integrated treatment approaches addressing both neurological and psychiatric components.

Introduction

Binge-eating disorder (BED) is the most prevalent eating disorder globally, with lifetime prevalence averaging 1.9%. It affects 0.6–1.8% of adult women and 0.3–0.7% of men, with higher rates (25–75%) among individuals seeking obesity treatment. BED is characterized by recurrent binge-eating episodes occurring at least weekly for 3 months, marked by loss of control, rapid consumption, eating beyond fullness, and subsequent distress, without the compensatory behaviors seen in bulimia nervosa [1].

Despite its prevalence, BED carries an increased mortality risk (SMR 1.50–1.77), with only 10–50% of patients receiving adequate care. Approximately 94% of individuals with BED receive an additional psychiatric diagnosis, most commonly mood disorders, substance use disorders, and anxiety disorders. Research indicates higher dissociation levels in eating disorder patients, with dissociation potentially facilitating binge-eating by reducing self-awareness and negative emotions [1, 2].

Emerging evidence suggests connections between BED, dissociative states, and neurological conditions. Studies show frequent co-occurrence of binge-eating symptoms in individuals with functional seizures. Additionally, approximately 7% of adolescents with epilepsy experience eating disorders (11.3% females, 3.1% males), with eating disorder onset averaging 1.6 years after epilepsy diagnosis (i.e., [3]).

From a neuropsychological perspective, patients with BED show poorer performance on tasks assessing cognitive flexibility, inhibitory control, attention, and planning [4]. This case report presents a young woman with BED and previously unrecognized epilepsy, where binge-eating episodes coincided with absence seizures, offering insights into the complex interplay between these conditions.

Case report

N.A., an 18-year-old girl diagnosed with BED, presented at our  Eating Disorders ward in June 2024 with worsening symptoms. With a BMI of 33 kg/m², she reported increased binge frequency (several times daily) and occasional incomplete purging attempts. She maintained adequate academic performance and social relationships. Her father, a military man concerned about metabolic risks due to family history (his father died at 45 from myocardial infarction), insisted on regular gym attendance for his children.

N.A. had shown unhealthy eating patterns since childhood, becoming overweight by age 8–9. During the 2019 COVID lockdown, she independently lost 10 kg through restriction. In 2021, she began psychotherapy with intermittent participation. BED onset occurred in 2023, characterized by binges beginning with sweet foods and continuing with salty items, accompanied by loss of control, guilt, and frequent memory lapses described as “absence of awareness”. Some binges were planned, occurring between home and gym at a nearby supermarket, followed by asthenia and social withdrawal.

In December 2023, she began fluoxetine 20 mg/day, reporting mood improvement but minimal effect on binge eating. We proposed inpatient admission, which she accepted. During the 20-day hospitalization, careful observation revealed that her apparent dissociative symptomatology following binges was actually compatible with epileptic absence seizures. Parents had not suspected this, but N.A. recalled childhood episodes of finding herself several meters ahead while walking without memory of the transition. As a diagnostic investigation, N.A. underwent an MRI, which revealed a very small gliotic focus in the left cerebellar peduncle. No pathological enhancement after contrast medium administration. The ventricular system was of normal morphology and size, aligned with the midline. Normal representation of periencephalic cerebrospinal fluid spaces (Fig. 1).

Fig. 1.

The MRI showed a very small gliotic focus in the left cerebellar peduncle. Ventricular system of regular morphology and dimensions, aligned with the midline. Normal appearance of periencephalic CSF spaces

EEG confirmed typical absence seizure features. Specifically, tracing is characterized by the presence of slow abnormalities, with an angular appearance, rarely configured as isolated sharp wave and spike-wave elements in the right temporal region. We initiated lamotrigine therapy, titrated to 200 mg/day.

After discharge, N.A. reported complete remission of home binges occurring during absence episodes, with reduced frequency of planned binges outside the home.

Written informed consent was obtained from N.A. prior to conducting the neuropsychological evaluation, in accordance with ethical guidelines and institutional protocols.

Neuropsychological assessment

We conducted a comprehensive neuropsychological assessment to evaluate general cognitive functioning and specific domains, including attention, executive function, memory, and visuospatial processing (Table 1). N.A. reported additional executive control impairments, including compulsive purchasing and frequent distractibility in studying and daily life activities, including following and carrying on conversations. This may reflect a dysexecutive pattern in real-life contexts, which standardized tasks cannot fully capture due to the complexity and cognitive demands of the real world [5, 6]. Therefore, we also collected self-reported cognitive symptoms and quantitative behavioral observations to identify potential functional deficits not fully reflected in psychometric scores. This multi-method approach allowed for a more ecologically valid description of the patient’s cognitive functioning across all domains [6]. Initial assessment revealed borderline intellectual functioning (IQ = 78) with significant working memory impairment (WMI = 69) and mild processing speed reduction (PSI = 83). Verbal comprehension (VCI = 86) and visuoperceptual reasoning (PRI = 90) were relatively preserved [7]. Pathological performance emerged in divided attention, particularly in response time in the visual modality (raw score = 907;1st percentile) with multiple omissions (raw score = 9; 1st percentile), and in working memory deficit with frequent omissions (raw score = 3; 4th percentile: TEA; [8]) (see Table 1).

Table 1.

Neuropsychological assessment conducted pre-treatment (July 2024) and follow-up (October 2024)

Test	Pre-treatment (July 2024)		Follow-up (October 2024)
	N.A.’ raw score	ESa/cut-offb/Pc/standard scored/Z-scoree	N.A.’ raw score	ESa/cut-offb/Pc/standard scored/Z-scoree
Attention
TEA alertness tonic	232	58c
TEA alertness phasic	206	66c
TEA FAS	0.075	62c
TEA GoNoGo median	501	34c
TEA GoNoGo errors	0	> 58c
TEA GoNoGo omissions	0	> 10c
TEA divided attention auditory	624	16c
TEA divided attention visual	907	1c	813	24c
TEA divided attention omissions	3	4c	2	8c
TEA divided attention errors	1	79c
TEA working memory median	733	16c
TEA working memory errors	3	31c
TEA working memory omissions	9	1c	2	54c
Executive functions
Tower of London (ToL) Tot	35	− 0.69e
ToL planning time	84	− 0.78e
ToL execution time	149	− 0.37e
ToL rule breaks	1	− 0.14e
ToL perseverations	2	0.91e
ToL self-monitoring	15	− 0.96e
Wisconsin card sorting test (WCST) errors (%)	13%	61d
WCST perseverative errors (%)	8%	58d
WCST non-perseverative errors (%)	5%	61d
WCST categories completed	6	> 16c
WCST numbers of attempts on the first category	11	> 16c
WCST inability to maintain the set	0	> 16c
WCST learning to learn	− 2.79	> 16c
Stroop test error interference	0	4a
Stroop test time interference	13	4a
Brixton spatial anticipation errors	12	− 0.847e
Language
Phonemic fluency	23	1a
Semantic fluency	45	3a
Alternate fluency	29	2a
Memory
Rey Word List immediate recall	55	3a
Rey Word List delayed recall	15	4a
Rey Word List recognition	15	4a
Rey Word List fakes	1	3a
Rey Word List delayed recall (ALF)	12	4a
Rey Word List recognition (ALF)	15	4a
Rey Word List fakes (ALF)	0	4a
Rey Osterrieth Complex Figure immediate recall	30	4a
Rey Osterrieth Complex Figure delayed recall	29	4a
Praxis abilities
Rey Osterrieth Figure copy	30	4a

Tests are standardized for use with individuals who speak Italian. Pathological scores are marked in bold

^aEquivalent scores adjusted for sex, age, and years of education. An equivalent score equal to zero should be considered pathological

^bCut-off. The reported score represents the threshold below which performance should be considered pathological

^cPercentile rank. Performances below the 5th percentile should be considered pathological

^dStandard scores. Performances below 84 should be considered pathological

^eZ scores. Performance that deviates by more than ± 2.0 z scores should be considered pathological

These results aligned with N.A.’s descriptions of binge-eating behavior during absence seizures. She reported frequent forgetfulness, word-finding difficulties, behavioral automatism, and circumscribed amnesia during binges, with intact memory for immediately preceding and following events.

Follow-up assessment

Three months post-pharmacological treatment, significant cognitive improvements emerged (see Table 1). WAIS-IV scores improved substantially: WMI increased to 94 and PSI to 97 [7]. Divided attention response times improved (raw score = 813; 24th percentile), with significant reductions in omission rates in both working memory (raw score = 2; 54th percentile) and divided attention (raw score = 2; 8th percentile).

Critically, N.A. experienced no new dissociative episodes or amnesia during treatment. She reported a significant reduction in impulsive behaviors (e.g., shopping and binge eating) and improved self-monitoring and inhibitory control.

Discussion

This case highlights the relationship between neurological conditions and eating disorders. The relationship between seizures and binge-eating, along with improvements from antiepileptic treatment, sheds light on the neurobiological factors underlying this comorbidity.

The diagnostic evolution underlines the importance of a comprehensive neurological evaluation in eating disorder patients, particularly with altered consciousness or memory lapses. N.A.’s “momentary memory lapses” were misinterpreted as BED symptoms but actually reflected absence seizures. This misattribution is not uncommon, given that dissociative symptoms are well-documented in eating disorders and may serve as a mechanism for initiating binge-eating behavior by reducing self-awareness and negative emotional states (e.g., [9]). People with functional seizures have more severe binge-eating symptoms than healthy controls, similar to those with anxiety and depression. Depression and dissociation are linked to binge-eating in functional seizure patients, with “perseveration” as a key predictor, indicating a compulsive aspect. Functional seizure patients also report higher childhood trauma and distinct personality traits [10].

The substantial reduction in home binges with lamotrigine treatment, while planned binges showed minimal improvement, indicates neurological factors may critically contribute to eating pathology. Altered consciousness during seizures may reduce cognitive control mechanisms, facilitating impulsive eating. Seizures create vulnerability windows for binge episodes. Additionally, shared neuroanatomical substrates—limbic structures regulating impulse control, emotional regulation, and feeding behaviors—may contribute to both conditions. Epilepsy and eating disorders may share neurotransmitter abnormalities, particularly GABAergic and glutamatergic systems, explaining their co-occurrence and lamotrigine’s therapeutic response [11]. Neuropsychological improvements following pharmacological intervention—in working memory, processing speed, and attentional control—suggest that underlying seizure activity significantly contributed to cognitive dysfunction. These improvements, alongside clinical remission of dissociative symptoms and binge episodes, suggest potential neurobiological connections between executive dysfunction and dissociative binge-eating behaviors. The observed amnesia and behavioral automatism may result from temporary disruptions to the attention and working memory networks rather than purely psychological dissociation. These findings emphasize the importance of integrating cognitive rehabilitation strategies alongside pharmacological treatment within comprehensive therapeutic approaches. Marked improvements across multiple cognitive domains suggest seizure activity significantly contributed to cognitive dysfunction, supporting the hypothesis that addressing neurological components provides broader benefits beyond seizure control through restored neural network efficiency. This treatment may contribute to the restoration of disrupted prefrontal cortical processes, which play a critical role in inhibitory control and self-monitoring. When talking about eating disorders, the correct functioning of frontal and prefrontal brain areas is pivotal. Impaired executive functioning can restrict the ability to control eating behaviors and resist impulsive urges [4]. Moreover, the improvement in processing speed aligns with an advancement in neural efficiency, which may facilitate enhanced real-time decision-making and behavioral regulation. Clinicians should screen for binge-eating in these patients due to potential unreported distress and the need for targeted therapy.

The persistence of some planned binge-eating behaviors despite neurological treatment indicates that while seizure activity contributed, other psychological and behavioral BED components require continued attention through integrated approaches.

“Limitations and future directions”

The temporal relationship between seizures and binges, while clinically compelling, remains correlational rather than definitively causal. Concurrent psychological treatment and hospitalization, as well as environmental changes, may have contributed to observed improvements.

These findings highlight the need for increased awareness among clinicians regarding the potential co-occurrence of eating disorders and epilepsy, and the importance of integrated treatment approaches that address both neurological and psychiatric components of such complex presentations. Further research is needed to better understand the mechanisms underlying this relationship and to develop evidence-based treatment strategies for patients with co-occurring conditions. Prospective studies using continuous EEG monitoring during binge-eating episodes could provide more definitive evidence of temporal relationships.

Conclusion

This case report contributes to the limited but growing literature on the intersection between eating disorders and neurological conditions. The identification of previously unrecognized absence epilepsy in a patient with BED, and the subsequent improvement in both conditions following appropriate neurological treatment, underscores the importance of comprehensive medical evaluation in complex psychiatric presentations. The neuropsychological improvements observed following lamotrigine treatment suggest that addressing underlying neurological dysfunction may have broader therapeutic benefits beyond seizure control.

Author contributions

L.P., A.B., I.M., M.P., MB.M, and R.R. contributed to the study’s planning and design. L.P., A.B., M.B.M., R.R., and I.M. wrote the original draft, prepared, reviewed, and edited R.R. and MB.M. performed data collection. A.B. conducted the statistical analysis. L.P., I.M., and M.P. supervised and read the final version of the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

No funding.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Competing interests

The authors declare no competing interests.